Compendium of

TRAINING ON PET ANIMAL PRACTICE

DECEMBER 9-20, 2004 Course Director

Dr. Suresh Chander

Director TVCSC College of Veterinary Science CCS HAU, Hisar

Course Coordinators Dr. Prem Singh

Associate Professor

& Compilation

Dr. Parveen Goel

Associate Professor

Dr. N.K. Rakha

Associate professor
College of Veterinary Science CCS HAU Hisar

Dr. A.P. Singh

Dean
College of Veterinary Science

CCS Haryana Agricultural University, Hisar 125004 2004

Table of Contents 1. REQUIREMENTS OF A PET CLINIC 2. GENERAL AND SYSTEMIC EXAMINATION OF PET ANIMALS 3. THERAPEUTIC MANAGEMENT OF SOME COMMON AILMENTS OF DOGS 4. RABIES- SOME MUST KNOW FACTS 5. INFECTIOUS DISEASES OF PET ANIMALS 6. VACCINATION OF PETS AND CAUSES OF ITS FAILURE 7. THERAPEUTIC MANAGEMENT OF CLINICAL CASES OF POISONING IN CANINES 8. COMMON DERMATOLOGICAL PROBLEMS IN CANINES AND THEIR MANAGEMENT 9. CONTROL OF ECTOPARASITES IN DOGS 10. COMMON ORTHOPAEDIC PROBLEMS OF PET ANIMALS 11. TREATMENT OF COMMON EYE AND EAR DISORDERS IN PET ANIMALS. 12. COMMON SURGICAL AFFECTIONS OF GI TRACT AND THEIR MANAGEMENT 13. SURGICAL CONDITIONS OF URO-GENITAL SYSTEM IN DOGS 14. MANAGEMENT OF ANAESTHESIA IN PET ANIMALS. 15. POSTOPERATIVE MANAGEMENT OF THE SURGICAL PATIENT. 16. RADIOGRAPHIC DIAGNOSIS IN PET PRACTICE. 17. OVARIOHYSTERECTOMY IN BITCH 18. CLINICAL ENDOCRINOLOGY IN FEMALE DOGS 19. INFERTILITY IN BITCH 20. PSEUDO-PREGNANCY AND CYSTIC ENDOMETRIAL HYPERPLASIAPYOMETRA COMPLEX IN BITCHES 21. INFERTILITY IN THE STUD DOGS 22. USE OF HORMONES IN CANINE REPRODUCTION 23. MANAGEMENT OF DYSTOCIA IN PET ANIMALS 24. CAESAREAN SECTION IN BITCH 25. ULTRASONOGRAPHIC DIAGNOSIS OF REPRODUCTIVE DISORDERS IN CANINES 26. CLINICAL PATHOLOGY OF COMMON DISEASES OF DOGS 27. SURGICAL AFFECTIONS OF TEETH IN DOGS 28. PAIN MANAGEMENT IN PET PRACTICE 29. FORMULATION OF DIETS FOR DOGS PRASAD 30. PARASITIC INFESTATIONS IN CANINES 31. HEAP A TOBILIAR ULTRASONOGRAPHY IN DOGS 32. MANAGEMENT OF EMERGENCY CASES IN CANINES

REQUIREMENTS OF A PET CLINIC

Dr. Naresh Kumar Rakha Teaching Veterinary Clinical Service Complex CCS HA U Hisar Objectives: The pet animals hold an important place in the hearts of human beings and particularly those who keep them. Providing health care to the pets is a compassion and highly rewarding profession for veterinarians. The pet clinic is set up mainly with the following objectives. To provide health care services to pet animals particularly dogs & cats To provide vaccination facilities against all preventable diseases To create awareness amongst pet owners regarding benefits of good management, proper nutrition, early treatment and control measures against deadly diseases. Location If someone is interested in establishing a new Pet Clinic, it should be based in urban or semi-urban areas where sizeable pet population exists and people are conscious of and concerned with the pet problems. Requirements Infrastructure Clinic equipments and general supplies. Laboratory equipments and supplies Medicines and Vaccines Marketing strategies Infrastructure To start up a pet clinic, adequate space is required for the following Veterinarian's consultation room Examination-cum-Injection room with wash basin Surgical activity area (small operation theatre if possible, or glass partitioning) Dispensary-cum-store for medicine, vaccines, pet foods, pet accessories etc Waiting area/room and toilets Arrangements should also be made for emergency lighting like inverter or generator, adequate lighting in the clinic, land line for telephone and internet, exhaust fan and cooling. Furniture including Doctor's table, examination and operation table (One each, at least), Chairs, stools, bench for the pet owners in waiting area, Cupboards (two) for storing and displaying medicine, vaccines, pet foods, accessories etc. Clinic equipments and general supplies Refrigerator Sterilizer Shadowless lamp Infrared lamp,

 UV Lamp, Insect killer lamp Trolley and trays to carry surgicals Autoclave Autoclavable tin boxes Fumigator Weighing machine Disposable syringes, needles, I. V. Sets, SV Sets, Nail cutter, Surgical packs for major and minor surgeries Supplies of cotton, gauze, bandages, plaster of Paris Illuminator for viewing radiographs Thermometer, Stethoscope, Ophthalmoscope, Otoscope, endoscopes etc Personal items like towel, towel stand, detergents, antiseptics

Add on Facilities
X-Ray Machine and radiograph processing apparatus and chemicals Ultra-sound machine in air conditioned room Kennel cages for indoor/ quartine patients Laboratory equipments and supplies Microscope with light source and regulator Centrifuge Machine Hot air oven Haematology requirements: Haemometer, haemocytometer, haematology reagents, stains, chemicals and glassware Urine analysis reagents and kits Medicine and Vaccine Common drugs including antibiotics, analgesics, anti-pyretic, antiinflammatory, anti-viral, life saving drugs, local anaesthetics, hormonal preparations etc. etc. Commonly used vaccines properly stored in referigerator Food supplements, pet foods, toy bones etc. Pet accessories like belts, collar, chain, winter clothing, food bowel, bedding etc. Marketing strategies . Circulating pamphlets and displaying posters highlighting the facilities available in the clinics and "Must know" information about the pets for knowledge of owners Circulating pamphlets to create awareness regarding the economic and health benefits of vaccination. Advertisement in local news papers, cable network TV Channel, FM Radio and other public media. Putting up banners and posters at social public functions, public places. Organising dog show, pet health camps, clinical conferences By individual contacts through post, e-mail and sending information, greeting cards and vaccination calls and also posting information on websites

Displaying posters at reception counter of the clinic highlighting services provided and facilities available. Pictorial and video presentation of the technical activities conducted at the clinic Organizing vaccination and deworming campaigns in the area and region in collaboration with pharmaceutical/ Biologicals companies, banks etc. Tie ups Poly clinics, College clinics, Diagnostic laboratories, Vaccine institutes Veterinary colleges Pharmaceutical companies, Banks Other agencies

GENERAL AND SYSTEMIC EXAMINATION OF PET ANIMALS

Dr. V. K. Jain, Rakesh Kumar, Sridhar, Parveen Goel and Yudhbir Singh Department of Veterinary Clinical Medicine, CCS H. A.U. Hisar-125 004 (India) General observation of the patient In the beginning the patient should be watched as it is kept in the waiting room or it enters the treatment room. Visual examination should be continued while collecting the history. Observe the general body condition and abnormalities in attitude, posture, respiration and behaviour. Vital signs Body weight should be recorded as many drugs require accuracy in dosage especially in debilitated animals. Record the rectal temperature in the beginning otherwise it may rise because of anxiety or excitement. In emergency situation early attention should be given to hypothermia/hyperthermia. Examine the bulb of thermometer for any blood. Pulse rate and its quality and heart rate should be examined for presence of arrhythmias and pulse deficit, if any. Examine the respiratory rate and pattern simultaneously. Sometimes dyspnoea may become worse due to additional stress of restraint and examination resulting in life threatening condition, therefore, first of all oxygen therapy should be instituted to stabilize the respiration then continue rest of the systemic physical examination. To assess hydration status of the animal looks for the sunken eyes or if the third eyelids are protruding bilaterally or the mucous membranes are dry/ tacky. Evaluate skin turgor by gently lifting the skin over the dorsal thorax. Geriatric or cachectic patients should be examined carefully because of loss of skin's natural elasticity; these may appear to be dehydrated when only skin turgor test is applied. Physical examination: Body systems approach The pattern of physical examination should be the same as for the history taking. One may start with patients head and then proceed caudally examining one system at a time, so that no system is left unexamined. This also involves the verification of what owner has already observed. HEAD Visual examination and palpation of head \\Till reveal about any asymmetry or localized swelling / mass and its nature (firm or fluctuant, mobile or attached). Examine the posture of the head and neck. Ventroflection of head and neck may be indicating towards conditions like thiamine deficiency, chronic organophosphate poisoning, polymyopathies and hypokalemia in cats. Pain and resistance to movements of head and neck may be observed in dogs suffering from cervical intervertebral disc protrusion. EYES If the problem is unilateral then examine the unaffected eye first. Look for abnormalities of size and symmetry of eyes. Chronic glaucoma results in larger then normal eyes, whereas, congenital m.icrophthalmoia or acquired phthisis bulbai results

in smaller than normal eye. Abnormal positions of the eyes may be enophthalmos (may be secondary to microphthalmia, loss of orbital fat pad e.g. cachexia; Homer's syndrome, dehydration, or acute ocular pain e.g. in acute uveitis); exophthalmos (may be because of space occupying lesion of the orbit e.g. abscess, neoplasia or cellulites; buophthalmos (glaucoma), myositis or breed predisposition; or strabismus. Ocular discharge may be present which may be serous, mucoid or purulent depending upon the complications. Examination of eyelid may reveal abnormalities like any swelling or gro\vth, distichiasis, entropion or ectropion. Examine for any abnormal pigmentation or mass involving conjunctiva or sclera and also look for hyperemia (examination of superior conjunctiva is more reliable than the inferior one), chemosis, pallor or jaundice. Protrusion of the third eyelid may be indicating towards enophthalmos or Haw's syndrome in cats. There may be any growth or prolapse of gland of nictitans. Cornea should be examined for cloudiness, pigmentation, vascularization or other defects. Anterior chamber should be examined for presence of aqueous flare, hypopyon, hyphema, or abnormal mass. A pen light may be helpful in detecting the subtle aqueous flare when anterior chamber is viewed from a lateral aspect. Pupil size and symmetry should be examined. Evaluate direct and consensual pupillary light reflexes. Persistent pupillary membranes may be identified. A darkroom is helpful in such examination. Examine the iris for hyperemia, pigmentary changes, swelling, roughening, synechia (which may be associated with the anterior uveitis), tumors or cysts. Direct or indirect ophthalmoscopic examination of lens may reveal cataract, displacement or lenticular sclerosis. Fundus can be examined after dilating the pupil with short acting mydriatic. Look for fundic vascularity, haemorrhages, pigmentary changes, retinal detachment, chorioretinal dysplasia or hypoplasia. Optic disc should be examined for any changes in ~olour, size, vascularity, fissures or colobomas / abnormal growths. Evaluate vision by moving a cotton ball across the table or floor or by dropping it in front of the patient. Menace response may not responded well by young normal puppies and kittens. ORAL CAVITY Thorough oral examination should be done and if required sedate the patient. Examine colour, moisture, capillary refill time of mucous membranes of oral cavity. Also look for hyperaemia, congestion, cyanosis, jaundice, pallor, petechae, gingival masses, ulcerations, pigmentary changes etc. Teeth should be examined for the presence of callus or exudates at the gingival margins. Examine the tongue for presence of any trauma or growth. Examine the sublingual area in a vomiting cat for the presence of any linear foreign body. Examine hard palate in neonates for clefts. The soft palate is examined for its elongation or any growth. Examine the pharynx for inflammation, trauma, foreign bodies, growths, asymmetry, tonsilar enlargement etc. NOSE Examine the nose for asymmetry or swelling. If any swelling or mass is present it should be palpated carefully to determine whether it is firm or fluctuating. Examine the nasal discharge which may be unilateral or bilateral, serous, mucous, purulent or haemorrhagic in nature. Examine the nostrils for the patency either by placing a whip of cotton in front of each nostril or by condensing the expired air on the mirror and any stridor, if present.

EARS Inspect both the inner and external surfaces of pinna for skin lesions, alopecia, erythema or swelling. Examine the external ear canal for erythema, discharges, odour, parasites (ear miters and ticks), any growth mass, foreign bodies etc. Palpate the ear canal cartilage for any growth, pain and any other abnormality. Otoscopic examination of vertical and horizontal ear canal will be helpful in detecting any mass, foreign bodies, discharges, parasites, and rupture of tympanic membrane or otitis media (erythema or protrusion). NECK One should palpate the paratracheal area extending from larynx to thoracic inlet. Place the thumb and forefinger on either side of trachea and slide them down the length of trachea to detect the thyroid nodule (normal thyroid is not palpable) especially in middle aged and older cats which may suffering from hyperthyroidism or dogs suffering from thyroid carcinoma. Trachea should be palpated for collapse, soft cartilage, or flattening. If gentle encircling the trachea with one hand and applying pressure on the tracheal muscles dorsally elicit cough, it indicates tracheal collapse or tracheobronchitis. Evaluate the jugular vein for distension or jugular pulse extending more than the lower one third portion of neck (moistens the neck with .alcohol or clips the hair to detect these abnormalities). THORAX Evaluate the respiratory rate, rhythm and efforts (dyspnoea/ apnoea/ polypnoea/ hyperpnoea etc). Palpation of thorax should be done to find fractured ribs, congenital malformations, (pectus excavatum), subcutaneous emphysema and masses. Artificial sound must be identified and ignored. These may be rumbles due to shivering and crackles from the stethoscope rubbing against the hair. Closing the patient's mouth for some time will reduce the upper respiratory noises. Sinus arrhythmias are typified by increase in cardiac rate during inspiration and decrease during expiration. While auscultating the heart evaluate the femoral pulse for quality and deficits. Note split heart sounds, murmurs and clicks. Auscultate all cardiac valve areas, because some murmurs are localized such as mitrial, aortic and pulmonary on the left hemithorax and the tricuspid on the right. Muffling of heart sounds may be due to obesity, pleural effusion, pericardial effusion, thoracic mass or diaphragmatic hernia. Normal broncho-vesicular sounds may be intensified in nervous or tachypnaeic patient when pulmonary auscultation is performed on both sides of chest. Abnormally quiet or dull areas are suggestive of pleural effusion, pneumothorax, thoracic mass and pulmonary consolidation. Crackles or rales are produced by air passing through partially obstructed bronchi because of accumulation of fluid or mucous or the thickening of the bronchial wall. Percussion of the pulmonary area help in examining the resonance (pitch and tone) of sound produced by a series of quick taps of uniform force at various points on the chest wall using a finger or a percussion hammer. Increased resonance (Tympany) is indicative of pneumothorax and decreased resonance (dull sounds) suggests pleural effusion, diaphragmatic hernia, large pulmonary mass, or area of lung consolidation. ABDOMEN External appearance of abdomen should be examined for any distension or asymmetry. If abdomen is distended, perform percussion to differentiate peritoneal

effusion, air (gastric dilatation or volvulus), obesity or a mass. In order to palpate the abdomen in standing position, either one hand technique (in small sized animals) or two hand (each hand on either side) technique (in large sized animals) is applied in cranial to caudal direction so that nothing is overlooked. The cranial abdomen is palpated for presence of gastric distension. Usually normal stomach is not palpable. Tympany is indicative of presence of gastric dilatation of volvulus, which requires rapid perusal. Distention due to overeating may be felt as doughy or fluid- filled stomach in the left middle region of the cranial abdomen. In normal animal caudal edges of liver are smooth, well defined and rarely palpable while in cases suffering from hepatomegaly the rounded edges extend beyond the costal arch. Such palpation may be conducted in lateral recumbency or the animal should be standing on the hind legs. Spleen may not be always palpable in normal animal as it is located in mid abdomen. It is palpable as a mass in case of splenomegaly or it may be irregular in appearance. Mesenteric lymph nodes are usually not palpable in normal cases and marked enlargement is encountered in lymphosarcoma. Palpate the thickness of the bowel wall and ascertain the presence of the gas, fluid, foreign bodies or masses. Plication and clumping of the intestine may be appreciable in the cases harbouring string foreign body. Kidneys can be palpated in the dorsal region of the abdomen. The right kidney is cranially situated than the left one and may be obscured by the last rib. Palpation becomes possible when cat's thorax is elevated (do not mistake them for any mid abdominal mass). Compare both the kidneys for their size, shape, firmness and surface irregularities/growths. Kidneys are not easily palpable in dogs and only sometimes the caudal poles or lateral aspect may be identified. Colon can be palpated in the dorsal caudal region of the abdomen. Faeces can be differentiated from any growth by applying gentle pressure to test the deformability of stool. Quality and consistency of faeces help in assessment of constipation. Urinary bladder is present in the central caudal abdomen and patient does not resist palpation of normal bladder. Asses size, turgidity and thickness of bladder wall (normally the bladder wall is thin). Careful palpation will help in identifying cystic calculi. Normal uterus is usually not palpable. In pyometra or late pregnancy it gets enlarged markedly (tubular in shape) and lie in mid-to-ventral abdomen often extending from pelvic inlet to diaphragm. In mid gestation, the individual fetuses may be palpable. Prostate gland can be occasionally palpated in caudal abdomen, central to colon and caudal to urinary bladder. It should be evaluated for its size shape and surface irregularities. RECTAL EXAMINATION Prostate of all mature intact male dogs should be examined per rectally. It is bilobed (characterized by the presence of the median raphe), smooth and non painful. Enlarged prostate may extend slightly over the brim of the pelvis or lie in the abdominal cavity. Abnormal masses associated with urethra or uterus may some times be detected on rectal examination of bitches. Enlargement of sublumbar lymph node in the dorsal aspect of pelvic canal is usually suggestive of metastatic neoplasia or any other mass should be examined for its size, position and consistency. In trauma victims always look for the symmetry of the pelvis to detect the palpable fractures. Look for perineal hernia or abnormal masses. Examine the anal sacs for any distension or growths. Note the anal sphincter tone and consistency of the faecal material.

MUSCULOSKELETALSYSTEM Observe the patient when in motion to find out lameness. Observe patient's posture with special attention to the head carriage, arching of back or stilted gait. If lameness is present examine/ palpate the foot for evidence of trauma, abnormal toenails or nail beds also look for interdigital erythema, swelling or abnormality of drainage tracts and foreign bodies. Proceed proximally by palpating each long bone for fractures, pain, swelling and abnormal masses. Examine joints for evidence of effusion, swelling, crepitation or pain with flexion and extension. Examine the stifle and note the position of the patella in extension and flexion. Extension of the stifle usually aid in mobilizing the patella. Palpate the patella for evidence of a cranial drawer sign. Palpate vertebral column for signs of pain by applying pressure to either side of the dorsal spinal process of each vertebra. NERVOUS SYSTEM Observe the mental state and behaviour of the patient. Evaluate the posture and gait while the patient is standing and walking. Evaluate and compare postural reactions in all limbs, including propioception, "wheel barrowing," hopping, extensor postural thrust and placing reaction. Evaluate and compare spinal reflexes in the calm patient in the lateral recumbency and important segmental reflexes are triceps, biceps, patellar, cranial tibia reflexes, as well as the flexor (withdrawal) reflexes of the thoracic and pelvic limbs. Evaluate the panniculus reflex by pricking the thoracic or lumber skin. SKIN Inspect the general appearance of the hair coat for its luster and presence of alopecia. Symmetrical alopecia is seen in endocrine disorders. In pruritic and psychogenic alopecia remains of broken hair are present. Note the erythema, if present. Location of skin lesions is helpful in diagnosis in establishing the diagnosis e.g. localized demodicosis can be identified by patches of alopecia involving head and forelegs. In sarcoptic mange scaly partial alopecia is present on the pinnae, elbow and hocks. Also examine the interdigital spaces and foot pads. To recognize the immune mediated diseases examine the mucocutaneous junctions e.g. lips, anus, vulva, prepuce etc. Skin lesions should be classified as primary or secondary. Common primary conditions may include papules, nodules, wheal, macules and vesicles. Common secondary lesions include scales crusts, ulcers, excoriations, lichenifications, hyperkeratosis and hyperpigmentations. Look for external parasites. Search for fleas or flea dirt, especially at the tail head region (a flea comb is often helpful in discovering small amounts of flea dirt). LYMPH NODES Generalized lymphadenopathy usually indicates about a systemic disease e.g. neoplasia, immune mediated diseases and systemic fungal Infections. Local lymphadenopathy is indicative of regional infection (abscess). Mandibular lymph nodes are located at the angle of the mandible. These are situated slightly cranial and ventral to the parotid and submaxillary salivary glands. Salivary glands are irregular in on palpation while lymph nodes have smooth and ovoid texture. Superficial cervical or prescapular lymph nodes can be palpated just beneath the anterior border of the scapula. In obese and heavily muscled patients there may be some difficulty in palpating these lymph nodes. Axillary lymph nodes are not always palpable as these are disc shaped and surrounded by

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musculature. Superficial inguinal lymph nodes are located at the junction of the abdominal wall and the medial thigh. Popliteal lymph nodes are palpable caudal to the stifle joint. These may appear larger than their actual size because of the surrounding fat especially in cats. Trunk and extremities should be palpated to identify abnormal masses or swellings

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Therapeutic Management of Some Common Ailments of Dogs

. Dr. Sridhar, Dr. Rakesh Kumar and Dr. V.K. Jain Department of Veterinary Clinical Medicine GASTRITIS Aetiology: Symptoms: Treatment: Ingestion of contaminated or spoiled foods, toxic plants, chemicals etc. Vomition and anorexia, Uncommon signs include enteritis and abdominal pain 1. Withhold food and water for 24 hours. 2. Fluid therapy 3. Antiemetics- Prochlorperazine(inj.Stemetil) or Metoclopromide(inj. Perinorm) parentrally Domperidone ( Tab. Domstal) orally 4. H2 blockers like ranitidine(inj aciloc 1 ml parentrally) 5. Supportive therapy in form of Vitamin B-complex ENTERITIS Aetiology: Symptoms: Treatment: Poor diet, abrupt dietary changes, infectious agents, chemicals, parasites Diarrhea or dysentery 1. Fluid therapy 2. Antimicrobials like furazolidone, quinidochlor, metronidazole, norfloxacin etc 3. Deworming in cases of parasitic infestations by combination of praziquantel and anthelmintics like pyrantel pamoate and fenbendazole (Tabs Plozin, Fentas plus or syrup Nemocid) 4. H2 blockers like ranitidine EPISTAXIS Physiological, hereditary, ehrlichiosis etc Bleeding from nose (unilateral or bilateral), anaemia in prolonged 1. Cold pack plug on nose 2. Haemostatics like adenochrome (Chromostat I-2ml i/m or i/v), nbutanol/citric. acid combination( Revici : 3-5 ml any route), ascorbic acid 2.0 g i/v, ethamsylate (Inj. Cosklot Iml i/m or i/v) etc 3. Homoeopathic drug Hamemelis (mother tincture) 2 ml orally BID. 4. Vitamin K orally( Tab Cadisper-C TID) or parentrally (Inj. Menadione 1 ml /m or i/v) 5. Haematinics in cases of severe loss of blood (Syrup Haem up or Inj. Imferon) 6. Treatment of specific disease, if any

Aetiology: Symptoms: illness Treatment:

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CONSTIPATION Aetiology: Change in routine, inactivity, pain in rectal/ perineal area, excess fibre in dehydrated animal, abnormal diet (hair, bones), obstruction in colon (tumour, granuloma etc.) , spinal cord trauma, severe dehydration Hard and scanty feces or no defaecation Rule out any serious causes 1. Liquid paraffin or castor oil orally @ 15-30 ml 2. Drugs like bisacodyl (Dulcolax 5mg tab orally) in cases where above treatment is not effective. 3. For evacuation of rectum phosphate enema should be given. 4. Isabgol husk in warm water. PARVOVIRAL ENTERITIS Aetiology: Symptoms: Treatment: Parvovirus Pyrexia and haemorrhagic gastroenteritis mainly, anorexia, some cases vomition also, anaemia in prolonged illness 1. Fluid therapy 2. Antibiotics intravenously (e.g. ampicillin /cloxacilin combination, chloramphenicol or cefotaxime etc.) 250-500 mg 3. Haemostatics (IN) as mentioned above 4. H2 blockers as mentioned above 5. Vitamin -C @ 2.0 g IN per adult dog 6. Antiemetics in cases of vomit ion 7. Oral norfloxacin / metronidazole or tinidazole combination if there is no vomition (sy. Powergyl / Tab Norflox -tz) CANINE DISTEMPER Aetiology: Symptoms: CD virus, mainly young animals are affected Biphasic fever, cutaneous lesions in form of pustules on belly, sequelae sometimes accompany the disease (chorea, blindness, hind limb paralysis Very difficult to diagnose early cases 1. Antibiotics parentrally as above to ward off the possibility of secondary infection 2. Antipyretics like al1algin (Naval gin 0.5-2ml i/m or i/v) 3. Vitamin- C @ 1.0-2.0 g IN 4. Corticosteroids like dexamethasone (Dexona 1mg/kg i/m or i/v ) 5. Sequelae of the disease are incurable ASCITES Aetilology: Symptoms: Treatment: Hepatic insufficiency, congestive heart failure Fluid retention in peritoneal cavity, pot belly condition, edema of dependent parts 1. Diuretics- Frusemide (Tab.Lasix) I mg/kg for several days 2. Liver tonics -Liv-52, Livosin or Livosil-B 5ml BID for 20 days

Symptoms: Treatment:

Treatment:

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like

3. Oral amino acidsupplements (Astymin-3 or Verol syrup, 5ml BID for 20 days 4. In cases of extensive fluid accumulation evacuate by syringe 5. In cases of congestive heart failure give enalapril maleate (Tab.Envas 2.5 mg orally OD) for 10 days and evaluate the benefit 6. In cases of infectious liver ailments give hepatoprotectives silymarin (Tab. Silybon, BID orally for 20 days) EPILEPSY

Aetiology: Symptoms: Treatment:

Neurological disorder, cause not fully understood Convulsive seizures in episodes lasting few minutes Frequency is variable 1. complete cure is not possible. 2 Aim is to keep nervous system under sedation 3. Phenobarbitone sodium ( Gardenal 30mg tab OD for 15 days followed by half the dose for further 15 days if there is improvement. 4. Ayurvedic drug Anxocare (Himalaya) BID orally for 20 days is also beneficial in some cases ALLOTRIOPHAGIA (PICA)

Etiology: Gastrointestinal worm infestation/dietary mineral deficiency Symptoms: Feeding on unnatural objects (faeces /soil / wood /clothes etc. Treatment: 1. Deworming 2. Mineral supplementation (Tab. Riconia / Rave-3), - 1 orally OD for 15 days RICKETS Aetiology: Symptoms: Treatment: Deficiency of calcium and Vitamin D-3 Soft pliable bones, bending and curvature of long bones, swollen joints 1. Calcium supplement orally (Ostocalcium pet, Capsola or Calpep 5ml bid for 2 months 2. Vitamin D-3 injectable (Arachitol 0.5-1ml i/m per week for 4 weeks) 3. Vitamin D-3 orally (Calcirol granules 0.25-0.5g per week for 8 weeks) 4. In cases where the clinical signs are severe leading to extreme weakness, Anabolic steroid like nandralone, Inj. Durabolin 0.5 ml i/m per week may be given EHRLICHIOSIS Aetiology: Symptoms: Rickettsial parasite Ehrlichia canis transmitted by ticks (Rhipicephalus sanguineus brown dog tick) High fever unresponsive to routine antibiotics, anaemia, serous or mucopurulent oculonasal discharge, anorexia, weight loss, lymphadenopathy, epi-5taxis in chronic cases Confirm the diagnosis by

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Treatment:

examination of dry blood smear (See in cytoplasm of the monocytes for morulae) 1 Oxytetracycline hydrochloride is the drug of choice (Terramycin or Tero-DS @ 10mg/kg b.w. intravenously.one or two doses 2. Follow the above with oral administration of doxycycline (Tab. Doxy1, 100 mg BID for 4 days followed by 100mg OD for another 8 days (never give these tablets empty stomach. 3. Vitamin B complex syrup (Sy. Polybion) should be given along with doxycycline tablets. 4. Imidocarb dipropionate (Inj. Imizol @ 5-7mg /kg b. w. i/m once or twice over a period of 14 days is also effective 5. Haematinics 6. Appetite stimulants like cyproheptadine (Ciplactin tablets BID for 3 days) BABESIOSIS Haemoprotozoan parasite Babesia canis, Transmitted by ticks High fever unresponsive to antibiotics, anaemia, No or rare haemoglobinuria Diminazene aceturate (Berenil @ 3.5-5.0 mg/kg bw, s/c Or Imidocarb @ 5.0mg/kg b.wt. i/m along with supportive therapy with haematinics and Vit B Complex injections ANTIDOTES FOR POISONINGS/TOXICITIES

Etiology: Symptoms: Treatment:

1. LEAD: 2. ARSENIC: 3. ZINC PHOSPHIDE: 4. ORGANOPHOSPHATES: 5. ORGANOCHLORINES: 6. SNAKE BITE:

Calcium versenate 25mg/kg sic repeated doses for 4-5 days odium thiosulphate 5mg/kg i/m TID till recovery Sodium benzoate 50mg i/m, Gastric lavage with KMn04 soln. (1:2000) Atropine sulphate (0.05mg/kg sic), rifluopromazine (Siquil lmg/kg) Calcium sandoz 5-IOmg i/v, gastric lavage. Inj Nikethamide (Coramine) 0.5-1.0 ml i/card or i/v Drain the blood by giving incision on site; Apply tourniquet above the bite. Inj. F. D, Polyvalent antivenom serum 1ml I/V, (Serum Institute Pune.)

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RABIES- Some must know facts

N. K. Rakha Teaching Veterinary Clinical Service Complex CCS HAU Hisar Rabies is a preventable viral disease of mammals most often transmitted through the bite of a rabid animal. Aetiology It is caused by rabies virus of genus Lyssa of family Rhabdoviridae. Rabies virus infects the central nervous system, causing encephalopathy and ultimately death. It has six genotypes. There are two strains of virus: Fixed virus- refers to those strains that have fixed incubation period and have been adapted to secondary hosts for experimental use and whose biological behavior is reproducible and characteristic of strain. Street viruses are those strains that are isolated from naturally infected warmblooded animals. EPIDEMIOLOGY It occurs in all farm animals world widely except Australia and New Zealand, which have never had the rabies, and Britain, Hawaii and Scandinavia are currently free. Rabies is common in developing countries in Asia, Africa, and Latin America where dogs are the major reservoir of rabies. The vast majority of rabies cases are reported in dogs however, cases do occur in human beings, cats, cattle, buffaloes, sheep, goats, pigs, camel, horses etc and in wild animals like raccoons, skunks, bats, jackals, and foxes. HOST SUSCEPTIBILITY Rabies virus causes acute encephalitis in all warm-blooded hosts, including humans, and the outcome is almost always fatal. Although all species of mammals are susceptible to rabies virus infection, only a few species are important for as reservoirs for the disease in nature. Several distinct rabies virus variants have been identified in terrestrial mammals, including major terrestrial reservoirs in raccoons, skunks, foxes, and coyotes. In addition to the terrestrial reservoirs for rabies, several species of insectivorous bats also serve as reservoirs for the disease. SEASONAL SPREAD Highest incidences are in late summer and autumn because of movement of animals for breeding and food. TRANSMISSION Transmission of rabies virus usually begins when the infected saliva of a host is passed to an uninfected animal. Most animals get rabies from being bitten by a rabid animal. If animal has broken skin, like a scratch, which comes in contact with animal

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saliva full of rabies virus, that animal may get infected. But rabies also can be spread in the air, as has occurred in caves where infected bats live. Other various routes of transmission have been documented and include contamination of mucous membranes (i.e., eyes, nose, and mouth), aerosol transmission, and corneal transplantations. The most common mode of rabies viral transmission is through the bite and virus-containing saliva of an infected host. PATHOGENESIS Following primary infection, the virus undergoes an eclipse phase in which it cannot be easily detected within the host. This phase may last for several days or months. Investigations have shown evidence for direct entry of virus into peripheral nerves at the site of infection, as well as evidence for indirect entry after viral replication in non-nervous tissue (i.e., muscle cells). It is during this time that host immune defenses may playa role in the outcome of viral infection because rabies viral antigens are good simulators of cell-mediated immunity. The uptake of virus into peripheral nerves is important for a progressive infection to occur. Following uptake into peripheral nerves, rabies virus is transported to the central nervous system (CNS) via retrograde axoplasmic flow. Typically this occurs via sensory and motornerves involved at the initial site of infection. The iflcubation period is the time of exposure to onset of clinical signs of disease. The incubation period may vary from a few days to several years, but typically lasts 1 to 3 months. Dissemination of virus within the CNS is rapid, with early involvement of limbic system neurons. Active cerebral infection is followed by the passive centrifugal spread of virus to peripheral nerves. The amplification of infection within the CNS occurs through cycles of viral replication and cell-to-cell transfer of progeny virion. Centrifugal spread of virus may lead to the invasion of highly innervated nerve sites of various tissues, including the salivary glands. It is during this period of cerebral infection that classic behavioural changes develop.

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SIGNS AND SYMPTOMS Several factors may contribute to the outcome of rabies exposure. These include the virus variant, dose of virus inoculum, route and severity of exposure, location of exposure, host species, and individual host factors, such as age and host immune defenses. It occurs in two forms: Paralytic form: - there is knuckling of fetlock joint of hind limb, sagging and swaying of hind quarter while walking, flaccidity of tail, tenesmus with paralysis of anus resulting in sucking in and blowing out of air, drooling of saliva and yawing movement. Furious form: - Animal has tense alert apearance, hypersensitive to sound and movements, violently attack on animals and inanimate objects, increased libido as animal mount on inanimate objects. CATTLE AND SHEEP Major clinical finding are- excessive salivation, bizarre behavior, muzzle tremors, bellowing in cattle and bleating in sheep, hyperesthesia, hyperexcitability, tresmus, wool pulling in sheep and recumbency.

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HORSE Muzzle tremors, abnormal posture, lameness, weakness, depression, ataxia, pharyngeal paralysis, hyperesthesia, biting of objects, loss of anal sphincter tone, recumbency and death in 4-6 days. PIGS Excitement, attack, twitching of nose, clonic convulsions, paralysis, rapid chewing movement In general the first symptoms of rabies in animals may be nonspecific flu-like signs - malaise, fever, or headache, which may last for days. There may be discomfort or paresthesia at the site of exposure (bite), progressing within days to symptoms of cerebral dysfunction, anxiety, confusion, hypersalivation and agitation, progressing to delirium, abnormal behavior, hallucinations, and insomnia. The acute period of disease typically ends after 2 to 10 days. Once clinical signs of rabies appear, the disease is nearly always fatal, and treatment is typically supportive. PATHOLOGY Pathology of rabies infection is typically defined by encephalitis and myelitis. Perivascular infiltration with lymphocytes, polymorphonuclear leukocytes, and plasma cells can occur throughout the entire CNS. Common with rabies infection is the presence of cytoplasmic eosinophilic inclusion bodies (Negri Bodies) in neuronal cells, including pyramidal cells of thehippocampus and Purkinje cells of the cerebellum, and within neurons of the cortex and other regions of the CNS, including the spinal ganglia. These inclusions have been identified as areas of active viral replication by the identification of rabies viral antigen. DIAGNOSIS Diagnosis of rabies is one of the most difficult and important duties that a veterinarian is called upon to perform. Since in most cases there is a probability of human exposure, failure to recognize the disease may place human life in jeopardy. Several tests are necessary to confirm or rule out rabies in animals intra-vitam (while living). No single test can be used to rule out rabies with certainty as no specific test is there. Tests are performed on samples of serum, spinal fluid, skin biopsies from the nape of the neck, and saliva. Routinely, Serum and spinal fluid are tested for antibodies to rabies virus. The skin biopsy specimen is examined by dFA for the presence of rabies antigen in cutaneous nerves at the base of hair follicles. Saliva may be tested by virus isolation or Nested Reverse Transcription Polymerase Chain Reaction (RT -PCR) methods. Dot- ELISA The Direct Fluorescent Antibody test (OF A) is most frequently used to diagnose rabies. This test can be performed on impression smear of brain tissue,

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preferably hippocampus, medulla, cerebellum or gasserian ganglion, of animals suspected of being rabid. Histopathological search for presence of Negri Bodies in tissue section of brain mainly from hippocampus and cerebellum Some of serological tests are used like virus neutralization, passive haemagglutination (PHA), complement fixation test (CFT), radioimmunoassay (RIA), and immunoperoxide test. The importance of routine rabies tests The rapid and accurate laboratory diagnosis of rabies in animals is essential for timely administration of post exposure prophylaxis. Within a few hours, a diagnostic laboratory can determine whether or not an animal is rabid and inform the responsible medical personnel. The laboratory results may save a patient from unnecessary physical and psychological trauma, and financial burdens, if the animal is not rabid. In addition, the laboratory identification of positive cases may aid in defining current epidemiological patterns of rabies and in recognizing the need for the development of rabies control programs. TREATMENT Once clinical signs of rabies appear, the disease is nearly always fatal, and treatment is typically supportive and no specific treatment. Disease prevention is entirely prophylactic and includes passive antibody (immune globulin) and vaccine. Management of wound Clean and irrigate the wound and scratches immediately with soap or 20% soft soap sol and water to remove saliva from the area to prevent the infection. If soap is not available, for example, when hiking, you can use water alone. But be sure to wash with soap and water as soon as possible. Allow the wound to bleed, which also will help to clean it. Post exposure vaccination should be done but is unlikely to be of value in animals, as death usually occurs before appreciable immunity has had time to develop. Available vaccines 5% Sheep brain phenolised vaccine (simple's vaccine) - HVVI Flurry egg passaged vaccine-low or high passaged (Rhabdomun) Chemically inactivated and stabilized rabies vaccine (Durarab) Tissue culture vaccine BPL inactivated vaccine (Annumune)

BPL inactivated vaccine rabies virus grown in purified chicken embryo cell culture (Candur-R) PREVENTION AND CONTROL The main goal of rabies control in domestic and wild animals is reduction or elimination of human rabies. The approaches are: -

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* Keep your pets under direct supervision so they do not come in contact with wild animals. If a wild animal bites your pet, seek veterinary assistance for the animal immediately. * Keep vaccinations up-to-date for all dogs, cats and ferrets. This requirement is important not only to keep your pets from getting rabies, but also to provide a barrier of protection to you, if your animal is bitten by a rabid wild animal. Avoid direct contact with unfamiliar animals and don't touch them even when they are dead. * Call your local animal control agency to remove any stray animals from your neighborhood. They may be unvaccinated and could be infected by the disease. * Spay or neuter your pets to help reduce the number of unwanted pets that may not be properly cared for or regularly vaccinated. * Enjoy wild animals (raccoons, skunks, foxes) from afar. * Do not handle, feed, or unintentionally attract wild animals * Never adopt wild animals or bring them into your home. Do not try to nurse sick animals to health. Call animal control or an animal rescue agency for assistance. * Teach children never to handle unfamiliar animals, wild or domestic, even if they appear friendly. "Love your own, leave other animals alone" is a good principle for children to learn. * Prevent bats from entering living quarters or occupied spaces in homes, churches, schools, and other similar areas, where they might come in contact with people and pets. Seal basement, porch, and attic openings and cap chimneys to prevent animals from entering your home. * When traveling abroad, avoid direct contact with wild animals and be especially careful around dogs in developing countries. For farm animal, there are 3 useful control techniques: * Prevention of exposure by destruction of wild animals, muzzling, restraint and vaccination of all dogs and cats in that premises. * Vaccination of domestic animals. * Quarantine and biosecurity. DIFFERENTIAL DIAGNOSIS Cattle and sheep Lead Poisoning- Blindness, convulsion, champing of jaw with production of frothy saliva, twitching of eyelids and ears, stupor, head pressing, grinding of teeth, bellowing. Lactation Tetany- Occurs in lactating cattle on lpsh green pasture in spring season during cold and windy weather, which is characterized by tremors, hyperesthesia, convulsions, recumbency and rapid death. Vitamin A deficiency- In young cattle of 6-8 months; characterized by blindness in ocular form, episode of tremors, convulsion. Polioencephalomalacia- In cattle and sheep characterized by blindness, nystagmus, opisthotonus, convulsion, bellowing, loss of sensation, tenesmus.

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 Listeriosis- In cattle and sheep, disease is manifested by localizing signs of circling and facial nerve paralysis. Enterotoximia- In sheep, confined to lambs on heavy carbohyrate diets. Pregnancy Toxemia- In pregnant ewes, differentiated by presence of ketosis. Louping IIl- In sheep, transmitted by insect, has a seasonal occurrence localized geographical distribution. Horses Viral Encephalomyelitis- Occur in summer, by insect vector (Mosquitoes), characterized by mild fever, circling and walking, mental depression, feed hanging from mouth, unable to shallow, paralysis and weakness. Tetanus- There is fever, hyperesthesia, protrusion of third eyelid, trismus, and recumbency, followed by titanic convulsion and death with in 5-10 days. Herpes Virus Myeloencephalopathy- It occurs as outbreak and as upper respiratory tract disease. There is ataxia, paresis, bladder paralysis, and spontaneous recovery. Hepatoencephalopathy- Animal is commonly ill for 2-3 weeks, develop slowly. Signs are depression, pushing, ataxia, yawing, compulsive walking, loss of weight and icterus. Horse Tail Poisoning- History of ingestion of plants, incoordination, swaying from side to side, muscle tremors, recumbency, bradycardia and cardiac arrhythmia

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Infectious diseases of pet animals

Yudhbir Singh Department of Clinical Veterinary Medicine, College of Veterinary Sciences, CCS HAU, Hisar 1. Parasitic Infestations: Internal: a) Hook Worm (Ancylostoma): Anemia and melena are the most Common signs. b) Round Worm (Toxocara): Diarrhoea, abdominal pain and pot belly. c) Whip Worm (Trichuris): Bloody diarrhea(acute and chronic) d) Tape Worm (Taenia, Dipylidium, Echinococcus) Majority of cases are symptom less Occasionally anal pruritis Control / Management: Hook, round and whip worm require Pyrantel pamoate- 5mg/Kg orally. Fenbendazole 50mg/Kg for 3 days, Mebendazole 22mg/Kg for 3 days. lvermectin .5mg?kg SIC. Praziquantel 5 mg/kg or 5 mg/kg epsiprantel (Deworming-2weeks of age, 4 weeks of age, than after every 3 months/6 months depending on prevalence). 2. Vaccination Schedule: Vaccine Distemper, Hepatitis, Parvo Leptospira and Parinfluenza Rabies 1st dose 6-8 weeks Booster dose 1 After 3-4 weeks Booster dose 2 After 3-4 weeks Revaccination Annual

3 months

After 1 year

Annual

Common Viral infections of Canines 1. Viral Infections: A) Parvoviral: 2 formsEnteric form: fever, vomition, diarrhea 50% (hemorrhagic) Myocardial from: - Early age infection, heavy mortality, congestive heart failure. Treatment: > GI rest, Fluid therapy- 66-110ml/kg Iday i/v, sc, i/p. > Antibiotics- Ampicilline/Amoxy. (Ampi/amoxy+ Amikacine or ampi +enroflox or > Ampamoxy+Cefotaxine in more severe cases) > Haemostat- Chromostat, coskclot, Ravici, cadisperC, Styplon tablets. > Dextrose 25% 0.5-1.0 g/kg i/v > Antiemetic metachlopramidel chlorpromazine / prochlorperazine 0.5mg/kg i/m tid

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> Antidiarreals bismuth subsalicylate .5-1ml/kg or loperamide 0.1-0.2mg/kg t.i.d > Shock- Dexamethasone 1-2mg/kg i/v or prednisolone 1020mg/kg i/v Multisystemic disease, >60-70% cases are subclinical. Fever, depression, occulonasal discharge, keratoconjuntivitis, coughing, vomition, diarrhea, neurological signs, seizures, paraperesis, chorea, optic neuritis. In young age - enamel ypoplasia and cardiomyopathy Treatment: 1 Fluid therapy, 2 Antibiotics qhloramphenicol/tetra/ genWkana/noyobiocin 3 Prednisolone 1-2 mg/kg sid for 3 days followed by Yz dose for a week in neurological form 4. Bronchodialators and antitussive 5. Vito C Seizures, chorea, optic neuritis are sequeles of distemper. Keratoconjuctivitis siccaPilocarpine drops 1 % p.o. 1-4 props in food 0.025 0.125% local application Artificial tears C) Infectious Canine Hepatitis: Common in < year of age. Signs: Fever, vomition, diarrhea, abdominal pain, pharyngitis, laryngitis, head neck and dependent part edema, petechial and ichimotic haemorrhages, epistaxis, melena, corneal edema and opacity during recovery stage. Treatment: 1. Fluid therapy Dextros i/v orringer lactate (20 mEq/L of fluid 2 coagulopathy Vit.K1: 2.2 mg/kg s/c followed by 1.1 mg/kg s/c 12 hourly 2 doses Fresh blood plasma 10 ml/kg i/v Heparin 100 U/kg sic 6-8hrsly 3. GIT hemorrhage Cimetidine 5-10 mg/kg i/m or sic t.i.d. Omeprazole .5-1 mgikg po sid Sucralfate 1 g/kg os 8-12 hrsly 4. Septicaemia Ampi/amoxy 22mgikg + kana5mgikg or genta 3mg/kg tid 5 Seizures 25-50% glucose .5-1 g/kg i/v 6. Toxaemia Enema 10 % povidone iodine 20 ml/kg Neomycin 10-20 mgikg or Metronidazole 10 mgikg bid p.o. Lactulose .5-1 mgikg orally tid (dose adjusted 2-3 soft stooll day) 7. Ascites Total Kcal 60-100 mg/kg/day LowNa diet + rice + cottage cheese + vit ABCDEK Zn Furosemide 1-2 mg/kg folloew by Spiro lactone 2-4 mg/kg bid B) Distemper: Signs:

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Paracentesis of ascitic fluid

2. Bacterial infections of skin:

(Staph, E. coli, Proteus & Pseudomonas) Surface infection erythema and papules Impetigo Sub corneal pustule on axillary and inguinal area. Superficial folliculitisHair saft in the centre of pustules Deep folliculitis, furunculosis and cellulitesBreakage of hair follicles, pus and pus tracts Treatment: Cephadroxyl 20mgikg, cephalaxin 30mgikg, erythromycin 15mgikg, Oxaciline 20mgikg BID.Amoxy-clav 20 mgikg X 21-180 days Sampoo-benzyle peroxide, salicylic acid, chlorhexidine, Mupirocin 3. Fungal Diseases: (Microsporum, Trichophyton, Candida) Alopecia, crusts and nodules are characerstics of fungal infections Classical ring worm form- Circular patch of 1-4cm in diameter Generalised formPustules and folliculitis KerionLocalised swollen area with pus PseudomycetomaCutaneous and subcutaneous nodules Treatment: Local application of antifungal- captan, miconazole, ketoconazole, povidone-iodine, chlorhexidine Systemic: ketoconazole 10 mg/kg os for 6-8weeks Malassezia: Treatment: erythema, hyperpigmentation and lichenification. Pruritis on muzzle, neck, abdomen and axillae Ketoconazole 10 mgikg for 30 days Ketoconazole, selenium disulfide, chlorhexidine sampoos Inflammation of epithelium of external ear canal. (Otodectic, scabies, demodex mites, scabies, staph, pseudomonas, proteus and E. coli, Malassezia, atopy) Infective, Reactive Pain, head shaking, scratching of ear, foul smell, brownish wax exudates Cleaning with .5% chlorhexidine, 10% Povidone iodine, white vinegar, diluted with water in 1: 1 ratio, 70% Isopropyl Alcohol.2% hydrogen peroxide solution Cauterisation: 5% silver nitrate/ tanic acid/ salisylic acid. Ivermectin 300ug/kg SC repeats after 3 weeks. Steroids, Gentamicin and ketoconazole. + amitraz (Taktic).

Otitis externa:

Stages: Signs: Treatment:

Ear drops-

Protozoan and other common problems of Canines 1. Protozoan and Rickettsial: a) Babesiosis: (Babesia gibsoni, Babesia canis). Anemia, fever, pale mucus membrane, petechial and ichymotic haemorrhages,

25

hemoglobinuria, hemoglobenemia, hepatomegaly and spleenomegaly. Malaise appearance, weight loss and intermittent low grade fever. Diagnosis: Parasite in RBCS on stained Blood slides. Treatment: Berenil 3.5mg/kg i/m X 3 days. Imidocarb- 5mg /kg i/m or s/c once Pentmidine Isethionate: 10-15 mg /kg sc bid X 2 days. b) Eherlichiosis: (Eherlichia canis): Lethargy, depression depression. Fever, tendencies, petechiation. Rarely edema of dependent part and CNS signs and arthritis Thrombocytopenia, anemia, leucopenia. (Leucocytosis in chronic) Presence of morulae in leucocytes Doxycyclines (drug of choice) 5mg /kg BID for 2 weeks, Oxytetracyclines 22mg/kg t.id 3weeks, Prednisolone 1-2mg/kg orally bid for 5 days. Androgenic steroids-nandrolone 1.5mg/kg week oxymethalone 2mg/kg orally o.d. Imidocarb - 5mg /kg i/m or s/c repeat after 14 days.

Diagnosis:

Treatment:

2. Fading Puppy Syndrome: There is neonatal death upto 2 weeks of age. 1. under weight 2 Hypothermia Puppy shows 96 F-100F) 3. Hypoglycemia 4. Dehydration. 5 Herpes viral infection 6 Other viral infections like, distemper and hepatitis, 7 Neonatal sepsis 8 Hook worm and Round worm infestation. 9 Death may occur due to Dystocia 10. Suffocation Control/Management: Warm up the puppy upto 97-98 F. Inject warm Rintose 1 ml/30gm body weight S/C or I/P or 5-10% glucose 0.25ml/30gm Antibiotics- Penicillin's are the choice/Cephlexin (Phexin) paediatric drops Contraindications- Amino glycosides- tetracyclines, chloramphenicols Canine Herpes virus (CHV) TransmissionVenereal (adult dogs) Transplacental, ingestion Respiratory and genital tracts Clinical signs- Less than 2 weeks puppy-more severely affected Depressed, anorectic, yellow-green diarrhea, abdominal pain, crying, petechial haemorrhages, vesicular/popular

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lesions on oral cavity, ventrum, genital neurological signs, cataract and blindness Treatment:

tracts,

1. Puppies should be housed in an environment at 36.637. 7c to maintain the body temperature over 101F 2. I/P - 1-2ml of Hyperimmune serum 3. Kennel cough: (canine Infectious Tracheo-bronchitis) It is an acute highly contagious respiratory disorder of dogs affecting the larynx, trachea, bronchi and occasionally lower respiratory tract. Aetiology: Para influenza virus, Bordetella broncheseptica, mycolplasma, herpes, distemper and hepatitis virus also involved. Symptoms: Cough of the sudden onset of high pitch known as honking cough. Mucopuruilant nasal discharge, conjunctivitis, complicated ITB dyspnoea, weight loss, lethargy, Treatment: Antibiotics- tetra, cephalaxin, amoxy, Steroids- prednisolone- to be given foe a minimum of 710 days Antitussive- Hydroicordon and butophenol Aminophyline and theophylline. Bacterial Pneumonia Aetiology: -

Clinical signs: Treatment: Organism Gram -ive bacteria Gram +ive bacteria Fungal Bronchodilators-

Herpes virus, parainflenza, canine adenovirus-2, Bordetella bronchiseptica, E. coli, Klebsiella, Pasteurella, Streptococcus, Staphylococcus, Aspergillosus Cough, depression, dyspnea, nasal discharge Antimicrobials chloramphenicol, Tri-sulpha,, Gentamicin, amicacin & Enrofloxacin oxacin, chloramphenicol, Tri-sul hadroxil, cephazolin Ketokonazole/Itrakonaz 5-10 mg/Kg b.i.d. orally

Theophyllin: 20mg/kg b.i.d. Aminophyllin: 10 mg/kg Terbutalin: 1.25-5.0 mg b.i.d. Ephiderin: 2.0 mg/Kg Prednisolone: 0.5-1.0mg/Kg UTI infections: Aetiology: Organism %age E. coli 38 Staphylococcus 15 Streptococcus 12

Treatment Sulpha-Trimethoprim, Cephalxin Ampicillin, Amoxycillin Ampicillin, Amoxycillin

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Proteus Klebsiella Pseudomonas Enterobactor

13 8 3.5 2.6

Ampicillin, Cephalxin Cephalxin Teteracycline Sulpha-Trimethoprime

Clinical Signs: Pollakiuria, haematuria, dysuria Antibiotic treatment should be given for 2 weeks. If pyelonepharitis is suspected then treatment should be continued for 3-6 weeks. 4. Hemorrhagic Gastroenteritis (Acute Hemorrhagic enteropathy): Signs: Bloody diarrhea, vomition anorexia. Fever is common, PCV > 60%. Management: 1 Ringers lactate- 90ml/kg in first instance 2 Antibiotics: Gentamicin / Amikacin + Amoxycillin 3 Cortocosteroids- Dexona 1-2ml/kg i/v 4 Plasmal plasma expander(plasma/ 6%dextran/ 6% hetastarch/@ 10-20 ml/kg or 7.2% hypertonic saline@ 5 ml/kg i/v External: (Tick, lice, Fleas and mites) a) Scabies: Nonseasonal, intense purities and alopecia and erythema on elbow, hock, ventral abdomen, chest anq Pinnae. Treatment: Ivermectin- .5mg/Kg SIC. b) Demodecosis: LocalizedIt is of2 types- localized and generalized. It occurs as one or more small circum scribed erythematous, scaly nonpruritic to pruritic areas of alopecia most commonly on face (periocclar area, commissure of mouth, chin and forelegs. Generalised- Covers large areas on head, leg and abdomen. Treatment: > Imitraz 3ml in 30ml mineral oil after cleaning with Benzyl peroxide shampoo. > Ivermectin- 0.5mg/Kg SIC for 3 to 4 times on week interval. > Milbemycin oxime- 1mg/Kg orally for a week some times up to 30-90 days. walking dandruffpruritis and scales on dorsal mid line all acaricides are effective (pyrethrins, carbaryl, ivermectin ect.) It is a hypersensitive reaction to antigen present in flea saliva. Average age 3-6 years, compulsive biting and licking. Lesions are concentrated on rump area. > Spray of common insecticides on animals and > Cythiorate and lufeneuron are given orally. (Not available in India, presently) > Flea collars-impregnated with insecticides > Beticol-spread over mid line

c) Cheyletiellosis: Treatment:

d) Flea allergy dermatitis: LesionsControl / Management: premises.

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e) Atopy: It is a cutaneous hypersensitivity to environmental allergens. Commonly occurs in between 1-2 years of age. Symptoms: pruritis characterized by licking, biting, rubbing and scratching. Lesions are present on pinnae, mouth, inguinal axillary interdigital spaces.

Treatment: > Immunotherapy 60-70% effective > Prednisolone 0.5 1 mg/kg to break the itch cycle. > Fatty acids -3 fatty acids (eicosapentaenoic acid) and -6 fatty acids (linolenic acid) > Antihistaminic: Hydroxygine 1-2mg/kg tid, chlorpheniramine .5mgikg bid, Diphenhydramine 2.2mg/kg, clemestine .04-.1 mg/kg > Terfenadine 30 60 mg total dose in dogs > Astemizole 1 mg/kg

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VACCINATION OF PETS AND C'AUSES OF ITS FAILURE

Drs. Parveen Goel and Pardeep Kumar Department of Clinical Veterinary Medicine College of Veterinary Sciences, CCS HAU, Hisar Vaccination refers to stimulation of immune responses against infectious diseases. It is also referred as immunoprophylaxis. It also includes the immunopotentiation of the pre-exposed antigen. Immunopotentiation should be differentiated with immunotherapy, wherein the immune response is increased nonspecifically in an already infected animal. Immunoprophylaxis is more common in case of viral and bacterial diseases where as immunotherapy is common for protozoan and fungal diseases. Active Immtinisation (Vaccination): a) Live vaccines: The live organisms are attenuated in such a way where they loose their pathogenecity while retails immunogenecity and ability to replicate in the intended host. These are usually lyophilized which makes them more stable and increase their keeping quality. These vaccines should be stored at 0C. b) Inactivated vaccines: These are the vaccines produced like live ones but their active agents are denatured without loosing their immunogenicity. Usually, adjuvant (aluminum Hydroxide, Aluminum phosphate, alum, New Generation- ISCOM and Quil A) are added to these vaccines to increase their duration and level of immunity they produce. Due to their nonreplication properties, these must be given at least twice. It takes several days to get a good immune response. Initially it is through the production of cytokines like interferon (IFN) more specifically IFN and later on by antibodies. The primary response consists of mainly IgM whereas secondary response is of IgG. The cellular immune responses are better than the humeral immune responses. Failure of Vaccination: a) Maternal antibody: Presence of maternal antibodies at the time of vaccination is a major cause of vaccine failure in young animals. The pups in their early days of life are protected by the antibodies they get inutero from their immune dams and later on by the antibodies absorbed through colostrums. Maternal antibodies usually are IgA, IgM and IgG, which are subsequently lost in the same order. The amount of immunoglobulin received by a pup is inversely proportional to size of the litter. Multiples vaccines are used at an interval of 2-3 weeks to break through the maternal immunity before exposure to virulent strain. Frequently given vaccines may accelerate the exhaustion of maternal antibody present in the neonates. Another way to overcome the interfering effects of maternal antibody is to use the antigenically related vaccines such as measles for canine distemper.

30

b) Cytotoxic drugs or Glucocorticoides: These drugs are responsible for the decreased response to vaccines. Steroids primarily affect the primary response whereas booster response is unaffected. c) Body temperature: Elevated temperature interferes in the initiation of immune response. Although no study is available which shows for the in-vivo effect of hypothermia, but in-vitro studies clearly indicated for the decrease in CMI d) Frequency of administration: Too frequent vaccination interferes with immune response. It is always better to administer several attenuated vaccines simultaneously rather then at an interval of 1-4 days. In case of too frequent administration, the vaccine given first will block the effect of vaccine delivered few days later. This is probably due to the interferon produced by the first antigen. Therefore modified live vaccines should never be administered in the other infectious diseases. A time gap of2-3 weeks is sufficient enough to overcome this problem of interference. e) Route of administration: Some of the ML V vaccine requires specific route of administration e.g. Rabies, measles and feline respiratory vaccines works better when given intramuscular rather than subcutaneous. The reason for this not know but for Rabies vaccine, the virus replicates better in innervated muscles rather than less innervated subcutaneous tissue. There are some other factors for failure of vaccination like- handling on the part of vet, storage of vaccine at higher temperature then required both at chemist shop as well as during transportation, wrong strain, excessive attenuation, vaccines do not protect 100% of population - protection of 65-95% is acceptable. Vaccination against following diseases of pets a) Canine Distemper: Primary vaccination should be done with ML V at the age of 6-8 weeks. Booster is recommended 2-3 weeks after first dose. Most vaccines are able to breakthrough maternal antibody by the age of 12 weeks. Those who are deprived of colostrums should be vaccinated at 2-3 weeks of age. b) Infectious canine hepatitis: Vaccination schedule is similar as that of canine distemper. It is usually given along with distemper. ICH vaccine containing canine adenovirus -1 (CA V-I) may produce anterior uveitis (blue eye). c) Canine parvovirus enteritis: Its schedule is similar to canine distemper and hepatitis; moreover it is given along with others. A Parvo-vial vaccine has the ability to breakthrough maternal antibody earlier than other vaccines i.e. as early as by the age of 6 weeks. It is advised to do vaccination of pups until the age of 18 weeks. It requires more booster than others to counter the prolonged maternal antibody interference. Pups from the breeds like Doberman; Rottweiler should be vaccinated till the age of 16-18 weeks as these breeds are more prone to this infection. d) Leptospirosis: It. schedule is similar to that of CD, ICH. It is allergenic in nature. Anaphylaxis may be noted within an hour. It does not produce a high level or long

31

duration immunity. It is available in liquid form and usually used to reconstitute the other lyophilized vaccines. e) Rabies: These days, it is a ML V vaccine rather then inactivated vaccine. It is not injected before the age of 3 months in dogs and cats. Booster is given after 6 months or 1 year or 3 years interval period, depending upon the local conditions. f) Feline panleukopenia: Both inactivated and ML V vaccines are in use. Two doses of inactivated are required for the single dose of ML V. Two ML V and 3 inactivated doses at an interval of 3-4 weeks are required. The first dose is injected at the age of 8-9 weeks. Inactivated vaccines are preferred in pregnant queens. g) Feline Respiratory disease: Calicivirus & rhinotracheitis virus vaccines are available as ML V and inactivated parentaral, ML V as intranasal products. Intranasal vaccine provides protection within 48 hours; however there are chances of post vaccinal mild contagious respiratory illness. The preferred age for vaccination is 9-12 weeks. Further reading to update knowledge about Vaccines: The Vaccine, Cell, Immunology, Infection and Immunity Journal of Immunology (cutting edge) Trends in Immunology (earlier Immunology Today)

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Therapeutic management of clinical cases of poisoning in canines

Rakesh Kumar Department of Veterinary Clinical Medicine, Ethics and Jurisprudence, CCS Haryana Agricultural University, Hisar-125004 (Haryana) It has been observed that small animals, particularly dogs and cats are exposed to variety of poisonous substances causing clinical illness / toxicity and even death if the patient is not attended timely. Further, pesticides have the largest contaminant group for canine exposures followed by plants, prescription medications and over-the-counter medications. Although there are different treatment approaches for different types of toxicities, yet there are certain general principles that apply to all cases of poisoning and these are discussed briefly here. The basis principles of treatment / management of poisoning cases are: 1. Removal of residual poison from skin If there is skin exposure, the poison may be removed by washing skin with soap and water to prevent further percutaneous absorption of poison. 2. Removal of residual poison from alimentary tract This can be achieved adopting the following the following approaches. a) Induction of emesis If the patient has ingested a poison within the past 2 hours and is asymptomatic, then an emetic such as 3 % hydrogen peroxide (2m I / kg orally, maximum of 45 ml) or syrup of ipecac (1 -2 ml / kg in dogs and 3.3 ml in cats) is given. Emesis from hydrogen peroxide is reliable if there is adequate ingesta in stomach and so hydrogen peroxide should be administered after feeding the moistened meal. These emetics usually initiate vomiting within 5-15 minutes. b) Gastric lavage As alternative to use of emetic, gastric lavage is employed, if animal is anaesthetized or unconscious. A rubber tube, with a funnel attached to proximal end is inserted directly through the mouth into the stomach. Raising the funnel allows liquid to the stomach; lowering it allows it to flow out. The stomach is washed out several times with water or normal saline and finally with some adsorbent material such as suspension of activated charcoal or universal antidote ( a mixture of activated charcoal 1 0 g, light magnesium oxide 5 g, kaolin 5 g and tannic acid 5 g) . c) Oral administration of adsorbents and cathartics: Removal of residual poison from alimentary tract can also be done by oral administration of activated charcoal (1-4 g I kg) combined with a saline (magnesium or sodium sulphate 250 mg I kg) or osmotic (70 % sorbitol 3 ml I kg) cathartic along with water. Magnesium based cathartics may be associated with CNS depression. Activated charcoal adsorbs organophosphate compounds, chlorinated hydrocarbons, mycotoxins and plant alkaloids, the common feed additives, antibacterial

33

agents and bacterial toxins. It does not adsorb heavy metals, halogens nitrites alcohols, caustics and sodium chloride or chlorate. 3. Neutralization of residual poison in alimentary tract This can be affected in some cases. For example: a) Oxidizing agents or tannic acid preparations are effective in precipitating alkaloids. b) Proteins including milk & eggs are effective chemical antidotes to protein coagulating poisons c) Lead is precipitated by the addition of sulfates to the alimentary tract. 4. Provision of chemical antidotes to the poison that has been absorbed Poison that has been absorbed can in some instances be inactivated or its excretion facilitated by the provision of chemical antidotes. For instance: a) Combined sodium nitrite (6 mg/kg) and sodium thiosulphate (60 mg I kg) when given i.v. with water are effective systemic antidotes to cyanide poisoning. Treatment may have to be repeated. Sodium thiosulphate is given orally to prevent absorption of cyanide content. b) Calcium versenate (I ml I kg as 6.6 % solution i/v in divided doses 2-3 times daily for 3-5 days) is an effective antidote for lead poisoning. It combines with lead to form soluble chelates readily excreted by the kidney. c) Atropine sulphate and 2-pyridine aldoxime methchloride (2-PAM) are effective antidotes for organophosphate and carbamate poisonings. The muscarinic effects of organophosphate compounds are blocked with atropine sulphate (0.2-0.5 mg I kg b. wt.) every 3-6 hours until clinical signs disappear. On third of the initial dose should be given slowly i/v and the remainder sic or i/m. Nicotinic cholinergic effects, muscle fasciculations, and muscle paralysis will not be alleviated with atropine. An improved treatment combines atropine with the cholinesterase reactivating oxime, 2-P AM. The dose of 2-P AM is 2550 mg I kg b. wt. given as 10 % solution i/m or by slow i/v injection repeated as needed. Response to cholinesterase reactivators decreases with time after exposure; therefore treatment with oximes must be instituted as soon as possible (within 24-48 hours). 5. Provision of supportive treatment It aims at keeping the vital organs of body functional until the poison is neutralized or eliminated either by suitable antidotes or by the body's own detoxification mechanisms. In general, it consists of treating the clinical signs of poisoning. Thus, convulsions can be treated with diazepam (0.5 mg kg i/v or i/m, doses may be repeated every 10 minutes for 3 doses). Phenobarbital (6 mg I kg i/v) or pentobarbital may be required. Coma, if deep, can be dealt with stimulants such as amphetamine or methyl amphetamine (0.25 mg I kg sic). Dehydration due to persistent vomiting or diarrhea as well as hypotension may be treated by parentaral administration of normal saline or Ringer's lactate solution. Acidosis (such as seen in ethylene glycol, metaldehyde and aspirin toxicity) may be treated with i/v sodium bicarbonate (1-3 mEq / kg administered in fluid over 1-3 hours).

34

Bradycardia occurring in organophosphate I carbamate poisoning may be treated with atropine (0.0 I -0.02 mg I kg i/v or i/m). Alkaline poisoning is treated by dilute acid (5 % acetic acid or vinegar). Similarly, acid poisoning is treated by means of dilute alkali (2 % sodium bicarbonate, lime water, chalks etc.). Irritation may be allayed by the administration demulcents. These may be anything from mixture of eggs, sugar and milk to linseed tea or oatmeal gruel. 6. Ion trapping It is a well known fact that alkaline urine generally favours increased excretion of acidic drugs and vice versa. Alkalinization of urine has been used successfully to treat ethylene glycol, salicylate and Phenobarbital poisonings. Forced alkaline diuresis is generally achieved with sodium bicarbonate at the dose rate of 1-2 mEq / kg administerd intravenously every 3-4 hours. Similarly, ammonium chloride (100 mg / kg ii dogs and 20 mg I kg in cats, bid) is used orally to acidify the urine in strychnine toxicity.

35

Common Dermatological Problems in Canines and Their Management

R. KHURANA Teaching Veterinary Clinical Service Complex CCS Haryana Agricultural University, Hisar It is commonly stated that in an average small animal practice, approximately 30 per cent of all cases are dermatological. Some of these cases will be obvious presenting no diagnostic difficulty e.g. heavy tick/lice/flea infestation. However, in many cases, a systematic approach is required for correct diagnosis of skin problem. The diagnosis is best made by careful history (most important), a general physical examination followed by a dermatological examination and by the use of laboratory and other techniques. In this lecture, attempts have been made to acquaint the field veterinarians about common dermatological problems encountered in dogs and their clinical management in brief. 1. ACUTE MOIST DERMATITIS CAUSE: It is also known as Pyotraumatic dermatitis, Hot spots and Wet eczema. It is produced by self-induced trauma as the patient bites or scratches at a part of its body due to some pain or itch. Majority of cases are complications of flea -bite hypersensitivity. Other underlying causes include: 1. Allergic skin diseases 2. Other ectoparasites like ticks, lice etc. 3. Anal sac problems 4. Inflammations such as otitis externa 5. Foreign bodies in the coat 6. Irritant substances 7. Dirty unkempt coats 8. Psychosis and painful musculoskeltal disorders CLINICAL FEATURES: Can occur in any breed but dogs with dense hair coat like German shepherd, Labrador, Collie, Spitz, Pomeranian, St. Bernard are more susceptible. More incidences in hot and humid weather i.e. July to September. Self-trauma perpetuates the problem (itch- lick- chew cycle). Rapid development of lesions, which may appear within hours. Typical sites include neck, face tail base, back and hind legs. Typical lesion is red, moist and exudative. Hairs are lost from the area, but the margins are sharply defined from the surrounding normal skin and hair. There is intense pain that prevents further self-trauma. DIAGNOSIS: History of acute onset

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Physical appearance and association with a primary underlying cause flat, eroded to ulcerated lesion CLINICAL MANAGEMENT: Therapy is effective if applied promptly and vigorously. Sedation or anesthesia may be needed for thorough cleaning of the area. Cleaning with povidone-iodine (betadine) or chlorhexidine (hexiprep) after clipping of hair. In unclipped area, antiseptics in form of shampoo (surgiscrub) can be used. Topical ointments containing glucocorticoids with antibacterial agents (betnovate-G, spectrazole, neomycin-H, eclospan etc.) for 7 days. Parentral administration of glucocorticoids (prednisolone @ 1.1 mg/kg B W) for 7 days. Recovery occurs in 7-10 days. Elimination or treatment of underlying cause. Constant attention to grooming, hygiene, baths, parasite control and periodic cleaning of the ears and anal sacs helps in prevention. 2. IMPETIGO CAUSE: It is also known as Juvenile pustular dermatitis and Puppy pyoderma. It is sub corneal pyoderma (pustules) that affects sparsely haired areas of the skin i.e. ventral abdomen and axillae. It is a bacterial disease caused by Staphylococcus organisms. Young dogs before or at the time of puberty are affected. This disease is non-contagious In some dogs it is secondary to parasitism, viral infections, a dirty environment, immune-mediated disease or poor nutrition. CLINICAL FEATURES: Small superficial pustules that do not involve hair follicles are not painful and rupture easily. Pruritus is not common. Papules and yellow scabs are also present Relatively benign problem, which may be asymptomatic. CLINICAL MANAGEMENT: Impetigo may regress spontaneously, but therapy can hasten the healthy process. If lesions are few and separated, topical antibacterial creams or povidone-iodine or chlorhexidine are effective. If numerous pustules, antibacterial shampoos (e.g. surgiscrub) can be used

37

Recovery occurs in 7-10 days. Systemic antibiotics are rarely required. 3. SUPERFICIAL BACTERIAL FOLLICULITIS CAUSE: Bacterial infection at the level of and incll,lding the intact hair follicle. Mostly caused by Staphylococcus intermedius. It may result from: 1. Local trauma 2. Brushing or scratching 3. Contamination due to dirty coats or poor grooming 4. Demodicosis 5. Hormonal factors (hyperadrenocortism or hypothyroidism) 6. Local irritants or allergies Pruritus mayor may not occur. 3 most common etiological agents are: staphylococci, dermatophytes and demodectic mites. CLINICAL FEATURES: It can occur in any breed and age but more common in young dogs. Variable lesions like pustules with hair protruding, papules, crusts, localized 'moth-eaten' alopecia, hyper pigmentation. DIAGNOSIS: History and physical examination Examination of stained smears of pus and/ or bacterial culture. .Examination of skin scrapings for mites and fungus. CLINICAL MANAGEMENT: Identify and treat the underlying cause if possible. Antibacterial therapy both topical and parentral for about 3 weeks. 1. Topical with chlorhexidine, povidone-iodine or benzoyl peroxide. 2. Parentral with any broad-spectrum antibiotics like erythromycin, enrofloxacin, amoxycillin with clauvinic acid, lincomycin, gentamicin, cephalexins etc. Do not use glucocorticoids. 4. INTERTRIGO (SKIN FOLD PYODERMA) CAUSE: It is frictional dermatitis that occurs in areas where two skin surfaces are apposed. Poor ventilation in association with a warm humid environment favour bacterial multiplication. This condition is seen in certain specific breeds of dogs only. The condition is found in various sites:

38

a) Lip fold pyoderma: Occurs in Spaniels, St. Bernard. b) Facial fold pyoderma: Occurs in brachycephalic breeds like Pekinese, Bulldogs & Pug etc. c) Body fold pyoderma: It occurs in obese dogs, Basset hounds and Chinese Sher pei dogs. d) Vulvar fold pyoderma: It occurs in obese older female an animal in which spaying has been done at a young age. e) Tail fold pyoderma: It occurs in English bulldogs, Boston terriers due to pressure of corkscrew tails on the skin of perineum. CLINICAL MANAGEMENT: Application of benzoyl peroxide or sulphur-based products in the form of gel, ointment or shampoo (e.g. Persol forte gel, Persol forte cream). Application of antibacterial talcum powder (e.g. Nebasulf). 5. Contact Dermatitis CAUSE: It is quite common in dogs. Very large variety of substances is capable of causing irritation. These are divided into two types: 1. Absolute: -acids and alkalis 2. Relative: - soaps, detergents and solvents, gravel, sand and flea collars etc. CLINICAL FEATURES: Erythema, papules, crusts and excoriation of skin at the site of contact Common sites are the ventral surface of the abdomen, axilla interdigital space, perineum, scrotum and any other area where hair is sparse. Hairy skin is relatively unaffected unless the irritant is a shampoo or spray. DIAGNOSIS: History is most important. Physical examination. Elimination and provocative exposure tests. CLINICAL MANAGEMENT: Removal of irritant substance. Bathing with water. Topical application of glucocorticoids ointment (e.g. Betnovate).

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6. Atopy (Atopic Disease, Allergic Inhalant Dermatitis): CAUSE: It is inherited predisposition to develop IgE antibodies to environmental allergens resulting in allergic dermatitis. Common 10 dogs and cats. Many allergens may be responsible including: house dust, dandruff, pollens, fungi, moulds, feathers etc. It can occur in any breed but certain breeds like Scottish terrier, Dalmatian, Pug, Labrador, Boxer, Lhasa apso, Boston terrier and Sher pei are predisposed. CLINICAL FEATURES: Most cases occur between 1 and 3 years of age. Clinical signs may be seasonal I Pruritus is the principal complaint. Typically the sites affected are face, ventrum, axilla and the feet. There may be erythema, pyoderma, seborrhea, lic;henification and alopecia. Self-trauma is common. Other features are salivary staining of the coat as a result of constant licking, conjunctivitis and otitis externa. DIAGNOSIS: Rule out the possibility of parasitic involvement particularly scabies and fleas, food hypersensitivity. Intradermal allergy testing. Major factors: At least 3 should be present. 1. A breed predilection. 2. A familial history of atopy. 3. Pruritus. 4. Facial and / or digital involvement. 5. Chronic or chronically relapsing dermatitis. 6. Lichenification of tarsus or carpus. CLINICAL MANAGEMENT: Avoidance of allergens. Systemic glucocorticoids like prednisolone @ 1.1 mg/kg B W on alternate day life long. Essential fatty acid supplementation (e.g. Nutricoat). 7. DERMA TOPHYTOSIS (RINGWORM) CAUSE: It is cutaneous fungus infection with species of Microsporum, Trichophyton or Epidermophyton. Fungi attack the keratin of the hair only. In dogs mostly caused by M canis and T. mentagrophytes.

40

CLINICAL FEATURES: More in hot and humid weather. Infection is by direct contact with infected animal or contaminated material (hair, scales, fomites) from the environment. More in young animals. Variable lesions that include circular patchy alopecia, erythematous plaques, folliculitis, scales and crusts. Lesions may be localized or diffused. Nails may also be involved. Hair loss and scarring due to secondary infection. Lesions may commonly occur on face, pinnae, paws and tail. DIAGNOSIS: 1. Examination of bright green fluorescence in infected hair produced by M. canis with Wood's lamp. 2. Examination of potassium hydroxide (10%) preparation. 3. Cultural examination. 4. Biopsy examination. CLINICAL MANAGEMENT: Spontaneous resolution in some cases within 4 months. Clipping of hair around lesions. Topical therapy: 1. Focal lesions: Topical application of antifungal ointments containing clotrimazole, miconazole, ketoconazole (e.g. spectrazole, nizoral, conaz, eclospan, zovate-M, lobate -OM, quadriderm etc.) at an interval of 12 hours. 2 Multifocal or generalized skin involvement: Weekly application of antifungal shampoos (e.g. Nizoral, Konaz, Danrut) or lotions (e.g. Wokazole, Konaz) or both. 3. Chlorhexidine (e.g. Hexiprep) and povidone-iodine (Betadine, Wokadine) are also effective if applied for 2 weeks daily. Systemic therapy: Dogs not responding to topical therapy after a 2-4 week course of treatment shoQld receive systemic therapy. Griseofulvin (e.g. grisofil) @ 25-60mg/kg BW b.i.d. for 4-6 weeks along with a high fat diet. Or Ketoconazole (e.g. ketazole, funazole) @ IO-15mg/kg BW once daily for 3-4 weeks. 8. ALOPECIA DUE TO OTHER PROBLEMS A. Hormones: 1. Hypothyroidism: - Lymphocytic thyroiditis - Seen in 6-10 years of age

41

- More in Bulldog, Great Dane, Doberman, Poodle, Dachshund, Afghan hound and Golden retriever -Bilateral symmetrical alopecia, hyper pigmentation, dull coat, thickening of skin -Treatment: Thyroxine sodium @ 10-20~g/kgBW b.i.d. life long. 2. Hyperadrenoconicism (Cushing Syndrome): - Excess secretion of cortisol due to adrenocortical hyperplasia - Excess use of glucocorticoids - More in Boxers, Dachshunds, Toy and Terrier breeds. - More in middle to old age and in female dogs. - There is polyuria, polydypsia, polyphagia, skeletal muscle atrophy, hepatomegaly, anestrus, testicular atrophy, panting and lameness. - Bilateral symmetrical non-pruritic alopecia (not on head or feet), hyper pigmentation, very thin skin on ventr~l abdomen, which tend to wrinkle, poor wound healing. - Treatment by bilateral adrenalectomy and use of anti-cancerous drugs (e.g. Vincristine). B. Nutrition: 1. Protein deficiency 2. Essential fatty acid deficiency 3. Deficiency of vitamin A, E and B (Biotin, Niacin, Riboflavin) 4. Zinc deficiency, which may occur due to over supplementation of calcium and soybeans. Zinc deficiency can be treated by administration of Zinc sulphate @ 10mg/kg BW daily for 3 weeks. C. Neoplasms: 1. Papillomas, histiocytoma 2. Squamous cell carcinomas 3. Melanoma, mast cell tumor 4. Fibromas, fibrosarcomas 5. Sweat gland tumors 6. Transmissible venereal tumors Treatment by Vincristine @ 0.0 125-0.025mg/kg BW i/v weekly for 3-4 weeks. D. Autoimmune disorders: e.g. Pemphigus complex E. Hypersensitivity: e.g. food and contact hypersensitivity,

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CONTROL OF ECTOPARASITES IN DOGS

R. KHURANA Teaching Veterinary Clinical Service Complex CCS Haryana Agricultural University, Hisar Animal skin is exposed to attack by many kinds of animal parasites. Each species has a particular effect on the skin; the effect can be mild, as in the case of an isolated fly or mosquito bite, or severe, as in the case of demodicosis or scabies. Ectoparasites can be vectors or intermediate hosts of bacterial, rickettsial or parasitic diseases. A severe local or systemic reaction may result when toxins are injected into the skin (e.g. tick paralysis). Most of the ectoparasites produce irritation and sensitization. The reaction of the skin to these ectoparasites living in or on the skin results in inflammation, edema and an attempt to localize the foreign body, toxin or excretory products of the parasite. These reactions are often allergic and cause itching and burning sensation. In this article, treatment and control of some of the common ectoparasites affecting dogs are given briefly. 1. CANINE SCABIES (SARCOPTIC MANGE) CAUSE: It is a non seasonal, intensely pruritic, transmissible infestation of the skin of the dogs. The mite Sarcoptes scabiei var. canis causes it. Sarcoptic mange is transmissible to human beings. CLINICAL FEATURES: Pruritic, reddish papulo-crustous eruptions having thick yellowish crusts. There is intense itching, excoriation of skin due to scratching and biting. Lesions mainly on ventral portion of abdomen, chest and legs. Ears and elbows are almost always affected. Disease spreads rapidly and can involve the entire body. But dorsum is usually not affected. Itching is more in warm environments. Erythema in early stages, alopecia, thickening of skin and folds formation, which gives appearance of elephant skin. Initially localized, if untreated becomes generalized. In Human beings there are pruritic erythematic papules on the trunks and arms that regress spontaneously in 12-14 days if in contact affected dogs are treated. DIAGNOSIS: By history and clinical signs. Skin scraping examination. Pinnal -pedal reflex. Response to therapy.

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CLINICAL MANAGEMENT: Ivermectin @ O.2-0.4mg/kg BW orally or s/c every 14 days until recovery. Recovery usually occurs with 2 injections. Ivermectin should not be given in Collies and sheep dogs. Doramectin (Dectomex) @ 0.2-0.4mgikg BW i/m every 14 days until recovery. Amitraj (e.g. Taktic, Ectodex) 0.03% application twice a week for 4-6 weeks. Spray of insecticides such as carbaryl (0.5%), malathion (0.5%), cypermethrin (150ppm), deltamethrin (25ppm) etc. twice weekly. [Notix, Butox, Clinar, Cyprol, Tikout, Ectomin etc. Spray of kennels with above insecticides in double concentration fortnightly. Administration of systemic Corticosteroids e.g. prednisolone @ 1.1 mg/kg BW daily for 2-3 days. 2. DEMODECTIC MANGE CAUSE: It is also known as Demodicosis, Follicular mange and Red mange. Mite Oemodex canis causes it. It is normal inhabitant of canine skin but is found in much larger numbers indiseased dogs. The mites inhabit hair follicles and occasionally sebaceous glands. Cigars shaped mites live entirely on host. Any breed, age and sex affected but more common in purebred dogs and in short haired breeds. But can occur in English sheep dog, Afghan hound, German shepherd and Collie. Transmission occurs from bitch to neonates. CLINICAL FEATURES: Three types -Localized, Generalized and Pododemodicosis. Localized: 1. One to several small circumscribed, mild erythematous, scaly non-pruritic to pruritic areas of alopecia. 2. Lesion most commonly on face (Periocular area and oral commissures) and forelegs. 3. Later hyper pigmentation occurs. 4. Most cases in pups of 3-6 months age. 5. In majority of cases spontaneous regression occurs. Generalized: 1. Occur in adult dogs (2-5 years). 2. It covers large areas of body. 3. Occur in dogs in which spontaneous recovery of localized lesions does not take place. 4. Numerous lesions on head, legs and trunk.

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5. Lesions are alopecic patches, scaling, erythema and lichenification. 6. Pyoderma is a common complication 7. Immunosuppression is also there in such cases. Pododemodicosis (Demodectic pododermatitis): 1. Foot lesions are common in generalized demodicosis. 2. In some cases only foot lesions occur. 3. Thickening of the skin of paws with hyper pigmentation and secondary pyoderma. 4. Pain and edema may be there. 5. May result from a generalized case of demodicosis. DIAGNOSIS: History and clinical signs. Microscopic examination of deep and extensive skin scrapings. Squeeze affected skin before collection of skin scrapings. CLINICAL MANAGEMENT Localized: 1. Spontaneous recovery in 6-8 weeks. 2. Topical ointments containing insecticides (e.g. Himax-D, Gammexine). 3. Use of insecticide solutions (e.g. Notix, Butox, Clinar, Cyprol, Tikout, Ectomin etc.) Generalized: 1. Amitraj (Taktic, Ectodex, Ridd) 0.03% application weekly for 4-6 weeks after clipping of hair and removal of crusts. 2. Shampoo before application of Amitraj. 3. A course broad-spectrum antibiotic (erythromycin, enrofloxacin, cephalexin, amoxycillin, cloxacillin etc.). 4. If pododermatitis is there, dip the paws in the Amitraj solution. 5. Use of insecticide solutions (e.g. Notix, Butox, Clinar, Cyprol, Tikout, Ectomin etc.) 3. FLEAS CAUSE: The disease is known as Fleabite hypersensitivity or Flea allergic dermatitis. It is pruritic, papular dermatitis in dogs. It is a common cause of skin disease in the dog. Caused by Ctenocephalides canis or C. felis. More in winter season. CLINICAL FEATURE All breeds and both sex are susceptible.

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 More common in 3-5 years of age. Hypersensitivity develops to haptens in the saliva. Both immediate and delayed hypersensitivity responses occur. Wheals, erythema and papules develop at the site of flea-bites. Common sites are dorsum, tail head, hind legs and ventral abdomen. Self-trauma from licking and scratching causes acute moist dermatitis in the early stages. In chronic cases seborrhea, lichenification and alopecia occurs. DIAGNOSIS: Physical examination. Identification of fleas or flea excrement by placing excrement on wet blotting paper. A reddish tinge diffuses out from the flea excrement. Lesions in typical sites. Response to therapy. CLINICAL MANAGEMENT: Administration ofPridnisolone @ I.Img/kg BW daily for 5-7 days and then on alternate days till recovery. Administration of antihistaminics like Chlorpheniramine @ O.4mg/kg BW 8 hourly orally or Diphenyl hydramine @ 2.2mg/kg BW 8 hourly orally. Treat the dog and in contact dogs with insecticides in the form of shampoos (e.g. Cisaflux, Clinar, Notix), sprays (e.g. Notix, Butox, Clinar, Cyprol, Tikout, Ectomin etc.), soaps (e.g. Asuntol, Notix, Tetmosol, Petmosol etc.) or powders (e.g. Notix etc.) Use of flea collars (e.g. Kiltix, Preventic etc.), but these have limited use. Regular spray of house or kennels with insecticides for control of fleas in environment. 4. PEDICULOSIS CAUSE: Pediculosis is infestation with lice. Lice are host specific. Lice survive only for few days if separated from the host. Life cycle entirely on host. Lice are either biting (Trictodectes canis) or sucking (Linognathus setosus). Spread either by direct contact or by contaminated brushes, combs or bedding. CLINICAL FEATURES: High irritation and intense itching. Sucking lice produce anemia and severe debilitation in young animals. Secondary alopecia and excoriation. Mouse like odor of the coat.

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 Hair coat is dirty, matted and ill-kept indicating poor sanitation. DIAGNOSIS: Physical examination. CLINICAL MANAGEMENT: Treat the dog and in contact dogs with insecticides in the form of shampoos (e.g. Cisaflux, Clinar, Notix), sprays (e.g. Notix, Butox, Clinar, Cyprol, Tikout, Ectomin etc.), soaps (e.g. Asuntol, Notix, Tetmosol, Petmosol etc.) or powders (e.g. Notix etc.) Repeat after one week. Ivermectin @ O.2mg/kg BW sic once. Treat the environment with the insecticides. Improvement of animal's living condition. 5. TICKS CAUSE: 2 classes: hard and soft ticks. All breeds, ages and both sex are susceptible. More common in summer months. Ticks are not host specific. CLINICAL FEATURES: There are various possibilities: 1. Asymptomatic. 2. Owner notices them. 3. Skin irritation due to bites. 4. Hypersensitivity reactions. 5. Anemia if infestation is high. 6. Paralysis. 7. Vectors for bacterial, rickettsial, viral and protozoal diseases. DIAGNOSIS: Physical examination. CLINICAL MANAGEMENT: Treat the dog and in contact dogs with insecticides in the form of shampoos (e.g. Cisaflux, Clinar, Notix), sprays (e.g. Notix, Butox, Clinar, Cyprol, Tikout, Ectomin etc.), soaps (e.g. Asuntol, Notix, Tetmosol, Petmosol etc.) or powders (e.g. Notix etc.) Manual removal: apply an ether swab first or spray with an insecticidal agent. Care must be taken to remove the entire tick or a foreign body granuloma will develop. Treat the environment with the insecticides. Prophylaxis by regular spraying of the environment and the use of insecticides as sprays, powders, shampoos or collars on the animal.

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Common Orthopaedic Problems of Pet Animals

Dr. Prem Singh Department of Veterinary Surgery and Radiology Orthopaedic problems can be divided into four main groups for the sake of convenience: A. Problems of the bone B. Problems of the joints C. Problems of the muscles and tendons D. Problems of the foot. A. Problems of the bone: The bone problems can be classified into Traumatic Infectious Neoplastic Metabolic

a.

Traumatic conditions of bone

The most important traumatic condition is fracture.

Fracture Any break in continuity of bone, may be complete or incomplete, will constitute fracture disease. Fractures are of various types: (Compound) open or closed (simple) Complete or incomplete (green stick), Comminuted or multiple Spiral or transverse If not attended well in time then may complicate into: 1. Delayed union After immobilization, clinical union takes place within 6-8 weeks but due to inadequate reduction, immobilization, and the period gets prolonged and makes it a case of delayed a union. 2. Non-union (fibrous union) Sometimes fibrous tissue gets filled between the fractured fragments resulting in complete absence of the union and there will be free movement in between the two fractured fragments. The condition is known as l1on-union. 3. Mal union (angular deformity)

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Healing of fractured fragments in an abnormal position. 4. Avascular nerosis When blood supply set interrupted. The cases of fracture and its complication can be diagnosed by radiography and can be treated by: Plaster cast Thomas splint Intramedullary pinning; Nailing Plating

b.

Infectious condition of bone

Common infection of the bone is Osteomyelitis. May be due to: Compound fracture Through haematogenous route Through surgical instrumentation Osteomyelitis denotes an inflammatory process of periosteum (periostitis), cortex (osteitis) and medullary cavity (myelitis) of bone. May be bacterial, fungal, parasitic or viral. The bacteria after entry into the bone marrow will initiate on inflammatory response resulting in accumulation ofneutrophils, macrophages at the site. This stage is called acute stage of osteomyelitis. The administration of antibiotics at this stage will be helpful in eradication of the bone infection. The bacteria when get trapped into the blood vessels will cause is ischemia and necrosis of the bone. This necrosed portion of bone is called sequestrum. This necrosed portion is surrounded by new bone to contain the infection. This formation of new bone is called involerum. The formation of sequestra and involerum are characteristic of chronic osteomyelitis. The condition can be diagnosed by radiography and treated by antibiotics and surgical debridement. c) Neoplastic condition of bone Tumors of the bone are commonly seen in the dogs and nearly most of them are malignant. Tumors may be benign or malignant. i) Benign tumor There are osteoma, chondroma and osteoclastoma. 1. Osteoma There are two varieties. Firstly, there is the osteoma eburneum, which arises from the compact bone and is a single, small and round, and secondly there is osteoma spongiosum, which arises from spongy bone & is generally multiple & large.

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2. Chondroma Chondroma occurs near the articular surfaces between the epiphysis and diaphysis. 3. Osteoclastoma These are slow growing tumors. So, the bone is slowly resorted and only a shell of cortex remains and it is on account of this formation that they are often referred to as 'egg shell' tumors. ii) Malignant tumors known as Osteosarcomas Osteosarcomas in dogs have a very definite breed and site incidence. The larger breeds such as the Great Dane, St. Bernard, Hound, Alsatian and Retriever are especial prone to osteosarcomas. Most common sites are distal extremity of radius, and femur, the proximal extremity of the humerus and both extremities of the tibia. The condition can be diagnosed by radiography and corrected by surgical intervention. d) form of: Ricket Renal ricket Ostemalacia Osteoporosis Panosteitis 1. Ricket Disease of young animals in which the newly formed bone matrix continues to grow but fails to calcify. The conditions attributed to lowered concentration of Ca and inorganic P in serum due to deficiency of vitamin D3 (choJecalciferol). The cholecalciferol is in inactive form and get activated in liver (25 hydroxyl cholecalciferol) and kidney (I, 25 dihydroxy cholecalciferol) which is required for absorption of Calcium from gut. In diseases of liver and kidney also ricket develop due to non conversion of (1, 25 dihydroxy cholecalciferol from cholecaciferol). If kidney is involved than the term renal ricket is used. Diet of dog must include vitamins, dicalcium phosphate, bone meal, cereal, meat, milk, cheese, egg, wheat germs etc. 2. Osteomalacia This is an adult form of rickets. The condition is due to lack of Vito D or deficiency of Ca and P. So the bone became soft and pliable. 3. Osteoporosis It is a non-specific term and occurs as a result of an imbalance between bone formation and bone resorption. Metabolic conditions of the bone Metabolic bone diseases are commonly observed in young and adult dogs in

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4. Panosteitis This disease is also called eosiniphilic panosteitis, enosteitis and servile osteomyelitis. This is a common disease of long bone in large breed of young dog especially German shepherd. It is a self limiting disease therefore gets better by itself. Blood picture of such patient will reveal eosinophillia and radiography will depict granular density, sclerotic density in metaphyseal areas

B. Problems of the joints

The problems of the joint can also be classified as: a) Traumatic b) Infectious c) Hereditary a) Traumatic ProblemsTrauma to the joint can cause: 1. Rupture of joint capsule, ligaments specially, cruciate ligament of stifle joint. 2. Fracture of articular surfaces followed by osteoarthritis. 1. Rupture of cruciate ligament: The cruciate ligaments are two strong bands situated in the intercondyloid fossa of the femur. Their function is to stabilize the stifle joints. When the dog takes a turn sharply with its stifle in a state of flexion either anterior or posterior cruciate ligament get teared making the joint free. The rupture of cruciate ligaments can be diagnosed by drawer test by drawing the affected hind limb either interiorly or posteriorly, the free articular surfaces of stifle joint can be felt. The free stifle joint can be stabilized by drilling a hole through articular surfaces and patting carbon fiber through it. 2. Fracture of articular surfaces resulting in osteoarthritis: Due to trauma, the articular surface of the joint get fracture and sometimes portion float into the joint cavity. The fracture or teared portion can incite an inflammatory response setting formation of bony changes. These bony changes first appear near the periphery putting pressure over the joint capsule and finally start obliterating the joint space. Diagnosis: By radiography Surgical treatment Debridement Arthrodesis

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 Arthroplasty Neurectomies b) Infectious problems When joint fluid cavity gets infected than the term used is septic, suppurative, pyogenic arthritis. The synovial fluid get contaminated by a. Haematogenous route b. Exogenous route When infection is through hematogenous route then multiple joints get involved and term polyarthritis is used. Polyarthritis (Joint ill) is common sequelae to navel ill. Following the introduction of infection in to the joint cavity, there will be an inflammatory response and the synovial fluid will contain 10,000 leucocytes/cmm. Due to change in composition of synovial fluid. There will be interference in transport of nutrition to the articular surface. The articular surface will loose its shiny appearance and become ulcerated and finally ligament will become loose and painful making the joint prone to dislocation. The condition is diagnosed by: 1. Clinical signs 2. Cultural exam 3. Radiography As a principle after culture exam and sensitivity testing antibiotics such as penicillin, ampicillin, neomycin, kanamycin, gentamicin, tetracycline are administered. c. Hereditary The common problem encountered in German shepherd affecting the hip joint is hip dysphasia. Hip dysphasia is an abnormal development or growth of the hip joint manifested by: Defect in the shape and size of acetabulum which becomes flat and shallow i. e. malformation of acetabulum. Malformation of head and neck of femur. The femoral neck becomes short and at a different angle and joint capsule will become flaccid. Clinically, the joint will be unstable on palpation and joint capsule will be flaccid. There will be swaying of hind quarter. Diagnosis: by radiography Acetabulum will be flat and shallow Femoral neck short and at an obtuse angle. Treatment include 1. Excision arthroplasty 2. Hip prosthesis

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C. Problems of the muscle and tendon

Problems of the tendon can also be seen in the same pattern as for bone and joint. a) Traumatic b) Congenital a. Traumatic problems: can be seen in form of: i. Inflammation of tendon (tendonitis) ii. Rupture of tendon i. Tendonitis A sprained or strained tendon is commonly used to describe inflammation of tendon following excessive stress. The tendonitis may be: Acute Chronic 1. Picture sprained tendonitis The acute injury can be due to over extension of the tendon following a slip or fall. The lameness is more marked in sprain of the deep digital flexor than other flexors. The most common site of sprain of the d-d-flexor tendon is near its function with the sub carpal check ligament. The use of anti inflammatory drugs will serve the purpose. 2. Chronic sprained tendon In chronic cases of tendonitis. The tendon becomes thickened in the mid portion giving it a bowed appearance which is due to thickening of the tendon following its repair by fibrosis. Use of blister, cautery & special shoes are vhelpful. ii) Rupture of tendons Following injuries, the tendon can be ruptured. The ruptured tendon may be: Superficial digital flexor tendon Deep digital flexor tendon Gastrocnemius etc. The ruptured tendon can be repaired and limb is put into the plaster cast. b) Congenital problems Most important condition is the contracted tendon popularly known as knuckling. The contracted tendon can be severed and limb can be put in to plaster cost.

D) Problems of foot
The bearing surface of foot can be injured on many occasions and can cause. 1) Sore pad There is due to injury of foot or cracks/ulcers in between digits. Only way is cleaning, application of emollient and rest. 2) Foreign bodies The foot pad became swollen and painful due to penetrating foreign bodies which can be removed. 3) Split or broken claws

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The abnormal position of claw split or broken claws are the potent source of lameness in dogs. These can be removed for normal gait of the animal.

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Treatment of Common Eye and Ear Disorders in Pet Animals

Kuldip Singh Professor & Head Department of Veterinary Surgery & Radiology College of Veterinary Sciences CCSHAU, Hisar, Haryana Ophthalmologic Examination & Diagnostic Procedures History Animal Restraint Examine Cornea, anterior & posterior chambers, iridocorneal angle by gonioscopy, Shape & size of pupil Wide pupil-indicates glaucoma, iris atrophy, retinal & optic nerve diseases Miotic pupil- indicates iridocyclitis, anterior uveitis Irregular/off centre pupil-lens subluxation, posterior synechia Examine Aqueous humour-Blood, parasites, inflammation Examine Vitreous -liquifaction, fine filaments in old animals Use Direct ophthalmocopy, slit lamp biomicroscopy, indirect ophthalmocopyFor cornea, iris, lens, fundus Nasolacrimal Duct Obstruction-dacrorhinocystography. Electroretinography- retina. Schinner Tear Test-Quantify tear flow (10-25mm wetting in one minute) Tonometry-15-25mmHg Intraocular Pressure in dogs. Ultrasonography- Foreign bodies, eye evaluation in corneal opacity Fluorescein dye is used to see normal tear drainage through NLD and angiography of retinal vessels. Rose Bengal dye is used to stains conjunctival defects, corneal ulcers and keratitis. Anticollagenase agents-Acetycysteine, Penicillamine used for corneal ulcers and dry eye disease. Tear replacement-Artificial tear solution stabilize pre-corneal tear, use for dry eye, keratitis. Examples-Methyl cellulose, polyvinyl alcohol. Other Drugs Used Tropicamide -Mydriasis is caused for 20 minutes, used for intraocular examination Homatropine -Mydriasis-Use prior to cataract surgery Phenylephrine -Pupil dilated Pilocarpine -Use in dry eye, glaucoma, decrease aqua Humour, increases its out flow Corticosteroids -Suppress acute inflammation (Not use in corneal defects and primary glaucoma). Use 3-4 times a day for 3-4 weeks. Can be used subconjunctivally.

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 Antibiotics-Chloramphenicol, sulphacetamide, cephalosporin, methicillin, gentamicin, neomycin have better penetration in eye tissues but Bacitracin, tetracycline, penicillin, streptomycin have poor penetration in eye. Hereditary DisordersEntropion, ectropion, luxation of lens, cataract, glaucoma, progressive retinal atrophy, retinal dysplasia, persistent pupillary membrane, retinal atrophy in cats. 40% abnormalities in dogs. 25% are abiotrophic (blindness in later life). 2/3rd of blindness in man is hereditary. Affections of Eye Ball & Lid Proptosis of globe- Protrusion of eye ball due to shallow orbit, blunt trauma. Enophthalmos -Reduce globe size & reduction in orbital contents-Injuries Phthisis bulbi- atrophy of eye-Injuries- reduction in Aqueous Humour formation, damage to retina and optic nerve Microophthalmia-inherited defect, microcornea present Buphthalmos- Excess fluid in anterior chamber leading to buldging of eyeball Lagophthalmos- Eye can not be closed completely due to growth on cornea, prolapse of 3rd eyelid, injury to 7th cranial nerve, inflammation of lacrimal gland, staphyloma Strabismus -Not common ,impaired vision, pupil is close to medial canthus Dermoid-Involves eye lids, conjunctiva and cornea. Enucleation of eyeball- for removing eye ball completely in glaucoma, trauma, tumour etc. Evisceration of eye ball- Removal of intraocular tissues leaving sclera and cornea and insert artificial eye (silicone) Ankyloblepharon-Fusion of upper and lower eye lids (Normal in dogs for 10 to 15 days of life) Ophthalmic neonatorum-Fused eyelids appear swollen with exudates due to Staph. Infection. Blepharospasms-contraction of orbicularis oculi muscle in response to stimulation of trigeminal nerve- keratitis, foreign body, conjunctivitis, ectropion Trichiasis-Hair touching cornea and conjunctiva-entropion, dermoid. Distichiasis- cilia originates from abnormally located follicle, inherited in Boxer Alsatian cocker Spanial sheep dog Hordeolum- localized suppurative inflammation of lid adenoidal adenexaStaphylococcus infection External Hordeolum- (Stye)- involves glands of zeis and moll Internal Hordeolum-(Chalazion)- involves meibmian glands, localized on conjunctiva surface of eye lids Orbital cellulitis-Frontal sinusitis, foreign bodies. Signs are oedema of conjunctiva, fever, prolapse of 3rd eyelid, exophthalmia Keratoconjunctivitis sicca (Dry Eye Disease) -Deficiency of tears by lachrymal glands and glands of nictitaing membrane (in dogs only). Average Schirmar tear wetting per minute 206 mm but in this disease the values are 0-5 mm per minute. 0.5% Rose Bengal dye can detect devitalized epithelium of cornea and conjunctiva and seen by slit lamp biomicroscopy. The signs are pain, ulcers, conjunctivitis, blepharospasm, hyperaemia of conjunctiva and nictitaing

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membrane, staphyloma, iridocylitis, aqueous flare, hypopyon and corneal vascularization and finally blindness and thick cionjunctiva. May be cuased by trauma, canine distemper, drug toxicity, inheritable, congenital. Prognosis is grave. Treated by artificial tear (Methyl cellulose), pilocarpine twice acrymal daily (stimulate tears). In chronic cases parotid duct transposition technique is adopted and flaps of nictitating membrane or conjunctiva over cornea. Affections of Conjunctiva: Chemosis: common condition. Edematous swelling of bulbar conjunctiva. Chronic Conjunctivitis: Cauterization with 1-2% silver nitrate followed by normal saline irrigation. Follicular Conjunctivitis (Trachoma): Enlargement of follicles of conjunctiva and 3rd eyelid. May lead to corneal ulcer. Use beta ray therapy or copper sulphate cautery or surgical removal. Parasitic Conjunctivitis: Thelazia, Californiensis in conjunctival sac, under 3rd eye lid, lachrymal duct, cornea. Other parasites Habronema, Onchocerca. Mycotic Conjunctivitis: Nystatin eye ointment b.i.d. for 4 weeks. Pterygium: - Growth of conjunctiva extending towards cornea. Tumours: - Viral pappiloma, hemangioma, melanoma, squamous cell carcinoma and dermoid cyst. Duct Obstruction and dacrocystitis -Epiphora-Excessive flow of tears due to conjunctivitis, stricture of lacrymal duct, dacrocystitis (inflammation of lacrymal sac). F lush out the NLD with 22-25 gauge needle and normal saline solution. Glaucoma-Leading cause of blindness in dogs. If not treated immediately lead to irreversible blindness. Increased intraocular pressure due to lens displacement, synechia, cataract, tumours, secondary to intraocular inflammation, iridocorneal angle closure due to uveitis, congenital glaucoma in Cocker Spanial. Signs-Cloudy cornea, dilated pupil, congestion of vessels in conjunctiva, blindness, thinning of retina causing hyperreflectivity. Treatment-Carbonic anhydrase inhibitors, mannitol (20%) 1-2 gm/kg IV in 20 minutes, pilocarpine (2-4%) but not recommended in animals with uveitis. Generally surgical procedures are adopted since majority not controlled by medication surgical treatment is recommended for all blind and painful eyes-Ciliary body ablation is done with laser beam. Intravitreal injection of gentamicin causes reduced aq. humour production. Uveitis-Inflammation of iris and ciliary body resulting into anterior. & posterior Uveitis. Signs- Miosis, corneal neovascularisation, aqueous flare, hyphema, hypopyon, hyperaemia of conjunctiva, epiphora, blepharospasm, photophobia, cataract, glaucoma, retinal oedema, vitreal debris, decreased vision. Causes- Distemper, herpes, toxocara, hypertension, lens rupture, fungal, lyme disease, leptospira, brucella, toxoplasma, septecaemia, tumours. Treatment- Hydrocortisones, atropine, to alleviate pain secondary to spasms of ciliary bodies, aspirin (10 mg/kg), and antimicrobial drugs.

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Corneal Ulcer-Complications-Corneal fistula, synechia, staphyloma (Iris out), keratocele, (protrusion of descemet membrane), corneal opacity. TreatmentConjunctival flap over cornea indicated. Corneal Opacity (Ulcerative Keratitis)-Most common, painful, blepharospasm. It can be diagnosed by fluorescein. Fluorescein does not stain the epithelium but if is broken the dye will enter stromal intercellar spaces surrounding the defects. It can be caused by infection, bum, foreign body, trauma, keratoconjunctivitis, sicca (Dry eye disease). Treatment-Corticosteroids are not to be used as they enhance the collagenase activity by 11 times which further aggravate the condition but antibiotics like chloramphenicol, sulphacetamide, gentamicin, and benzyl penicillin are indicated. Keratectomy may be indicated. Superficial Punctuate Keratitis- Circular large coarse white opacity in cornea seen in poodle, German Shepherd breeds of dogs. May be associated with long standing keratoconjunctivitis. Treatment is not specific. Chronic Superficial Keratitis: - (Degenerative Pannus) -Common in dogs with no definite cause, may be due to hypersensitivity reactions. Treated by dexamethsone 34 times a day for 4-7 days. Treatment may be continued for 3-4 weeks. Entropion: - Inversion of eyelid margins. Treated by Hotzcelsus technique. Ectropion: - Eversion of lower eyelids. Treated by 'V -Y' blepharoplasty. Cataract: - Opacity of lens. Congenital. Acquired-(Diabetic, distemper, old age, bacterial parasites in anterior chamber. Treatment -1. Surgical, extra capsular technique is preferred, and with hyper mature lens intracapsular technique is preferred. Advantage of extracapsular technique is the posterior lens capsule remains intact which remains attached to anterior hyloid membrane (Absent in humans, so technique not preferred). 2. Phacoemulsification- High frequency vibration to break lens into smaller fragments and aspirated from anterior chamber through suction. Complications- Iridocyclitis, corn~al edema, uveitis, secondary glaucoma, bacterial endophthalmitis. Retinal Degeneration (Atrophy): - can be diagnosed by indirect ophthalmoscopy. Hereditary. Degenerative-Old age, diabetes, glaucoma, deficiencies, Toxoplasmosis, canine distemper. Signs - Pupil dilated, reacts sluggishly to light, Blood Vessel fine and thread like, optic disc becomes pale, increase palpebral reflectivity, total blindness. Other affections are optic nerve edema and atrophy, optic neuritis (papillitis), tumors of optic nerve. Diseases like hypertension, aging, canine distemper also lead to retinal atrophy. No treatment possible. Retinal Detachment: - Due to diseases, tumours, parasites, vitreous loss, lens displacement, poisoning, uraemia, toxicity due to chloroquine, hypertension etc. Prognosis is grave.

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Vitreous Humour Affections: - Degenerative, opacity, abscess, haemorrhage. Opacity is due to haemorrhage and synchysis scintillans (Old age), cholesterol crystals are present, vision impairment, may lead to lens subluxation and retinal detachment. Astroid Hyalitis: - Solid bodies suspended in vitreous humour. Ocular Manifestation of Systemic Diseases Canine distemper-(retinal degeneration, keratitis, ulcer, dry eye disease, and conjunctivitis). Infectious canine hepatitis- (uveitis). Leptospirosis, fungal infections, Cryptococcus (hyphema and retinitis), blastomycosis (retinal detachment and uveitis), coccidiodidomycosis (keratitis), chlamydial and mycoplsma leading to conjunctivitis, heart worm larvae in anterior chamber (uveitis), Ehrlichiosis, diabetes (retinal degeneration and cataract. Affections of Ear External ear: Otitis externa Middle ear (Tympanic cavity): Otitis media Internal ear (Labyrinth) Aural Haematoma Ear lacerations Tumours / polyps Congenital anomalies: Anotia, microtia, dystopic ear Otitis Externa

Common condition, 15% incidence .Inflammation of external auditory canal: ear mites, fungus (Malassezia dermatitis-Yeast), FB, bacterial Signs: Lumen blocked, ulcerated epithelium, copious secretions from glands, debris in the meatus of the ear Otoscope for examination Treatment Antibacterial agents and flushing of ear canal Surgical, if no response then Zepp operation is done For congenital atresia, ulceration/proliferation ablation of ear canal may be undertaken for tumour removal

Otitis Media Most common Chronic inflammation of pharynx, tonsils Bacterail and fungal infectioin, allergy, perforation of tympanic membrane Polyps in cats Tumours of pharynx and tonsils resulting in obstruction of Eustachian tubes Tumours (Adenoma, papilloma, carcinoma, histiocytoma, basal cell tumour Signs: Head sacking affected ear tilted discharge, loss of hearing, facial paralysis, Horner syndrome (Miosis, ptosis, enophthalamitis, protrusion of 3rd eye lid, limited jaw opening due to pain. Diagnosis: History, oral cavity examination, CT scan of tympanic bulla, hearing loss asessment Treatment: Ear cleaning, antibiotics, antifungal agents,

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Surgical treatment: Bulla oesteotomy for drainage 90% successful Otitis Interna Infectious, non-infectious (Trauma, tumours, hypothyroidism, antibiotic toxicity (Degeneration of auditory receptors), polyneuropathy, head trauma Signs: Loss of balance, tilt head, rolling toward the side of lesion, hearing loss, vomition, nystagmus Diagnosis: Radiography of bulla/pterous temoral bone, otoscopic examination and cytological examination Difficult to treat

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COMMON SURGICAL AFFECTIONS OF GI TRACT AND THEIR MANAGEMENT

S.M. Behl Department of Veterinary Surgery & Radiology CCS Haryana Agricultural University, Hisar -125 004 Gastric foreign bodies: Gastric foreign bodies are found in dogs and cats of all breeds and ages. The incidence may be high as animal consume foreign bodies like rubber ball, bone pieces, mango seeds etc. Clinical signs: Most characteristic sign is vomiting, it is intermittent because the vomiting reflex is only triggered when foreign body is located in pyloric antrum. If foreign bodies located in the fundus of the stomach, than there are no vomiting. If they are lodged in the pyloric portion, gastric emptying may be impaired. Cannot be detected on abdominal palpation. Laboratory findings: There may be dehydration and electrolyte and acid base imbalances -most common abnormalities metabolic acidosis, but hypokalemic alkalosis may occur with pyloric obstruction. Diagnosis: Gastric foreign bodies are diagnosed by radiographic finding. Plain radiograph is adequate in diagnosing radiopaque foreign bodies. Radiolucent foreign bodies can not be diagnosed on radiography. Increased width of a localized portion of stomach may indicate presence of foreign bodies. Barium meal studies may be helpful in diagnosing foreign bodies. Gastrotomy: Gastrotomy is most common procedure for removing foreign bodies. The patient should be evaluated for fluid and electrolyte imbalances, these should be corrected before operation. Following is the surgical procedure: The operation is done under general anaesthesia. After preparing the animal for aseptic surgery, the dog is placed on dorsal recumbency. Ventral midline incision extending from the xiphoid to umblicus given to enter the abdomen. The stomach is grossly inspected and is exteriorized from the abdominal cavity. Stomach is walled off with moist drapes to prevent spilling of gastric contents into the abdomen.

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The incision is given on the relatively less vascular area, on the ventral aspect of the stomach between lesser and greater curvatures. After removing the foreign bodies, the stomach is closed in two layers. The first layer consists of cushing pattern and second layer is lambert pattern using 2/0 or 3/0 chromic catgut. Then abdominal cavity is closed in routine manner Post operative care: Feed and water is with held for next 24 hrs. during that period fluid therapy is given intravenously. Soft diet can be started for second or third day onwards. Chronic gastric outflow obstruction: Gastric outflow obstruction results due to antral polyps, neoplasia and pyloric stenosis. Pyloric stenosis may be acquired or congenital usually results from hypertrophy of the pyloric sphincter muscles or hypertrophied mucosal folds after chronic gastritis. Signs: History of chronic vomiting. Projectile vomiting typically does not occur in most cases of outflow obstruction. Unless pyloric obstruction is complete. If mucosal ulceration occurs, the vomitus may contain blood. Chronic vomiting may cause electrolyte and acid base imbalance. Prerenal azotemia, , hypochloraemia, metabolic alkalosis or acidosis, anaemia and dehydration may occurs. Diagnosis: on the basis History, signalment Radiography provide the most definitive diagnosis. Plain radiograph may demonstrate a normal to markedly distended fluid filled stomach with caudal extent ion of gastric fundus and body and increased diameter of pyloric lumen. Delayed gastric emptying, pyloric intralumal filling deficits and thickening of pylorus and radiographic signs. Pyloromyotomy: This is done to increase the diameter of the lumen Patient is placed on dorsal recumbency and a ventral incision is given extenting for xyphoid to umblicus to enter the abdominal cavity. The stomach and pylorus are then exteriorised through the incision. Then approximately 5 cm long incision is given on the least vascular area of the pyloric canal, pylorus and proximal duodenum. The pylorus is mid point of the incision. This incision extends through the tunica serosa and muscle layer. Then muscle layer is cut and seprated with blunt dissection, care is taken not to cut the mucosa.

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Gastric dilation-volvulus syndrome: It occurs most commonly in large breeds and also reported in small breeds. Mostly present in older dogs. It occurs secondary to gastric distention and malpositioning. Pathophysiology: This syndrome is usually initiated by gastric accumulation of gas, fluid, or both with some degree of functional or mechanical obstruction to gastric outflow. Aerophagia is most likely source of gas accumulation. Bacterial fermention of carbohydrate, gas production form gastric acid- bicarbonate reaction also contributes towards gas accumulation. Fluid components of gastric contents is a combination of ingesta, gastric secretion and transudate for venous obstruction As gastric dilation progress, the normal means of relief, such as eructation, vomiting or pyloric emptying fail to occur. Gastric dilation usually precedes volvulus of the stomach. Progressive dilation of stomach may allow simple dilation to progress to gastric volvulus. A clockwise: or counter clockwise rotation of the stomach occurs. Common in clockwise rotation (when viewed dog in dorsal recumbency), maximum amount of rotation that can occur is between 270-360. The degree of rotation is determined by the shift in the normal axis of the pylorus and cardia on the sagital plane. Counter clockwise rotation of the stomach is rare. The maximum amount of rotation that occurs is 90. In this type of malpositioning, the pylorus and antrum displace dorsally along the right abdominal wall, locating adjacent to the oesophagus. Clinical signs: Dog with this syndrome has a progressively distended and tympanic cranial abdomen, non productive retching, hypersalivation, restlessness, depression. Hypovolemic shock, pale mucous membrane. Abdominal palpation reveal various degree of gastric distention and splenomegaly. Partial or chronic gastric gilationvolvulus syndrome infrequently occurs but should be considered in large dogs prevented with history of intermittent vomiting, anorexia and weight less, gastric dilation is not a consistent feature associated with this aspect of the syndrome. Diagnosis: Based on radiographic evaluation and clinical signs: The right lateral survey abdominal radiograph is best view to confirm the diagnosis of GOV. The radiographic sign of GDV includes a large, distended stomach, the pylorus located cranial or dorsal to the stomach, a tissue density line dividing the gas filled stomach into compartment, splenomegaly and splenic malposition. The most significant finding is a gas filled pylorus located dorsal to the fundus of the stomach. Preoperative care: The initial treatment is gastric decompression and therapy for shock to increase the venous return to the heart, which increases cardiac output and tissue perfusion.

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Gastric decompression: Gastric decompression can be accomplished by: Needle trocarizaiton, 18G needle is thrust percutaneously through the patient's right or left abdominal wall, at the point of greater distention and into stomach lumen. The stomach wall is against the body wall and other viscera have been displaced, therefore, risk of injuring other tissues is minimal. 2-4 needles can be inserted. Other method is to pass the stomach tube. Lubricated stomach tube is passed down the oesophagus and into the stomach. Passage of stomach tube into stomach is difficult in case of GDV of higher rotation. Surgical treatment: Surgical treatment has three main goals: Correction of gastric malposition, assessment of gastric and splenic ischemic injury and prevention of recurrence by permanent fixation of the stomach to the abdominal wall. The dog is positioned in dorsal recumbency and a ventral midline incision is made from the xiphoid cartilage to a point between the umbilicus and pubis. If necessary, a large bore 15 or 16 gauge needle can be used to remove air and fluid. Reporitioning can generafly be performed without empting the stomach via a gastrotomy. After decompression, the stomach is repositioned. The pylorus and greater curvature are identified exteriosed through the incision. Then the fundus is pushed into the abdominal cavity. Gastropexy: to prevent the recurrence the pylorus antral region is fixed to right abdominal wall. Intestinal obstruction: Obstruction of the intestinal lumen may occur with foreign bodies, intussciption, neoplane and less commonly adhesions. Intraluminal intestinal haematoma causing obstruction has been reported in dogs. Clinical signs: Nature and site of the obstruction influence the clinical signs. An object lodged in the proximal small intestine stimulates vomiting, with loss of acid from the stomach and alkalifle secretions from gall bladder, pancreas and duodenum. Dehydration and electrolyte imbalance can be expected. Animal that are vomiting may have either normal pH or primary metabolic acidosis. Primary metabolic acidosis is probably due to relatively greater loss of base fluids from duodenal, pencreatic and bile secretions than that of acid from gastric juice during vomiting. Primary metabolic acidosis may also occur in animal with severe dehydration and inadequate perfusion of splanchic viscera, skin, and muscle. Obstruction of the distal jejumum or ileum may not stimulate vomiting but result in distention of the intestinal lumen with fluid and gas. This originate from three sources: > swallowed atmospheric air (approximate 70 %), > decomposition of intestinal contents (10%) and > diffusion from blood into the intestinal lumen (20%).

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Strangulation of the intestine can be produced by incarceration on the neck of hernial sac or by twisting of the mesentry. The mesenteric circulation is blocked, and tissue necrosis follows. The necrotic area allows bacteria and their products to pass into peritoneal cavity and the systemic circulation. The strangulated segment is purple to black, foul smelling and friable. In strangulation there is severe abdominal pain, a severe systemic reaction, often including shock that is out of proportion to that with intestinal obstruction and poor response to supportive therapy. The clinical course of strangulation obstruction depends on the degree and extent of vascular obstruction, volume of blood lost, and proliferation and absorption of bacteria and toxinis. Causes death is it not promptly corrected. Pressure produced by a foreign body or intussception may cause venous stain and oedma followed by disruption of arterial and necrosis of the intestinal wall. Once the intestinal mucosa is damaged, the alimentary canal is no longer segregated from the systemic circulation. Bacterial products enter the systemic circulation and can produce endotoxic shock. Radiographic findings: Obstruction of the distal small intestine produces greater dilation with more accumulation of fluid and gas than does obstruction of the proximal small intestine. An additional standing lateral projection easily demonstrates gas fluid interfaces in dilated loops of obstructed small intestine. Radiopaque foreign bodies are easily identified. Contrast examination of small intestine permits confirmation of the diagnosis. Diagnosis: The diagnosis of foreign body obstruction is based on history, careful abdominal palpation and abdominal radiograph. Treatment: The treatment of foreign body obstruction is exploratory celiotomy. The abdomen is exposed by ventral midline abdominal incision of sufficient length to permit adequate inspection of the entire gastrointestinal tract. If the foreign body had not caused vascular obstruction of the intestinal wall, it is removed through an enterotomy distal to the foreign body and slightly over it. If the foreign body has caused necrosis of the intestinal wall or it visibility is in question, resection with end to end anastomosis is indicated. Intussusception: Intussusception is produced by a vigorous contraction that forces the intestine into the lumen of the adjacent relaxed segment. The components of an Intussusception include the invaginated section called the intussusceptum, and the enveloping segment called intussusceptions. The mesentery and blood supply to the intussusceptum are included in the invagination; venous obstruction can progress to arterial occlusions and necrosis. An Intussusception can progress, so that small intestine protrudes from the anus. Intussusception occurs most frequently in young animals, at ileocaecal junction.

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Signs: Signs are vomiting, abdominal pain, and passage of bloody mucoid stools and palpation of a sausage-shaped, minimally painful abdominal mass. Radiographic finding: Radiographic findings are similar to mechanical obstruction. Contrast radiography is usually necessary to differentiate an Intussusception from other cause of intestinal obstruction. Treatment: The treatment is exploratory celiotomy. The entire small and large intestine is carefully examined. An attempt can be made to reduce the Intussusception manually. One of following will occur. Can be successfully reduced The Intussusception cannot be reduced, or the intestines are not viable, resection and anastomosis are necessary. Small-intestinal anastomosis: Reconstruction of the intestinal tract after resection can apply to end to end, end to side, or side to side techniques. The side to side and end to side techniques are technically more demanding and more time consuming, involve two or three more suture lines and do not reconstruct the intestinal tract in a physiological fashion. Although used in other alimentary tract procedures, a side to side or end to side technique has no advantages over an end to end anastomosis for the small intestine. Technique for anastomosis: The intestines are exposed by a ventral midline abdominal incision of sufficient length to examine the entire length of the intestine. The procedure of choice is end to end anastomosis. The segment of intestine to be removed is selected after the vascularity of the intestine is assessed. The jejunal branch of the cranial mesenteric artery that supplies the segment of intestine are doubly ligated with 3-0 chromic catgut. A space between the ligatures is left for transaction. Intestinal clamps are placed across the intestine at the terminal arcade ligature adjacent to the diseased segment. Before there clamps are placed, the intestinal clamps are milked away from the resection site. The intestine is transected with a scalpel blade, using the crushing clamps, as guide line. The mesentery is transected with scissors, between each pair of ligatures on the jujunal artery branches. A simple continuous suture pattern is started adjacent to the mesenteric border, the mesenteric border is sutured and the pattern is continued around the circumference of the intestines. Using simple interrupted sutures, the first two sutures are placed at the mesenteric and antimesentric borders. Mild traction is applied to there two sutures, the edges are aligned and additional sutures are placed. Sutures are placed approximately 2 to 3 mm from the cut surface and 3 to 4 mm apart. The sutures are passed through the wall to penetrate the submucosa avoiding the mucosa, with appositional tension only. The anastomosis is inspected and gaps or excess mucosal eversion is corrected by placement of additional sutures. The anastomosis is washed with warm saline and wrapped with oruentum. The abdominal cavity is closed in routine manner.

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Anal and Rectal Prolapse: It occurs secondary to tenesmus resulting from urogenital or anorectal disease. Can occur at any disease in any breed of animal? Predisposing factors or disease causing rectal prolapse include cystitis dystocia, prostatitis, perineal hernia, prostatic hypertrophy colitis, rectal foreign bodies, proctitis, rectal or anal tumour, urolithiasis and post operative tenesmus following perineal or urogenital surgery. Clinical signs: With anal (partial) prolapse, only the mucosa protrudes from anal opening. In rectal (complete) prolapse, a double layer invagination of the rectum protrudes through the anal canal. The prolapsed mass is cylindrical with a luminal opening at the end. Treatment: The prolapse is treated depending on tissue viability and the number of previous recurrences. In animal with normal viability the mucosal surface is gently cleaned using warm isotonic solution. Massage reduces the swelling of the prolapsed mass. Using general anaesthesia or epidural anaesthesia the prolapse is reduced and a purse-string suture is places at the anocutaenous line using non absorbable suture material. The canal sacs and ducts are avoided. The purse-string suture is loosely tied, allowing insertion of a lubricating finger generally and soft faeces can pass through the opening. A liquid diet is given and laxative is also given. The purse string suture is left in place for 3 to 5 days. In animals that have viable tissue and in which manual reduction of the prolapse is difficult or after two to three unsuccessful attempts at treating the prolapse with a purse string suture, an abdominal colopexy should be performed. Colopexy: Routine caudal mid line celiotomy is performed and the prolapse manually reduced by applying traction on the colon. Once the prolapse is reduced, several sutures 1 to 2 cm apart in a single or double row are placed into seromusclac wall of the descending colon and the transverse abdominal wall. Rectal amputation: When the prolapsed segment is devitalized, necrotic or severely traumatized amputation and rectal anastomosis are performed. General and epidural anaesthesia is used. The animal is placed in sternal recumbency. Stay sutures are placed full thickness through all layers of the prolapse to help prevent retraction of the cut ends of the rectum and to aid in suture placement. The prolapsed tissue is resected 1 to 2 cm distal to the anus. A simple interrupted suture pattern in a single or double layer can be performed using absorbable 2-0 or 3-0 suture material. Complication after surgery includes dehiscence, leakage and stricture formation. Perianal fistulation: Perianal fistula or anal furunculosis is characterized by multiple chronic, ulcerating or fistulous tracts involving the peritoneal region. The exact cause of perianal fistualiton is unknown.

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Clinical signs: Dogs with perianal fistula have a history of dyschezia, haematohezia, conslipation, mucopurulent discharge, pain associated with elevation of the tail, excessive licking of the perianal region. Examination of area revealed multiple clraining ulcers, sinuses or fistula with formation of granulation tissue. Groove director is used to determine the extent and depth of each tract and degree of communications. Fistulous tracts from anal sac disease are few and communicate directly with the anal sac. Surgical excision of perianal fistulas is one of the more favorable methods for treating the disease. The main objective of this technique is to excise all diseased tissue while preserving as much of the external anal sphincter as possible. After excision of all diseased tissue, the wound is thoroughly lavaged with isotonic fluid. This may be allowed to heal by second intention or closed primary. In severe cases with multiple sinuses and fistulas involving the anus and external anal sphincter, partial or complete excision of the anus and sphincter may be required (i.e. partial or complete anoplasty). Post operative complication associated with surgical excision include fecal maintenance, flatulence, tenesmus diarrhoea, incisional dehiscence, constipation and stenosis and recurrence of disease. Anal sac disease: Diseases of the anal sac occur frequently in dogs and infrequently in cats. Disorders of the anal sac include impaction, sacculitis, abscesses and neoplesia. Diagnosis: Non-neoplastic and sac disease consists of three type, impaction, sacculitis and abscesses. Clinical signs: The characteristics signs of anal sac impaction or infection include frequent dragging or rubbing of the anus on the ground or carpet. The affected animal often persistently licks or bits at the anus, tail base, or skin on the side of the peritoneum, resulting in acute moist dermatitis. Treatment: The treatment for anal sac disease depends on the type of disease. Anal sac impaction and acute anal sacculitis are often treated conservatively. Recurrent episodes of severe impaction, and sacculitis, abscesses and anal sac adenocarcinouma are indication for anal sacculectomy. Analsacculectomy: Before surgical excision of an infected anal sac, the infection is treated medically. If surgery is performed during the acute inflammatory state, excessive friability of the anal sac may be encountered, resulting in incomplete removal of the anal sac and bacterial contamination of surrounding tissues. Surgical techniques for anal sac excision are closed or open. The closed technique is performed by making a vertical incision over the anal sac and bluntly dissecting the sphincter muscle until the sac in reached.

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The open technique for anal sacculectomy is easy and quick to perfQrm. This technique permits exposure of the secretory lining of the anal sac and helps ensure complete anal sac and duct removal. Post operative complications: Careful surgical technique is necessary to prevent complications, including faecal incontinence, chronic draining tracts, tenesmus and dyschezia. Chronic draining tracts following anal sacculectonJies result from incomplete excision of the mucosal lining of the anal sac or its duct. Rectocutaenous fistula: They are tract between rectum and skin surrounding the anus usually in the distal rectum. They are caused by external trauma such as a bite wound or a penetrating object, internal trauma secondary to a fractured pelvis or a rectal foreign body. Pararectal abscesses or ruptured anal sac can evolve to rectocutaneous fistulas. Diagnosis: The primary sign of rectocutaneous fistula is the presence of fecaJ material passing through the anus and the pararectal wound. Treatment: Surgical treatment involves placing tissue forceps into the rectum via the anus and grasping the rectal wall at the cranial edge of the wound. The rectal wall at the cranial edge of the wound is gently undermined sufficiently to retract it. The mucocutaneous junction without tension. The mucus membrane between mucocutaneous junction of the anus and the caudal border of the fistula is excised to provide a vascular base to the transposed rectal wall, and the cranial edge of the fistula is sutured to the mucocutaneous junction of the anus with non-absorbable sutures. The fistula resolves spontaneously once the rectal defect is eliminated.

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Surgical Conditions of Uro-Genital System in Dogs

Dr. PREM SINGH Department of Veterinary Surgery and Radiology C.O.V.S., C.C.S. H.A.U., Hisar. Indications for surgery of urogenital system in pet animals are relatively high. The surgical intervention is mainly required for cases of obstructive urolithiasis, tumourous growths (venereal granuloma) and to make the animal sterile (spaying and castration). In canine, the kidneys are smooth surfaced and bean shaped. The right kidney is placed below the last rib up to 2nd or 3rd lumbar transverse process. The position of left kidney is variable (2nd, 3rd and 4th lumbar vertebrae). The blood is supplied to the kidney is directly from aorta by the renal artery and leaves the kidney via renal vein which empties directly into the caudal vena cava. The kidney receives its nerve supply from the vagus and splanchic nerve via coeliac ganglion. The kidneys regulate the internal environment through 3 processes, the renal filtration, selective resorption and excretion of waste and foreign substances. The passage for urine from urinary bladder to external meatus is straight. The straightness of the urethra is maintained by two paired bones in the penis and the penis is known as ospenis. The kidney may suffer from congenital or acquired anomalies. a) The congenital anomalies may be: Agenesis of kidney, hypoplasia of kidney and fusion of kidney. b) The acquired anomalies may be: 1) Renal cyst (Retention cyst) The renal cyst is globular in outline with smooth border and can be diagnosed by radiography. Sometimes they are small and multiple. 2) Renal abscess (Pyelonephritis) Renal infection is caused by corynebacterium. This pyogenic bacterium is carried to the kidney by the blood stream. Some renal abscesses are sequelae to trauma and may be the result of renal haematoma. Clinically, there will be Fever, Hematuria, Leacocytosis, Kyphosis and Bacterimia. Treatment will include Nephrectomy combined with chemotherapy. 3) Hydronephrosis It is due to obstruction of outflow of urine by stone etc. Urine stoppage result in dilatation of the urinary tract including kidney and the kidney will become enlarged due to backflow of urine. Treatment is made by removal of the cause. 4) Renal tumour Main renal tumours are carcinoma, sarcoma and nephroblastoma.Because of its rich blood supply; the kidney is site for metastatic tumours. 5) Renal parasite The giant kidney worm is Dictiophyma renale.

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Diagnosis is made by clinical symptoms, radiography and ultrasound. Treatment of all these conditions is usually done by nephrectomy. After filtration, the urine will be stored in urinary bladder through ureter and voided through urethra. Any obstruction will affect the outflow of the urine. Most common causes of obstruction are calculi formation and enlargement of prostate gland. The calculi can lodge in kidney, ureter, urinary bladder and urethra and can affect any age group, but enlargement of prostate is seen mostly in old age group. The prostate gland surrounds the neck of urinary bladder. This gland is not essential for life or fertility. It secretes fluid which adds to the volume of semen. Its hyperplasia will put pressure over the urethra. Other causes of obstruction of urine flow can be infection of urinary tract and pressure from external growth. Obstructive urolithiasis; Most of the time nidus for stone formation starts in the kidney followed by its mineralization. Small concretions are flushed through urethra along with urine. When the size become large, they get lodged in ki-dney (nephrolith), ureter, urinary bladder (cystolith) or urethra. The causes of urinary calculi are obscure. Many theories concerning the cause have been documented. Bacterial infection and vitamin A deficiency may contribute to the formation of nidus. Feed and water rich in mineral will promote the mineralization of nidus. Most of the time clinical signs become evident, when the calculi get lodged anywhere in the urinary passage. The urinary calculi usually get lodged at the caudal end of the os-penis or get trapped in between the groove of the bones of the penis. Clinical signs: In cystolith, sometime no sign ofretension of urine. In nephrolith, signs of acute colic and hematuria. In urolith, urination either drop wise or complete stoppage. The dog will be reluctant to move prefer sitting. Acute abdomen. Attempt to pass a catheter usually unsuccessful.

Diagnosis by clinical symptom, radiography and ultrasonography. Line of treatment: Vitamin A is beneficial in prevention of disease. Change of urine pH is also very beneficial. Lithotrity i.e. crushing of stone by an instrument or by rays and flushed by normal saline back in urinary bladder. Standard method is of removal stone by surgical intervention. For nephrolith, Kidney is exposed and calculus is removed toward renal pelvis by giving a short nick.

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 For cystolith, Urinary bladder is exposed through mid line incision. Stay sutures are applied and bladder is punctured. The cystotomy incision is closed by Lambert or lock stitch using chromic cat gut number 1. For urolith, a sterile polyethylene catheter can be placed to know the location of the calculi. An incision is given over the calculi to expose it and take it out. When catheter reaches to the urinary bladder and urine start coming out it indicates clearance of urethra. Urethra is sutured by lock stitch using 3/0 or4/0 chromic catgut. Urine can be collected and send for cultural examination and sensitivity testing. Post-operative care include adequate fluid, antibiotics, analgesics supplemented with urinary antiseptics, cystone etc. Management of urine pH is important because it affects the antimicrobial activity. Activity of amino glycoside gets increased in alkaline pH. Oral sodabicarb is used for alkalinisation of pH. Activity of tetracycline gets increased in acidic pH. Hexamine or ammonium chloride can be used as urine acidifier. MALE GENITAL SYSTEM The main components of the male genital system are testes, spermatic cord, and os-penis and prepuce. The penis is made up of 2 parts, the bulbous glandis and the pars longa gland is. The bulb consists of erectile tissue which also surrounds the os-penis and urethra. The blood supply to the penis is derived from the internal pudendal artery. The sensory nerve of the penis is the terminal branch of the pudendal nerve. Conditions of penis and prepuce: The condition can be congenital or acquired. The congenital lesions can be: 1) Hypospadiasis: This is a condition in which the external orifice of urethra is situated on the ventral aspect of the penis. The condition is usually not corrected in a dog. 2) Persistence of the penile frenulum: Connective band between skin and prepuce does not break and the penis get curvature on ventral side. The band is cut to make the penis straight. The acquired lesions can be: a) Traumatic injury: In male dog, the penis and prepuce are more prone to injuries resulting in prolapse of_mucosa of prepuce, hematoma of penis, phimosis, paraphimosis and priapism. 1) The Prolapse of mucosa of prepuce: The prolapse of mucosa can be corrected by reducing_it back and by applying purse string using silk no.! on the prepuce followed by douching with povidone-iodine and aqministration of antibiotics and non-steroidal anti-inflammatory drugs. When the inflammation get subsided and prolapsed mucosa get retained then the sutures can be removed. If penile hematoma also persists

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simultaneously then it can also be removed by surgical intervention before putting the prolapsed mucosa back in to the prepuce. 2) Phimosis: In this condition, the animal is unable to protrude the penis from the preputial orifice. The preputial stenosis can be dilated by cross section and stenosed mucosa is also incised to dilate it and some lubricant jelly is infused to facilitate easy protrusion of penis. 3) Paraphimosis: In this condition, the protruded penis can not be retracted into the preputial sheath. The protruded_penis will become swollen and oedematous. The oedema of the penis can be reduced_by application of cold and anti-inflammatory antibiotic cream. A longitudinal incision is made over the tight constricted band to relea~e the pressure and to separate the penis. The lubricatants are applied and the penis is retracted in to the preputial sheath. 4) Priapism: This term refer to persistent erection of the penis without sexual excitement. The priapism usually follows urethritis, constipation and lesion of the spinal cord. b) The tumour of the Prepuce and Penis: The most common tumour of prepuce and penis is canine transmissible venereal tumour. It is known by different names such as venereal granuloma, infectitious sarcoma, canine. condyloma, contagious lympho sarcoma. As it is a contagious disease so incidence of this disease is higher in free roaming population of dogs. It is transmitted through coitus and mostly affects dogs of around one year of age. Females are observed to be more susceptible than males. Clinical signs: Constant bleeding from genitelia sometimes mixed with urine. The dog is in habit of licking the genitelia. Sometimes, there is a protrusion of red mass also when a forceful attempt is made for urination. Diagnosis: Diagnosis can easily make on the basis of history, clinical signs and cytologic findings. Treatment: 1) Surgical excision either alone or supplemented with autogenous vaccine. 3) Radiotherapy. 4) Chemotherapy i.e. Vincrystine sulphate is given @ 0.025mgs/kg b. w. intravenously at a weekly interval. 5) Episiotomy and spaying of female bitches. Conditions of testes and spermatic cord: The conditions of the testes may be congenital or acquired. The congenital anomalies include; anorchidism (absence of both testes), monorchidism (absence of one testes), cryptorchidism. The acquired conditions can be orchitis, tumours of testes (seminoma, sertoli cell tumours, and tumours of interstitial cells). Other conditions can be scrotal hernia and hydrocele etc. The operation carried out for all these conditions is castration. The other indication for this operation is to make the animal sterile. The spermatic cord is other structure upon which vasectomy is performed to make the animal docile. The structures comprising the spermatic cord are: vas deferens, lymph vessels, nerve, and arterypampiniform plexus and cremaster muscle. In vasectomy, vas-deferens are cut and ligated. FEMALE REPRODUCTIVE SYSTEM Diseases of the female reproductive system can also be divided into similar two categories: congenital and acquired. First part is diseases of vulva and vagina. Congenital anomalies include: Atresia of vagina. Stenosis of vagina. Persistent hymen. Anomalies associated with hermaphrodism, agenesis and double vagina.

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Acquired anomalies include: * Vulvitis, trauma, neoplasms, prolapse of vagina. Second part covers diseases of the uterus. Congenital abnormalities can be: * Agenesis of uterus. * Atresia of uterus * Hypoplasia of uterus. * Uterus unicornus. * Double cervix. Acquired abnormalities can be: - Trauma, prolapse of uterus and pyometra etc. Main operation carried out on female genital tract is OVARIOHYSTERECTOMY (spaying) which means complete removal of the uterus, uterine horns and the ovaries. Indications: 1) to make the animal sterile. 2) In cases of pyometra, metritis, salpingitis. 3) Ovarian tumours or cysts. 4) Mammary tumours. 5) To avoid recurrences of venereal tumours. Surgical method: Under general anesthesia, spaying can be carried out either through - Flank incision -Mid line incision. (Linea Alba) After opening of the abdomen, the genitelia can be removed by three clamp method or by ligation. Post-operative complications: 1) Hemorrhage 2) Peritonitis 3) Omental hernia 4) Evisceration 5) Recurrent estrus 6) Uterine stump pyometra.

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Management of Anaesthesia in Pet Animals

Ashok Kumar Department of Veterinary Surgery & Radiology CCSHAU, HISAR Selection of an anaesthetic is based on the patient's physical status and temperament, the type of procedure for which anesthesia is being considered, the anaesthetist's familiarity with the anesthetic drugs, the type of facility, and the available equipment and technical assistance. There is no single best method for anesthetizing dogs and cats, but familiarity with just one anesthetic technique limits the veterinarian's ability to perform the myriad surgical and diagnostic procedures commonly called for in a modem veterinary practice. Some breeds respond atypically to routine administration of an anaesthetic drug. For example, sighthounds are less tolerant to thiobarbiturate than comparably sized mixed- breed dogs. The one thing that should not vary among anesthetic procedures is the degree of monitoring vigilance. Early warning of an impending anesthetic emergency is the single most important factor for decreasing anesthetic related morbidity and mortality. PREANAESTHETIC CONSIDERATIONS The history and physical examination are the most important components of the preanaesthetic evaluation of small animals. Signalment Sighthounds are sensitive to barbiturates. Brachycephalic breeds have their associated airway problems and can present anaesthetic challenges. Toy breeds require special attention to maintenance of body heat. Furthermore, a toy breed requires a relatively greater drug dose per kilogram than does a giant breed. Generally, there is no sex-related difference in the response to anaesthesia. A history of the estrous cycle identifies recent estrus and its associated enlarged and vascularized uterus, which would cause concern for potential blood loss during an ovariohysterectomy. Age is an important consideration. Generally the very young (1 week) and the aged (> 80% of the expected life span) do not metabolize anaesthetic drugs as well as the young, healthy patient does. Healthy geriatric patients should receive sedatives, hypnotics, and tranquilizers at 15 to 30% of the dose given to a comparable young healthy animal. Geriatric dogs and cats should receive intravenous fluids perioperatively to maintain optimal perfusion of the vital organs. History In addition to questions concerning organ system function, the owner should be asked about any previous anaesthetic episodes and past and current medication history, including heartworm prophylaxis. The time since the last feeding should be noted. Physical Examination The preanaesthetic physical examination should be thorough, and all body systems should be considered. Any abnormality discovered or suggested by the medical history should be followed up with the appropriate laboratory test or other suitable

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diagnostic test. The assessment of the animal's temperament is critical. A vicious or aggressive dog requires a different approach to anaesthesia than does the quiet relaxed individual. Laboratory Evaluation Young healthy dogs require minimal laboratory tests, haemoglobin (Hb), packed cell volume (PCY) and plasma protein. Middle-aged to older animals should be checked for kidney functions by doing blood urea nitrogen and creatinine. Physical status of patients should be classified according to relative anaesthetic risk. A system of classification has been adapted from suggestions by the American Society of Anaesthesiologists (ASA). At physical stage I or II, patients are at less risk for anesthetic complications. At physical stage III through V, patients are at relatively greater anesthetic risk. This is not to imply, however, that stage I and II patients are at no risk of unanticipated anaesthetic mishaps. Anaesthetic Risk Anaesthesia is not a naturally occurring state and its induction with drugs which are never completely devoid of toxicity must constitute a threat to the life of the patient. This can be a major threat depending on the circumstances. The state of health of the animal: Animals presented for anaesthesia may be fit and healthy or suffering from disease; they may be presented for 'cold' surgery or as emergency cases needing immediate attention for obstetrical crises, intractable haemorrhage or thoracic injuries. In the US the American Society of Anesthesiologists has adopted a classification of physical status into categories, 'E' being added after number when the case is an emergency. Category I Category II Category III Category IV Category V Normal healthy patient with no detectable disease. Slight or moderate systemic disease causing no obvious incapacity Slight ot moderate systemic disease causing mild symptoms (e.g. moderate pyrexia, anaemia or hypovolaemia). Extreme systemic disease constituting a threat to life (e.g. toxaemia, uraemia, severe hypovolaemia, cardiac failure). Moribund or dying patients.

This is a useful classification but it is most important to appreciate that it refers only to the physical status of the patient and is not necessarily a classification of risk because additional factors such as its species, breed and temperament contribute to the risk involved for any particular animal. The influence of the surgeon: Inexperienced surgeons may take much longer to perform an operation and by rough technique produce intense and extensive trauma to tissues thereby causing a greater metabolic disturbance. Increased danger can also arise when the surgeon is working in the mouth or pharynx in such a way as to make the maintenance of a clear airway difficult, or is working on structures such as the eye or larynx and provoking autonomic reflexes.

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The influence of available facilities: Crises rising during anaesthesia are usually more easily overcome in a well equipped veterinary hospital than under the primitive conditions which may be encountered on farms. The influence of the anaesthetist: The competence, experience and judgment of the anaesthetist have a profound bearing on the degree of risk to which the patient is exposed. Familiarity with anaesthetic techniques leads to greater efficiency and the art of anaesthetic administration is developed only with experience. Patient Preparation Fasting: Healthy dogs and cats should receive no food for at least 6 h before being anaesthetized. Water should be allowed free choice until just before anesthesia. Dogs and cats younger than 8 weeks of age and those weighing < 2 kg should not fast longer than 1 or 2 h. They should also receive intravenous fluids containing dextrose during any prolonged anaesthesia (> 15 min). Patient Stabilization: When possible, life-threatening disturbances should be corrected before administering anaesthesia. Venous Access: Advantages of having an intravenous catheter in place include the following: Tissue-toxic drugs, such as the thiobarbiturates, can be administered without perivascular administration. Intravenous fluid administration is facilitated. The circulation is immediately accessible for administration of emergency drugs. The most common site for catheter insertion is the cephalic vein. The lateral and medial saphenous veins are also easily accessible. The jugular vein can also be used. Intravenous Fluids: The purpose of preanaesthetic administration of intravenous fluids is to maintain vascular volume, which is decreased as a result of anaesthetic drugs, blood loss, and insensible fluid loss. For routine use, a balanced electrolyte solution such as lactated Ringer's solution is most suitable, because most fluid loss during anaesthesia is isotonic. The patient's disease process may warrant the use of other fluids, such as normal saline, fluids containing dextrose, or a colloid solution (e.g., whole blood, plasma, or a plasma expander). Several styles of fluid administration sets are available. An administration set with a 10 or 15 drop/mL drip chamber is most convenient for patients weighing> 5 kg. For smaller patients, a 60 drop/mL drip chamber allows a more precise estimation of proper fluid rate. It is convenient to calculate the number of drops per minute necessary to deliver the calculated hourly fluid amount. A danger of perioperative fluid administration to very small animals is inadvertently administering too much fluid by improperly adjusting the drip rate. This problem can be minimized by attaching a measured volume administration set to the fluid line. The Anaesthetic Plan: The anaesthetic technique chosen depends upon a variety of considerations. Some of the more commonly used techniques include the following: 1. Local anaesthesia is usually accompanied by mild to strong sedation and is used more frequently in dogs than in cats. The techniques most commonly used are lumbosacral epidural block, local infiltration or linear block.

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2. Injectable anaesthesia may be induced by either the intramuscular or intravenous routes. The intramuscular route is often used with opioids, ketamine, and benzodiazepines. The thiobarbiturates and propofolare always given intravenously. 3. Inhalation anaesthesia is usually initiated after induction of injectable anesthetics but may be administered from an induction chamber or by use of a face mask. 4. For procedures < 15 min in duration, the following methods can be used: a. The thiobarbiturates are relatively inexpensive and are suitable for short-term restraint of most healthy dogs and cats. The disadvantage of their use is that full recovery usually takes up to 1 h and can be associated with ataxia and disorientation. These effects are reduced when the thiobarbiturate is preceded by a tranquilizer, such as acepromazine. Another disadvantage is that they must be administered intravenously, a problem with fractious or uncooperative animals. b. Alternatives to the thiobarbiturates include propofol, etomidate, and the combination of diazepam and ketamine. These drugs are more expensive than the thiobarbiturates; and the duration after one bolus dose is shorter, generally < 10 min. preceding these drugs with a sedative or tranquilizer such as acepromazine, xylazine, or diazepam decreases the dose and improves the quality of recovery. c. Neuroleptanalgesic combinations are suitable for short-term restraint for mildly invasive procedures or for procedures not requiring general anaesthesia. An advantage is that one or both components of neuroleptanalgesia are reversible, allowing rapid return to preanaesthetic mentation. d. The relatively cumbersome nature of inhalation anaesthesia makes it less suitable for very short procedures. The rapid induction and recovery associated with isoflurane, however, make it the most suitable of the approved inhalants for short-term restraint. 5. For procedures between 15 and 60 min (intermediate duration), the drugs described above can be used; and re-dosed to effect. Typically, one-third to onehalf the original dose is administered to prolong the anaesthetic effect. The thiobarbiturates should not be repeatedly re-dosed, however. Although their initial duration of action primarily depends on redistribution away from the brain to other tissues, such as muscle, when the tissues are saturated, metabolism is ultimately responsible for awakening. Again inhalation anaesthesia is also appropriate for procedures of intermediate duration. 6. Procedures> 1hour (long duration) are best managed with inhalation anaesthesia. Awakening from halothane and isoflurane anesthesia is predictably rapid. Even sick and debilitated patients recover from prolonged periods of inhalational anaesthesia relatively quickly. Premedication Inhalation anaesthesia can be initiated without premedication; however, premedication with a sedative, tranquilizer, or other injectable drug is recommended. Preanaesthetic drugs aid in restraint, reduce apprehension, decrease the quantity of potentially more dangerous drugs used to produce general anaesthesia, facilitate

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induction, enhance analgesia, and reduce autonomic reflex activity. Drugs for premedication are usually administered intramuscularly or subcutaneously 15 to 20 minutes before induction. The choice of premedication depends on species, temperament, physical stage, the procedure to be performed, and clinician's preference. For procedures associated with significant postoperative pain, premedication should include an analgesic such as an opioid or alpha2-agonist. When analgesia is provided before initiation of a painful stimulus (pre-emptive analgesia), need for postoperative analgesics is lessened. Tranquilizers and Sedatives Drug Acepromazine Xylazine Medetomidine Dosage (mg/kg) 0.025 0.2; i.v./i.m. 0.3 2.2; i.v./i.m. 0.01 0.02; i.v./i.m. (Canines) 0.02 0.03; (felines) 0.2 0.4; i.v. 0.1 0.3; i.v./i.m. Comments Mild to moderate sedation, duration 1 2 hours Moderate to deep sedation and analgesia, duration 20 60 minutes Similar effects to xylazine, duration 1 3 hours

Diazepam Midazolam

Most useful when combined with other sedatives, opiods or ketamine. Similar to diazepam, but also useful i.m.

Opioids and Neuroleptanalgesic Combinations Drug Morphine Butorphine Bupenorphine Pentazocine Fentanyl Acepromazine Butorphanol Acepromazine Buprenorphine Midazolam Butorphanol Xylazine Butorphanol Fentanyl Droperidol Dosage (mg/kg) 0.2 0.6; s/c, i/v 0.2 0.4; s/c, i/m, i/v 0.006; i/v, i/m 1.0 3.0 mg; i/m 0.001 0.007; i/v 0.05/0.2; i/v, i/m 0.3 -/0.01; i/v 0.1 0.2/0.2; i/v, i/m 0.4 0.6/ 0.2 0.4; i/v, i/m 0.001 0.007/ 0.125 0.5; i/v, i/m Comments Mild sedation when used alone, duration 1 4 hours Minimal sedation when used alone Long duration of action Duration 2 hours Duration 20 30 minutes Can be combined in the same syringe, duration 15 60 minutes Moderate sedation, duration 2 3 hours Can be combined in the same syringe, duration 15 40 minutes Both drugs are reversible, duration 30 40 minutes Exellent for aggressive dogs, dose dependent sedation, duration 30 60 minutes

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Induction Induction is most easily accomplished with an ultra-short-acting barbiturate or other equally short-acting drug(s). Advantages to this method of induction include rapid loss of consciousness and ability to quickly intubate. Alternatives to rapid induction are chamber or mask induction and opioid induction. These techniques can be useful in special circumstances; but for routine use, their disadvantages outweigh their advantages. Opioid Induction: A disadvantage to opioid induction is the attendant relatively slow loss of consciousness. Advantages include good cardiovascular stability and the attenuation of the stress response associated with anaesthesia and surgery. Opioid induction works best in debilitated dogs and is not recommended in cats or young healthy dogs that are not well sedated. Low doses of oxymorphonc or fentanyl are alternated with low doses of diazepam or midazolam until the dog can be intubated. Injectable Anaesthetic Drugs Drug Thiopentone Propofol Dosage (mg/kg) 8.0 20.0; i/v 4.0 6.0; i/v 0.4-0.8 mg/kg/minute 2.0 10.0; i/v, i/m Comments Use lower dosage after premedication Duration 5 10 minutes after single bolus dose, apnea with rapid injection Not useful alone in dogs Useful restraint in cats; lasts 5 30 minutes

Ketamine

Maintenance The maintenance phase of anaesthesia begins when unconsciousness is induced and continues through the time the patient is disconnected from the anaesthesia breathing circuit. After the loss of consciousness, a properly sized cuffed endotracheal tube is inserted. Adequate cardiovascular function is verified, and the anaesthetic vaporizer is turned on. The initial and subsequent anaesthetic vaporizer settings vary with the condition of the patient, the type of vaporizer, the type of breathing circuit, and the fresh gas flow rate. The relatively high fresh gas flow rate and vaporizer setting that are initially used after induction are decreased to maintenance settings when the palpebral reflex disappears and the heart rate begins to decrease. The vaporizer setting is adjusted according to signs of anaesthetic depth, which include muscle tone (assessed by opening mouth to its full extent), heart /respiratory rates, and systemic blood pressure. Recovery Recovery begins when the procedure for which the patient has been anaesthetized is finished and the anaesthetic drugs have been discontinued.

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Antagonists of Various Classes of Sedative Drugs Drug Dosage (mg/kg) Alpha 2 Adrenoceptors Yohimbine 0.1; i/v, i/m Atipamizole 0.04-0.05, i/m Benzodiazepine Flumazenil 0.2-0.05; i/v Opiod Naloxone 0.003-0.01; i/v, i/m Patient monitoring should occur regularly during the recovery period until the patient is alert and extubated and the heart rate, respiratory rate, and body temperature have returned to normal. Young, healthy animals undergoing routine procedures need not receive supplemental oxygen during recovery unless nitrous oxide was used. If nitrous oxide was used, the breathing circuit should be repeatedly flushed with oxygen, and the patient should be allowed to breathe an oxygen-enriched gas mixture for the first 5 to 10 min to help prevent diffusion hypoxia. Sick or debilitated dogs and cats benefit from supplemental oxygen during recovery. Shivering signifies increased oxygen consumption. Some loss of body heat is unavoidable during anaesthesia and surgery, and the patient should be warmed during recovery. The endotracheal tube cuff should be deflated and the gauze securing the tube should be untied when the patient is disconnected from the anaesthetic machine. This permits extubation in the event that the patient rapidly awakens and begins chewing. Dogs and cats should be extubated as soon as the swallowing reflex returns, unless there is some specific contraindication to removing the endotracheal tube. Dogs and cats should be constantly observed when the endotracheal tube is still in place. Occasionally, a dog or cat will be disoriented when it awakens from anaesthesia and will vocalize, paddle, and appear incoherent. This is most often caused by emergence delirium or pain. Emergence delirium occurs most frequently in nonpremedicated animals and, in particular, patients awakening rapidly from anesthesia. Dogs and cats suffering from emergence delirium will usually become quiet and more comfortable within a short time (10 min.). A quiet, reassuring voice and restraint are all that is generally necessary to guide the animal through this period of excitement. Occasionally, a low dose of acepromazine (0.05 mg/kg IV) is needed to quiet the animal. If the apparent excitement is the result of postoperative pain, the animal should receive a systemic analgesic or some other analgesic technique. In rare instances, delirium may be associated with a drug effect that can be reversed with an antagonist

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Postoperative Management of the Surgical Patient

Ashok Kumar Associate Professor Department of Veterinary Surgery & Radiology College of Veterinary Sciences CCSHAU, HISAR The outcome of any surgical procedure is determined by the efforts made during pre-, peri-, and post-operative period. Some of the important points to be taken care of during postoperative period are summed up here. Care of the surgical patient does not end with the termination of surgical procedure. The ultimate outcome is determined by the postoperative care of the patient. Postoperative care involves normalizing homeostasis, controlling pain, and recognizing complications early. Early recognition of complications facilitates treatment and ultimately recovery. Following points should be considered after surgery: The patient after surgery should be shifted to quiet recovery room and closely watched till complete recovery from the effects of anaesthesia. If the patient is slow to recover, it may be stimulated by rubbing, flexing and extending the limbs. The animal's position should be changed frequently to prevent hypostatic congestion, atelectasis of lungs and decubital ulcers. Geriatric patients, ill or debilitated patients and patients that underwent along surgical procedure should be maintained on intravenous fluid8 until they are able to eat and drink. Close attention must be paid to the fluid rate and urinary losses to prevent volume depletion, severe electrolyte imbalances, acid-base disorders, or all three conditions. Appropriate analgesic agent should be administered for atleast 3 days to reduce pain, better to administer analgesic one hour before surgery. It reduces the number of postoperative administration. Tranquilizers may be used with caution if the animal is distressed. Diazepam should not be used in buffaloes as it is not safe in this species. Temperature, pulse and respiration should be monitored at least every hour until the temperature is normal and the animal is alert. Hypothermic animals may need to be effectively rewarmed with heated cages, hot water bottles or warmed blankets. Evaluation of hematocrit, blood gases, bl99d pressure or oxygen saturation may be necessary. Oxygen supplementation by means of oxygen cage, nasal insufflation or mask should be considered for hypoxaemic patients. The respiratory rate and tidal volume should be adjusted to maintain the PaCO2 between 30 -40 mm Hg and PaO2 over 60 mm Hg. Excessive airway pressure should be avoided. Haemorrhage may be a result of surgery or of the underlying disease. Severe haemorrhage reduces the circulating blood volume and oxygen- carrying capacity, eventually resulting in cardiovascular collapse. The clinical signs of severe haemorrhage may be obvious, but occult haemorrhage into a body cavity may be hard to recognize. Pale mucous membranes, a slow capillary refill time, weak pulse, and a high heart rate are non-specific signs of haemorrhage. These parameters should be

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monitored closely after surgery. Normal healthy animal can loose approximately 10% of their blood volume without severe consequences, many post-operative patients are unable to tolerate this much haemorrhage. Ongoing haemorrhage should be eliminated are minimized and blood volume replaced. In case, the dressing becomes wet from external contamination or wound discharges, it should be removed and fresh, clean, sterile dressing should be done. The sutures or dressing should be protected so that the patient may not bite or tear the wound or dressing. In dogs, the use of Elizabethan collar or an improvised collar of a card-board box fitted to the neck or side-stick or cradle in large animals may be helpful in protecting the site of operation from self-mutilation. Splints are, sometimes, used to immobilize the limb. The patient should be given easily digestible nutritive diet either orally or parenterally. To prevent bacterial infection, a prophylactic course of broad spectrum antibiotic should be given for 5 to 7 days. Skin sutures are generally removed 8 to 10 days after complete healing has taken place.

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Radiographic diagnosis in pet practice

Dr. Rishi Tayal Dept. of Surgery & Radiology, CCSHAU, Hisar Diagnostic radiology remains the primary modality used to image diseased animals in veterinary practice. It is a rapid, non-invasive means of supplementing information obtaining by clinical and laboratory examination. Specialized techniques such as diagnostic ultrasound, computed tomography, nuclear medicine and MRI are becoming more widely available and used, but diagnostic radiology continues to be the main stay of veterinary imaging. Thus, a firm understanding of the principles of diagnostic radiology is essential for students of veterinary medicine. Radiographic diagnosis involves careful reading of a quality radiograph under satisfactory conditions with the background of normal radiographic anatomy, pathophysiologic processes, clinical picture and results of other diagnostic procedures. The ability to read radiographs thoroughly and accurately comes only with practice and attention to detail. Competent radiologic practice presupposes the availability of good quality radiographs. Familiary with the basic principles underlying the production of radiographs is a prerequisite for the radiologist. Accurate positioning of the animal under investigation, correct exposure factors, the use of grids and other ancillary aids, and good dark room technique all influence the quality of a radiograph. The use of a technique chart is essential for consistent results. An ideal quality radiograph should have excellent detail, correct density, proper scale of contrast, sharpness, least magnification and distortion of the image. Magnification, distortion and blurring of the image can be minimized by placing the part being studied as near to the film as possible and at a standard acceptable distance of 90-100 cm from the source of radiation. A radiograph is a two dimensional image of a three dimensional structure and hence at least two views at right angles to each other, are made as far as possible. Some of the limiting factors in obtaining a quality radiograph in veterinary practice are: i) A natural handicap that an animal cannot be held totally mobile. ii) ii) Motility of organs or certain degree of muscle tremor cannot be eliminated. iii) iii) The possibility of reducing the exposure time by using high mA is often limited by the thickness of the subject. iv) iv) Large area to be covered requires higher focal-film distance (FFD). Radiograph viewing: 1) Radiographs should be interpreted in an isolated and quiet environment. Distractions cause one's diagnostic accuracy to decrease. 2) To assist in developing a mental picture of normal radiographic anatomy, radiographs should always be placed on the illumator in a standard manner i) Lateral views of any part should be viewed with the cranial aspect of the animal to the viewer's left.

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ii) Ventrodorsal or dorsoventral radiographs should be placed with the cranial part of the animal positioning up and with the left side of the animal to the viewer's right. iii) Dossopalmer, dorsoplanter, caudocranial or craniodorsal radiographs of the exterimities should be placed on the illuminator with the proximal end of the extremity at top. 3) At least two illuminators are desirable so that at least two views can be evaluated simultaneously. 4) Avoid interpreting radiographs by holding them towards an overhead light or a window. 5) A wet film contracts on drying and definition of the image improves and details are enhanced. Therefore, the x-ray film should be reexamined after drying. 6) The radiograph should be viewed on an illuminator with uniform light so that all parts of it receive equal intensity of light. 7) A spot light device should be used to examine overexposed areas like soft tissue around a hone. It can be helpful in detection of early stage of new bone formation and other lesions. 8) A magnifying lens should be kept handy to differentiate finer details on a radiograph. 9) Direct light should not fall on the film. Subdued light in the room helps in better visualization of the lesions on a radiograph. 10) The radiographs should not be viewed from too close distance. Viewing from a slight distance helps to locate suspected lesions. 11) Faint shadows of metallic foreign bodies are visualized better if the radiograph is held at an angle to the viewer. Principles of interpretation: Radiographic interpretation is neither mysterious nor difficult if certain basic procedures are followed. Interpreting a radiograph is a matter of compiling all the evidence, analyzing it, and arriving, at reasonable conclusions. Important steps: 1) Signalment and Case historyAs in any phase of clinical diagnosis, the breed, gender, and age as well as complete knowledge of the medical history of the animal should be known for accurate radiographic assessment. Radiographs should never be interpreted without access to history and signalment. 2) Physical examinationA radiographic examination should be performed only after a clinical opinion of the patient's health has been formed. Generally the purpose of a radiographic examination is to confirm a clinical diagnosis or impression, not to make the diagnosis. A detailed and complete physical examination is necessary to establish a reason for radiographic evaluation and to determine the part or parts of the animal to be examined radiographically.

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3) Correct radiographic procedure: If a radiographic examination is technically inadequate because of insufficient number of views, improper exposure factors ,inadequate equipment such as cassettes and screens, or poor dark room technique, important information may be overlooked, and the correct diagnosis may be missed. A poor quality radiograph is at best inconclusive and at worst misleading. 4) Evaluating the radiograph: In the process of trying to determine whether or not an abnormality exists, the entire radiograph must be evaluated. The organ approach or the area approach may be used. In the organ approach, the evaluator makes a conscious effort to evaluate every organ on the radiograph. In the area approach, the evaluator evaluates the radiograph by starting the analysis centrally and working toward the periphery or vice versa. Whether to use the organ or area approach is an individual decision. Nevertheless, whichever approach is adopted, the entire radiograph should be interpreted in a systematic manner. In veterinary practice, it is difficult to memorise 'normal' radiographic appearance of all regions of various species and breeds of animals. Developmental, senile, individual and postural variations also do occur. It is prudent on the part of radiologist to keep these factors in mind and ~to consult standard text books showing normal radiographic anatomy. Better still, is to maintain a library of normal x-ray films for this purpose. While viewing a radiograph for suspected lesions, one usually looks for the following anatomical changes. i) Changes in the size and shape of the structures or organs e.g. enlarged heart. ii) Deviations in the location either due to organ itself i.e. hernia, or due to an adjacent growth e.g. a tumour pressing the trachea. iii) Variations in radiographic density of a structure e.g. in an abscess. iv) Break in the continuity of a structure e.g. in case of fracture or diaphragmatic hernia. v) v) Variations of texture e.g. in case of osteoporosis, osteosarcoma, rickets etc. A radiograph should not be viewed with preconceived ideas. After viewing the whole radiograph, history of the case and clinical data should be consulted. Information regarding the breed, sex, and age, results of physical examination and laboratory tests done should be sought. The radiographic findings should be correlated with clinical data and then radiographs viewed again for finer details. If progression or regression of a disease is in question, a series of radiographs spread over days, weeks or even months, will be required. Jumping to conclusions with

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preconceived ideas or observing only the major variations on a radiograph often lead to erroneous radiological interpretations. Radiography can provide valuable information about a wide variety of disorders in canines. The chest radiography remains a major diagnostic window offering clues to the nature of both symptomatic and asymptomatic pulmonary diseases. Many conditions of lungs such as pneumonia, tuberculosis, pulmonary emphysema, bronchiectasis, atelectasis, metastatic neoplasias and pleurisy etc. can be diagnosed successfully by this technique. The radiographic detection of cardiomegaly is potentially of great value as it directly correlates with many cardiac diseases. Other disorders of the chest, which can be diagnosed radiographically, include pericardiac effusion, hydrothorax, pneumothorax, hiatus hernia etc. Radiographic examination of the abdolrten of the dog provides an interesting, but challenging problem. Demonstration of different visceral structures depends entirely upon slight difference in density of the various abdominal organs. It is a useful method of diagnosing pathological enlargements of the liver, spleen and kidneys. An upper gastrointestinal (UGI) examination using barium sulphate suspension is a popular contrast radiographic procedure to evaluate partial and complete gastrointestinal obstruction in canines with vomiting and/or diarrhea. In addition, VGI examination can be used for detection of functional changes by studying gastric emptying times and small intestine transit times. Retrograde contrast radiography provides increased diagnostic capability and has become an integral part of the diagnostic examination. Barium enema technique is very valuable in diagnosing ileocolic intussusceptions, large bowel neoplasia, strictures and other related disorders. Triple contrast studies of the stomach and the urinary bladder, using both positive contrast media and air, alongwith pneumoperitoneum, are of immense value in detecting both mucosal and serosal lesions of the wall. Pneumoperitoneum alone lends itself very nicely to clear and detailed examination of the external contours of the kidneys and liver in canines. Intravenous pyelography can be effectively used to diagnose both pathological and functional disorders of the the renal system. Careful radiographic assessment offers a real basis for the identification of lesions in cases of cervical and thoracolumbar disc disease. The use of myelography has become an essential requisite in a dog, showing clinical signs of the disc disease for the assessment of possible surgical treatment. The extremities of animals are examined radiographically more often than any other part of the body. The technique can be successfully used to diagnose most conditions of congenital, metabolic, traumatic and neoplastic origin such as hip dysplasia, rickets, osteoporosis, osteochondritis dissecans, fractures, dislocations, degenerative and infective arthritis, osteomyelitis, osteosarcoma etc. Osteomedullography is a reliable clinical technique in evaluating the repair process of the canine long bone. It can be effectively used to investigate the delayed or non-union of fractures. One can decide whether conservative treatment should be continued or surgery should be performed.

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Special radiographic techniques, such as the use of contrast media, media, nonroutine positioning and various technical manipulations, have greatly increased the usefulness of radiography. A few examples of such techniques include the use of iodine compounds to outline the kidneys, air to outline the urinary bladder, barium sulfate to outline the gastro-intestinal tract and oblique angles in taking radiographs. 1. Pneumonia: (a) Irregular patches of density or granular appearing infilteration (pneumonic consolidation). (b) May be unilateral and may involve a part. 2. Pneumothorax: Presence of air or gas in the pleural cavity (a) Collapse of lung lobes away from chest wall (b) Air in pleural space more radio-lucent than lungs @ Depression of diaphragm on side of tension. 3. Pulmonary tuberculosis (a) Poorly or well defined nodule shadows of varying size and density (b) in miliary form small nodule shadows distributed uniformly (c) hilar Iymphnode enlarged 4. Hydrothorax, pyothorax (a) Ground glass appearance of thorax due to free fluid (b) level offluid seen on standing lateral view 5. Lung abcess (a) dense centre with a hazy and poorly defined periphery (b) roughly circular with radio-lucent small shadows 6. Lung cyst (a) Air filled rounded radio-lucency -different size (b) fluid filled rounded cavity with air fluid level. 7. Pericardial effusion (a) increase in size of cardiac silhouette (b) ground glass appearance due to fluid 8. Diaphragmatic hernia (a) Diaphragmatic line not continuous (b) presence of visceral organs in thorax (c) confirmation by barium meal study 9. Chronic gastritis and peptic ulcers (diagnosed by Ba meal study) (a) Enlarged rugal folds (b) Filling defects -ulcer (c) Hyperactivity -early evacuation 10. Gastric torsion (a) Distended stomach with gas (b) Fluid level on standing lateral view (c) No passage ofBa meal 11. Hepatomegali and splenomegali (a) Increased radio-opacity of liver and spleen (b) Enlargement of liver and spleen 12. Oesophageal dilation (a) Barium meal will outline enlargement of oesophagus 13. Intestinal obstruction

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(a) Dilatation of bowl with gas (b) Passing of barium only upto the area of obstruction 14. Hydro-nephrosis (a) Enlarged kidneys (b) Contrast medium not cleared for a long time 15. Ruptured urinary bladder (a) Free fluid in peritoneal activity (b) Confirmed by contrast radio-graphy. 16. Chronic cystitis (a) Thickened bladder wall on contrast cystography 17. Fracture (a) Break in continuity of bone (b) Overriding of bone fragments 18. Hip dislocation (a) Increased space between acetabulum and femoral head (b) Femoral head out of acetabulum 19. Rickets (a) Lack of adequate mineralisation (b) Bowing of long bone (c) Widening of metaphysic and radiolucent epiphyseal plate 20. Infectious arthritis (a) Early joint space widened due to destruction of cartilage (b) Lysis of adjacent bone by septic process 21. Osteo-arthritis (a) Uneven joint space with narrowed width. (b) Subcartilagenous sclerosis of bone (eburnation) (c) Extensive peri-articular new bone formation. 22. Osteo-myelitis (a) Zone of bone lysis (b) Zone of increased density (sclerosis) surrounding zone of lysis (c) A chip of bone with increased radio-lucent density (sequestrum) 23. Bone cancer (a) Destruction of cortical bone (b) Large tumor mass (c) Periosteal elevation (d) Sun-bust appearance 24. Malunion (a) Abnormal position of fractured ends. (b) Bone deformity, overriding or rotation (c) Secondary joint changes due to deformity 25. Non-union (a) Bone ends fail to unite -no bridging (b) Smooth round fractured ends

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OVARIOHYSTERECTOMY IN BITCH
Dr. Suresh Chander Teaching Veterinary Clinical Service Complex, CCS Haryana Agricultural University, Hisar -125 004 Indications: 1. Elective sterilization 2. As treatment for uterine diseases such as Pyometra Uterine torsion Uterine prolapse Uterine rupture Diffuse/ localized cystic endometrial hyperplasia Uterine neoplasia 3. To prevent the recurrence of vaginal hyperplasia. 4. In diabetic or epileptic dogs to prevent hormonal changes that can interfere with medication. 5. As a protective factor reducing the incidence of mammary gland tumours. Ovariohysterectomy before the first estrous cycle decreases the incidence of mammary neoplasia to 0.5%. Risk factor is 8% after one estrus and after two estrous cycles the risk increases to 26 per cents. Procedure: 1. Make a midline incision extending from the umblicus approximately 5 cm caudally. If the uterus is enlarged the length of incision may be increased. 2. Locate the right uterine horn by using either an ovariohysterectomy hook or the index finger. 3. Place a clamp on the proper ligament of the ovary to retract the ovary while the suspensory ligament is stretched or broken. Tension must be directed caudally along the dorsal body wall rather than perpendicular to the incision to avoid tearing the ovarian A V complex. 4. Make a window in the mesovarium caudal to the ovarian vessels. 5. Triple clamp or double clamp the ovarian pedicle (A V complex). 6. Severe the ovarian pedicle between the clamp closest to the ovary and the middle clamp (when 3 clamps are used) or between the middle clamp and the ovary (when 2 clamps are used). 7. Place a circumferential suture loosely around, the clamp most distant from the ovary. 8. Remove the clamp while the circumferential suture is tightened so that the ligature lies in the groove created by the clamp. Absorbable suture material is to be used for the ligature. 9. Grasp the pedicle with a small hemostat and remove the remaining clamp. 10. Inspect the pedicle for bleeding. If no bleeding occurs replace the pedicle into the abdomen. 11. Repeat the procedure on the other ovarian pedicle. 12. Make a window in the broad ligament adjacent to the uterine artery and vein.

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13. Grasp the broad ligament and tear it. 14. Ligate the large vessels in the broad ligament before clotting it. 15. Place three clamps on the uterine body just cranial to cervix. 16. Severe the uterine body between the proximal and middle clamp. 17. Ligate the uterine arteries and veins individually caudal to the most caudal clamp. 18. Apply a circumferential suture around the distal clamp. Remove the clamp and tighten the suture in the groove of the clamped tissue. 119. Grasp the uterine pedicle with a small hemostat above the clamp and remove the clamp. 20. Inspect the uterine pedicle for bleeding and replace it gently into the abdomen. 21. Close the abdominal incision. Complications: 1. Hemorrhage Causes (i) (ii) (iii) (iv) (v)

Rupture of ovarian vessels when suspensory ligament is stretched. Tearing of large vessels in broad ligament. Tearing of large vessels by excessive traction on the uterine body. Improperly placed ligatures or Accidental releasing of a clamp before placement of ligatures.

Prevention (i) (ii) (iii) (iv)

Careful strumming of the suspensory ligament. Individual ligation of large vessels in the broad ligament. Lengthening the abdominal incision. Double ligation of ovarian pedicle and uterine stump

2. Uterine Stump Pyometra Cause It the entire uterine body or a portion of either uterine horn is not removed and the animal has elevated blood progesterone levels. Prevention Complete excision of the uterine horns and body. 3. Recurrent Estrus Cause Functional residual ovarian tissue after incomplete ovariohysterectomy Treatment Exploratory laparotomy preferably during estrus and excision of residual ovarian tissue. Prevention

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By maintaining constant digital contact with the ovary during application of clamps to the ovarian A V complex. 4. Urinary Inconsistence Cause (i) Adhesions or granulomas of the uterine stump that interfere with urinary bladder sphincter function. (ii) Low systemic estrogen level. Treatment Estrogen responsive urinary inconsistence may be treated by oral administration of diethyl stilboesterol @ 0.1 to 1 mg per day for 3-5 days followed by 1 mg per week. 5. Body Weight Gain Most common long term sequalae of ovariohysterectomy Cause (i) Low systemic estradiol level after ovariohysterectomy that lead to fat deposition (ii) Inactivity and increased food intake. 6. Eunuchoid Syndrome Seen in working dogs after ovariohysterectomy characterized by decreased aggression, interest in work and stamina. Prevention Auto transplantation of ovary to subserosa of stomach which is drained exclusively by portal vein. Circulating levels of estradiol are inadequate embedded in reactive tissue, the entire mass is removed.

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Clinical endocrinology in female dogs

Dr. S. K. Khar Animal Reproduction, Gynecology and obstetrics As in all other animal species, successful reproductive function is dependent on an intricate inter-play of a host of hormones and the response they elicit from the respective target organs. Essentially the hormones are the same, but what differs is probably their level and in some cases the response produced. Whereas appropriate levels at appropriate times ensures normal reproductive functions; deficiencies and / or inefficient report can and do result into aberrations which need to be corrected at the earliest A. Reproductive hormones 1. GnRH; Hypothalmic hormone, pulsatile release, reaches anterior Pituitary via portal circulation. Attaches to a cell which produces FSH / LH. Effect on receptors is temporary, low binding affinity, quickly metabolized. Synthetic analogues are more potent. 2. FSH Stimulation of growth of ovarian follicles. Factors which initiates the release are not known and circulating levels are not well documented. 3. LH It is released in short bursts/ pulses. Increase in pulse frequency is seen 1-2 weeks before proestrus. It causes Maturation, leutinization and ovulation of ovarian follicles. Circulatory concentrations peak about 48 hours before ovulation. Peak levels are generally observed in late proestrus or early estrus. It also acts as leutotropic. 4. Estrogens It is produced from growing follicles, mainly 17. and 17, also estrone. Circulating levels rise for a few days before the beginning of pro-estrus. Sharp increase occurs later, peaks about 48 hours before LH surge. It causes changes observed in proestrus. 5. Progesterone It is produced from mature follicles and corpora lutea. Circulating levels begin to rise around the time of estrogen peak. High concentrations are observed at the time of ovulation and highest levels at 20 days post end of estrus (irrespective of the pregnancy status. Thereafter gradual decline, until basal levels are reached by day 70 (60-70). 6. Prolactin It is produced from anterior pituitary. It stimulates milk production. Its concentration is inversely proportional to progesterone. In nursing animals its concentration remains high for sometime after whelping. It also has luetotropic properties. 7. Androgens Functions in females are unknown. Testosterone peaks parallel with LH peaks. During met-estrus and pregnancy androstendione levels are high and closely follow progesterone.

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8. Prostaglandins Spontaneous PGF2 a. from uterus is not responsible for luteolysis. Corpora lutea becomes non-functional gradually over a period of time either due to lack of tropic support (LH/Prolactin) or because of limited inherent life span. Yet causes final lysis of corpora lutea of pregnancy, which in any case are producing very little progesterone, in later days. B. Clinical endocrinology and mating a. Average bitches experiences LH surge on day 10 (Day 1 is the first day of bloody discharge) b. Ovulation occurs on day 12. c. Best conception days are day 14/15. d. Traditionally bitches are mated on day 14 post onset of proestrus. e. Most bitches demonstrate "Tail flagging" and "Standing estrus" on this day. f. Other signs like "softening of flesh of swollen vulva" indicates "onset of ovulation" g. For multiple matings -breed on days 12 & 14 or 11, 13 and 15. h. These schedules are generally adequate; yet some do not breed optimally (Ovulation from day 5-25). i. Many times, these approaches are not absolutely clear cut. j. Some subjects may 'phantom proestrus' -with no or little external signs. k. Some subjects may 'flag and appear receptive throughout proestrus' or to be 'willing to mate even after ovulation.' I. An unsuccessful mating causes at least 6 month's loss. m. Even cytological analysis may also prove to be poor indicator of ovulation, because ovulation may occur 3-5 days before to 5 days after onset of estrus. Estimation of serum progesterone levels (quantitatively/ qualitatively) in the best option in such subjects for accurate determination of the various events and organization of the 'mating schedule'. Conventional progesterone assay is generally time consuming costly method which requires highly sophisticated laboratory and equipment. ELISA has been developed which are easy to perform cheap and afford immediate results. Although the basic principle and procedure underlying all available systems is the same, the end points may differ. The following schedule highlights the main features. Vaginal smears from the subject are examined periodically from the onset of proestrus for cornification of vaginal epithelial cells -resqlt of increasing estrogen levels. When 60% cells show cornification, testing for serum progesterone should begin. Specified quantity of either whole blood or serum is added to a specified quantity of the' test indicator' (treated with progesterone monoclonal antibodies.

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Color changes are interpreted as follows: 1. Strong blue color: early proestrus (p4 levels 0- 1 ngiml) 2. Light blue color: Late proestrus, early estrus (p4 levels 1-2 ngiml). 3. White color: about two days after LH surge (p4 levels 5 ng/ml or above, confirma ovulation). * In late pro-estrus decline in estrogen levels, LH surge and progesterone increase above 1 ng/ml occurs on the same day) . Limitations: False positivel negative reactions Greatest inaccuracy in measuring levels between 1.5-3 ngiml. Occasionally a test indicates a medium P4 (LH Surge) but low levels on the next day, apparently the former test was false. Once the levels start rising, they should continue to rise To eliminate such problems, testing on two consecutive days should show high levels before mating schedule is decided. Further confirmation can be done by testing on the mating day for levels above 5 ng/ml. Kits for LH- ELISA are also available. These work on the same principle. However time factor is important as LH remains high for only 24 hours, necessitating repeated short interval sampling; which is not feasible. If used, the following schedule is recommended LH surge Ovulation Mating Day 0 Day 2 Day 4/5

Pregnancy * No pregnancy specific gonadotrophin hormone. * Progesterone levels can't be utilized as concentrations start decreasing about twenty days after peak levels. * Relaxin is secreted by the canine placenta and is specific for pregnancy. * Relaxin is not present in non-pregnant animals. * Concentrations increase from 25 days after breeding and peak at 40-50 days. * Blood samples are drawn on day 25 (Day 22-26 after LH surge). * ELISA test is highly positive detecting pregnancy, no false positive results. * Can also be used to differentiate between pregnancy and pseudopregnancy. Thyroid insufficiency * Irregularities in the reproductive cycle * Persistent anoestrus * Silent heat (mild bleeding minimal vulvar swelling) * Prolonged pro-estrus * Ovulation failure

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* Thyroid hormones are involved in numerous positive and negative feed back loops that have direct or indirect effects on other hormone levels and also metabolism. Less thyroid hormone levels promote high 'prolactin' which in turn inhibits GnRH. Possibly one of the several ways in which hypothyroidism blocks estrus and ovulation. For accurate diagnosis of hypothyroidism: * Measure levels of free thyroid hormone in serum. * Monitor the response to administration 9f TSH and * Monitor anti-thyroid antibodies. Hormone replacement therapy is successful for restoring cyclicity within 3-6 months. Ovarian cysts * Persistent estrus is sometimes associated with luteal cysts * Ovarian cysts should be suspected when P4 levels above 2 ng/ml persist for more than 2 months. * Symptoms of abnormal cycles and finding of enlarged ovaries on ultrasonography. Pituitary insufficiency * Pituitary function is critical for thyroid, adrenal and ovarian function * Numerous endocrine abnormalities * Animal retains the size, haircoat and dentition of a puppy * Persistent anestrus.

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INFERTILITY IN BITCH
Umed Singh, Assoc. Prof. Deptt.of Animal Reproduction Gynaecology & Obsts, CCS Haryana Agricultural University, Hisar Reproductive pattern in female dog is remarkably different from those of farm animals. Bitch is monoestric i.e, one estrous in each breeding season, followed by anestrous. Ovulation in majority of females occurs at beginning of estrous. Uterus has no major role for regression or maintenance of CL of cycle. Puberty is attained is attained between 9 to 16 months when first estrous is displayed. Higher incidence of breeding is observed during early or late spring, otherwise throughout the year. A litter of 5 to 8 puppies is average. Proestrus is considered to begin when the bitch discharges blood from the vulva and the bitch is excitable, restless loss of appetite, increased water intake and urination, attractive to male. Proestrus lasts on an average of 9 days (2to 15d).During estrus female is receptive and accept male for mating and it lasts on an average of 10 days (3toI2d). Diestrus begins with refusal of bitch to mate and CL is fully grown during this period. Bitches that are not mated or mated with sterile dog may develop pseudo pregnancy. In the bitch conception is possible whether breeding has occurred on the first or on the last day of estrous. Ovulation is spontaneous and usually occurs within 5 days after the onset of estrus (40% within 2d, 70% within 3d). VAGINAL CYTOLOGY It is good indicator of stage of estrous cycle. Take a smear from the suspected bitch, air dry it and stain with Giemsa. Number of layers epithelial cell layers increases with increase in the conc. of estrogens. Epithelial lining of vagina during anestrus is 2-3 layers thick but at the beginning of proestrus it is stratified (6-8 layers) and the growth continues and by the time estrus occurs the epithelial lining may be 12-20 cell layers. Desquamation of epithelium begins by late estrus. During Anestrus Proestrus Exfoliated cells i.e. foam cells (cytoplasm vacuoles) and leukocytes are observed. Number of cornified epithelial cells (pyknotic nucleus) increases There are numerous RBCs and sparse leukocytes. Mostly cornified cells (flakes) and moderate number of RBCs. Number of leukocytes increases. Change from superficial cells (keratinized) to basal cells.

Estrus Diestrus

PSEUDO-PREGNANCY False pregnancy is commonly observed if bitches are not mated or mated with sterile male. The CL of the non pregnant bitch remains functional for an extended period after ovulation. In such cases there is development of uterus just like that of pregnant, uterus enlarges and abdomen is relaxed. Mammary glands also develop and relaxation of pelvis and external genitalia is similar to that during pregnancy. Pseudo pregnancy often lasts as long as or longer than a normal pregnancy. During later stages

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psychological manifestation is intense and bitch may attempt to build a whelping nest and even in some cases lactation begins and bitch may adapt to nurse puppies from other bitch. These signs are manifested because of high levels of prolactin. Progesterone levels are similar to that of pregnant but higher than that of non pregnant, Diagnosis: 1. Breeding history. 2. Abdominal palpation for enlargement of uterus. 3 X-Ray Ultrasonography Administration of Bromocryptine (Cryptal-l.25 or 2.50 mg tab .twice daily orally for 7 days) may result in suppression of overt sign or alternatively such females can be treated by administration of 1. Testerone 1-2 mg/kg i/m single injection 2. MGA (melengestrol acetate) 2 mg/kg orally daily for 7 days. 3 Mibolerone oral androgen. Ovario-hysterectomy

Treatment:

Prevention:

ABORTION The common causes of abortion are poor nutrition, hypothyroidism, foetal abnormalities, progesterone deficiency and infections like Brucellosis, E. coli, Streptococi, Canine herpes virus. Affected female exhibits abdominal contractions, expulsion of live or dead foetuses and there is vaginal discharge. Some or all fetuses may be aborted and remaining live fetuses may be born at term. Treatment: Collect blood, Urine for analysis and also collect material like uterine or vaginal discharge or foetal tissues for culturing and following line of treatment can be adopted for handling affected cases. 1. If the bitch is in shock, then supportive therapy like i/v fluid should be given. 2. Give Broad spectrum antibiotics like a) Sinulox 2-3 mI. 11m single injection or b) Biotex 250-500 mg i/m + Amikacin 100-250 mg i/m twice daily for 37 days 3. Give Oxytocic drugs to aid uterine evacuation a) Ergonovine (Methergin) 0.2 mg orally t.i.d for 2-3 days or b) Oxytocin 1 i.u/kg i/m or 1 i.u i/v or 10-20 i.u i/m daily for 2-3 days or c) PGF.2a 0.25 mg/kg sic or 50-100 ug/kg sic d) 4.Abortion can be prevented by providing good nutrition, exogenous thyroxin (Thyroid tab) or by giving Progesterone 2 mg/ kg i/m every third day. RETAINED PLACENTA Normally in majority of cases pup is accompanied by its placenta, if not then within 15 minutes after expulsion of pup, placenta should be delivered. Retention is suspected when discharge is copious and dark green to black in color. Green discharge is also sometimes normally present at the time of whelping, however, it disappear

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within few hours. If it persists for 12 h or more, then it is due to retention of placenta. It may lead to toxaemia, uterine distension, Metritis and death within 4-5 days. Treatment If diagnosed before 12 h - Give 1. Oxytocin 10-20 i.u. 11m or slow il v in 500 ml DNS. 2. Methergin 0.2 mg orally t.i.d for 2 to 3d. 3. I/U antibiotics or Nitrofurazone 1-2 gm with the help of syringe and pipette. 4. Systemic antibiotics for 3-5 days If there is any evidence of necrosis, which may occur in long standing cases, hysterectomy should be performed. SUB-INVOLUTION OF UTERUS It is failure of the uterus to undergo normal reduction and occurs when uterus fails to contract after whelping due to which placental fluids and debris are retained. Uterine inertia is the main cause of this condition. Sub involution is not a main hazard to the bitch but retained placental fluids and debris after 72h in the uterus, result in protein break down and resultant products are absorbed from the uterus and are excreted in the milk and when this milk is suckled by pups it causes a typical disease of puppies where they become restless, crying and develop bloat and may die. Treatment: First thing is remove the pups from the bitch for 24h and immediately give the bitch oxytocic drugs for emptying of the uterus i.e Metheregin 0.1 -0.2 mg t.i.d. orally for 2-3d, along with systemic antibiotics and I lu infusion of 1-2 gm of antibiotic dissolved in 10-20 ml of distilled water. After 24h of start of treatment allow feeding of pups by dam. METRITIS Mostly occurs within first week following parturition or abortion. Commonly occur due to infection or using unsterilised hands or instruments at the time of whelping. Metritis results in to depression, anorexia, toxaemia, elevated temperature and greenish discharge from the vulva and the bitch frequently licks the vulva. Treatment: If toxaemia occurs then prognosis is poor because of chances of rupture of uterus and peritonitis. However, following line of treatment can be adopted in the bitches suffering from Metritis. 1. Calcium (Sandoz) 10-20 ml i/v 2. Oxitocin 5-10 i.u in500 ml, of DNS i/v 3. Estradiol valerate 5 mg i/m 4 Methergin 0.1-0.2 mg orally t.i.d. for 2-3 days 5 I/V antibiotics 1-2 gm in 10-20 ml DW for 2-3 days 6. Systemic antibiotics Treatment should be continued for 2-3 days. CYSTIC ENDOMETERIAL HYPERPLASIA- PYOMETRA COMPLEX It is the disease of the luteal phase and mostly observed between 5-80 days after end of estrus. There is glandular and cystic endometrial hyperplasia. Subsequently

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infection mainly by E. coli results in to pyometra. During early stage bitch becomes lethargic, reduced appetite, increased thirst, vomiting are subsequently observed. There may be discharge of pus and the abdomen is distended. Inmost of the cases cervix is closed and animal may die due to toxaemia. In some cases cervix is open and pus comes out and such females do not suffer from toxaemia. Diagnosis: 1. Abdominal palpation- horns are turgid and solid 2. Ultrasonography- uterus filled with fluid. 3. Radiography -enlargement of the uterus 4. Hematology -elevated total leukocytic count 5. Rectal examination -distended uterus per rectum 1. Ovariohysterectomy, if the case is long standing or diagnosed late. 2. If diagnosed earlya. Broad spectrum antibioti~s in DNS, IN b. Methergin 0.1-0.2 mg orally tid for 3 days or c. Prostaglandins 0.25 mg/ kg sic daily for 2-3 days. ANESTRUS Anoestrus may be due to delayed puberty or prolonged diestrus /anestrus. Bitches witch do not reach puberty by 2 years (normal 5-24 months) of age are considered to have delayed puberty. Normal inter-estrus period is between 26- 36 weeks, if longer than this or anticipated, and then it is prolonged estrus. Poor nutritional plane and body weight, prolonged use of progestogens, androgens and anabolic steroids and hypothyroidism are the major causes. Treatment Estrus can be induced by DES (diethylstilbe~trol) 5 mg orally daily until 2 days after signs of proestrus develops. If no response by day 7 then increase the dose to 10 mg for further 7 days. DES for 7 days with 5 mg LH on day 5 and 10 mg FSH on day 9 and 11. Prolactin antagonist. Prolactin inhibits or interfere with gonadotrophins rel~ase, therefore, inter-estrus interval is prolonged.Antagonist like Bromocryptine (Proctinal) 1.25 -2.5 mg b.i.d. for 3-5 days orally is given. SPLIT / SILENT ESTRUS Sometimes there may be silent estrus without obvious external signs or split estrus i.e bleeding from vulva for short duration and after few weeks exhibits estrus again. For both these conditions proper follow up along with vaginal cytology for detecting ovulation is required. PROLONGED ESTRUS OR PROESTRUS Normal interval between the onset of proestrus and ovulation varies from 5-30 days (Majority ovulate by day 14 after onset of proestrus) , if it is longer than this period, then considered prolonged estrus.

Treatment

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No treatment is required, best is careful assessment of ovulation by vaginal cytology or induction of ovulation may be attempted by administration of 20 i.u of hcg ( Chorulon) / kg. PREVENTION OF ESTRUS If the owner does not want that bitch should not exhibit estrus, then estrus can be prevented by administering1. Progesterone (Proluton Depot) 2-3 mg /kg 11M every 2-3 weeks or using single injection of oily preparation like 'Depot Provera" 2. MGA 2.2 mg orally for 4 days 3. Testosterone 1 mg / kg oral or i/m weekly 4. Mibolerone Synthetic oral androgen, 30 ug /kg for bitches up to 10 kg and for heavier than this 200 ug /kg daily.

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PSEUDO-PREGNANCY AND CYSTIC ENDOMETRIAL HYPERPLASIAPYOMETRA COMPLEX IN BITCHES

N.S.BUGALIA 1 Department of Animal Reproduction, Gynaecology and Obstetrics, CCS Haryana Agricultural University, Hisar- 125 004 Bitches attain puberty at the age of 9 to 12 months. Pubertal bitches usually show short and irregular oestrus cycles associated with short oestrus periods, prolonged oestrus periods and split oestrus periods during early breeding season due to variation in pituitary gonadotropin secretion and this is followed by regular cyclicity following establishment of functional coordination of hypothalamic-pituitary-gonadal axis to initiate follicular growth, maturation and ovulation. Pseudo-pregnancy and "cystic endometrial hyperplasia-pyometra complex" are the hom1onal disorders of the cyclic bitches along with secondary bacterial infection resulting in infertility. Pseudopregnancy usually resolves spontaneously but bitches affected with "cystic endometrial hyperplasia-pyometra complex" rarely recover without treatment and recurrence is most common. Medical treatment, if instituted, in early phase of the disease in bitches affected with pseudo-pregnancy and "cystic endometrial hyperplasia-pyometra complex", gives encouraging results and post-treatment recurrence is also much rare. However, the cyclic bitches prone to recurrence of pseudo-pregnancy and "cystic endometrial hyperplasia-pyometra complex" are recommended for ovariohysterectomy. Pseudo-pregnancy: It is a hormonal disorder of late dioestrus associated with declining levels of peripheral progesterone profiles and characterized by mammary gland development, sero-sanguineous to milky secretion from mammary gland, mastitis, nesting behavior, mothering of toys, depression and irritability. The condition most commonly occurs during late dioestrus or following dioestrual ovario-hysterectomy or after cessation of progesterone therapy in bitches. Pseudo-pregnancy can be diagnosed by the history (cyclic bitch with overt oestrus during past 2 months and followed by development of signs of false pregnancy) and clinical symptoms (abdominal distension, mastitis, abnormal nesting behaviour, inapetite and nervous symptoms- restlessness, depression and irritability). The differential diagnosis with the pregnancy can be made by radiography and ultrasonography on the basis of absence of litter and uterine enlargement due to accumulation of viscous mucoid exudate. Pseudo-pregnancy resolves spontaneously in bitches. Oral administration of bromocryptine (10 j.lg/Kg body wt. SIC tid for 5 days) resolves mammary development associated with Pseudo-pregnancy in bitches. The hormonal treatment (Repositol progesterone-1 mg/Kg body weight. 1M single dose; Mibolerone 40 j.lg/Kg body weight. orally daily for 5 days) can be used to suppress destructive nesting behavior and concurrent mastitis. Progesterone therapy also suppresses symptoms during treatment but relapse after cessation of the treatment have

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been commonly reported in treated bitches. Ovariohysterectomy is the only permanent preventive measure in canine Pseudo-pregnancy. Cystic endometrial hyperplasia (CEH) -pyometra complex: It is the hormonal disorder of dioestrus phase of oestrous cycle along with occurrence of secondary bacterial infection of the uterus in bitches. The pyometra also develops as a sequele of uterine infection following breeding and whelping in bitches. Further, institution of progesterone therapy to suppress the oestrus in bitches also has been reported to develop the "cystic endometrial hyperplasia-pyometra complex". The defect in the metabolism of ovarian steroids (oestrogen and progesterone) by the uterus has been implicated in the development of canine pyometra rather than excessive production of progesterone. Further, a change in the number or affinity of the endometrial receptor sites leads to the abnormal accumulations of the ovarian steroids within the uterus as evidenced by uterine histological changes in the canine pyometra. Uterine morphological changes primarily induced by ovarian steroids results in cystic hyperplasia of the endometrium followed by accumulation of the endometrial secretions into the uterine lumen along with secondary bacterial infection of the uterus, resulting in the development of the pyometra. CEH is considered to be the sequele of exaggerated response of the uterus to progestational stimulation during the luteal phase of the oestrous cycle. Prolonged progesterone stimulation produces an acute inflammatory reaction aggravated by bacterial infection. The luteal regression is followed by decline in peripheral progesterone profiles, resolution of acute endometritis and infiltration of plasma cells. Secondary bacterial infection is a frequent complication of CEH. The most frequent bacterial isolate of the canine pyometra is Escherichia coli and others less frequent uterine bacterial isolates are Staphylococci, Streptococci, Proteus spp., Klebsiella spp. and Salmonella spp. The source of uterine bacterial infection is either from urinary tract or perineal region and infection often occurs during oestrus and bacteria multiply during metoestrus. The presence of specific endometrial and myometrial receptors for Escherichia coli antigens enhances colonization of bacterial population into the uterus of the affected bitches. Spontaneous recovery occurs following regression of the corpus luteum, relaxation of the cervix and drainage of uterine exudate. However, such bitches are prone to recurrence of the disease during subsequent oestrous cycles. Bitches affected with "CEH-pyometra complex" often develop renal dysfunction. Pre-renal azotemia develops in pyometra bitches secondary to dehydration or shock. Occurrence of glomerulonephropathy in bitches affected with "CEH-pyometra complex" is caused by immune-complex deposition in the glomerular capillary walls and glomerulonephropathy is reversible following removal of the diseased uterus. Impaired renal tubular water absorption despite of adequate circulating antidiuretic hormone in canine pyometra referred as "renal diabetes insipidus". Epithelial surface of Bowman's capsule and renal tubules are reported to have an affinity for Escherichia coli antigens and thus, the immunological factors are associated with the aetio-pathology of renal dysfunction in canine pyometra.

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Functional disturbance of bone marrow, liver, spleen, and adrenals are recorded in canine pyometra. The bone marrow dysfunction is evidenced by marked increase in the myeloid : erythroid ratio due to hyperplasia of the myeloid elements. The chemotactic effect of endometritis in CEH causes massive outpouring of neutrophils into the peripheral circulation. Severe toxaemia in "CEH-pyometra complex" causes bone marrow depression and resultant decreased WBC count along with neutrophilia (presence of immature neutrophils) and mild to severe anaemia. The liver, spleen and adrenals often show evidence of extramedullary myelopoiesis due to bone marrow depression. Canine pyometra occurs most often in bitches over 6 years of age and develops in 4 to 6 weeks after last estrus. The common clinical symptoms are inapetite, abdominal distension, mucopurulent to purulent vaginal discharge with yellow-grey or reddish-brown colour and fetid odor, polydipsia, polyurea, dehydration, depression and nocturea. The subnormal temperature is observed in severely toxic bitches. Immature neutrophilia and leucocytosis (WBC count- 20,000 to 100,000/c mm) is most common in "CEH-pyometra complex". Bitches with close cervix pyometra and infected uterine contents along with toxaemia show higher WBC count. Rarely, normal WBC count is observed in severely toxaemic bitches but there is severe degenerative left shift (Presence of immature neutrophils). Occasionally, normal TLC and DLC are recorded in bitches with sterile clear mucoid like uterine exudate and the condition is classified as "mucometra" or "hydrometra". Distinct rise in WBC count (two to three times of pre-surgical values) is observed in canine pyometra following ovariohysterectomy, due to pre-operative stimulation of bone marrow. Mild to moderate normochromic anaemia (PCV-Iess than 36 per cent) in "CEH-pyometra complex" is the sequele of toxic bone marrow depression or loss of R6C's into uterine lumen or both. Moderate to severe hyperproteinemia is entirely due to increase in gamma globulins. Pre-surgical monitoring of Blood Urea Nitrogen (BUN) and serum creatinine concentration should be done due to concomitant high incidence of renal failure in canine pyometra. Potential vulnerability of pre-renal or primary renal failure in "CEHpyometra complex" warrants complete urine analysis in conjunction with BUN and serum creatinine concentration. Hyposthenurea and proteinurea are most frequently associated with canine pyometra. Vaginal cytology in cyclic bitches between 10th to 25th days of metestrus reveals non-cornified flat epithelial cells with vacuolated cytoplasm. Vaginal cytological smears from pyometra bitches evidence massive neutrophilia and bacteria, persist-ing till late metestrus and anestrus. Abdominal radiograph serves as confirmatory diagnosis in bitches with diagnostic history and clinical symptoms. Abdominal enlargement associated with uterine enlargement permits evaluation for pyometra induced renal failure (enlargement of the kidney, renal calculi, and tumors of the abdominal organs) in affected bitches. Radiography demonstrates homogenous dense tubular mass in caudal abdominal region. Pyometra can be distinguished from pregnancy and Pseudo-pregnancy by evidencing uterine enlargement along with accumulation of dense uterine exudates mucoid in nature. Fetal skelton can be visualized by Day 45 of gestation.

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Other diseases associated with polydipsia and polyurea are required to be differentially diagnosed with pyometra are renal failure and diabetes mellitus (BUN, serum creatinine and urine analysis- biochemical and microbiological investigation) and hepatic disorders (Liver function tests- SGOT, SGPT and billirubin and haemogram haemoglobin, TLC and DLC). Transmissible Veneral Tumor, vaginitis or vaginal hyperplasia can be ruled out by clinical examination and vaginal cytology of the affected bitches. Medical treatment for canine pyometra includes treatment with oestrogen, testosterone and oxytocin. Oestrogen induces cervical dialata-ion, increases uterine muscular tone and initiation of uterine contractions and promotes expulsion of uterine exudate. Testosterone (25 mg 1M twice weekly) was effective in the thera-peutic management of "CEH-pyometra complex" within 3 weeks. Testoste-rone causes ovarian atrophy by eliminating the luteal source of progesterone to prevent endometrial hyperplasia. Therapeutic management of canine pyometra with oxytocin (5 IV 1M bid for 5 days) and ergonovine maleate (0.2 mg 1M b.i.d. for 10days) along with pretreatment with oestradiol valerate (5 mg bid 1M for 5 days- 2 hours before the administration of oxytocin and ergonovine maleate dose) was found to be successful in the affected bitches. Potential therapy in "CEH-pyometra complex" constitutes institution of "Prostaglandin treatment regimen". PGF2oc is recommended along with parentral antibiotic therapy and deep vaginal antibiotic douches in canine pyometra. Bitches with open cervix pyometra respond well to PGF2oc whereas PGF2oc treatment in close cervix pyometra can rarely cause peritonitis due to forceful evacuation of uterine contents through oviduct before occurrence of cervical dilatation. PGF2oc is administered at the dose rate of 25 g/Kg body weight S/C daily for 5 days. Treatment response should be evaluated on 3rd Day post-treatment by observation of evacuation of uterine contents. Failure to observe evacuation of uterine contents warrants thorough clinical examination involving radiography and ultrasonography to ensure prevention of development of peritonitis. Most of the bitches affected with pyometra respond within 3 to 5 days of treatment. Treatment response is confirmed by reduction in neutrophilia, return of normal leukogram, cessation of pussy vulvar discharge and drop in progesterone level (<1 ng/ml). However, rarely, some bitches require 2nd treatment regimen. Prognosis for future fertility is worst for bitches requiring treatment longer than 6 days. I Recent investigations on therapeutic management of "CEH-pyometra complex" revealed encouraging results with Diethylestilbesterol (1 mg ora.ily bid for 10 days) and ergonovine maleate (2 mg orally bid for 10 days) along with parentral and intra-uterine adminisiration of antibiotics for 4 to 6 weeks. Ovariohysterectomy is preferred in chronic pyometra due to its recurrence. Ovariohysterectomy is recommended in bitches non-responding to medical teatment. Parentral administration of broad spectrum antibiotics along with administration of polyionic fluid therapy and non-steroid anti-inflammatory drug is recommended for 7 to 10 days post-operation. Complications of Ovario-hysterectomy in canine pyometra are peritonitis and uterine abscesses. Flushing of abdomen with Ringer's lactate and intra-

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peritoneal infusion of antibiotics along with parentral antibiotic treatment should be done to prevent further post-operative complications in the affected bitches.

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Infertility in the Stud Dogs

N.S. BUGALIA College o/Veterinary Sciences, CCS'HaryanaAgricultural University, Hisar-125004. Infertile dog is often reported with the history of either conception failures in three to five bitches following breeding on two to three successive oestrus periods during the current breeding season as well as in preceeding breeding season. Some dogs are reported with the history of azoospermia beginning between 3 to 5 years of age. An infertile dog records poor conception rates or low fertility in fertile bitches bred on schedule on two to three occasions during receptive period of oestrus (Day 4 to Day 6 pf oestrus or 2 days after cessation of bloody vaginal discharge of proestrus). Oligospermia or necrospermia (live sperm count- 40 to 60%) or normo-spermia with poor motility and high sperm abnormalities (above 20%) are the common feature of semen evaluation report in infertile dogs. Testicular semen production is affected by inguinal hernia with omentum or intestines passing into the scrotum, prostatic infection or retrograde ejaculation or progressive testicular degeneration leading to partial to complete testicular damage. Low libido with low testosterone, hypothyroidism or psychic impotency accounts for subfertility in dogs. Treatment schedule in canine male infertility constitutes medical approach involving antibiotics and hormone therapy, and the surgical management or correction of infertility comprising orchidectomy, repair of stenosed lumen of epididymis and ductus deferens due to formation of spermatic granuloma or spermatocoele or segmental aplasia of ducts. Primary infertility: Pubertal dogs with oligospermia or azoospermia and good libido along with small testes should be suspected for testicular hypoplasia. Segmental aplasia of the epididymides can be detected by careful palpation. This defect causes azoospermia with normal sexual behviour. Some dogs often suspected for cryptorchidism were diagnosed as sterile due to absence of testes and vas deferens. Aquired infertility: High fever, scrotal dermatitis, orchitis, epididymitis and cryptorchid testes increase the testicular temperature and adversely effect the spermatogenesis in dogs. High scrotal temperature up to 10 days do not produce irreversible damage and dog recovers from testicular degeneration. Testicular torsion produces ischemia along with loss of spermatogenesis within 1 to 2 hours. However, the few leydig cells are functional provided partial circulation is maintained. Dogs over 10 years of age suffer from senile testicular ~trophy and subsequent degeneration of the testes. Chronic diseases, testicular neoplasia, most common in older dogs, cause gradual loss of fertility and libido. Hyaline degeneration of testicular arteries in older dogs often predisposes to testicular degeneration. Testicular degeneration ranges from deficiency of germinal epithelium to complete disappearance of epithelium along with sertoli cells. Focal testicular necrosis is also observed in severe vascular lesions.

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Dogs subjected to frequent semen collection (once or twice daily) often suffer from low fertility due to reduced sperm concentration in the ejaculate. However, semen collection every other day maintains normal sperm concentration. Occlusion of efferent ducts, epididymal ducts, ductus deferens, prostatic ducts, and urethra causes azoospermia or oligospermia due to partial to complete blockage of testicular fluid and semen. However, the testicular size and histology are normal. Chronic epididymitis can OQs~ruct transfer of testicular fluid and sperm through epididymis, and fibrous scar in epididymal lumen and obliteration or distorsion of the duct lumen also blocks transfer of testicular fluid and sperm during normal maturation process, occurring in a gradual and slow rate in epididymides. The recurrent acute or chronic infection of the testes causes development of microabscesses, scrotal sinuses or spermatic granulomas, further preventing flow of testicular and epididymal contents. Orchitis occurs consequential to trauma, exposure of testes to adverse temperature, epididymitis and prostatitis. Mild testicular trauma most. commonly results in decreased sperm output and poor motility. The tail defects of sperm are most common following testicular trauma (bent tails, proximal cytoplasmic droplets) Complications of testic\11ar trauma are secondary infection, systemic exposure to sperm antigens resulting in testicular atrophy. Spermatoceles and sperm granulomas develop from testi- cular sperm caused by congenital or aquired blockage of ducts. The degeneration and rupture of these ducts is most common in diseased conditions causing immunological infertility. The damage of blood testis barrier results in lymphocytic orchitis and epididymitis and prostatitis. Focal degeneration, segmental atrophy, and diffused atrophy of the testis can be recorded in lymphocytic orchitis. Brucella canis causes scrotal dermatitis, epididymitis, or orchitis in 55 per cent of the affected dogs. Semen records high sperm abnormalities (30 to 80 %) within 2 to 5 weeks of initial infection. Large clumps of inflammatory cells, neutrophils, macrophages are common in ejaculates, and these cells adhere on phagocytosed sperm. Bent sperm tails, head-tail detachment and head-to-head agglutination predominante by 15 week of infection with severe infertility in bitches bred to affected dog. The lymphocytic orchitis often develops in canine brucellosis leading to severe testicular damage and subsequent degeneration. Orchitis and epididymitis of longer duration during prepuberal period cause sterility in male dogs. Radiation adversely affects the spermatogenesis in dogs. Spermatogonia are the most radiosensitive cells of the seminiferous epithelium. Subsequently, the older sperm cell types of the spermatogenesis continue to mature and disappear in the order in which they are formed till thecomplete degeneration of testis has occurred. Both the single large dose or a sublethal dose or multiple doses of radiation completely damages the germinal epithelium of the seminiferous tubule. Acute distemper disturbs semen production and serum testosterone level drops and testicular function is restored following recovery from the disease. The renal failure, liver cirrhosis, diabetes mellitus and metastatic neoplasia alter hormone metabolism and subsequent development of infertility in dogs. Hyperadrenocorticism causes testicular atrophy. Gluco-corticoids are known to have anti gonadotropic action

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on leydig cells membrane and drastically drop testosterone profiles in dogs. Hypothyroidism affects both libido and semen production in 50 to 60% of affected dogs. Lymphocytic orchitis was recorded concurrent with lymphothyroiditis. Testicular degeneration and atrophy can also occur in dogs following development of neoplasia of hypothalamus or pituitary gland interfering with the production and secretion of gonadotrophins. Sertoli cell tumor, seminomas, interstitial cell tumor are found in older dogs between 8 to 10 years of age. Testicular tumors occupying the mediastinum testis interfere with the semen passage due tometplastic involvement of the region. Testicular neoplasms are associated with prostatic enlargement and diseased condition of the epididymis and ductus deferens. Diagnosis: Infertility can be diagnosed by the history of infertile services (failure to sattle the bitches in oestrus and conception failures in mated bitches during past 2 to 3 months). Clinical examination includes palpation of the scrotum, testes, epididymides, prostate, penis and prepuce for detectable abnormality. Tests for brucellosis and endocrine status (functional tests for testicular steroidiogenesis- testosterone and thyroid activity- T 3 and T 4) should be compulsory for evaluation of fertility of the stud dog. Sexual behaviour: The mating behaviour and coupulatory reflexes can be evaluated by careful observation of the stud dog near a receptive bitch. Prolonged reaction time (above 5 minutes; absence of courtship, sexual displays, sexual arousal, erection and incomplete mounting attempts; and partial erection with weak thrust are indicative of low libido and subfertility), incomplete coital lock, premature ejaculation and ejaculate with low volume and watery consistency with poor sperm concentration are suggestive of infertility in stud dog. Sometimes intromission fails to occur despite of strong libido of the stud, indicates examination of bitch for persistent hymen, vaginal hypoplasia and hyperplasia and vaginal tumors. Semen evaluation: The semen is collected by masturbation (presperm and sperm rich fractions appear milky in colour and are collected in the same tube and the postsperm fractioncrystal clear prostatic secretion is collected separately) and examined for motility (60 to 80 per cent), pH (7.4), total sperm count (1730 millions/ml), live sperm count (80%) and abnormal sperm count 20 per cent). TLC (above 20,000/cmm) and DLC (neutrophilia- 85 to 92%, eosinophil-5 to 10%, lymphocytes- 5 to 15% basophils 1% and monocytes- 2 to 5%) reflect infection of the genital tract while degenerating sperm cells and spermatozoa with pyknotic nuclei are recorded in testicular degeneration. Retrograde ejaculation is diagnosed due to presence of large numbers of sperm in the urine; consequential to stenosis of the sperm passage between the efferent tubule to the pelvic urethra, the blockage most commonly involves epididymides and occasionally the vas deferens and rarely the efferent tubules and the urethra.

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Cytology: Epididymal cellular contents are collected by needle puncture from cauda epididymis. Azoospermic dogs with normal sperm in tail of the epididymis usually have defect in sperm transport beyond cauda epididymis. Epididymitis is detected due to prensence of neutrophils, macrophages and bacteria. The testicular needle puncture samples often reveal disrupted architecture of seminiferous tubule, making it difficult to interpret sperm cell types on testicular puncture smear and warrants evaluation through testicular biopsy. Azoospermia associated with arrested spermatogenesis or slow rate of spermatogenesis can only be diagnosed by testicular biopsy and it also indicates aetiology and severity of testicular degeneration. Hormones: Testosterone (0.5 to 9 ng/ml; leydig cell tumor- above 5.0 ngiml), oestradiol (1.1 to 8.8 pgiml; sertoli cell tumor and seminoma- above 10.0 pgiml), luteinizing hormone (LH- 0 to 174.7 ngiml; LH profiles above 150 pg/ml- deficiency of androgen receptor in pituitary gland or abnormal negative feed back of androgen from the testes), follicle stimulating hormone (FSH- 20 to 130 ngiml; FSH levels above 250 ngiml- severely damaged seminiferous tubule or complete depletion of germinal epithelium of the tubules), thyroid hormones (T 3 -8.20 to 15.35 ngiml; T 4 -6.55 to 18.45ng/ml) and cortisol profiles (0.45 to 2.75ngiml) in circulation are of diagnostic value in detection of aetiopathology of canine male infertility. Treatment: The infection of the testis and epididymides requires treatment by broad spectrum antibiotic. Unilateral orchidectomy is a valid approach in involvement of single testis, where prognostic value of prolonged antibiotic medication appears to be futile. Stud suspected for brucellosis, on confirmation should be neutered and euthenised with medication. Quarantine and institution of medical treatment along with sexual rest is recommended for systemic diseases. Surgical intervention is warranted in preputial stenosis, persistent ventral frenelum and inguinal hernias. Semen picture returns to normal after 10 to 12 weeks of surgery. Fertility can only be restored after unilateral orchidectomy in testicular neoplasms along with 10- to 12-week post-surgical sexual rest. Renal failure, hepatic cirrhosis, metastatic neoplasia, diabetes mellitus, hyperadrenocorticotropism and cardiac disease should be strictly managed on recommended treatment schedules and treatment response should also be periodically evaluated both by laboratory and clinical evaluation. Fertility can return to normal within 3 to 6 months of successful medical treatment. Thyroid supplementation in hypothyroidisxn corrects seminiferous tubule and leydig cells function in the affected stud. PMSG has been advocated in azoospermic and oligospermic stud dogs. However, (azoospermic do not respond to PMSG but oligospermic dogs improved fertility with the treatment (PMSG- 200 to 500 IU IV at 3- to 6-day intervals or FSH- 25 mg SC once a week)

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Primary testicular failure with elevated gonadotrophins profiles (FSH), usually fails to respond to hormonal treatment in dogs. Studs affected, with secondary testicular failure with decreased circulatory pituitary gonadotrophins levels (FSH and LH), respond well to the gonadotrophin replacement therapy. Dogs with normal gonadotrophins output but with other andrological disturbances like occlusion, retrograde ejaculation, acute and chronic infections of the genital tract should be treated with standard surgical and scheduled medical treatment regimen under strict periodic evaluation of instituted treatment.

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Use of Hormones in Canine Reproduction

J.B. Phogat Department of Animal Reproduction Gynaecology and Obstetrics Endocrinology of canine estrous cycle Pro-estrous: This is the stage of the estrous cycle prior to estrous when bitch attracts male but is not receptive to mating. A serosanguineous discharge passes from the swollen turgid vulva. The average duration is 9 days (3-17 days). During this time concentration of estradiol rise and usually reaches to peak value 1-2 days before the end of pro-estrous and start to decline when first acceptance to male is observed. Progesterone remains low prior to and during first few days of pro-estrous and 2-3 days prior to acceptance it starts increasing may be due to lutenization of pre-ovulatory follicle. Serum LH remains near base line during most of the proestrus, however, slight level above base line may be observed during early anoestrus in some bitches. FSH also remains at base line during late pro-estrous. Oestrus: It is the period of the reproductive cycle when bitch accepts the male. Average length is 9 days (3-21 days). Bitch becomes receptive to male when serum estradiol begins to fall and concentration of progesterone begins to rise. Similarly, pre-ovulatory LH surge is mediated by decline in estradiol and rise in progesterone. As per some studies LH surge occurs at the onset of estrus but others say there is no such correlation. The period of pre-ovulatory LH surge ranges from 24-96 hours. Ovulation in bitch occurs 0-96 hours after onset of LH surge but most ovulations occur between 24 -72 hours after LH surge. As stated earlier, progesterone starts to rise during late pro-estrous but after LH surge there is gradual increase in progesterone for approx. 10 days. Unlike most other species, the bitch ovulates the primary oocyte rather than a secondary oocyte. The first meiotic division begins about 1 day after ovulation usually in the mid piece of oviduct and maturation of oocyte occurs within 3 days of ovulation. After ovulation viable life span of secondary oocyte is 24 hours. Diestrous: It starts with the first day bitch refuses to accepts to male. During early diestrus, serum concentration of progesterone continues to increase until approximately day 15 of diestrous and then continue to decline gradually for 5-6 weeks. The canine uterus/uterine prostaglandins have got no role in maintenance and regression of CL since hysterecomised bitches have same luteal phase as of intact bitches, however, exact mechanism is not clear. Anestrous: It had been referred as quiescent phase of the reproductive cycle. However, recent work I suggests that neither ovary nor pituitary gland is quiescent at this time. Oestradiol decreases & LH increases just before on set of proestrus. FSH is high in anestrus bitches compared to bitch in heat. Progesterone remains at base line at this time. Although mechanisms for terminations of anestrus & initiation of new follicular phase are not completely understood, concentrations of LH appear to increase prior to

112

the onset of pro-estrus and may be important lin inducing a new follicular phase. During anestrus, serum FSH is high in bitches & that is why in anestrus bitches fertile estrus with FSH cannot be induced. Endocrinology of Pregnancy: The patterns of peripheral levels of hormones during pregnancy are very similar to those observed during non-pregnant cycles with prolonged phases of progesterone secretion. Oestradiol levels comes down during and following LH surge and throughout most of estrus and then rather undramatically increases during pregnancy to reach elevations (20-30 pg/ml) prior to parturition that are considerably below than those seen in late pro-estrus. Oestradiol falls abruptly to basal levels (5-10 pg/ml) following parturition. Progesterone levels rapidly increase over 1 ng/ml during the onset of the pre-ovulatory LH surge and continue to increase throughout estrus to reach initial peak level of 15-85 ng/ml by 15-30 days after the LH peak. Following implantation and placental development when progesterone is at their initial apex or declining, there is second peak of progesterone during the 4th or 5th week of pregnancy. During the last third of pregnancy, progesterone levels slowly decline to 4-16 ng/ml, which is maintained for 1-2 weeks until abrupt decline to 1-2 ng/ml, 1-2 days before parturition. Thus, broadly, we can say that during the second half of pregnancy, progesterone is higher than non-pregnant bitches. Conditions for which reproductive hormones are used: Estrus induction: GnRH in pulsatile form at the rate of 140 ng/kg/pulse every 90 min for 11-13 days with the help of programmable pump can be used for fertile estrus induction in bitches. Alternatively, 1.7-2.5 micro gm/kg/day of GnRH agonist as continuous infusion also induces estrus in anestrus bitches but its results are variable. Another protocol has also been tried by others. Diethylstilbesterole -5mg orally was given daily until 2 days after the onset of vaginal bleeding and it was followed by 10 mg FSH/bitch or 5mg/bitch LH i.m. on day 5, 9 and 11 after on set of bleeding. This protocol gave very encouraging results in the form of fertile estrus induction. Induction of ovulation: There are certain circumstances when bitch comes to heat normally but fail to ovulate. A single injection of GnRH (50 micro gm/bitch i.m.) can induce ovulation of mature follicles. Alternatively, 500-1000 IV of hCG i.m. can induce ovulation when given at the time of heat. However, above treatments should be given when more than 90% of the exfoliative vaginal cells appear cornified for at least 3 days. Luteal insufficiency: It leads to low progesterone profiles in the circulation, which is not enough to sustain pregnancy. So either the fetus is resorbed or abortion takes place. So in such cases external supplementation of progesterone is must to sustain the pregnancy. A progesterone blood level of at least 5 ng/ml is must to maintain the pregnanc)'. Supplementation of progesterone in oil (3 mg/kg/day i.m.) will maintain progesterone concentration at 10 ng/ml that is enough to maintain the pregnancy. This progesterone supplementation should be stopped 3 days before the expected date of whelping.

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Follicular cyst: Follicular cysts produce estrogen and may cause prolonged proestrus, nymphomania and possibly estrogen toxicity with bone marrow aplasia. It should be confirmed by ultrasonography and blood oestradiol levels. To treat the condition, GnRH 50 micro gm/bitch i.m. for three days or 500-1000 IV of hCG i.m. will luteinize the cyst and terminate the estrus behaviour. Cryptorchidism: When testicles fail to descend in to sacrotum and it may be unilateral or bilateral. To treat the condition, GnRH- 50-100 micro gm/pup sic or i.m. can be tried and if no response is observed the same therapy should be repeated after 46 days. Alternately, hCG 100 - 1000 IU/dog i.m. can be given 4 times over 2 weeks duration i.e. on days 1, 5, 10 and 15. The above treatment is more effective in dogs of less than 16 weeks of age. Estrus suppression: Megestrol acetate, 2.2 mg/kg administered for 8 days starting 3 days after the onset of sanguineous discharge and vulvar swelling. This therapy prevents the heat but chances of occurrence of pyometra increases. Alternately, Mibo1irone, a synthetic androgenic compound at a dose rate of 30 micro gm/day for bitch weighing 1-12 kg body weight and up to 180 micro gm/day for bitches with weight of 45 kg or above' can be used for long estrus suppression and the therapy should be started one month before the pro-estrus. This treatment may lead to clitoral hypertrophy, mucoid vaginal discharge and atrophy of the glandular epithelium. Medroxyprogesterone is another hormone which can be used for this purpose but again treatment should be initiated two month before the next heat. Pregnancy prevention/mismating: If accidental mating takes place and owner does not want to have the bitch pregnant in such cases diethylstilbesterole at dose rate of 0.5 mg/kg (up to 25 mg total dose) should be given within 5 days of coitus. Oestradiol benzoate or valerate may be given 0.1 mg/kg (not to exceed 3 mg total dose) up to 5 days following mismating. The above treatment causes pyometritis so owner must be informed about its side effects. Another protocol if bitch is brought within 24 hours of mating then Tab. Oncotam (Tamoxiphine citrate) 10 or 25 mg b.i.d. depending upon size of bitch for 5 days should prevent the conception. Pseudo-pregnancy: In this condition bitch is not actually pregnant but shows signs of late pregnancy like nesting, mammary gland development, fluid secretion and mothering behaviour with toys or other animals. Some bitch becomes aggressive and agitated. To treat the condition, reposital testosterone 1 mgikg i.m. only once or 40 micro gm Mibolerone orally for 5 days will subside the symptoms. If not treated after some time automatically symptoms subside after few days. Induction of parturition: If bitch is at full term and owner wants or due to some other diseases if it is necessary to initiate the whelping then; first 10-100 ml of calcium (Sandoz) i.v. dependimg upon the size of bitch followed by 5 IV of synthetic oxytocin SIC and repeat it after 30 min or 5-10 IV of synthetic oxytocin in. 1 liter dextrose saline i. v. should be given. This therapy should initiate the whelping within half to two hours of start of treatment.

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Role of prostaglandins: They are used in canine reproduction for luteolysis and smooth muscle effects that results in cervical dilatation and uterine contraction. For luteolysis and abortion, a dose of 30 micro gm/kg at 12 hours interval for 3 days can induce abortion 30 days onward within 56-80 hours after initial treatment. Early corporalutea are resistant to prostaglandins and results related to abortion induction are very poor in early pregnancy. To treat the cases of closed-cervix pyometra or open case of metritis, prostaglandins 25-50 micro gm/kg for 3-5 days is recommended to evacuate the uterus. However, parental antibiotics should also be given to treat the infection. Apart from its beneficial effects, this drug has very severe side effects like salivation, vomiting, diarrhoea, hyperpnoea, ataxia, urination & anxiety.

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Management of Dystocia in Pet Animals

S.K. Khar and R.A. Luthra Department of Animal Reproduction, Gynaecology and Obstetrics, CCS Haryana Agricultural University, Hisar -125 004 Any impediments, irrespective of their nature, which prevent the progress of fetal expulsion from the uterus, through the maternal birth canal, after completion of gestation, constitute -"DYSTOCIA ". In order to understand the various possible factors, which can lead to such a situation, it is necessary to outline the events in "Normal Parturition".

1. Intense uterine contractions 2. Dilatation of cervix 3. Clear/White vaginal discharge Second Stage Labour: 1. Beings within 24 h of temperature drop. 2. Strong abdominal contractions. 3. Expulsion of pups. 4. Head first, occasionally feet first or even breech presentation. 5. Each pup followed by individual placenta. 6. Pups born in succession at intervals of minutes/l hour. 7. Intervals greater than 20 minutes, contractions decrease in frequency/intensity.

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8. Allowing already born pups to nurse between deliveries -stimulates uterine contractions. 9. Full bladder/rectum slow down the process. Leash walking allowing urination/defection hastens the process. 10. During interludes -allow some water to prevent dehydration and some source of sugar to replace the depleted energy resources. 11. Total duration of second stage labour could be several minutes to several hours. 12. Uterine contractions stop after the expulsion of last pup and placenta. Whelping -When? a. First day of mating: Range 57 to 72 days b. Monitor LH surge: 65 1 day c. Monitor ovulation: 63 1 day Parturient Complications 1. Primary uterine inertia 2. Pre-eclampsia / eclampsia (Hypocalcaemia) 3. Pelvic obstruction (Anatomical defects/foetal oversize) 4. Premature placental separation 5. Secondary uterine inertia 6. Uterine torsion/rupture 7. Fetal distress Non emergencies Due date reached? But: a. No decrease in body temperature. b. No signs of first stage labour (Generally uterine contractions/cervical dilatation must begin within 12 to 18 hours after body temperature decrease).

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Emergencies a. 6 to 8 hours after first stage -failure to progress to second stage Straining for more than 20 minutes, weak intermittent abdominal contractions for about 60 minutes. No pups born. No pups born, thick, black-green discharge Heavy persistent flow of fresh blood from vulva Muscle weakness, spasm, tremors, muscles rigid More than 60 minutes between delivery of pups; no further signs of active labour; pups still present Obstruction

b.

Obstruction

c. d. e. f.

Premature placental separation Haemorrhage/uterine rupture Uterine inertia Uterine inertia

g.

Evidence of intense abdominal pain, Uterine torsion symptoms of shock -pale mucosa, sudden drop in body rupture/massive temperature (below 99F); collapse haemorrhage

Questionnaire? Age: Previous chronic Medical conditions Serum progesterone Vomition Color of vaginal discharge Whether oxytocin has been given? Breed Reproductive history (Previous litters, previous caesarean section) Pre-ovulatory LH peak Last feed and drink Urination/defecation

Overdue Patient Possible causes 1. Late mating 2. Inaccurate information/calculation 3. Primary uterine inertia .f 4. Non-Pregnancy/resorption Investigations 1. Mating date 2. Abdominal palpation 3. Fetal heart beats 4. Radiography -pups visible, viability unknown; bones in stomach of patient delivery and eating of pups 5. Ultrasonography

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6. Serum progesterone levels higher than 2mg/ml -incomplete gestation. Therapy 1. If pups are viable, give more time. Condition of vagina -dry and tight body temperature suggestive. 2. Dead pups -caesarean section, oxytocin may be tried -but likely to fail. 3. In primary uterine inertia (temperature fall has occurred more than 48 hour earlier but no signs of labour) or evidence of placental separation. Try oxytocin, but caesarean section is more successful. Haemorrhagic discharge at term (no signs of labour): Possible causes 1. Primary inertia with at least one fetal death. 2. Placental separation 3. Aged pet with only one pup. 4. Death of all fetuses in mid to late pregnancy followed by haematic mummification. 5. Cause unknown, but pups die at different development stages. Investigation Palpation Radiography Ausculation Ultrasonography

Therapy: Caesarean section/hysterectomy Non Productive Straining: Second stage labour has commenced, patient exhibits labour of reasonable intensity, no pups born for more than sixty minutes (First pup may survive upto 6 hours after onset of straining, but subsequent ones die after about 2 hours). Possible Causes 1. First pup too large (small litter) 2. Fetal monster 3. Ventral flexion of nose -poll engages pelvic inlet. 4. Lateral deviation of head/neck. 5. Pup not able to get up to inlet level, bitch with pendulous abdomen. 6. Dead pup. 7. Pup in vagina, does not progress further due to large size (Small vagina). 8. Posterior presentation. 9. Straining not intense. 10. Vaginal tumor/polyp. 11. Pelvic exostosis (previous fracture). 12. Congenital vaginal stenosis. Investigation 1. Digital exploration of vagina 2. Vagina relaxed and moist, but no pup present. Manipulation of caudal abdomen may make palpation easy. 3. Fluid filled amnion in vagina. 4. Part of pup in vagina.

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5. Radiology/ultrasonograpy -viability and number of pups. Therapy 1. If nothing felt in the vagina -caesarean section. 2. Amnion palpable in vagina -lift the foetus wall to induce uterine contractions. 3. Vaginal occlusion/stenosis/pelvic exostosis/tumor -caesarean section 4. Fetal malposition -obstetrical manipulation Patient with some pups born; restless/larger litter expected Possible causes 1. Pup in cranial vagina causing no contractions. 2. Secondary uterine inertia 3. Normal rest between pups 4. No more pups. Investigation 1. Digital exploration per vaginum 2. Bimanual palpation, involuting uterus quite turgid and can be mistaken for a pup. 3. Radiography and Ultrasonography Therapy 1. Pups present and no discharge -oxytocin 2. Pups present and vaginal discharge is suggestive of placental breakdown consider immediate caesarean section. Oxytocin Therapy 1. Oxytocin leads to rhythmic contractions, although it has short half life, contractions induced are powerful. 2. Initially used in small doses -5 I.U. 3. If there is no effect after 10 to 20 minutes, repeat same or larger dose. 4. If one pup is born after oxytocin, it may be necessary to repeat for other pups. 5. If large number of pups are yet to be born, consider caesarean section. 6. Contraindicated in obstructive dystocia. Obstetrical Manipulation Failure of labour to progress is generally caused by one or two fetuses obstruction in birth canal. Oversized fetus Fetal malposition Two fetuses presented simultaneously Intervention Fingers are the best and safest instruments. Whelping forceps -use sponge over teeth. Ensure asepsis as far as possible. Finger manipulation -pushing the fetus caudally is important. Depending upon the availability, head or hips are grabbed between fingers. Drying of vagina is avoided by using a water soluble lubricant.

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 If a pup appears to be stuck, slight rotation may assist delivery. Traction should be applied when the dam is straining. When forceps is used -ensure avoiding vaginal damage, compression of foetus (particularly skull) and amputation of extremities. In case no progress is made after 15 mi~!:1tes, vagina gets traumatized, dam is distressed, there is fetal distress (heart rate less than 150 BPM) or many pups are yet to be born consider caesarean section. Calcium Therapy For proper function and response, neuromuscular tissue depends upon a proper balance of electrolytes. Uterine contractions depend upon adequate calcium levels. When calcium metabolism stands compromised (inadequate diet, extended period of labour) - depletion of serum calcium could interfere with uterine contractions. Grossly lower levels may lead to life threatening complications, Tetany and Seizures. Monitor calcium levels. Recognize clinical symptoms. Administer calcium S/C - I/V may be dangerous (Cardiac arrhythmia/sudden death). I/V administration recommended only in cases with life threatening hypocalcaemia (Muscle spasm, muscle rigidity, seizures, convulsions). I/V fluid therapy if excessive vomiting/dehydration IN fluid therapy must for cases of caesarean section to combat hypertension. Nervous Inhibition of Labour The patient is either in first or second stage of labour, but does not settle to whelp. Possible causes 1. Unfamiliar place 2. Introduction to whelping box too close to term. 3. Absence of owner Presence of strangers. Remedy 1. Allow the patient to whelp where she wants (inconvenience?) Ensure Owner's presence until whelping is over

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CAESAREAN SECTION IN BITCH

Dr. Suresh Chander Teaching Veterinary Clinical Service Complex, CCS Haryana Agricultural University, Hisar -125004 Delivery of puppies by hysterotomy is required when dystocia cannot be relieved by medical management or manipulation of fetus per vaginum. The operation is relatively safe for both bitch and puppies when performed at the appropriate time. Caesarean section in the bitch is usually an emergency procedure as prolonged dystocia adds risk to the life of the mother and neonate. Ideally, the operation should be done when the dog is in relatively good health and should not be used as a treatment of last resort. Caesarean section can be planned and performed before the onset of active labour when dystocia is likely to occur because of abnormalities that narrow down the birth canal. Indications: 1. Prolonged gestation, when normal parturition is not likely to occur after 70 days of gestation. 2. Primary uterine inertia. 3. Incomplete primary uterine inertia, if several puppies remain and ecbolics have failed. 4. Secondary uterine inertia. 5. When abnormalities of mate mal pelvis or soft tissues exist that interfere with the passage of foetus e.g. pelvic fractures, vaginal tumour. 6. Relative and absolute foetal oversize. 7. Monstrosities 8. Malpositions of foetus (Transverse presentation, head flexion etc.) 9. Foetal death with putrefaction. Pre operative preparation: The patients selected for caesarean operation are often in poor physiological condition at the time of presentation and should be carefully examined. X-ray examination helps in ascertaining the presence and number of foetuses thus .prevents leaving a foetus in the uterus or pelvic canal inadvertently by the surgeon. Animal's packed cell volume, total plasma protein, BUN and specific gravity of urine may be measured. These tests assist in evaluating the need for corrective fluid therapy. An intravenous fluid infusion should be established before any anaesthesia is given. Dehydrated or toxic bitches should be stabilized with fluids, corticosteroids and antibiotics prior to anaesthesia. All volume deficits should be corrected with balanced electrolyte solution such as ringer's lactate @ 10ml/kg/hour I/V. The surgeon should discuss with the client before surgery, the nature of surgical procedure, its possible complications and the issue of simultaneous ovariohysterectomy. The advisability of an additional operation for ovariohysterectomy should be carefully considered.

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Surgical Procedure: Site of operation Two surgical approaches are used for cesarean section: The ventral midline abdominal approach and the flank approach. The ventral abdominal approach provides better exposure of the uterus and requires less haemostasis. However, the flank approach reduces the chances of wound dehiscence and does not interfere with lactation. Technique 1. Prepare the ventral abdomen of the dog for aseptic surgery by shaving from xiphoid 'to pubis and scrubbing before induction of anaesthesia to reduce anesthesia time. 2. Long "incision to delivery" time is associated with increased fetal asphyxia and depression so operative speed is important in caesarean section. 3. Place the animal in dorsal recumbency. 4. Tilting the dam 10 to 200 to the right or left is not required as supine hypotension syndrome does not occur in the pregnant bitch. 5. After preparing the surgical site for aseptic surgery, drape the surgical field. 6. Make a ventral midline incision commencing at the umblicus and extending to a length sufficient to exposure the uterus. 7. Take care not to invade the mammary tissue while making skin incision, as the mammary glands are hypertrophied. 8. A void injury to the underlying viscera as the abdominal cavity is entered. 9. Exteriorize the uterine horns one by one by careful lifting through the incision. 10. Pack the uterus from the surrounding viscera with moistened laparotomy pads to avoid contamination of peritoneum by foetal fluids. 11. Make a longitudinal incision on the dorsal midline of the uterine body long enough to allow removal of the foetuses. 12. If it is dystocia, remove the foetus present in the uterine body first. 13. Bring each foetus to the incision by gently "milking it down" the uterine horn. This is done by squeezing the uterine horn cranial to the enlargement. 14. Once the fetus is near the incision, grasp it and apply gentle traction to facilitate rapid removal from the uterus. 15. As each foetus is removed, break the amniotic sac to allow breathing to begin. 16. Clamp the umbilical vessels and cut approximately 2 cm from the fetal abdomen. 17. Place the neonate on a sterile towel and pass to an attendant. 18. Remove the associated placenta from the endometrium slowly by gentle traction to minimize hemorrhage. 19. Repeat this procedure until all fetuses and placentas have been removed. 20. If considerable difficulty is encountered in mobilizing the fetuses down the uterine horns, additional incisions can be made in the horns. 21. Before closing the uterus, palpate it from the pelvic canal to each ovary to ensure that all fetuses and placentas have been removed. Vaginal canal should also be inspected.

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22. Once all fetuses have been removed, the uterus rapidly begins to contract. If the uterine contractions are absent administer oxytocin @ 1-2 units/kg I/M or I/V or ergonovine maleate 0.02 to 0.1 mg/kg I/M. 23. Close the uterine incision with one or two layers of continuous absorbable suture, using an inverting Lembert or Cushing pattern. 24. Clean the uterine surface with warm sterile saline solution and inspect the closure before returning the uterus to the abdomen. 25. Close the laparotomy incision with simple interrupted sutures in the ventral rectus sheath using absorbable sutures followed by placement of subcutaneous sutures. The skin is closed with non absorbable sutures. Resuscitation of neonates: 1. Clamp the umbilical cord (if it has not been done previously). 2. Remove the oral and nasal secretions by gentle suction or cotton swabs. A gentle downward swing of the neonate may help to clear the fluid from the upper airways. 3. Towel dry the infant. 4. Vigorous rubbing of the puppy usually stimulates respiration. However, it the puppy fails to breath artificial respiration may be attempted. 5. One to two drops of respiratory stimulants like dopamine (0.25 to 1 mg) may help initiate breathing. 6. Narcotic antagonists such as naloxone (0.01 mg/kg) placed on the tongue will reverse the effect of narcotics used for anaesthesia. Post Operative Complications Complication Hypovolemia and hypotension Hemorrhage Control/Treatment Vigorous fluid therapy or blood replacement a. Administration of oxytocin or ergonovine maleate b. Whole blood transfusion in severe hemorrhage c. Ovariohysterectomy in case hemorrhage is persistent a. Careful surgical technique peritonitis b. Intraoperative abdommallavage c. Antibiotics a. Normal milk flow usually occurs within 24 hours b. Oxytocin @ 0.5 units/kg I/V or I/M may be administered.

1. 2.

3.

Post operative peritonitis

4.

Agalactia

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Ultrasonographic Diagnosis of Reproductive Disorders in Canines

Dr. R. K. Chandolia Department of Animal Reproduction, Gynaecology & Obstetrics, College of Veterinary Sciences, CCS Haryana Agricultural University Hisar 125004 Introduction In veterinary sciences, ultrasonography is an emerging tool for the benefit of reproductive biologists, practicing veterinarians and academicians (Goddard, 1994). For the veterinary practice in India, the use of ultrasonography is still very less; the reason may be high cost of equipment and lack of proper training of the veterinarians in this field. In the recent past, this tool is being employed in the small animal practices, particularly bitches for diagnosis of various reproductive disorders and estimation of gestational status. In the past, veterinarians had limited assistance for assessing reproductive status of this animal. Pregnancy diagnosis in a bitch was possible either with the use of X-rays or transabdominal palpation, but that too at a advanced stage of gestation. These methods could provide information either about presence of pups in vitro, or their number, but assessment of fetal viability was not accurately predicted with these traditional methods. With the use of X-rays, there was always risk of harmful effects on the health of mother and fetus. As far as reproductive disorders are concerned, most of them remained either undiagnosed due to the lack of proper access to the internal organs or were diagnosed with a guess. In the recent past, with the advent of diagnostic ultrasound in veterinary field, a solution to the above problems appears possible. Diagnostic ultrasound is a valuable alternative imaging system that can provide more accurate information about the canine pregnancy and reproductive disorders in comparison to traditional methods. Ultrasonography is of many kinds such as A-mode, B-mode, M-mode and Doppler ultrasonography. For diagnostic purposes, B-mode ultrasonography is commonly employed. In this mode also, various frequencies are available. In bitches, frequencies of 4.0 to 7.5 MHz are used for scanning of reproductive tract. Preparation of the animal: The ultrasonographic scanning in bitches is done from lower abdomen/pelvic area. In this area, there are hairs that interfere in obtaining good quality images; therefore shaving of this area with a sharp razor is advised. Most of the bitches follow instructions from the pet owner, but for precaution (to avoid biting), the mouth of the animal should be tied with a cotton rope or a bandage. Light sedation is not usually required, but may be used if animal is not co-operative or pet owner is not accompanying the pet. Type of transducer: For scanning of reproductive organs of a bitch, a sector scanner should be used. Either a linear sector scanner or a convex sector scanner can be selected as per the availability. If a scanner of switch-able frequency is available, use that, it will be helpful in getting desired magnification and depth area of the tissue/organ. A transducer having frequency of 5.0 and 7.5 MHz can serve the purpose.

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Ultra scan gel: These water-based gels are available at a price ranging from Rs. 20 to 40. The quality of gel should be checked before making large purchases. Some gels are very thin and do not stick to the animal body; therefore are not useful. The gel should be of good quality that can serve the purpose of excluding air from the space between the transducer and animal skin. Scan area: The ultrasonography in the bitch is performed trans-abdominal/transcutaneous. The scan area ranged from pubis to cranial of the umbilicus or beyond umbilicus in pregnant animal. Procedure of scanning: 1. Keep the animal in dorsal or lateral recumbency. One person should take care of forelimbs and neck, while other should hold hind limbs. 2. The monitor of ultrasound machine should be at eye-level. 3. Apply gel on transducer and animal body. The transducer is moved from caudal to cranial direction. The area of movement of transducer should be between and around two rows of mammary glands. The urinary bladder should be taken as landmark to locate reproductive organs. 4. The image of non-pregnant uterus can be obtained in the area between two rows of mammary glands, while during early pregnancy; images are obtained by moving transducer lateral to mammary glands. 5. In .large bitches and pregnant animal, scanning can be performed in standing position, but in our experience, respiration and movement of animal interfere with scanning. There is also a problem of holding transducer in upside direction and one may loose contact easily, while moving transducer from one to another place. PREGNANCY STATUS: Investigators are of the opinioi1 that pregnancy can be detected from 17-21 days after the surge of plasma luteinising hormone, but real-time ultrasonography is a reliable method for pregnancy diagnosis in bitches from 21-22 days of pregnancy and for litter size estimation the most appropriate time is between day 25 and 30 of pregnancy. With advancing knowledge in this field, now it is possible to diagnose early pregnancy from day 18 onwards in Indian conditions, but one requires a good quality ultrasound machine. In our situations, where LH estimation is not always possible, there is a difficulty in ascertaining the exact date of pregnancy. In such cases, an estimation of stage of gestation is assessed on the basis of fetal development. Otherwise, the last date of mating is also taken as approximation for judging fetal age. Scanning on day 18 of gestation, the embryonic vesicle appears as spherical anechoic structures of around 2 mm diameter. It is actually the yolk sac contents that has filled the chorionic cavity, which appeared as the anechoic structure and is the first ultrasound confirmatory image of early pregnancy. The conceptus is initially somewhat spherical in nature, rapidly increases in size and may becoming oblate in appearance. On day 22 we can first recognize the fetal heart beat as rapid flickering in the center of the embryonic mass. The heartbeat ranges between 192 to 216. Accuracy of counting depends upon high long one can keep in focus the heart. During the same period, a 2nd fluid filled region adjacent to the embryo is also observed. The echoic images of developing allantois and the amnion may appear on 25th day. Amnion membrane is

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easily diagnosed in the fluid, while allantois needs some experience. Fetal growth is more rapid in between 32nd and 55th day of gestation. Marked differentiation of cylindrical fetus into its head, trunk, tail and umbilical cord is visible on 30th day. Hyperechoic fetal bones and heart valves can be appreciated on 40th day. Greater blood vessels are also seen during scanning at this time. In general from day 40th onwards only trunk diameter exceeds the head diameter. The hyperechoic regions of lungs and liver could be clearly distinguished approximately 20 days before parturition and fetal stomach can be imaged as an anechoic structure caudal to the liver around the same period itself. On careful slow scanning, fetal urinary bladder is also observed around this time. Hyperechogenicity of the fetal skeleton get enhanced during late pregnancy. With advancing gestation, the fetal kidneys can be imaged and fetal vasculature becomes more pronounced. In late pregnancy intestinal loops may be detected. Around day 50, the images of bladder are easily obtained as a 2nd anechoic structure in caudal abdomen. One more, anechoic structure can be located within the liver, which is the gall bladder during the same stage. Fetal death/resorption: In cases of early fetal death, fluid volume is reduced along with changes in normal echogenic pattern and also there will be marked loss of the embryonic mass and absence of fetal heartbeat, thickening and inward bulging of uterine wall with collapsed and reduced conceptus when compared to adjacent conceptus (England, 1990). In cases of fetal resorption, uterine ultrasonographic picture will be similar to that of post partum uterus, that is it will appear as homogenous and moderately hypoechoic areas (England and Allen, 1989b; Yeager and Concannon, 1990a). The beginner ultrasonographer can predict, the ensuing mortality if there is sudden slowing down of heartbeat or growth of the pup retarded in comparison to others or the fetal fluid turns turbid. The internal uterine diameter can also be used to predict normal and abnormal development of conceptus. Abortion: Diagnosis of abortion can be done using ultrasonography with high percentage of surety. During fetal death, the echogenicity of fetal fluid will be increased along with thickening of the uterine wall. If fetus is still inside, one should identify fetus proper and presence or absence of heart beat. In later stages of fetal death, fetal fluid volume gets reduced and fetus appears as flecked because of fetal tissue breakdown. The investigator also reported that in such cases, the conceptual sac collapses along with thickening and inward bulging of uterine wall. If fetus is already expelled out or resorbed then, the uterine images will be just like that of non-pregnant status. There may be some amount of fluid in the uterus in late abortion cases. Dystocia and fetal distress: In clinics, many a time cases are presented having problem of dystocia. Owner wish to know, whether the pups are dead or live in overgestation cases. Sometime one pup is delivered then, it is desired, whether any other pup is inside or not and status of retained pup. In our clinics, such quiries were answered through ultrasonography. The diagnosis of status of pups by ultrasonography helped in deciding the line of treatment. Using ultrasound it was easy to detect fetal heart beats from day 22 onwards and generalized fetal movements from day 28 onwards. In late stage of dystocia, the veterinarian has limited option of focusing either on heart or head at one time. Overlapping of fetal parts make it difficult to ascertain exact number of fetuses in bitch in advance gestation. Scanning at advance stages dystocia cases is performed with

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3.5 to 5.0 MHz transducer. In such cases, the animal is shaved from lover abdomen and kept in standing or lateral recumbency. In standing position respiratory movements of mother interfere in obtaining good pictures of fetus. Therefore, lateral recumbency is the choice for scanning. If the fetal heartbeat is detected then it should be counted for 5 or 10 seconds and multiply it accordingly to convert it per minutes. From this fetal distress can be easily detected. If the fetal heart rate is less than twice than that of maternal rate, it is an indication of significant distress. In one case of dystocia, the animal showed severe straining without expulsion of pups. Uterine involution During first week after delivery, the horns showed multiple layers of varying echogenicity with discrete areas of enlargement with hypoechoic centers at regions of placenta. Measurement of uterine dimensions, particularly of uterine horns is considered helpful in knowing the proper involution of genitalia. Normal size of the uterus, equivalent to that of non-pregnancy i.e. anoestrus, is reached within 4 -6 weeks of whelping. Retaintion of Placenta: Scanning for such cases can be done using 5.0 MHz transducer. In such cases, there will be echogenicity due to soft tissue debris and blood clots. This will be seen as echoic spots in the unnechoic fluid within uterus (Pharr and Post, 1992). Again, one needs to have some experience for such diagnosis otherwise, confirmatory diagnosis of retained placenta will be very difficult. Visualisation of the abnormalities of the non-pregnant uterus: To obtain images of normal uterus during anoestrus in young nulliparous bitch is difficult due to small transverse diameter, which is less than, but with good quality machine and transducer of high frequency, it can be visualized on dorsolateral aspect of urinary bladder. In older, pluriparous bitch the scanning of uterus is comparatively easier. The uterine horns and body are having two distinct lyers, these in ultrasound can be visualised as centrally, relatively hypoechoic area, surrounded by hyperechoic layer, which are endomatrium with serosa. During oestrus, the transverse section of uterus appears more hypo-echoic as compared to images during anoestrus. The hypoechoic image is due to oedematous endometrial folds. Further drop in echogenicity of the uterus is seen in mated bitches during early pregnancy. Images at this time (Few days after mating) are show an increase in uterine diameter and presence of unechoic fluid. Continuous scanning during such early phase of pregnancy (also referred as dioestrus phase), there is continuous increase in diameters of cross sections of the uterus, but echogenic appearance of uterine wall remain similar to those images obtained during proestrus. Cystic Endometrial Hyperplasia (CEI-J): This condition is associated with high progesterone concentration and has been observed during luteal phase (diestrus) leading to the cystic hyperplasia of endometrium. Diagnosis of this condition requires skill of the operator and good resolution of the machine. Moreover, in certain cases of'CEH changes are not visualised due to small lesions. On careful visualization of the ultrasound image, one may find many small anechoic cysts, which are seen in many sections of the endometrium. In certain cases the diamensions of these cysts reaches up to 5 mm or larger due to coalesce of smaller lesions. There is need to differentiate these cysts from other anechoic images. Infect, these CEH cysts lack a well defined border and are asymmetrical. Pyometra: Ultrasonography is considered as wonderful tool for

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the diagnosis of pyometra. The ultrasonographic diagnosis of pyometra is possible even before the appearance of the clinical signs. In pyometra, one may obtain transverse or longitudinal sections that show large diameters in comparison to non-pregnant genitalia. Due to increase in diameter of these sections and folding up of the the endometrial layer, images of two or three sections of each horn are seen in a single plane. Enlargement of these sections of uterus depends upon the type of pyometra, being less in open than closed pyometra. In such cases, uterine wall will appear hyperechoic and there will be increase in its thickness. These sections contain anechoic fluid, but mixed with echoic particles of inflammatory debris. It is also reported that in case of pyometra scanning may reveal an outer echogenic area with an inner hypoechoic to anechoic ring and a central hyperechoic zone and they suggested that the hypoechoic region was as a result of vascular enlargement and secretory gland activity. Differential diagnosis of other causes of uterine fluid accumulation like mucometra and hydrometra is difficult and experience of images of these various conditions.

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Clinical Pathology of common diseases of dogs

Dr. K.K. Jakhar Teaching Veterinary Clinical Service Complex, CCS HAU, Hisar. Dog was the first animal to be domesticated because of its pleasing disposition, obedience, loyalty and fidelity. It is estimated that dog population in India is about 30 million with 1:30 dog to human ratio. With change in social attitude and increasing urbanization, veterinarians have to be alerted to needs of society for better canine health. With advanced .diagnostic techniques, diseases are being reported with increased frequency. In this lecture, I will be discussing clinical pathology of diseases frequently encountered in large number in clinics with an updated look. The important canine disease can be categorized into infectious and non infectious diseases. Infectious Diseases: Canine Distemper: Haemogram : Haemogram varies with stage of disease. In the early acute cases leukopenia due to lymphopenia and in later stages leukocytosis in 20% cases due to neutrophilic shift to left, thrombocytopenia (as low as 30000/ml) and regenerative anaemia. Distemper inclusions in lymphocytes (up to 3 m) and erythrocytes (light blue excentrically placed bigger than howell jolly body). Biochemical Tests: The changes are non specific. Hypoalbuminemia, Hyperglobulinemia, mild hypocalcemia (8.5 mg/dl) Cereberospinal Fluid: Increased protein (>25 mg/dl) and cell count predominantly lymphocytes (> 10 cell/dl) Biopsy: Intracytoplasmic and intranuclear acidophilic inclusions (5 m in diameter) in epithelial cells of respiratory system and urinary bladder are pathognomonic. Materials to be collected: Blood, serum, conjuctival/gum smear (swabs in Hank's medium) and tonsilar biopsy during clinical examination and liver, spleen, lung, lymph node and brain in Hank's medium and 10% formalin on post-mortem examination. Confirmation: Fluorescent antibody test (FAT), virus neutralization (VN), virus isolation (VI), complement fixation (CFT) and direct examination of blood smear (DEBS). Infectious Canine Hepatitis: Haemogram : A brief prefebrile leukocytosis precedes leukopenia. Leukopenia characteristic (2000-7000 ml) from second day post infection due to neutropenia and lymphopenia. Eosinophils may be entirely absent at peak of leukopenia. Leucopenia persists up to 5th day. During period of recovery i.e. 6th day onwards leukocytosis due to marked lymphocytosis and neutrophilia. There is an increase in immature lymphocytes. The PCV shows a continuous decrease. Thrombocytes are markedly reduced. Biochemical Tests: Hypoproteinemia, Increased serum AL T, AST, alkaline phosphatase, hyperbilrubinemia, hypoglycemia (20 mg/dl), decreased prothrombin and clotting time. Urine Examination: Bile pigment positive (Bilirubinuria) Cereberospinal fluid: Protein concentration -> 30 mg/dl and mononuclear cells > 10 cell/cumm.

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Biopsy/Necropsy: Intranuclear basophilic inclusions with margination of chromatin material of enlarged nucleus in heptocytes are pathgnomonic. Materials to be collected: Blood, serum, urine, nasal and tonsilar swabs in transport medium during clinical examination and visceral organs chiefly liver, kidneys, spleen and gall bladder in transport medium and in 10% formalin during post-mortem examination. Confirmation: FAT, VN, CFT, Haemagglutination inhibition (HI), DEBS. Canine Parvo Virus: Concurrent infection with opportunistic enteric organisms are not uncommon. Haemogram: Leukopenia (500-2000 cells/ml) due to lymphopenia (more) and neutropenia. Feces: Melena (blood positive). Biochemical tests: Decreased serum albumin, sodium, potassium and chlorides while increased serum AST, LDH anQ creatinine phosphokinase, serum IgG titre and blood glucose (more so in puppies upto 150 mg/dl) are consistent findings. Biopsy/Necropsy: Myocarditis and haemorrhagic gestroenteritis. Parvo virus particles in immunoelectroscopy. Materials to be collected: Blood, paired sera samples, and feces (50% glycerine saline) during clinical examination and intestines, heart, spleen, liver, mesenteric lymph nodes and thymus in 50% glycerine saline and 10% formalin at post-mortem examination. Confirmation: FAT, VN, VI, HI and Electron microscopy. Canine Corona virus: Haemogram: Non specific. Leucopenia is rare as compared to parvo virus. Feces: Yellow green to orange malodorous feces are characteristic. Materials to be collected: Blood, paired sera samples and feces (in 50% glycerine saline) during clinical examination and intestines (in 50% glycerine saline and 10% formalin) at post-mortem examination. Confirmation: FAT, VI, VN and Electron microscopy. Canine Tracheobronchitis (kennel cough): The disease is of multiple etiology and various agents implicated are parainfluenza, adenovirus 1 & 2, herpes, Mycoplasma and Bordetella species. Haemogram: Absolute neutrophilia leading to leukocytosis (16000 to 26000/ml) Biopsy: Aspiration of tracheal fluid contain large number of neutrophils. Materials to be collected: Blood, paired sera, nasal, pharyngeal and tonsilar swabs (in 50% glycerine saline) during clinical examination and liver, lung and kidney in 50% glycerine saline and 10% formalin at post-mortem examination. Confirmation: FAT, VI, VN, HI, HA. Rabies: Haemogram: Not specific. The number of leukocytes increases on the appearance of clinical signs reaching 15000 to 19000/ml (mainly due to neutrophilia) which declines on day of death. Biochemical: Nil. Cerebrospinal Fluid: Increased protein (110 to 150 mg/dl) and leukocytes (predominance of lymphocytes) - 120 to 240/cumm.

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Biopsy/Necropsy: Intracytoplasmic eosinophilic inclusion bodies (negri bodies) with clear halo around them (1-27 m with 1-20 bodies) in each neurons of Hippocampus of dogs are pathognomonic. The smear (corneal impression/mucosal scrapings) can be stained by Sellor's stain. Materials to be collected: Mucosal scrapings and corneal impression swabs in 50% glycerine saline on clinical examination and brain (hippocampus) and salivary glands in 50% glycerine saline and 10% formalin at post-mortem examination. Confirmation: FA "f, VI, VN, Mouse inoculation test and direct examination of impression smears. Eherlichiosis (Tick borne fever): It is caused by Eherlichia canis and E. gibsoni and transmitted by brown tick. Infection can occur concurrently with babesiosis. Haemogram: In acute cases usually normal but may reflect mild normocytic, normochromic anaemia, leukopenia, mild leucocytosis and thrombocytopenia. In chronic cases severe thrombocytopenia, severe leukopenia due to pancytopenia and non regenerative anaemia. Coccoid bodies in cytoplasm of monocytes usually and neutrophils and lymphocytes sometimes. Biochemical tests: Increased serum globulins. Biopsy/Necropsy: Aspiration biopsy from lymphnode reveal plasmacytosis and coccoid bodies in cytoplasm of monocytes usually and neutrophils and lymphocytes sometimes. Urine: Blood positive (haematuria) Feces: Blood positive (melena) Materials to be collected: Blood, buffy coat smears during clinical examination and lung, liver and spleen under refrigeration and 10% formalin at post-mortem examination. Confirmation: FAT and direct examination of smear from buffy coat/blood. Leptospirosis: Previously infection with Leptospira canicola and L. icterohaemorrhagica and recently L. pomona and L. grippotyphosa. Haemogram: Leukocytosis with marked shift to left is characteristic of acute form with total leukocyte count as high as 35000/ml after 5th day of infection. Leukocytosis may be absent in subclinical cases and transient leukopenia during febrile period. Lymphopenia, monocytosis and thrombocytopenia are also seen. In some cases decrease in Haemoglobin of 1 to 2 gm/dl with commensurate decrease in PCV, icterus and sometimes their may be increase in TEC, Haemoglobin and PCV due to haemoconcentration. Urine: Decreased volume, dark red colour, specific gravity increased, Albumin positive, acidic pH, glucosuria, casts (Hyaline, epithelial, leukocytic and erythrocytic), erythrocytes abundant and few leukocytes (pus cells). Biochemical: Azotemia, decreased sodium, chloride, phosphorous and increased serum AST, AL T, alkaline phosphatase, bilirubin and BUN usually high but variable. Materials to be collected: Blood, urine and paired sera samples during clinical examination and liver, kidney and spleen under refrigeration and 10% formalin on postmortem examination. Confirmation: Culture and direct examination of blood/urine.

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Tuberculosis: The dogs may be infected with Mycobacterium tuberculosis, M. bovis and occasionally M. avium. Haemogram and biochemical tests: Not specific except monocytosis. Biopsy/necropsy: Examination of sputum and discharges/peritoneal fluid for acid fast coccobacillary organisms. Tubercles in visceral organs lack calcification, langhan's giant cells but sarcomatous. Materials to be collected: Sputum, nasal discharges peritoneal fluid under refrigeration during clinical examination and lungs and liver under refrigeration and 10% formalin during post-mortem examination. Confirmation: Cultural examination and direct smear examination, Intradermal Tuberculin test. Babesiosis: Caused by Babesia Canis and Babesia gibsoni. Haemogram: Haemolytic regenerative anaemia, anisocytosis, poikilocytosis, polychromasia and nucleated erythrocytes, reticulocytes, parasite in erythrocytes (with few to many pyriform - 4-5 m shape organisms) and mild thrombocytopenia. Leukocytosis of varying degree may be present with associated neutrophilia. Urine: Granular and cellular cast in urine, blood positive (Haemoglobinuria), Proteinuria. Biochemical Test: Metabolic acidosis decreased CO2. HCO3 and lower blood lactate. Materials to be collected: Blood, urine during clinical examination. Confirmation: Direct blood smears examination. Demodicosis: Generalized. Confirmation by skin scrapings of demodex species with cigar shaped bodies and stumpy legs. Sarcoptic mange: Confirmation by skin scrapings with circular outline with four pairs of short and stumpy legs. Dirofilariasis: Seen in large breeds of dogs. There is a leukocytosis and eosinophilia. Confirmation: By blood smear and direct wet blood film examination for microfilarae. Ancylostomiasis: Haemogram: Microcytic hypochromic anaemia, marked leukocytosis with an absolute neutrophilia with right shift and eosinophilia is variable. Feces: Melena (blood positive). Confirmation: Faecal examination for eggs which are embryonated and strongyle like but smaller in size. Pyoderma: Secondary to ectoparasitism/allergic dermatitis/harmonal imbalance. Haemogram: Leukocytosis due to neutrophilia and eosinophilia. Biopsy/Necropsy: Massive infiltration of neutrophils in dermis and epidermis in skin. Materials to be collected: Discharges from skin under refrigeration and skin biopsy in 10% formalin during clinical examination. Confirmation: Aseptic culture. Pyometra: Multiple aetiology Haemogram: Marked leukocytosis (20000 to 100000 or more) with average of 50000/ml due to absolute neutrophilia (shift to left) with toxic granulation. PCV is normal but occasionally non-regenerative anaemia and

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haemoconcentration. Confirmation: By cultural examination of aseptically collected pus under refrigeration conditions. Ring worm: Caused by Trichophyton and Microsporum species. Confirmation: By culture of skin scrapings and demonstration of fungus. Pyelonephritis: Multiple aetiology. Haemogram: Leukocytosis occurs if large area of kidney is involved. Urine: Turbid colour (sometimes bloody), proteinuria, alkaline PH, blood positive, pus cells in masses. Erythrocyte and epithelial cells and clumped bacteria present. Confirmation: Cultural examination. Metritis: Multiple aetiology. Leucocytosis (25000/ml) due to neutrophilic shift to left. Confirmation by cultural examination of uterine discharge. Chronic renal (interstitial) disease: Multiple aetiology Haemogram: Leucocytosis (20000 to 30000 ml) due to neutrophilic right shift, monocytosis but lymphopenia and a non regenerative normocytic and normochromic anaemia. Urine: Increased volume, pale yellow colour, low specific gravity, mild proteinuria, few pus cells and erythrocytes and granular casts. Biochemical: BUN Normal/slightly increased. Confirmation: Cultural examination. Prostatic abscess: Haemogram: Leucocytosis. Urine: Cloudy urine, pH alkaline, erythrocytes and leucocytes numerous, epithelial cells present and bacteria seen. Confirmation: Cultural examination. Pneumonia: Multiple aetiology. Haemogram: During mild disease slight anaemia, marked leukocytosis due to neutrophilia but eosinopenia and lymphopenia while in severe disease, severe anaemia with marked leukopenia with relative neutrophilia and shift to left. Also decrease in eosinophils and lymphocytes. Non-infectious diseases: Hypertrophic osteodystrophy: Haemogram: During febrile state, a leukocytosis with neutrophilic shift to left and slight anaemia. Biochemical: Calcium and phosphorus imbalance. Lead Poisoning: Numerous nucleated erythrocytes with basophilic striplings in absence of severe anaemia, polychromasia and reticulocytes. Polycythemia vera: There is a absolute increase in number of erythrocytes, Hb and PCV values. Diabetes mellitus: Haemogram: Leucocytosis and increased PCV. Urine: Volume increased, specific gravity increased, colour yellow/orange/amber, glucose positive. Biochemical: Higher Glucose levels in blood and elevated BUN. Confirmation: By Glucose levels in blood.

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Allergic dermatitis: Increase in eosinophils. Obesity: Hormonal imbalances. Increased cholesterol in blood. Zinc responsive dermatitis: Pups over supplemented with calcium induce zinc deficiency. There is a significant lower levels of zinc in blood and no ectoparasite in skin scrapings. Hyper-parathyroidism: Pups fed on meat and organ tissue diets suffer from this disease because of continuous mobilization of calcium from bones. Hypocalcaemia is characteristic. Transmissible venereal tumor: Haemogram: Anaemia in chronic cases. Leucocytosis due to secondary infection. Biopsy: Cells in clusters with minimum connective tissue. Nucleus with fine chromatin, large nucleus and abundant cytoplasm. Urine: Erythrocytes in urine. Materials to be collected: Vaginal discharge and tumor tissue. Confirmation: By vaginal discharges/biopsy. Stress: Non regenerative anaemia, neutrophilic leukocytosis with lymphopenia and eosinopenia. So clinico-pathological picture is an important aid in diagnosis of canine diseases and future veterinary diagnostician will have significant role in improving canine health. References: Benjamin, M.M. 2001. Outline of Veterinary Clinical Pathology, Kalyani Publishers, New Delhi pp93-97. Greene, C.E. 1984. Clinical Microbiology and Infectious diseases of the Dog and Cat, W.B. Saunders Company, USA. Jakhar, K.K., Gupta S.K., Gera S. and Gulati B.R. 2001. Laboratory manual for Veterinary Laboratory Diagnosis, College of Veterinary Sciences, Haryana Agricultural University, Hisar (India). Varshney J.P. 2000. Clinical diagnosis of emerging djseases of canine, Monograph on diagnosis of emerging diseases of livestock, IVRI, Izatnagar, India.

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Surgical affections of Teeth in Dogs

Sukhbir Singh Department of Veterinary Surgery & Radiology College of Veterinary Sciences CCSHAU, Hisar Tooth The functions of teeth are prehension, mastication and weapon. Types of teeth: there are four types of teeth namely incisors, canines, premolars (P), molars (M) (Cheek teeth, sectorial or carnassial -4th maxi. P and 1st mandibular: M., Tuberculate teeth). Deciduous/temporary and permanent, mandibular, maxillary. Anatomy: Composition: Pulp, dentin, enamel/cement lodged in alveolus and held firmly by periodontal ligament.

Parts: Crown, neck, root. Neck is embraced by gingiva (gingival margin, gingival sulcus.) Surfaces: Labial, buccal, lingual, masticatory, contact/dental. Single root teeth: all incisions and canines, first Ps, mandibular 3M=22 Double root teeth: maxillary 2 & 3 P, mandibular 2, 3 & 4 P and 1 & 2 M=14. Triple root teeth: maxillary 4P and molars=6. Dentition Formulae Deciduous: 2(Di313, DC1Il, DP 0+310+3)=28 Permanent: 2(1313, C1Il, P414, M213)=42 Eruption of teeth: Primary or deciduous teeth 1. Born edentulous (without teeth) 2. Central & Intermediate incisors and canines-during the first month 3. Lateral incisors between 5 and 6 weeks. 4. Premolars (2, 3, 4) at 4 to 8 weeks.

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Secondary or permanent teeth 1. Incisors at 2 to 5 months 2. Canines at 5 to 6 months 3. Premolars A) First -at 5 to 6 months B) Second- at 6 months C) Third- at six months D) Fourth- between 4 and 5 months 4. Molars A) First- 5 to 6 months B) Second- 6 to 7 months C) Third- 6 to 7 months Dental Affections Developmental anomalies: e.g. abnormalities of shape, abnormal number: complete congenital absence of teeth, extremely rare condition in dogs. Polyodantia or supernumerary teeth: rare condition, more common in upper jawmay result in malocclusion and crowding as well as incomplete eruption or impaction of adjacent teeth, extraction of these teeth is the remedy. Retained deciduous teeth: quite common due to absence of corresponding permanent tooth and incomplete root absorption. Extraction is recommended. Injuries to teeth: Attrition: wearing away of dental substance due to occlusion contact and mastication, normal physiological process associated with aging. Attrition is usually minimal in carnivores that have a normal diet. Abrasion- it is pathological wearing away of dental substance due to abnormal chewing habits, cage or stone biting. It may predispose fracture of teeth. Dental fracture: common in dogs. Enamel or uncomplicated crown fractures are of little clinical importance. Soft tissue trauma due to fractured ends. Fractures involve the periodontal ligament and may lead to periodontitis, hence extraction is indicated. Caries/cavities: a microbial disease of calcified tissue of the tooth characterized by demineralization of inorganic portion and destruction of organic substance. May be in the form of brown or black pit or fissure on occlusal surface or at the neck. It may involve different structures depending on its depth. Clinical signs are -difficulty in eating and jaw chattering. Mostly 1st molars are affected due to large occlusal surface. Salivary pH and urea concentration is higher in dogs that neutralize the acid produced by bacteria. Periodontal disease: pathological condition involving the structures surrounding the tooth namely gingiva, periodontal ligament and the alveolus. Chronic presence of bacterial products around teeth results in gingivitis- deeper inflammation- loss of supporting alveolar bone-destruction of fibrous connective tissue- loss of tooth. Treatment: Preventive therapy- keep the teeth clean. Oral hygiene is important. Tooth brushing, antiseptic mouth rinses are recommended. Removal of plaque and calculus by scaling, smoothen the rough surfaces and hard diet is recommended. Surgery for root debridement is recommended when pocket depth is 5 mm or more. Endodontic therapy- recommended when tooth with necrotic pulp is to be retained. After the full development of tooth, pulp is not required. Indications are pulpitis, fractured pulp.

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Gingiva (Gums) Healthy gums are must for health teeth Gums massage is as important as teeth brushing. Special care to be taken for gingival sulci Conditions of gums: Gingivitis, gingival hyperplasia and neoplasms Dental Extraction or Exodontics Indications: Gross decay or carries Fractured tooth involving pulp Advanced periodontal disease Supernumerary teeth Malocclusion Retained deciduous teeth Teeth in fracture line (Mandible or maxilla) Periapical abscess Basic Principles Good accessibility to surgical site Good visibility Gentle tissue handling Thorough debridement Section or division of crown with bur in Dental Instruments for Extraction Dental elevators Dental drill/burs Extraction forceps Complications of Extraction Haemorrhage Fracture of mandible Root retension Necrosis of bone around extraction site Oronasal fistula Functional abnormalities Gingivallacerations Fracture of alveolus Local/systemic infection (Septicemia)

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Pain Management in Pet Practice

Kuldip Singh Professor & Head Department of Veterinary Surgery &Radiology COVS, CCSHAU; Hisar Pain is defines as (IASP 1979) Unpleasant sensory and emotional experience associated with tissue damage and initiated by stimulation of nociceptors (free nerve terminals of afferent fibres present in all tissues but abundant in viscera) Nociceptors are innervated by two types of afferent nerves -a -delta (myelinated, for fast pain-6-30 m/sec ) and c fiber (non-myelinated, for slow pain) C fiber are dull aching (0.5 -2 mtr./second) induces the release of mediators and neurotransmitters in dorsal horn of spinal cord that enhances further pain perception (central sensitization) Behavioral and Physiologic Responses to Pain Behavioral: Growling, whining Dilated pupil, Stare gazed, stare look Rigid, Hunched posture Aggressive, fearfulness behavior Decreased appetite Lick the injured area Unkempt appearance Physiolgical responses: Increased heart rate, blood pressure, vasocons. Increased respiration rate, shallow breathing Inappetance vomition, constipation or diarrhoea Tense muscles Increased catabolism Numerical Rating Scale Posture Vocalization Appetite and thirst Temperament Response to palpation Facial Expression Mental Status

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Classification of surgeries as per degree of pain Most painful Thoracotmy Pelvic fracture Nephroectomy Ear resection Amputation Spinal surgery Moderate to severe Mastectomy Disc surgery Abdominal surgery Fracture repair Mild to moderate of ear Castration Dental extraction Tracheotomy Fracture of radius, tibia

General Terms Allodynia- pain resulting from non-noxious stimulus -that does not normally provoke pain. Neuralgia -pain in nerves Neuropathy -pathological change in nerve. Nociceptor- a specialized afferent nerve ending which transduces painful stimuli (noxious) into nerve impulse. Noxieption -process resulting in conscious perception of pain Central pain- pain associated with CNS lesions. Hyperesthesia increase sensitivity of stimulation Hyperalgesia increased pain response to stimulation. Analgesia-absence of pain sensation. Anesthesia-absence of all sensory modalities. Pre-emptive analgesia- analgesia before onset of pain stimuli to prevent central/peripheral sensitization processes, if left unabated results in hyperalgesia. By administering analgesic before surgery, spinal cord is not exposed to barrage of afferent nociceptive impulses that induce spinal hyper-sensitivity and neuroplastic changes associated with development of allodynia/ hyperalgesia. Noxious stimulus- adequate to trigger nociceptive reaction (damaging to tissue) Physiological pain- Protective to animal-results from heat, cold, pressure. Somatic pain- well localized cutaneous pain (skin, joint, muscle, periosteum involved) Visceral pain- more defused, less localized originate from internal organs. Referred pain may occur with visceral stimulation for example: cramping, gnawing. Neuropathic pain- Due to damage to peripheral nerve or spinal cord, not responsive to treatment. Inflammatory pain- results from tissue damage due to surgery, hypoxia, freezing, burning and characterized by following terms. a. Primary hyperalgesia- sensitization of nociceptors at injury time (inflammatory mediators released) b. Secondary hyperalgesia- changes in sensory processing of peripheral of CNS term wind up and fecilitation. It is mediated by release of P-substance, glutamate, neuropeptide that activate N-methyl D asparatate, natural killer cell-!, receptors that promote central sensitization

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c. Allodynia- low threshold response. d. Field plasticity- poorly localized sensation. (Plasticity refers to ability of nervous system to modify function in response to different environmental stimuli. Peripheral and central sensitization occurs following injury.) Physiology of pain (Nociception) * Four physiological processes take part in processing nerve signals generated by stimulation of nociceptors finally resulting in perception of pain. 1. Transduction- receptors of mechano/thermo/chemo sensitive.-it is translation of noxious stimuli into electrical activity relayed to CNS via specific afferent nerve fiber. Inhibited by local anaestheti, opioid, NSAIDS. 2. Transmission: It occurs via peripheral afferent sensory nerve fiber and ascending pathways within spinal cord. Nerve amples is propagated through peripheral nerve system. Abolished by epidural injection, alpha2 agonists. 3. Modulation: Occur within spinal cord and from supraspinal areas fecilitatory pain receptors are substance P, glutamate, PG Spinal inhibitory receptors are GABA opioid (Mu, k, delta, alpha-2, .adenosine (A-l type receptors). Central sensitization is inhibiteed by opiods, local anaesthetics, choline estrase inhibitors. NSAID modulate spinal processing of painful stimuli 4. Perception: It is abolished by general anaesthetic, opioid and alpha-2 agonist. It is final process and integration of thalamo, cortical, reticular limbic function to produce pain. Pain Management Anaesthetic Induction agents (Propofol, etomidate + inhalent anaesthetics (Isoflurane/ sevoflurane- speedy recovery but no analgesia so supplement with analgesics. Acepromazine+butorphenol Diazepam+butorphenol Medetomidine+ morphine Acepromazine+oxymorphone Ketamine +xylazine or medetomidine are good analgesics Tranquilizers/sedatives: ACP good for acutely distress dog Benzodiazepine (Diazepam+midazolam) not good tranquilizers may cause excitement. Xylazine/medetomidine- cause profound cardiopulmonary effects. Pre-emptive analgesia is most effective mean of controlling pain e.g. meloxicam, piroxicam, ketoprofan, ketorolac, caprofen, butorphanol are effective drugs in dogs.

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Local anaesthetics Neural-blockade of sensory afferent nerves tract by local anesthetics-epidural, regional nerve block/infiltration. Epidural analgesia is good for high risk patient, c. section, amputation. Dissociative analgesia: ketamine effective in controlling pain arising from superficial surface but not viscera (1-2 mg/kg I/v). Results into interruption of ascending nociceptive input as it traverses thalamo neocorticol system. May lead to salivation, seizure, bronchodilation. NSAIDs analgesic agents for chronic pain, anti-inflammatory effect, decrease production of prostanoids which facilitate pain. Side effects are kidney, liver damage ulcers and blood clotting problems. Opioids Interfere with nociceptive neural transmission centrally. Butorphanol is good for peritonitis, pancreatitis (.4-1.0 mg/kg three times for three days), and minimum respiratory depression. Buprenorphine useful for mild to moderate pain. Effect last for 4-8 hrs. Codeine- not to be given in dog with liver disease. Morphine -effect for 3-4 hours (.1 mg/kg body wt.) Side effects are histamine release, decreased temperature, miosis, vomition, decreased heart rate, slow A V conduction. Fentanyl effective analgesic for short duration- good for critically ill-patient. Fentanyl 1-2 microgram per kg + midazolam 1-6 microgram per hour may be used constant infusion. Fentanyl patch provide relief for three days. Tranquilizers and Sedatives Drug Midazolam Xylazine Dosage (mg/kg) 0.2 0.1 0.5

Commonly used systemic Opioid Analgesics Drug Butorphanol Buprenorphine Fentanyl Morphine Hydromorphone Oxymorphone Dosage (mg/kg) 0.2 0.4 0.005 0.015 0.002 0.005 0.1 0.4 0.1 0.2 0.05 0.1

Dose recommendations of Opioids alpha-2 adrenergic agonist combinations for postoper.analgesia (Injected im or iv route)

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Drug Medetomidine + Butorphanol Xyalzine + Butorphanol Medotomidine + Morphine Xylazine +Morphine Medotimidine + Oxymorphone Xylazine + Oxymorphone

Dosage (mg/kg) Dog: 0.004 0.01 + 0.2 Cat: 0.01 0.03 + 0.2 Dog: 0.5 + 0.2 Cat: 0.75 1.0 + 0.2 Dog: 0.004 0.01 +0.5 Cat: 0.01 0.03 +0.1 Dog: 0.5 + 0.5 Cat: 0.75 1.0 + 0.1 Dog: 0.04 0.01 + 0.1 0.2 Cat: 0.01 0.03 + 0.1 0.2 Dog: 0.5 + 0.1 0.2 Cat: 0.75 1.0 + 0.1 0.2

Effect last for 2-6 hours Epidural dosages of various combinations used in the dog. Drug Dosage (mg/kg) Duration Morphine Morphine + Medetomidine Oxymorphone Fentanyl Lidocaine Bupivicaine Morphine + Bupivicaine 0.05 0.2 0.05 0.2 + 0.005 5 -84 10 164

0.05 0.15 8 12 0.005 0.04 0.5 1.0 1.0 ml/4.5 Kg 2.0 4.0 6 -12 1.0 ml/4.5 Kg 0.05 mg/Kg morphine diluted 8 -16 in 1 ml/4.5 kg of bupivicaine NSAIDS and corticosteroid dose recommendation Dosage (mg/kg) Drug Aspirin 10-20 fig/kg q 12 hr po Phenylbutazone 15-20 fig/kg q 8-12 hr PO Carpofen 2.2 fig/kg q 12 hr PO Etodo1ac 10-15 fig/kg q 24 hrs.PO Ketoprofen 1-2 fig/kg q 24 hrs PO for 5 days Meloxicam 0.2 fig/kg PO Piroxicam 0.3 mg/kg q 48 hrs PO Meclofenamic 0.1 mg/kg q 24 hrs PO Ketorolac 0.3-0.5 mg/kg q 8-12 hrs Flunixin meglumine 1.1 mg/kg q 24 hrs/PO Acetaminophen 15 mg/kg q 8 hrs. PO(Not to be given in cats) Prednisolone 0.5 -1.0 mg q 12-24 hrs. PO All leads to gastric irritation, kidney damage, ulcers.

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Formulation of diets for dogs

Dr. Dinanath Prasad Professor Deptt. of V ety. Clinical Medicine College ofVety. Sciences CCS Haryana Agricultural University, Hisar-125 004 Diets formulation for dogs has three components: 1. Nutrient requirements for various categories of dogs; 2. Nutrient composition of available feeds for dogs and 3. Knowledge of the individual dog i.e. current weight, adult weight and physiological state of the dog. Let us discuss one by one and finalize a broad guideline about dogs diet. 1. Nutrient requirements for various categories of dogs: The ideal way to provide dog with its nutritional needs is to incorporate its exact daily nutrient requirements into precisely that amount of food consumed each day to meet the animal's energy needs. This has led to the expression of nutritional requirements as so many units of a nutrient per 100 kcal of metabolizable energy (ME). An alternative is to express .nutrient requirements per kg of body wt per day. These bases for expression have been employed in the most recent edition (1985) of the standard work on dog nutrition-Nutrient Requirements of Dogs prepared by the Subcommittee on Dog nutrition of the Committee on Animal Nutrition of the National Research Council (NRC). The recommendations of that group are incorporated in TABLES 1 to 6. The use of energy or body weight as a basis for expressing nutrient requirements is intellectually satisfying but lacks a certain practicality when making comparisons between rations or making .recommendations to the dog owner. For those reasons, the older (1974) recommendations of the NRC for dogs of average size are presented in TABLE 1-6. PROTEIN The dog's protein requirement usually is met by commercial dog foods having a minimum of 22-28% of average quality protein, on a dry-weight basis. There is some evidence that' dietary levels of high quality, highly digestible protein of as low as 10% may be acceptable for adult dogs in a maintenance state. Lactating bitches should receive 28% of the diet as protein. Soybean meal, eggs, dairy products, muscle meats, and the less tendinous organs are all satisfactory sources of amino acids for dogs. The higher the quality of protein fed, the lower the percentage of total protein needed in the diet. Average quality protein should provide at least 18% of the diet's total calories for the mature, non-reproducing dog.

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Table-1: Minimum Nutrient Requirements of Dogs for Growth and Maintenance (Amounts per kg body Weight per Day) Protein Nutrient Arginine Histidine Isoleucine Leucine Lysine Methionine cystone Phenylalanine tyrosine Threonine Tryptophan Valine Dispensable amino acids Unit mg mg mg mg mg mg mg mg mg mg mg Growth 274 98 296 328 280 212 390 254 82 210 3414 Adult Maintenance 21 22 48 84 50 30 86 44 13 60 1266

The ability of a protein to meet the dog's amino acid requirements depends on its ability to supply them in the correct quantity and proportion. For this reason, the NRC does not make a recommendation for protein intake but cites required intakes of "indispensable" (essential) and "dispensable" (non-essential) amino acids. This approach is quite correct but lacks a certain practicality; it may be more useful to remember that an adult, non-reproducing dog requires about 22% of the diet dry matter as an average quality protein. CARBOHYDRATES The dog utilizes properly cooked carbohydrates with almost the same efficiency as man. Carbohydrates are economical sources of energy, and help to spare proteins from being used for energy. Carbohydrates may safely supply 60% of dietary calories without causing a deficiency of proteins, fats, minerals or vitamins. Dogs lack the ability to digest efficiently uncooked cereals or raw starches and these should be cooked during processing of dog foods. Lactose (milk sugar) is poorly digested by some dogs; therefore, large quantities of cow's milk should not be given to either puppies or adult dogs. Undigested lactose may ferment in the intestinal tract and cause diarrhea. Many species have what appears to be a "requirement" for carbohydrate or a level of carbohydrate that must be present in the diet if ketosis is to be avoided. Most dogs appear not to have a minimal requirement for carbohydrates and apparently can satisfy their caloric need from protein and fat alone. The exception to that rule appears to be in lactating bitches, which are not able to satisfy their need for glucose by gluconeogenesis because of the great amount of energy required to produce milk. Animals that are pressed to work very hard may have the same difficulty in meeting their complete glucose requirement from gluconeogenesis.

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FATS Dietary fat supplies concentrated energy and essential fatty acids, and makes the diet palatable. While only 2% fat as com or soy oil (50%. linoleic acid) s needed to provide the essential unsaturated fatty acids, fat levels of 6-8% on dry matter basis are frequently added to diets for palatability and to help meet the energy requirement. Dogs can tolerate rations containing up to 50% fat; however, these diets are not economically feasible or technically desirable. Rations that contain high levels of fat result in a proportionate reduction in total food intake and require that all other nutrients be increased proportionately to maintain proper ratios relative to the increased metabolizable caloric content. Table-2: Minimum Nutrient Requirements of Dogs for Growth and Maintenance (Amounts per kg Body Weight per Day) Nutrient Fat Linoleic acid Unit gm mg Growth 2.7 540 Adult Maintenance 1.0 200

The addition of com or soy oil with their high linoleic acid content will help alleviate the dry, scaly coat condition produced by a previous deficiency of unsaturated fatty acids; 1 ml/4 kg body wt added to the daily diet usually will effect improvement. Opened containers of food oil should be kept refrigerated to inhibit oxidative rancidity. Fats added during the manufacture of dry dog foods are stabilized with antioxidants to retard rancidity since rancidity also destroys fat-soluble vitamins, particularly vitamins A and E, and may precipitate deficiencies of these vitamins. This condition may be observed in show dogs when an excess of polyunsaturated oil is fed in an effort to produce an attractive hair coat. Evidence has emerged that work performance of dogs may be affected by the concentration of dietary fat. Fatty acids are the primary source of energy for the myocardium, ordinarily, and for skeletal muscle during exhaustive exercise. Consumption of a "high-fat" diet in comparison with a "high-carbohydrate" diet caused a 30% increase in the time required for exhaustion of Beagles working on a treadmill. ENERGY Energy, or the ability to do work, results in the evolution of heat equal to the amount of energy expended. For this reason, it is appropriate that it be ex- pressed in heat units, kilocalories (kcal), rather than electrical units, kilojoules (kj). The energy requirement of the dog is equal to the sum of the amounts required for basic life function (basal energy), growth, and activity. The energy required for gestation is considered as "growth"; lactation is considered an "activity". The energy required for growth is usually about twice that required for maintenance per unit of body weight. In the last trimester, gestation increases the energy requirement 110-130% over pregestational levels. Lactation may result in a 250-300% increase in energy requirements over maintenance levels. The most recent estimates of the energy requirement of dogs are presented, in TABLES 1-6.

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Table-3: Caloric and daily food allowance for maintenance of adult dogs Body weight (Kg) 1 2 5 7 10 15 20 35 50 Kcal ME/Kg bw 132 106 88 81 75 70 62 53 48 Dry Food (g) 36 62 126 160 213 297 350 524 678 WATER While water is one of the most important dietary factors for survival, it often is not considered in a discussion of nutritional needs. The dog has only limited ability to store or conserve water, and water loss is a primary mechanism of temperature regulation and detoxification. Dogs may obtain water in liquid form, from foods, and from the oxidation of hydrogen during metabolism. Oxidation of 100 g of protein, carbohydrate, or fat will produce 40, 55 and 107 ml of water, respectively. If an animal consumes 2000 kcal of metabolizable energy per day, about 200-320 ml of water will be produced. Consumption of liquid water is usual, and typically, an animal will consume 2-3 times its dry matter food intake as water. This may go to 4 times dry matter intake in hot weather and during lactation. Dogs should have a generous supply of fresh, clean water available to them at all times. VITAMINS Dogs require at least 13 vitamins. Although the precise requirements for some vitamins have not been determined definitively, satisfactory levels have been confirmed by years of satisfactory formulation use and are presented in TABLES- 1 -6. Semi moist (g) 45 73 154 202 263 364 454 650 840 Canned (g) 104 168 347 448 591 829 980 1465 1893

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Table 4: Minimum Nutrient Requirements of Dogs for Growth and Maintenance (Amounts per kg Body Weight per Day) Nutrient A D E K Thiamine Riboflavin Pantothenic acid Niacin Pyridoxine Folic acid Biotin B12 Choline Unit IU IU IU g g g g g g g mg Growth 202 22 1.2 54 100 400 450 60 8 1.0 50 Adult Maintenance 75 8 0.5 20 50 200 225 22 4 0.5 25

Ascorbic acid (vitamin C) is synthesized by most dogs. It has been theorized that during stress, requirements may exceed the amount synthesized; therefore, supplementation may be beneficial. However, there are no controlled studies confirming this theory. In contrast to previous speculation, vitamin C supplementation is of no benefit in preventing skeletal problems in rapidly growing, large dogs and, in fact, has been shown to be detrimental. Adding vitamin supplements to complete and balanced commercial rations for healthy dogs is unnecessary. Some diseases may increase specific vitamin requirements and reduce intake due to partial or complete anorexia. In such cases, vitamin supplementation may be useful. MINERALS The dog requires a number of dietary minerals (TABLES 1 - 6). Most balanced commercial foods contain these minerals in ample (and frequently excessive) amounts. Mineral deficiencies are usually noted when animals arc fed ill-constructed "home made" diets composed entirely of muscle or organ meats or table scraps. The metabolism of many minerals is interrelated and they are best utilized when provided in the proper ratio to one another. Calcium and phosphorus, e. g, are usually best utilized when provided in a ratio ranging from 1-2: 1 with adequate levels of vitamin D. Supplemental calcium should not be added to adequate rations, particularly for growing dogs, since excessive amounts of ingested calcium increase the requirement for phosphorus, manganese, zinc, and other nutrients. Excess absorbed calcium results in decreased bone .remodeling and causes bone abnormalities during growth and in all ages, may result in soft tissue calcification, arterial plaques, and arthritis, or be concentrated in the urine where it may contribute to urolithiasis.

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Table-5: Minimum Nutrient Requirements of Dogs for Growth and Maintenance (Amount per kg body weight per day) Nutrient Calcium Phosphorus Potassium Sodium Chloride Magnesium Iron Copper Manganese Zinc Iodine Selenium Unit mg mg mg mg mg mg mg mg mg mg mg g Growth 320 240 240 30 46 22 1.74 .016 .28 1.94 0.032 6.0 Adult Maintenance 119 89 89 11 17 8.2 0.65 0.06 0.10 0.72 0.072 2.2

Table-6: Examples of semisolid foods for dogs (%) Ingredients Cereal flour Soyabean/Groundnut meal Meat and bone meal (50% CP Skim milk Dried skim milk Eggs Sucrose Animal fat Water Propylene glycol Sorbitol Minerals & vitamin supplement Diet 1 10 15 45 20 05 02 02 01 Diet 2 05 15 15 10 15 05 30 02 02 01 Diet 3 10 15 15 20 02 33 02 02 01 Diet 4 10 15 15 40 20 -2 13 02 02 01

2. Nutrient composition of available feeds for dogs: Available foods in particular area can be collected and analyzed as per AOAC (1997) methods. Table values from published literature (NRC, 1985, ICAR, 1991, Prasad, 2000) may be taken as guidelines. Nutrient composition of some of foods of Indian origin has been given in Table-7.

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Table-7: Nutrient composition of food (g/100)

Food items Maize flour Rice Wheat flour Wheat bread Bengal gram dal Black gram dal Lentil dal Soyabean (whole) Groundnut cake Cabbage Spinach Milk, cow Milk, buffalo Eggs, hen Meat, goat Moisture (g) 14.9 12.2 12.8 40.8 9.9 10.9 12.4 8.1 8.2 90.2 91.7 87.6 81.3 73.7 715 Protein (g) 11.1 8.5 11.8 8.0 20.8 24.0 25.1 43.2 47.0 1.8 1.9 3.3 4.3 13.3 18.5 Fat (g) 3.6 0.6 1.5 1.1 5.6 1.4 0.7 19.5 4.4 0.1 0.9 3.6 8.8 13.3 13.3 Fibre (g) 2.7 0.6 1.2 0.8 1.2 0.9 0.7 3.7 6.1 1.0 0.6 CHO (g) 66.2 77.4 71.2 49.0 59.8 60.3 59.0 20.9 31.5 6.3 3.4 0.12 0.21 0.06 0.15 Calories (Kcal) 342 349 348 238 372 350 343 432 180 33 30 65 117 173 194 Ca (g) 0.01 0.01 0.05 0.02 0.06 0.20 0.13 0.24 0.28 0.08 0.06 0.09 0.13 0.22 0.15 P (g) 0.33 0.17 0.32 0.20 6.33 0.37 0.25 0.69 0.78 0.05 0.01 0.20 0.20 2.10 2.50

3. Knowledge of individual dogs: Nutrient requirements have been tabulated for maintenance for various weight categories. Various breeds of dogs have different adult weights. Considering the current weight of the dog, maintenance requirement of the dog can be ascertained. The physiological state of the dog (growing, adult, pregnant, suckling, work etc. demands extra nutrients. Such requirements are added up and complete nutrient requirements for a day can be tabulated. Now, let us take the nutrient composition table and complete diet that contains cereals, pulses, other protein foods such as eggs, meat, cakes etc. to fulfil the energy, protein, fat, fiber, L calcium and phosphorus requirements. For trace minerals and vitamins separate mixes can be prepared and added up.

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Table-8: Nutrient content of some of the home made foods and nutrient requirements for maintenance for different weight groups of dogs Weight (Kg) Foods Energy (Kcal) Roti (g) flour Dal (g) 100 25 150 38 200 50 Roti (g) Milk (ml) 100 100 150 200 200 300 Bread (g) Milk (ml) 200 100 300 200 400 300 Roti (g) Meat (g) 100 100 150 150 200 200 Roti (g) Eggs (g) 100 one 150 Two 100 Three Requirments/day (NRC, 1999) 441 662 882 402 630 858 530 822 1144 542 813 1084 434 694 954 440 660 750 Nutrients Protein Ca (g) (g) 17.0 25.5 34.0 15.1 24.3 33.5 19.3 36.6 41.9 20.3 45.4 60.6 18.4 24.9 43.4 28.0 42.0 55.0 0.10 0.16 0.20 0.14 0.26 0.37 0.13 0.24 0.35 0.20 0.30 0.40 0.17 0.32 0.46 1.5 2.0 2.5

P (g)

5.0 7.5 10.0 5.0 7.5 10.0 5.0 7.5 10.0 5.0 7.5 10.0 5.0 7.5 10.0 5.0 7.5 10.0

0.41 0.62 0.82 0.52 0.82 1.22 0.24 0.46 0.68 2.82 4.18 5.64 0.32 0.48 0.64 1.0 1.5 2.0

An attempt has been made in Table-8 for 5, 7.5 and 10 kg of dogs, to fulfill their energy, protein, calcium and phosphorus requirement. Their requirements have also been given in the table. This has been given for a practitioner to initiate diet formulation. It is hoped to be helpful.

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PARASITIC INFESTATIONS IN CANINES

S.K. Gupta Department of Veterinary Parasitology CCS Haryana Agricultural University, Hisar Man, has had a need for animal companionship, since the days he was walking on all fours, to semi-erect and now on his two feet and man dog relationship goes back to more than 14,000 years. While most people prefer dogs as pets, cats make equally good companion animals. They are ideal pets for people who live in apartments and for people who have very busy lifestyles and do not have the time that is required for looking after a dog. The pets may harbour various endo- and/or ecto-parasites. The endoparasites may be helminthes and/or protozoan. The helminthes include roundworms, tapeworms and flukes. A) Ascarids : Are common parasites of small intestine. Major species are Toxocara canis, T. cati and Toxascaris leonina. Toxocara canis can cause severe infections in puppies and a condition called visceral larval migrans in humans. Transmission: 1. By oral route 2. Via uterus: In the pregnant bitches dormant larvae become active and pass to the developing pups in the last fortnight of pregnancy. It is very likely that some dormant larvae present in the mother can infect pups in future pregnancies. 3. Via milk: Though not common, dormant larvae in the mammary glands may become active and pass in the milk. 4. Via rodents: By eating rats/mice carrying dormant larvae in their tissues. Transmission of T. cati is similar to that of T. canis except that trans-mammary transmission is the major source of infection in kittens and trans-placental transmission does not occur. Both dogs and cats can be infected with T. leonina by ingestion of either embryonated eggs or larvae encysted in tissues of paratenic hosts. Neither tracheal nor somatic migration occurs in the primary host. T. leonina usually occurs in adults. Clinical signs: Heavy infection with adult ascarids causes moderate enteritis, subnormal growth, and dry and dull hair coat. If left untreated, the worms cause pot belly and diarrhoea. Vomiting and respiratory signs frequently accompany heavy infection in pups. Occasionally neurologic symptoms and death occur. Heavy prenatal infections cause severe abdominal discomfort in nursing pups. Death may also be due to obstruction of intestine with worms or its rupture. In kittens in heavy T. cati infection, there is general unthriftiness, abdominal distension and intermittent diarrhoea. Toxascaris leonina, the least pathogenic of these ascarids, may provoke a mild inflammatory response associated with larval development in the intestine. Diagnosis: A history of weight loss accompanied by abdominal distension in pups is suggestive of T. canis infection. Demonstration of characteristic eggs in faeces confirms ascarid infection. In heavy infections, immature and adult worms may be excreted either in the faeces or vomitus.

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Treatment: Piperazine salts are commonly used for treatment, and are given orally @ 75110 mg/kg. This drug has no effect against somatic larvae in the bitch. Pyrantel pamoate and levamisole are also effective against T. canis. Benzimidazoles (fenbendazole, meben-dazole) display high efficacy against adult and larval infections in pups and adult animals. Fenbendazole is the most potent and safest in killing tissue-dwelling larvae and 1 preventing the occurrence of prenatal infection in the bitch. It is given @ 50 mg/kg for 3 days. Control: a) Pups are to be treated within 2-3 weeks of birth to prevent establishment of infection, repeat it every 2-3 weeks until the pup is 12 weeks of age. Kittens should be dosed at 4-6 weeks of age, followed by every 3 weeks until the age of 4 months. b) Dosing of fenbendazole @ 50 mg/kg from day 45-50 of pregnancy to day 14 post-parturition ensures ascarid-free pups. Pregnant cats should be treated during pregnancy to reduce the possibility of neonatal infections in kittens. c) Bitches and adult cats should be regularly dewormed to reduce environmental contamination. d) Strict hygiene must be observed in the premises. B) Hookworm infection: The two genera of importance in dogs and to a lesser extent in cats are Ancylostoma and Uncinaria. Transmission of A. caninum is oral or trans-mammary through colostrum/milk of infected bitches; by cutaneous route and also by ingestion of paratenic hosts. However U. stenocephala, primarily a problem in kennels, is acquired by direct ingestion and those larvae which penetrate the skin rarely complete their life cycle. All age groups are susceptible. In neonates and suckling pups, the clinical manifestation of infection is acute and is characterized by anaemia as an adult worm sucks about 0.8 ml blood/day. Because of secretion of an anticoagulant in the mouth of hookworms, blood keeps on flowing from ulcers at points of previous attachments, as worms move from feeding sites. Heavy infection in pups may be fatal. Lighter infections, common in older dogs, are characterized by haemorrhagic enteritis, anaemia and finally host becomes iron deficient. Other clinical signs are emaciation, diarrhoeic tarry faeces, dyspnoea and weakness. Mild anaemia may result from heavy infection with U. stenocephala. Larval penetration of skin can result in dermatitis in both the infections. At necropsy, there may be haemorrhagic enteritis with swollen intestinal mucosa that shows red bite marks and small ulcers as well as attached worms in acute cases. Intestinal contents may be dark and tarry. Diagnosis: a) Clinical signs of acute disease may be apparent b) b) Demonstration of typical eggs in faeces. Treatment and Control: 1. Severely affected animal requires supportive therapy including blood transfusion and iron supplementation. 2. Benzimidazoles (fenbendazole, mebendazole), febantel, milbemycin, pyrantel pamoate, dichlorvos, disophenol and levamisole in recommended doses are effective against hookworms.

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3. Fenbendazole @ 50 mg/kg from day 40 of gestation to day 14 postpartum greatly reduces trans-mammary transmission to pups. 4. Pups should be treated weekly up to 6 weeks of age and at 2 weeks interval from 6-12 weeks of age. 5. Older dogs at risk should be treated at 1-3 months intervals. 6. Sodium borate @ 0.5 kg/sq m is good for decontaminating the kennels. C) Strongyloidosis: Strongyloides species parasitize the small intestine of dog and large intestine of cat. These nematodes have both parasitic and free-living cycles. Clinical disease has been described in pups infected with S. stercoralis. Infections with S. tumefaciens and S. cati in cats are usually asymptomatic. Pups become infected with third-stage larvae which penetrate the skin/oral mucosa. Auto-infection may also occur. In young pups there is verminous interstitial pneumonia caused by larval migration, and enteritis due to adult worm activity in the small intestine. In cats, S. tumefaciens may cause nodular lesions in the wall of colon. Pups show emaciation, dehydration and diarrhoea (occasionally blood-tinged). There may be evidence of pneumonia. Penetration of the third-stage larvae into the skin may produce an intense local pruritus and erythema. Diagnosis: 1. Embryonated eggs/larvae in anal swabs. 2. Third-stage filariform larvae in faeces stored at room temperature for 24-96 h. The oesophagus of L3 is half the length of the entire larva. Treatment and Control: Give fenbendazole @ 50mg/kg orally, daily for 5 days. Alternative anthelmintics include ivermectin, pyrantel pamoate and mebendazole. D) Dirofilariosis: By Dirofilaria immitis (heart worm). Adults are found mainly in the right side of the heart and associated vessels. Females produce microfilariae, which are ingested by mosquitoes (Aedes, Culex). 3rd stage larvae are inoculated s/c into a new definitive host when the mosquito feeds. Other signs are dyspnoea, fever and ascites. Advanced cases may show signs related to chronic right sided cardiac insufficiency. If the number of worms is high in posterior vena cava, they may produce an acute jaundice, haemoglobinuria and death. In cats there may be anorexia, coughing, intermittent dyspnoea, vomiting, lethargy, weight loss and neurological signs. Right sided heart failure is rare in cats. Diagnosis: Microfilariae can easily be detected on microscopic examination of unstained blood film as well as micro-haematocrit blood sample, where motile microfilariae can be seen in the area close to buffy coat. This is more sensitive than unstained blood film examination. Other methods include: Modified Knott's technique, radiography, serological tests (ELISA) etc Treatment: Therapy to kill adult worms is hazardous particularly in cats and may result in thrombosis and fatality. Adulticide drugs are melarsomine (2.5 mg/kg, i/m for 2 days), thiacetarsamide (2.2 mg/kg i/v b.i.d for 2 days). Microfilaricide drugs are ivermectin, milbemycin and levamisole (has a narrow safety margin and toxicity is common in dogs and cats). Control: By prophylactic drugs (ivermectin, milbemycin, diethylcarbamazine) during mosquito activity periods as these inhibit larval development in tissues of definitive hosts.

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E) Spirocercosis: Not common, adults are found coiled in nodules in wall of oesophagus, aorta, stomach and other organs. Embryonated eggs are passed in the faeces and do not hatch until ingested by certain coprophagus beetles. Signs may be absent in mild infections or persistent vomiting may be caused by oesophageal obstruction. Sudden death from haemorrhages from aortic lesions may occur. Dysphagia, vomiting, oesophageal neoplasia, aneurysm of thoracic aorta may be associated with chronic S. lupi infection. Diagnosis: 1. Gelatin capsule like ova containing coiled larvae in the faeces. 2. By characteristic nodules in 20rta, oesophagus and other locations at autopsy. Treatment: Disophenol 7-10 mg/kg s/c twice at 1week interval. Levamisole and albendazole are also effective. F) Trichuriosis (whip worm infection): They parasitize the large intestine, sometimes inducing severe diarrhoea in dogs. Common species is Trichuris vulpis. Light infections are often symptom-less, heavy worm burden may cause typhlitis, weight loss, foetid diarrhea, abdominal pain, vomiting and anaemia. Feline whip worm infestations are of little clinical importance. Diagnosis: Thick - shelled eggs with bipolar plugs. Treatment and Control: Fenbendazole, mebendazole, febantel, dichlorvos, milbemycin are effective. Repeated treatments (at 3 wks and 3 months) may be required as juveniles are resistant. Since eggs remain viable for years, premises should be thoroughly cleaned to avoid re-infection. G) Tapeworms: Occur in the small intestine without producing severe clinical disease. Their life cycles are indirect and may have one or two intermediate hosts. Dogs are likely to become infected if they are fed uncooked meat or offal containing viable cysts. Dogs and cats can also be infected through scavenging or predation. Birds have been implicated in the dispersal of tapeworm eggs for up to 60 km. Transmission of Dipylidium caninum, one of the most common tapeworms of dogs and cats, is dependent on the density and activity of flea populations. Lice may occasionally act as vectors of D. caninum. Diphyllobothrium latum is likely to occur in areas where raw/undercooked fish is fed to pets. Clinical importance: Tapeworm infection may occur at any age as there is a minimal immune response even after repeated infections. The pathogenic effect of adult tapeworms in most cases is low, irrespective of their numbers or individual size. Occasionally, there may be intestinal irritation or diarrhoea. Motile segments of D. caninum cause pruritus as they pass to the exterior and may induce the dog or cat to drag its hindquarters along the ground. Heavy infestations with adult parasites lead to intestinal obstruction in young dogs. Diagnosis: By demonstration of egg capsules and/or segments in the faeces. Treatment: Praziquantel, niclosamide, fenbendazole, febantel, mebendazole, bunamidine are effective in recommended doses against Taenia, Echinococcus and Dipylidium. For Diphyllobothrium, high doses are required. Control: Periodic anthelmintic treatments, avoid feeding raw meat, fish or offal to pets and control of flea or lice infestations.

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H) Trematodes: Four species i.e. Opisthorchis noverca, O. caninus, O. tenuicollis and O. felineus have been reported from India. Infection is acquired by ingestion of infected raw or insufficiently cooked fish. They occur in bile and pancreatic ducts and sometimes in small intestines. Light infections are asymptomatic, while massive infection may cause papillomatous cysts and fibrosis in liver. Several cases of liver or pancreatic carcinomas in cats were related to eggs of O. tenuicollis. Weakness, jaundice and ascites are the generally observed clinical symptoms. Hexachlorophene (20 mg/kg) or Praziquantel @ 25 mg/kg b.wt for 3 days are effective drugs. For control, pets should not be fed raw or partly cooked fish. I) Babesiosis: Babesia canis and B. gibsoni are responsible for the infection in dogs. B. canis is a large species, typically pear-shaped. Multiple infections of the erythrocytes often occur. B. gibsoni is a small species. The infection is transmitted through ticks mainly by stage to stage transmission. However, transovarian transmission may also occur. The disease is more common during summer and rainy seasons owing to favourable climate for the development and survival of vectors. Though the disease has been seen in dogs of all age groups but it is more severe in pups. Pathogenesis and symptoms: Mortality is high amongst exotic dogs. Incubation period is 10-21 days. Clinical signs vary from a mild fever lasting several days before the onset of anaemia to an acute disease involving a sudden high fever, marked anaemia and haemoglobinuria, with a later development of jaundice. B. gibsoni usually produces a more chronic disease. Cerebral forms of babesiosis causing hyperexcitability can occur. Other clinical forms include episodes in which the alimentary tract appears to be involved, producing stomatitis, gastritis and enteritis; a predominantly respiratory form; a circulatory form which is marked by oedema; a form in which keratitis occurs; a muscular form in which the signs give the impression that the animal is suffering from rheumatism. Diagnosis: By history of tick infestation, clinical signs, detection of protozoa on blood smear examination and serological tests (IFAT, CFT). Treatment: Phenamidine, diminazene aceturate and imidocarb dipropionate are effective against B. canis. B. gibsoni is less amenable to treatment but large doses of diminazene aceturate (5-10 mg/kg) or imidocarb appears to be the most promising treatment. Care must be taken with high doses of certain drugs (diminazene, phenamidine) in dogs, as they may induce severe, sometimes fatal toxicity. Phenamidine : 10-15 mg/kg b.wt as aq. sol (5%) sic, may be repeated 24 hours later if necessary. Diminazene aceutrate: 3.5 -5 mg Ikg b. wt i/m repeat every alternate day, 2 to 3 injections. Diampron : 5 -10 mg/kg b. wt i/m or sic repeat every alternate day, 2 to 3 injections. Imidocarb dipropionate (Imizol) : 2-6 mg/kg b. wt sic or i/m, less toxic. Quinuronium derivatives (Acaprin, Babesan, Piroplasmin, Piroparv) : @ 0.25 mg/kg b.wt. safely margin is very low. Symptomatic and supportive therapy: Diuretics, antipyretics, laxatives and astringents as per the need, haematinics and multivitamins are also useful in improving the health. Prevention and Control: Includes control of vector ticks. Imizol can be used as chemoprophylactic agents in enzootic areas. An inactivated vaccine (Pirodog) against B. canis has been produced in France and has shown good results.

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J) Canine Ehrlichiosis: - It is a tick borne disease caused by a rickettsia, Ehrlichia canis, which infects monocytes. Ehrlichia infections have frequently been reported in dogs with simultaneous infections with B. canis. Incubation period is 8 20 days. In acute cases there is fever anorexia, depression, stiffness and reluctance to walk. There is generilzed lymphadenopathy, splenomegaly and thrombocytopaenia. Animal amy show respiratory signs like coughing and dyspnoea. There may be oedema of limbs or scrotum. In chronic infections there is glomerolonephritis, renale failure, meningitis, paresis and severe thrombocytopaenia. There may be haematuria, patechiae and echymoses of the skin. In some breeds epistaxis is common. Diagnosis: - Demonstration of organisms minute gram-negative cocci, stain dark blue to purple with Giemsa) within the cytoplasm of mononuclear cells. In acute phase there is consistent thrombopaenia with an increased proportion of large and regenerative platelets. Serological test (IFAT) is also helpful. Treatment: Tetracycline (22mg/kg b. wt., t.i.d. for 14 days in acute infection and for 1 2 months in chronic cases) and doxycycline (5 10 mg/kg b.wt. for 10-14 days). Imidocarb dipropionate @ 5-7 mg/kg b. wt. i/m, twice at 2 weeks apart, is also effective. If haemorrhage is extensive, platelet or whole blood transfusion may be required. Prevention and Control: Include effective tick control and chemoprophylaxis in endemic areas by tetracycline @ 6.6 mg/kg b.wt. orally, daily atleast for one tick season. K) Trypanosomiasis: is caused by Trypanosoma evansi. The infection is acquired by eating infected meat and through blood sucking flies. Disease is more serious and fatal in pups and exotic and delicate breeds. Clinical signs include intermittent fever, progressive anaemia, oedema of dependent parts followed by muscular atrophy, lumber paralysis, corneal opacity and incoordinated gait. Occasionally, in some cases there may be oedema of throat with hoarse voice and difficulty in swallowing. In chronic cases, the course is longer and untreated dogs invariably succumb to pressure. Tentative diagnosis is based on history and clinical signs. In acute or early stages, trypanosomes can be demonstrated in peripheral blood. The method of demonstrating trypanosomes in the blood is centrifugation of infected blood in a micro-haematocrit tube followed by microscopic examination of the interface between the buffy coat and the plasma under dark ground or phase contrast microscope. Serological tests (CFT, ELISA and IFA) may be helpful. Animal inoculation can also be tried so also culturing the parasite in NNN medium. Antrypol @ 0.3 g i/v for 6 days, quinapyramine sulphate, diminazene aceturate (5-10 mg/kg) on alternate days can be used. Prevention: Fly-proof kennels to reduce mechanical transmission through biting flies, proper disposal of faeces and insecticide treatment of breeding sites of vector to reduce the population of flies along with usage of chemoprophylactic agents. L) Giardiosis: Giardia is generally considered capable of causing enteritis and diarrhoea in dogs. Diarrhoea may begin as early as 5 days after exposure to infection. In cats, the trophozoites occur in jejunum and ileum instead of duodenum. Principal clinical sign is persistent diarrhoea. Diagnosis :By finding trophozoites in diarrhoeal faeces and cysts in formed stool. Phase contrast microscope is helpful in diagnosis.

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Treatment: Quinacrine (6.6 mg/kg b.i.d. for 5 days) is very effective; however, anorexia, fever, and lethargy may appear as side effects. Metronidazole (25 mg/kg orally b.i.d. for 5 days) and tinidazole (44 mg once daily for 3 days) are less effective but are relatively free of side effects. Control involves prevention of fecal contamination of feed and water, sanitation and disinfection of the environment with lysol (2 -5 %) or chlorine bleach (sodium hypochlorite, 1%). M) Coccidiosis: Many species infect the intestinal tract. All species except Cryptosporidium are host specific. The most common coccidia are Isospora spp which occur in dogs living in unhygienic conditions. More prevalent in pups aged between 516 weeks; mainly caused by Cystoisospora (=Isospora) canis in dogs and I. felis and I. rivolta in cats. Clinical signs, which may precede oocyst shedding, particularly in acute infections include dehydration, diarrhoea (sometimes bloody) and weight loss. Infection is usually self limiting. Diagnosis is based on oocyst morphology. Treatment in cats may not be required as they usually spontaneously eliminate the infection. In clinically affected cats, trimethoprim-sulpha @30-60 mg/kg for 6 days can be used. In dogs in severe cases, in addition to fluid therapy, give sulphadimethoxine @ 50 mg/kg on the first day followed by 25 mg/kg for atleast 1 wk thereafter. Sanitation is important in kennels and catteries. Cages, utensils etc should be disinfected regularly and avoid overcrowding. N) Toxoplasmosis: Caused by Toxoplasma gondii for which cats are the definitive hosts and the intermediate hosts are all warm-blooded animals including cats. In intermediate hosts, tissue cysts are formed in the brain, striated muscles, and liver and remain viable for the life of the host. Cats are also capable of developing systemic disease. The clinical signs are non-specific and may reflect damage to a number of organs/systems including CNS, lungs, liver, musculature and eyes. However, the presence of cysts in host tissues does not necessarily result in clinical disease. There may be transient diarrhea in cats. For treatment give clindamycin @ 10-40 mg/kg in dogs and @ 25-50 mg/kg in cats for 14-21 days. O) Sarcocystosis: Normally, the carnivorous host becomes infected by eating the infected flesh of herbivorous host. Sarcocystis usually causes no illness in carnivorous but schizogony in the endothelium of herbivorous may result in serious or fatal disease. The cycle of infection can be interrupted either by cooking meat scraps to be fed to dogs/cats or by preventing canine/feline fecal contamination of cattle feedstuffs. P) Neosporosis: Neospora caninum is a recently described parasite of the domestic dogs. It resembles T. gondii and causes neuromuscular disorders in dogs. The diagnosis is based on demonstration of parasites in stained tissue sections or isolation from freshly aborted foetuses. Sulfonamides combined with trimethoprime, pyrimethamine (1 mg/kg, daily orally for 4 weeks) and clindamycin (13.5mg/kg, 3 x daily. 10 days) are used in dogs for treatment. Q) Hepatozoon canis: Schizonts occur in the endothelial cells of spleen, bone marrow and liver. Gamonts occur in the leucocytes and are elongate, rectangular bodies and are surrounded by a delicate capsule. The dog is infected by the ingestion of

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infected vector tick, Rhipicephalus sanguineus, which contains sporocysts in its body cavity. The organism may be found in apparently healthy dogs, but sometimes it is associated with pathogenic effects. The clinical signs consist of an irregular fever, anaemia, progressive emaciation with enlargement of spleen. Lumbar paralysis has been described. Death occurs 4-8 weeks after the onset of clinical signs. Hepatozoon canis infection is diagnosed by the demonstration of the gametocytes in stained blood smears, or the schizonts in the spleen or borne marrow. For treatment imidocarb may be given and control is based on effective tick control.

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HEAPATOBILIARY ULTRASONOGRAPHY IN DOGS

Dr. Pardeep Kumar Teaching Associate, College of Veterinary Sciences Teaching Veterinary Clinical Service Complex, CCS HAU, Hisar-125004 (India) Introduction Ultrasonography is an important diagnostic technique in veterinary medicine. Diagnostic ultrasound is an imaging technique for soft tissues as it is: o Non-Invasive and painless for the patient. o Biologically safe for both the operator and patient. o Moreover, it provides valuable information the regarding the shape, size, position and interval architecture of soft tissues. It may be used to examine most structures in the small animal abdomen. Frequency of diagnostic utlrasound is between 2-10MHz. Scanner with 5.0 and 7.5 MHz transducer is optimal for examination of dog and cat abdomen. 5.0 MHz transducer provides visualisation of structures to a depth of 12 to 15cm and is used for large organs such as the liver. 7.5 MHz transducer has more limited range but provides greater detailed resolution of structures to a depth of 6 to 8cm. Liver Most vital and essential organs of the body. It guards interval environment of the body. Being the first to encounter and identify substances absorbed from the digestive tract. Metabolic functions: Synthesis and storage of carbohydrates proteins, fats, vitamins, detoxification of toxins, synthesis and secretion of bile and erythropoiesis. Since liver is subjected to a variety of onslaugts its dysfunction is commonly seen. Clinical signs: Anorexia, alimentary, tract stasis, discoloured faeces, epigastric pain, jaundice, oedema of dependent parts of the body, photosensitization, blood clotting disorders, nervous signs, vomition and diarrhoea. Diagnosis: Clinical signs Liver function tests

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Tests to evaluate liver function Type of disease Hepatocellular injury/reduced functional mass Cholestasis Appropriate tests SGPT BUN, albumin, clotting panel, BSP retention, serum ammonia. SAP, GGT, serum bile acids bilirubin (serum, urine)

Ultra sonography Histopathological examination Normal Ultrasonographic Appearance Hepatic Parenchyma: It is smooth, having sharp borders, homogeneous, slightly coarse and medium level echotexture. Hypoechoic when compared with spleen. Isoechoic to slightly hyperechoic wnen compared with renal cortex. Hepatic vasculature: It is anechoic tub\llar structure within hepatic parenchyma. Hepatic veins: Without detectable walls Portal veins: With hyperechoic walls. Hepatic arteries: Not seen Diaphragm and Falciform fat Diaphragm: Continuous, curvilinear hyperechoic structure. Falciform fat: Intensely hyperechoic Gall Bladder: Anecheic, smooth marginated, thin walled structure within liver just to right of midline. Size: Smaller in patients fed recently than in fasted or anorectic. Examination Technique Liver may be examined in dorsal, lateral recumbency or in standing position. Preparation of the patient: Sharing of the area between xiphisternum and umbilicus extending several cm to each side of the midline. Application of acoustic gel to ensure proper contact of scanner head with body surface Transducer is placed between the xiphisternum and angled craniodorsally. Rotation of the head of the transducer through 900 allows different planes of the section to be imaged. Liver is examined by dorsal right and lateral intercoastal approach. If liver is large: It is necessary to move the transducer caudally towards the umbilicus until tip of the ventral liver lobe is reached. If liver is small or gas in stomach or difficult visualisation due to small intestines, then image the liver through intercoastal approach. Images are frozen whenever clear and good images are obtained. Measurements are taken by electronic calipers of the machine using distance mode and trace mode for length, width and circumference.

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Indications for Hepatic Ultrasonogaphy Ascites, jaundice, hepatomegaly, weight loss, possible hepatic metastasis, ultrasound guided biopsy, fever of unknown origin and masses in the area of liver. Normal Structures Detectable By Hepatic Ultrasonography Hepatic parenchyma, portal veins, hepatic veins and gall bladder. Hepatic Parenchymal Abnormalities: Divided into focal and diffuse. Focal: If lesions have discrete borders should be termed as focal. Many focal lesions are termed as multifocal. Diffuse: Widespread parenchymal abnormalities causing alteration of architecture without discrete borders should be termed as diffuse. Hepatic Parenchymal Diseases Divided into benign and malignant. Benign: Predominant forms of benign liver diseases with reported sonographic findings include: Hepatic lipidosis, nodular hyperplasia, steroid hepatopathy, cirrhosis, hepatitis, abscess, cyst and neoplasia. Malignant: Divided into primary and metastatic neoplastic diseases Primary Neoplastic Diseases: Hepatocellular carcinoma-most common Choloagiocellular carcinoma- in cats Fibrosarcoma Haemagiosarcoma Metastatic Neoplastic Diseases: These appear spread from primary sites which include spleen, lymph nodes, adrenal glands, pancreas, bone marrow, gastrointestinal tract and mammary glands. Lymphosarcoma is most common metastatic neoplastic disease. Findings of multiple small hypoechoic/hyperechoic nodules within hepatic parenchyma are characteristics is hepatic metastasis but diagnosis can not be made without histopathological examination. Difference between the primary and metastatic neoplastic diseases can be made by liver enzymes. In metastatic neoplastic diseases liver enzymes are in normal range, if increased then extent is very small whereas in primary neoplastic diseases liver enzymes are increased to a greater extent. Gall Bladder Choleliths: Echogenic structure within gall bladder Cholecystitis: Thickening of the gall bladder wall.

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MANAGEMENT OF EMERGENCY CASES IN CANINES

Dr. Ashwani Kumar Teaching Associate, College of Veterinary Sciences Teaching Veterinary Clinical Service Complex, CCS HAU, Hisar-125004 (India) ANAPHYLACT.ICSHOCK This is an immediate type of hypersensitivity reaction in which death may occur rapidly due to respiratory and circulatory collapse. The main signs are due to activation of complement system with intensive vascular dilatation of smooth muscle. Release of histamine, serotonin, heparin, acetylcholine and bradykinin increases the severity of the problem. The most common signs in dogs are restlessness, diarrhea, vomiting, circulatory collapse, epileptiform seizures, coma and death. Agents that may cause anaphylaxis are penicillin, streptomycin, tetracyclines, chloramphenicol, erythromycin, antitoxins, oxytocin, vaccines, stinging insects, food and allergens. Treatment In severe cases, immediately administer an IV injection of 1: 10000 epinephrine hydrochloride (Adrenaline), 0.5 to 1.0 ml if needed, repeat in 20 to 30 minutes. Infiltrate subcutaneously at the entrance site of the allergen (insect bites) with 0.3 ml of 1:20000 epinephrine hydrochloride. Ensure a clear air passage by passing endotracheal tube Establish an IV line with lactated Ringer's saline solution or normal saline solution Administer an IV injection of a rapidly acting steroid such as hydrocortisone sodium succinate 100 to 500 mg or prednisolone sodium succinate 100 to 500 mg. Repeat the injection in 3 to 4 hours if needed. Give an IV injection of an antihistamine such as chlorpheniramine malleate slowly. Hospitalize and observe the patient closely following above mentioned treatment. If recovery occurs within 5 to 10 minutes after this treatment, then prognosis is good. ELECTRIC SHOCK Electric shock is usually the result of an animal chewing an electric cord, contacting defective electrical equipment or being struck by lighting. Electric current passing through the body can produce several maj or abnormalities such as: 1. Electrophysiologic abnormalities producing ventricular tachycardia and first and third degree heart block. 2. Tissue destruction by heat and electrothermal bums. 3. Acute pulmonary edema.

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Clinical signs include acute onset of dyspnoea with moist rales and localized bums with necrosis of lips and tongue. Additional signs are muscular contractions, loss of consciousness, pulmonary edema and Ventricular fibrillation. The first 12 hours are the most critical for the patient, and then the prognosis improves. Treatment Support respiration by passing endotracheal tube. Large doses of corticosteroids. IV injection of diuretics (furosemide) IV injection of bronchodilators (aminophylline) Antibiotics prophylactatically for possible Pneumonia. If pulmonary congestion is severe, consider performing phlebotomy and remove upto 10% of the blood volume. Sedate the animal with triflupromazine for anxiety only if needed.

POISONING There are basically three situations the veterinarians commonly face while attending poisoned animal. 1. The animal presented with unknown history and may have a range of symptoms. 2. The animal is presented with toxic symptoms to a known poison about which the veterinarian may know little or for which the antidote may not be readily available. 3. The animal is presented with toxic symptoms to a known poison with which the veterinarian is familiar and for which an anti dole exists. In dogs and cats most frequent reported toxicities are rodenticides (22.7%), human medicines (17%), insecticides (12%) and plants (9.8%). Every veterinarian should develop familiarity with the clinical management of rodenticides and insecticides and be a master of general poison management-emesis, lavage and catharsis as well as support of cardiovascular, respiratory and renal function in the critically ill patient. Advising clients who call for advice When a client calls about a poisoned animal, following questions should be asked. What is the suspected substance? How long ago was the exposure? Was it swallowed or is it on the animal's skin or eyes? How is the patient acting? How long has the patient been acting that way? First aid instructions to clients over telephone 1. Induce vomiting and if possible save the vomitus: a) Emetics on hand in most household include. i) Table salt: 1 to 3 t.s.f. in dogs.

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1-2 ml/kg body wt. PO in dogs. 3.3ml/kg body wt. PO in cats. Note: Do not induce vomiting if it appears that the animal has ingested corrosive substance such as strong acid or alkali or petroleum based substances such as kerosene or turpentine oil; instead give milk or water to dilute the poison. 2. If the animal has had skin or ocular exposure to toxic or corrosive material, the owner should be advised to immediately begin ringing the eyes unlimited volumes of warm water till animal is hospitalized. 3. If patient is excited or having convulsions, advice the owner to try to protect the animal from injuring itself. 4. Advice the owners to transport patient as soon as possible to nearest veterinary hospital. Essential principles of treatment in toxicities 1. Stabilize vital signs 2. Obtain history and evaluate patients. 3. Prevent continued absorption of the toxin. 4. Administer antidotes, if available. 1. Stabilize vital signs a) Maintain Respiration Provide immediate oxygen source if the patient demonstrates any degree of respiratory compromise. An intranasal cannula or endotracheal intubation or oxygen cage should be provided. Nikathamide can be given as respiratory stimulant. b) Maintain intr3venous fluid therapy An intravenous catheter should be placed immediately and should be used for fluid therapy and other intravenous medications c) Control central nervous system Excitation Diazepam at dose rate of 0.25-0.5mg/kg body wt. intravenously is drug of choice for initial control of CNS excitation, but may need to be followed shortly with muscle relaxant such as methocarbanol (150mg/kg body wt. IV). Phenobarbitone (4-8 mg /kg body wt. iv) can be used to control long term seizers. d) Control body temperature Animal may be presented either hypothermic or hyperthemic, depending upon toxins ingested and stage of toxicity. Hypothermia can be managed with heating pads and hot water bottles to provide a source of warmth Hyperthermia can be managed by quickly bathing the animal in lukewarm water until the rectal temperature reaches 102F. 2. When initial stabilization of vital signs has been accomplished, the veterinarian can then discuss the patient history with owner. It is important to systematically evaluate the patient's physical status, focusing particularly on clues associated with common poisons such as organophosphates and anticoagulant rodenticides.

ii) Syrup of Ipecac:

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3. Prevent continued Absorption of the toxins Removal of toxic substances from body or their prevention of continued absorption in body should be done as early as possible. Emetics Use emetics only if the animal's physiology is stable i.e. no seizuring, not in mental or respiratory distress. Do not bother giving the same emetics more than twice. If it does not work after two doses, switch to a different emetic or go to gastric lavage. Emetics are strictly contraindicated for petroleum products and corrosive substances because of risk of aspiration and of further damage to oesophagus. Following emetics can be used 1. Apomorphins at dose rate of 0.02 to 0.04 mg/kg body wt i/v or i/m. 2. Syrup of ipecac (7% ipecac) Dogs: 1-2ml/kg body wt PO Cats: 3.3 ml/kg body wt PO 3. Hydrogen peroxide (3% solution) Dose rate: 1-2ml/kg body wt PO 4. Xylazine at dose rate of 0.5 to 1mgikg bQdy wt. im. 5. Sodium chloride (table salt) for owners at home 1-3 tsp PO. Gastric lavage Patient should be sedated and then pass cuffed endotracheal tube to prevent aspiration of gastric contents. Pass stomach tube to serve as an egress tube for the lavaged contents. Then pass small bore stomach tube to serve as fluid ingress tube. This method sets up a circuit of fluid flew, allowing rapid and complete emptying of stomach. This will require 5-10 ml of water or saline/kg body wt. Enemas For this purpose, it is best to use simple Luke warm water. The fluid volume depends upon size of animal and stat of its lower GI tract. Cathartics: They are useful in hastening gastrointestinal elimination of undesirable substances and are particularly useful for most ingested solid toxicants such as compost, garbage or snail baits. e.g. Sodium sulfate: 200-500mg/kg body wt in a 10x volume of water. Paraffin oil: 5-15 ml/dog 2-6 ml/cat

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Administer antidote if available Generic name of Antidote 1. Potassium permagnate 2. Dimecaprol (BAL) Usage In strychnine poisoning Arsenic, mercury and other heavy metals except cadmium, lead, silver and selenium Carbon monoxide Cholirnergic agents and cholinesterase inhibitors e.g. organo-phosphates, Carbamate poisoning Lead poisoning Dose 500 2000 ml as lavage solution 2.5 5.0 mg/kg b. wt. i/m

3. Oxygen 4. Pralidoxime chloride (2-PAM)

Pure oxygen at normal or positive pressure 0.2 1.0 mg/kg b.wt. slow i/v or 20-50 mg/kg b.wt. i/m Maximum dose is 75 mg/kg b. wt./24hr as 5.0% solution i/v 0.1 mg/kg b. wt. i/v 1.0% solution of sodium nitrate (1.6ml/kg b.wt. i/v)

5. Calcium disodium edetate 6. Naloxone chloride 7. Sodium nitrate

Morphine and related drugs poisoning Cyanide poisoning

drkldahiya@rediffmail.com

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DOSAGE AND ADMINISTERATION OF DRUGS IN SMALL ANIMALS

Dr. K.L.Dahiya drkldahiya@rediffmail.com

http://info.med.yale.edu/yarc/vcs/drugs.htm

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Anaesthetics Analgesics and Sedatives Anti-Infectives Miscellaneous Drugs Parasiticides

170 - 183 184 - 199 200 - 224 225 - 245 246 - 256

Abbreviations used: NHP: Non Human Primates

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Anesthetics
Azaperone and ketamine (respectively) Mouse Rat 75 mg/kg BW IM and 100 mg/kg BW IM (duration of anesthesia approximately 1 h) (Olson and Renchko, 1988) 50 mg/kg BW IM and 87 mg/kg BW IM; give to 1 times this dose depending on the length of anesthesia required (approximately 1-6 h) (Olson and Renchko, 1988)

Benzocaine Amphibia Larvae: 50 mg/l bath (dissolve in ethanol first) (Crawshaw, 1993) Frogs and salamanders: 200-300 mg/l bath (Crawshaw, 1993) Fish 20-50 ppm in water (Green, 1982) Chloral hydrate Amphibia 1-2 ml of a 10% solution injected into dorsal lymph sac (Kaplan, 1969) Cat 300 mg/kg BW IV (Borchard et al., 1990) Dog 125 mg/kg BW IV (Borchard et al., 1990) Goat 50-300 mg/kg BW IV (Swindle and Adams, 1988) Guineapig 200-300 mg/kg BW IP of 10% solution (Green, 1982) Hamster 270-360 mg/kg BW IP (Hughes, 1981) Mouse 400 mg/kg BW IP (Borchard et al., 1990) Rat 200-300 mg/kg BW IP of 10% solution (Green, 1982) Sheep 50-300 mg/kg BW IV (Swindle and Adams, 1988) Swine 100-300 mg/kg BW IV (Swindle and Adams, 1988) Chloralose Cat 75 mg/kg IV (Borchard et al., 1990) Dog 80 mg/kg BW IV with 5 mg/kg BW IV thiopental sodium initially, then maintain anesthesia with additional chloralose (1 ml/s IV); respirator required at this dose of chloralose (Grad et al., 1988) Goat 45-62 mg/kg BW IV (Swindle and Adams, 1988) Mouse 114 mg/kg BW IP(Hughes, 1981) Rat 55 mg/kg BW IP (Borchard et al., 1990) Rabbit 80-100 mg/kg BW IV of 1% solution (Green, 1982) Sheep 45-62 mg/kg BW IV (Swindle and Adams, 1988) Swine 55-86 mg/kg BW IV (Swindle and Adams, 1988) 170

Equithesin Note: Combine 0.85 g chloral hydrate with 0.21 g sodium pentobarbital (4.2 ml Nembutal), 8.6 ml propylene glycol (4.2 ml Nembutal provides 1.68 ml of this amount), 2.2 ml 100% ethanol, and 6.7 ml water (for a total of 20 ml). Add ethanol and propylene glycol together, then add chloral hydrate, and last Nembutal. Ethyl alcohol Amphibia Frogs and toads: immerse in 10% solution (Kaplan, 1969) Etomidate Mouse 30 mg/kg BW IP (Green et al., 1981)

Etorphine (M-99) Reptile Turtles: 0.5-5.0 mg total dose (for approximately 1.8-kg animal) (Marcus, 1981) Snakes: 2-15 mg total dose IPP (Marcus, 1981)

Fentanyl and medetomidine (respectively) Rat Rabbit 300 g/kg BW IP and 300 g/kg BW IP (Flecknell, 1996) 8 g/kg BW IV and 330 g/kg BW IV (Flecknell, 1996)

Fentanyl and metomidate (respectively) Cat Gerbil Mouse 0.02 mg/kg BW IM and 20 mg/kg BW IM (Flecknell, 1996) 0.05 mg/kg BW SC and 50 mg/kg BW SC (Flecknell, 1996) 0.002-0.006 mg/kg BW SC and 60 mg/kg BW SC (Green et al., 1981)

Fentanyl/droperidol (Innovar-Vet) Chinchilla 0.20 ml/kg BW IM (Green, 1982) Ferret 0.5 ml/kg BW IM (Green, 1982) Guineapig 0.66-0.88 ml/kg BW IM (Hughes, 1981) 0.5-1.0 ml/kg BW IM (CCAC, 1984) Hamster Not recommended (Thayer et al., 1972) Mouse 0.05 ml/g BW IM (Hughes, 1981) NHP 1.0 ml/9 kg BW IM (Melby and Altman, 1976) Rat 0.02-0.06 ml/100 g BW IP (Wixson et al., 1987) 171

Rabbit Swine

0.3 ml/kg BW IM (Hughes, 1981) 0.10-0.50 ml/kg BW IM (Green, 1982) 0.10 ml/kg BW IM (Swindle and Adams, 1988)

Fentanyl/droperidol (Innovar-Vet) and diazepam (respectively) Hamster 1 ml/kg BW IP and 5 mg/kg BW IP (Green, 1982) Fentanyl/fluanisone (Hypnorm) Guineapig 0.5 ml/kg BW IM Note: Addition of 1-2 mg/kg BW IP or IM diazepam is advisable (Cooper, 1984). Mouse 0.5ml/kg BW IM Note: Addition of 1-2 mg/kg BW IP or IM diazepam is advisable (Cooper, 1984). Rat 0.5 ml/kg BW IM (Cooper, 1984) Fentanyl/fluanisone and diazepam (respectively) Gerbil 0.3 ml/kg BW IM, IP and 5 mg/kg BW IP (Flecknell, 1996) Guineapig 1 ml/kg BW IM, IP and 2.5 mg/kg BW IP (Flecknell, 1996) Hamster 1 ml/kg BW IM, IP and 5 mg/kg BW IP (Flecknell, 1996) Mouse 0.4 ml/kg BW IP and 5 mg/kg BW IP (Flecknell, 1996) Rat 0.6 ml/kg BW IP and 2.5 mg/kg BW IP (Flecknell, 1996) Rabbit 0.3 ml/kg BW IM and 1-2 mg/kg BW IM, IP IV (Flecknell, 1996) Fentanyl/fluanisone and midazolam (respectively) Rabbit Halothane Amphibia Terrestrial species: 4-5% in anesthetic chamber to effect (Crawshaw, 1993) Hexobarbital Amphibia 120 mg/kg BW intravascularly (Kaplan, 1969) Mouse 100 mg/kg BW IP (Taber and Irwin, 1969) Rat 100 mg/kg BW IP (Ben et al., 1969) 0.3 ml/kg IM and 1-2 mg/kg BW IP, IV (Flecknell, 1996)

172

Inactin Rat Isoflurane Amphibia Terrestrial species: 4-5% in anesthetic chamber to effect (Crawshaw, 1993) Ketamine (Used alone in mammals, we have found that ketamine is not usually adequate for deep anesthesia, Eds.) Amphibia 50-150 mg/kg SC, IM (Crawshaw, 1993) Bird 10-50 mg/kg BW IM (Fowler, 1978; Cooper, 1984) Note: Rarely used alone (Sinn, 1997). Chinchilla 44 mg/kg BW IM (Johnson-Delaney, 1996) Ferret 20-30 mg/kg BW IM (Green, 1982) 20-30 mg/kg BW IM for immobilization (Flecknell, 1987) 20-35 mg/kg BW IM (Andrews and Illman, 1987) Gerbil 200 mg/kg BW IM for immobilization (Flecknell, 1987) Goat 22-44 mg/kg BW IM (Swindle and Adams, 1988) Guineapig 44 mg/kg BW IM, atropine recommended (Weisbroth and Fudens, 1972) 100-200 mg/kg BW IM for immobilization (Flecknell, 1987) Hamster 10-30 mg/100 g BW IP (Strittmatter, 1972) 200 mg/kg BW IP for immobilization (Flecknell, 1987) Mouse 44 mg/kg BW IM for sedation (Weisbroth and Fudens, 1972) 100-200 mg/kg BW IP (Hughes, 1981) 200 mg/kg BW IM for immobilization (Flecknell, 1987) 50 mg/kg BW IV (Hughes, 1981) NHP 10-30 mg/kg BW IM (Welshman, 1985) African green (Cercopithecus spp.): 25-30 mg/kg BW IM (Cramlet and Jones, 1976) Baboon (Papio spp.): 7.5-10 mg/kg BW IM (Cramlet and Jones, 1976) Chimpanzee (Pan troglotydes): 10-15 mg/kg BW IM (Cramlet and Jones, 1976) Cynomolgus macaque (Macaca fascicularis): 20-25 mg/kg BW IM (Cramlet and Jones, 1976) Gorilla (Gorilla gorilla): 12-15 mg/kg BW IM (Cramlet and Jones, 1976) Patas (Erythrocebus patas): 5-7.5 mg/kg BW IM (Cramlet and Jones, 1976) Rhesus macaque (Macaca mulatta): 20-25 mg/kg BW IM (Cramlet and Jones, 1976) 80 mg/kg BW IP (Flecknell, 1987) 100-110 mg/kg BW IP (Ellison et al., 1987)

173

Squirrel monkey (Saimiri sciureus): 25-30 mg/kg BW IM (Cramlet and Jones, 1976) Rat 44 mg/kg BW IM (Weisbroth and Fudens, 1972) 100 mg/kg BW IM for immobilization (Flecknell, 1987) 75 mg/kg BW IP (Waterman and Livingston, 1978) Rabbit 44 mg/kg BW IM (Weisbroth and Fudens, 1972) 50 mg/kg BW IM for immobilization (Flecknell, 1987) 25 mg/kg BW intranasally for light surgical anesthesia (Robertson and Eberhart, 1994) Raccoon 5-27 mg/kg BW IM (use higher doses for longer anesthetic duration) (Evans and Evans, 1986) Reptile Snakes: 88-110 mg/kg BW IM (for 3.6- to 4.5-kg animals) (Marcus, 1981) Snakes: 22-44 mg/kg BW IM (for <0.9-kg animals) (Marcus, 1981) 50-130 mg/kg BW IM (Page, 1993) Tortoises and turtles: 15-60 mg/kg BW IM (Fowler, 1978) Tortoises: 20-80 mg/kg BW IM (Page and Mautino, 1990) Chelonians: 20-60 mg/kg BW IM (Page, 1993) Sheep 22-44 mg/kg BW IM (Swindle and Adams, 1988) Swine 15-25 mg/kg BW IM (Swindle and Adams, 1988) 15-20 mg/kg BW IV (Swindle and Adams, 1988) Ketamine and acepromazine (respectively) 10-25 mg/kg BW IM and 0.5-1 mg/kg BW IM (high-end dose for <250g bird) (Curro, 1998) Cat 20 mg/kg BW IM and 0.11 mg/kg BW IM (Flecknell, 1996) Chinchilla 40 mg/kg BW IM and 0.5 mg/kg BW IM (Morgan et al., 1981) Ferret 20-35 mg/kg BW IM, SC and 0.2-0.35 mg/kg BW IM, SC (Morrisey et al., 1996) Gerbil 75 mg/kg BW IM and 3 mg/kg BW IM (Flecknell, 1987) Guineapig 125 mg/kg BW IM and 5 mg/kg BW IM (Flecknell, 1987) Hamster 150 mg/kg BW IM and 5 mg/kg BW IM (Flecknell, 1987) Mouse 100 mg/kg BW IM and 2.5 mg/kg BW IM (Flecknell, 1987) NHP Varecia and Propithecus (not Lemur): 4 mg/kg BW IM and 0.4 mg/kg BW IM (Feeser and White, 1992) Rat 75 mg/kg BW IM and 2.5 mg/kg BW IM (Flecknell, 1987) 30 mg/kg BW IM and 3 mg/kg BW IM (Roman and Osborn, 1987) Rabbit 75 mg/kg BW IM and 5 mg/kg BW IM (Flecknell, 1987) 50 mg/kg BW IM and 1 mg/kg BW IM (Flecknell, 1996) Raccoon 8-10 mg/kg BW IM and 2.2 mg/kg BW IM (Evans and Evans, 1986) Bird

174

Ketamine and detomidine (respectively) Rat 60 mg/kg BW IM and 10 mg/kg BW IM in males (Cox et al., 1994) 40 mg/kg BW IM and 5 mg/kg BW IM in females (Cox et al., 1994)

Ketamine and diazepam (respectively) 10-50 mg/kg BW IM and 0.5-2 mg/kg BW IM (high-end dose for <250g bird) (Curro, 1998) 5-30 mg/kg BW IM and 0.5-2 mg/kg BW IM, IV (Sinn, 1997) 2.5-5 mg/kg BW IV and 0.5-2 mg/kg BW IM, IV (Sinn, 1997) Chinchilla 20 mg/kg BW IM, IP and 5 mg/kg BW IM, IP (Flecknell, 1987) 20-40 mg/kg BW IM and 1-2 mg/kg BW IM (Johnson-Delaney, 1996) Ferret 25 mg/kg BW IM and 2 mg/kg BW IM (Flecknell, 1987) 25-35 mg/kg BW IM and 2-3 mg/kg BW IM (Morrisey et al., 1996) Gerbil 50 mg/kg BW IM and 5 mg/kg BW IP (Flecknell, 1987) Guineapig 100 mg/kg BW IM and 5 mg/kg BW IM (Flecknell, 1987) Hamster 70 mg/kg BW IP and 2 mg/kg BW IP (Flecknell, 1996) Mouse 200 mg/kg BW IM and 5 mg/kg BW IP (Flecknell, 1987) NHP 15 mg/kg BW IM and 1 mg/kg BW IM (Flecknell, 1996) Rat 40-80 mg/kg BW IP and 5-10 mg/kg BW IP (Wixson et al., 1987) Rabbit 25 mg/kg BW IM and 5 mg/kg BW IM (Flecknell, 1987) 30-40 mg/kg BW IM and 2-5 mg/kg BW IM (Carpenter et al., 1995) 20-30 mg/kg BW IM and 1-3 mg/kg BW IM when used with isoflurane (Carpenter et al., 1995) Ketamine and medetomidine (respectively) (not for major surgical procedures) Cat 7 mg/kg BW IM and 80 g/kg BW IM (Flecknell, 1996) 2-3 mg/kg BW IV and 30-50 g/kg BW IV (Ko et al., 1997) 3-5 mg/kg BW IM and 40-80 g/kg BW IM (Ko et al., 1997) Dog 1-3 mg/kg BW IV and 10-20 g/kg BW IV (Ko et al., 1997) 3-5 mg/kg BW IM and 30-40 g/kg BW IM (Ko et al., 1997) 2.5-7.5 mg/kg BW IM and 40 g/kg BW IM (Flecknell, 1996) Ferret 5 mg/kg BW IM and 80 g/kg BW IM (Ko et al., 1997) 4-8 mg/kg BW IM and 50-100 g/kg BW IM (Wolfensohn and Lloyd, 1994) Gerbil 75 mg/kg BW IP and 0.5 mg/kg BW IP (Flecknell, 1996) Goat 1 mg/kg BW IM and 25 g/kg BW IM (Flecknell, 1996) Guineapig 40 mg/kg BW IP and 0.5 mg/kg BW IP (Flecknell, 1996) Hamster 100 mg/kg BW IP and 250 g/kg BW IP (Flecknell, 1996) Mouse 50 mg/kg BW IP and 1 mg/kg BW IP in males (Cruz et al., 1998) 75 mg/kg BW IP and 1 mg/kg BW IP in females (Cruz et al., 1998) 175 Bird

NHP

Rat Rabbit

Sheep Swine

Callithricidae: 5-7.5 mg/kg BW IM and 100-150 g/kg BW IM (Jalanka, 1993) Pongidae: 3-5 mg/kg BW IM and 70 g/kg BW IM (Jalanka, 1993) 75 mg/kg BW IP and 0.5 mg/kg BW IP (Flecknell, 1996) 5 mg/kg BW IV and 0.35 mg/kg BW IM; use with supplemental oxygen (Hellebrekers et al., 1996) 25 mg/kg BW IM and 0.5 mg/kg BW IM (Flecknell, 1996) 1 mg/kg BW IM and 25 g/kg BW IM (Flecknell, 1996) 10 mg/kg BW IM and 0.08 mg/kg BW IM (Flecknell, 1996)

Ketamine and midazolam (respectively) Bird Cat Mink Rat Swine 10-40 mg/kg BW IM and 0.5-1.5 mg/kg BW IM (high-end dose for <250-g bird) (Curro, 1998) 10 mg/kg BW IM and 0.2 mg/kg BW IM (Flecknell, 1996) 50 mg/kg BW/h IV and 2 mg/kg BW/h IV (4 mmol/(kg.h) sodium bicarbonate also required) (Wamberg et al., 1996) 75 mg/kg BW IP and 5 mg/kg BW IP (Flecknell, 1996) 10-15 mg/kg BW IM and 0.5-2 mg/kg BW IM (Flecknell, 1996)

Ketamine and xylazine (respectively) Bird 10-50 mg/kg BW IM and 1-10 mg/kg BW IM (high-end dose for <250-g bird) (Curro, 1998) 40 mg/kg BW IM and 10 mg/kg BW IM (Heaton and Brauth, 1992) 5-30 mg/kg BW IM and 1-4 mg/kg BW IM (Sinn, 1997) 2.5-5 mg/kg BW IV and 0.25-0.5 mg/kg BW IV (Sinn, 1997) Chichilla 35 mg/kg BW IP and 5 mg/kg BW IP (Johnson-Delaney, 1996) Ferret 25 mg/kg BW IM and 2 mg/kg BW IM (Moreland and Glaser, 1985) Gerbil 50 mg/kg BW IM and 2 mg/kg BW IM (Flecknell, 1987) Guineapig 40 mg/kg BW IM and 5 mg/kg BW SC (Flecknell, 1987) 50 mg/kg BW IP and 5 mg/kg BW IP (Strother and Stokes, 1989) Hamster 200 mg/kg BW IP and 10 mg/kg BW IP (Flecknell, 1987) Mouse 200 mg/kg BW IM and 10 mg/kg BW IP (Flecknell, 1987) Note: High mortality possible. 90-120 mg/kg BW IM and 10 mg/kg BW IM (Harkness and Wagner, 1989) NHP 10 mg/kg BW IM and 0.5 mg/kg BW IM (Flecknell, 1996) Rat 40-80 mg/kg BW IP and 5-10 mg/kg BW IP (Wixson et al., 1987) 37 mg/kg BW IM and 7 mg/kg BW IM followed by 1-1 mg/kg BW/min IV and 32-40 g/kg BW/min IV for up to 12 h (Simpson, 1997) 90 mg/kg BW IM and 10 mg/kg BW IM (Flecknell, 1987)

176

Rabbit

50 mg/kg BW IM and 10 mg/kg BW IM (Lipman et al., 1987) 10 mg/kg BW IV and 3 mg/kg BW IV (Flecknell, 1987) 10 mg/kg BW intranasally and 3 mg/kg BW intranasally (Robertson and Eberhart, 1994) 35 mg/kg BW IM and 5 mg/kg BW IM (Flecknell, 1996) Raccoon 5-8 mg/kg BW IM and 1.5-3 mg/kg BW IM (Evans and Evans, 1986) 5.5 mg/kg BW IM and 5.5 mg/kg BW IM (Evans and Evans, 1986) Ketamine, medetomidine, and diazepam (respectively) Rabbit 20 mg/kg BW IM, 300 g/kg BW IM, and 0.75-1.5 mg/kg BW IM (Ko et al., 1997)

Ketamine, tiletamine/lorazepam, and xylazine (respectively) Swine 2.2 mg/kg BW IM, 4.4 mg/kg BW IM, and 2.2 mg/kg BW IM (Ko et al., 1993)

Ketamine, xylazine, and acepromazine (respectively) Mouse Rabbit 30 mg/kg BW IM, 6 mg/kg BW IM, and 1 mg/kg BW IM (O'Rourke et al., 1994) 35 mg/kg BW IM, 5 mg/kg BW IM, and 0.75 mg/kg BW IM (Marini et al., 1989). Note: This provides approximately 30% longer anesthesia and recovery than ketamine-xylazine alone. 35 mg/kg BW IM, 5 mg/kg BW IM, and 1 mg/kg BW IM, SC (Flecknell, 1996)

Ketamine, xylazine, and butorphanol (respectively) Rabbit 35 mg/kg BW IM, 5 mg/kg BW IM, and 0.1 mg/kg BW IM (Marini et al., 1992)

Ketamine, xylazine, and guaifenesin (respectively) Sheep 1 mg/ml, 0.1 mg/ml, and 50 mg/ml in 5% dextrose IV; induction use 1.2 ml/kg; maintenance use 2.6 ml/(kg.h) (Lin et al., 1993)

Ketamine, xylazine, and oxymorphone (respectively) Swine 2 mg/kg BW IV, 2 mg/kg BW IV, and 0.075 mg/kg BW IV for minor surgery (Breese and Dodman, 1984)

177

Medetomidine and butorphanol (respectively) (not for major surgical procedures) Cat Dog Ferret 30-50 g/kg BW IV and 0.1-0.2 mg/kg BW IV (Ko et al., 1997) 40-80 g/kg BW IM and 0.1-0.2 mg/kg BW IM (Ko et al., 1997) 10-20 g/kg BW IV and 0.1-0.2 mg/kg BW IV (Ko et al., 1997) 30-40 g/kg BW IM and 0.1-0.2 mg/kg BW IM (Ko et al., 1997) 80 g/kg BW IM and 0.1-0.2 mg/kg BW IM (Ko et al., 1997)

Medetomidine and morphine (respectively) (not for major surgical procedures) Dog 10-20 g/kg BW IV and 0.07-0.1 mg/kg BW IV (Ko et al., 1997) 30-40 g/kg BW IM and 0.2-0.3 mg/kg BW IM (Ko et al., 1997)

Medetomidine and oxymorphone (respectively) (not for major surgical procedures) Dog 10-20 g/kg BW IV and 0.01-0.02 mg/kg BW IV (Ko et al., 1997) 30-40 g/kg BW IM and 0.05-0.1 mg/kg BW IM (Ko et al., 1997)

Medetomidine and propofol (respectively) Rabbit 0.35 mg/kg BW IM and 3 mg/kg BW IV (Hellebrekers et al., 1996) 0.25 mg/kg BW IM and 4 mg/kg BW IV (Ko et al., 1992)

Medetomidine, midazolam, and propofol (respectively) Rabbit 0.25 mg/kg BW IM, 0.5 mg/kg BW IM, and 2 mg/kg BW IV (Ko et al., 1992)

Methohexital Guineapig 31 mg/kg BW IP (Flecknell, 1987) Mouse 6 mg/kg BW IV (Flecknell, 1987) NHP 10 mg/kg BW IV (Flecknell, 1987) Rat 7-10 mg/kg BW IV (Flecknell, 1987) 10-15 mg/kg BW IV (Flecknell, 1996) Rabbit 10 mg/kg BW IV (Flecknell, 1987) Methoxyflurane Cat Dog 3% for induction; 0.5% by inhalation for maintenance (Kinsell, 1986) 3% for induction; 0.5% by inhalation for maintenance (Kinsell, 1986) 178

Metomidate Mouse 30-50 mg/kg BW IP (Green et al., 1981)

Pentobarbital and chlorpromazine (respectively) Mouse 40-60 mg/kg BW IP and 25-50 mg/kg IM (Harkness and Wagner, 1989)

Pentobarbital sodium Amphibia Frogs and toads: 60 mg/kg in dorsal lymph sac (Kaplan, 1969; Marcus, 1981) Bovine 12-28 mg/kg BW IV (Schultz, 1989) Cat 30 mg/kg IV to effect for anesthesia (Kinsell, 1986) Chinchilla 40 mg/kg BW IP (Mason, 1997) 30 mg/kg BW IV (Mason, 1997) Dog 30 mg/kg IV to effect for anesthesia (Kinsell, 1986) Ferret 36 mg/kg BW IP (Andrews and Illman, 1987) 30 mg/kg BW IV (Green, 1982) Gerbil 6 mg/100 g BW IP up to 6 mg maximum (Norris, 1987) Goat 25-30 mg/kg BW IV (Swindle and Adams, 1988) Guineapig 28 mg/kg BW IP (Croft, 1964) Hamster 9 mg/100 g BW IP, boost with 1.2 mg/100 g BW (Whitney, 1963) Mouse 40-85 mg/kg BW IP (Cunliffe-Beamer, 1981) 50 mg/kg BW IP followed by a dose of 25 mg/kg BW SC for longer procedures (45-50 min) (Taber and Irwin, 1969) Neonates (1-4 days): 5 mg/kg BW IP (Taber and Irwin, 1969) NHP 5-15 mg/kg BW IV (Flecknell, 1987) Rat 30-40 mg/kg BW IP (Wixson et al., 1987) 40-50 mg/kg BW IP (Flecknell, 1996) Rabbit 28 mg/kg BW IV, IP (Croft, 1964) Raccoon 30 mg/kg BW IP (Evans and Evans, 1986) Reptile Turtles: 16 mg/kg BW IC, IP (Marcus, 1981) Snakes: 15-30 mg/kg BW IPP (Marcus, 1981) Sheep 25-30 mg/kg BW IV (Swindle and Adams, 1988) 15-30 mg/kg BW IV lower dose for castrated animals (NCSU, 1987) Swine 25-35 mg/kg BW PO (Swindle and Adams, 1988) 30 mg/kg BW IP (Swindle and Adams, 1988) 20-30 mg/kg BW IV (Swindle and Adams, 1988)

179

Propofol Mouse NHP Rat Rabbit 20-30 mg/kg BW IV (Mason, 1997) 7.5-12.5 mg/kg BW IV (Flecknell, 1996) 10 mg/kg BW IV (Flecknell, 1996) 7.5-15 mg/kg BW IV (Adam et al., 1990) 1.5 mg/kg BW IV bolus followed by 0.2-0.6 mg/(kg.min) continuous infusion (Blake et al., 1988) Saffan (alphadolone and alphaxalone) Bird 8.0 mg/kg BW IV, with incremental doses up to 25 mg/kg BW maximum (Cooper, 1984) Cat 9 mg/kg BW IV initially, followed by multiple 3 mg/kg BW IV doses as needed to maintain anesthesia (from product information) 18 mg/kg BW IM initially, followed by multiple 3 mg/kg BW IV doses as needed to maintain anesthesia (from product information) Chinchilla 20-30 mg/kg BW IM (Green, 1982) Dog Not suitable for use in dogs (Glaxovet guide to Saffan) Ferret 12-15 mg/kg BW IM initially, followed by multiple 6-8 mg/kg BW IV doses as needed to maintain anesthesia (Green, 1982) Gerbil 80-120 mg/kg BW IP (Flecknell, 1987) Guineapig 10-20 mg/kg BW IV (Green, 1982) 40 mg/kg BW IP (Flecknell, 1987) Hamster 150 mg/kg BW IP (Flecknell, 1987) Mouse 5 mg/kg BW IV, with incremental doses up to 20 mg/kg maximum (Cooper, 1984) 90 mg/kg BW IP (Green, 1982) NHP 6-9 mg/kg BW IV initially, followed by supplemental doses to effect as needed to maintain anesthesia (from product information) 12-18 mg/kg BW IM initially, followed by multiple 6-9 mg/kg BW IV doses as needed to maintain anesthesia from product information) Rat 5 mg/kg BW IV, with incremental doses up to 20 mg/kg maximum (Cooper, 1984); has been given by slow IV drip for periods up to 10 h without tolerance or cumulation developing (Green, 1982) 10-12 mg/kg BW IV (Flecknell, 1996) Rabbit 6-9 mg/kg BW IV (Green, 1982); high mortality possible (Flecknell, 1987) Reptile 9mg/kg BW IV (Frye, 1981) 12-18 mg/kg BW IM (Cooper, 1984) Chelonians: 9-18 mg/kg BW IM (Page, 1993) Lizards: 9-18 mg/kg BW IM (Page, 1993) Swine 12 mg/kg BW IM, then 6-8 mg/kg BW IV every 30 min (Tongetal., 1995)

180

Thiamylal NHP 25 mg/kg BW IV (Hughes et al., 1975)

Thiopental Dog Goat Mouse 6-12 mg/lb BW IV; lower dose with preanesthetic tranquilization (Kinsell, 1986) 20-25 mg/kg BW IV (Swindle and Adams, 1988) 25-50 mg/kg BW IV (Taber and Irwin, 1969) 25 mg/kg BW IV (Hughes, 1981) 50 mg/kg BW IP (Williams, 1976) 15-20 mg/kg BW IV (Flecknell, 1987) 22-25 mg/kg BW (Hatch, 1966) 30 mg/kg BW IV (Flecknell, 1987) 28 mg/kg BW IV, IP (Croft, 1964) Snakes: 15-25 mg/kg BW IPP (Marcus, 1981) 20-25 mg/kg BW IV (Swindle and Adams, 1988) 24-30 mg/kg BW IP (Swindle and Adams, 1988) 5-19 mg/kg BW IV (Swindle and Adams, 1988)

NHP Rat Rabbit Reptile Sheep Swine

Tiletamine Raccoon 10-12 mg/kg BW IM (Evans and Evans, 1986) Tiletamine/zolazepam (Telazol) Bird Cat Ferret 7.7-26 mg/kg BW IM (Curro, 1998) 7.5 mg/kg BW IM and 7.5 mg/kg BW IM (Flecknell, 1996) 22 mg/kg BW IM (Payton and Pick, 1989) 12-22 mg/kg BW IM (Morrisey et al., 1996) Gerbil 60 mg/kg BW IM (Hrapkiewicz et al., 1989) Guineapig 10-30 mg/kg IM (Fowler, 1978) Hamster Not recommended (Silverman et al., 1983) Mouse Not recommended (Silverman et al., 1983) NHP 2-6 mg/kg BW IM (Ialeggio, 1989) Lemurs: 20 mg/kg BW IM (immobilization by dart) (Glander et al., 1992) Rat 20-40 mg/kg BW IP (Silverman et al., 1983) Rabbit Not generally recommended (except intranasally); nephrotoxicity (Doerning et al., 1990, 1992) 10-25 mg/kg BW IM (Fowler, 1978)

181

Reptile

Sheep Swine

10 mg/kg BW intranasally (no renal compromise) (Robertson and Eberhart, 1994) Chelonians: 10-20 mg/kg BW IM (Page, 1993) Snakes: 22 mg/kg BW IM (Marcus, 1981) Snakes: 10-20 mg/kg BW IM (Page, 1993) Lizards: 30 mg/kg BW IM (Page, 1993) 2.2 mg/kg BW IM (Schultz, 1989) 6.6-11 mg/kg BW IM following xylazine 2 mg/kg BW IM (Schultz, 1989) 6-8 mg/kg BW IM (Flecknell, 1996)

Tiletamine/zolazepam and xylazine (respectively) Hamster 30 mg/kg BW IP and 10 mg/kg BW IP (Forsythe et al., 1992) Rabbit 15 mg/kg BW IM and 5 mg/kg BW IM (Popuskis et al., 1991) Swine 4.4 mg/kg BW IM and 2.2 mg/kg BW IM (Ko et al., 1993) 6 mg/kg BW IM and 2.2 mg/kg BW IM (Braun, 1993) 2-7 mg/kg BW IM and 0.2-1 mg/kg BW IM (Flecknell, 1996) Tribromoethanol Gerbil Mouse 250-300 mg/kg BW IP (1.25% solution) (Flecknell, 1987) 125 mg/kg BW IP (0.25% solution) (Flecknell, 1987) 250 mg/kg BW IP (Taber and Irwin, 1969) 0.2 ml/10 g BW IP (1.2% solution) (Papaioannou and Fox, 1993) 300 mg/kg BW IP (Flecknell, 1987)

Rat

Tribromoethanol/amylene hydrate (Avertin) Note: No longer available commercially but can be made. For concentrated solution (66.66%), dissolve 1 g 2,2,2-tribromoethanol in 0.5 g amylene hydrate. Take 0.5 ml concentrate and mix with 39.5 ml sterile saline (this is now a 1.25% solution). If solution falls below pH 5.0, discard. Warning: Stored solutions are known to be unstable and potentially hepatotoxic. Frequent use may induce chemical peritonitis. 250-300 mg/kg BW IP of 1.25% solution (Flecknell, 1987) 0.2 ml/10 g BW IP of 1.25% solution (The Jackson Laboratory) 300 mg/kg BW IP (Flecknell, 1987)

Gerbil Mouse Rat

Tricaine methanesulfonate (MS 222) Amphibia Immerse in 0.1% solution (Kaplan, 1969) 50-150 mg/kg BW SC, IM (Crawshaw, 1993)

182

Fish Reptile Urethane

Tadpoles and newts: 200-500 mg/l bath to effect (Crawshaw, 1993) Frogs, salamanders: 500-2000 mg/l bath (buffer with NaHCO3) (Crawshaw, 1993) Toads: 1-3 g/l bath (buffer with NaHCO3) (Crawshaw, 1993) Immerse in 25-100 mg/l water (Kiontz, 1964) Snakes: 200-300 mg/kg BW IPP (Marcus, 1981)

Amphibia Frogs and toads: Immerse in 1-2% solution (Kaplan, 1969) Frogs and toads: Inject 0.04-0.12 ml/g BW of 5% solution into dorsal lymph sac (Kaplan, 1969) Ferret 1500 mg/kg BW IP for acute use only (Andrews and Illman, 1987) Fish Immerse in 5-40 mg/l water (Klontz, 1964) Guineapig 1500 mg/kg BW IV, IP (Flecknell, 1987) Hamster 1-2 g/kg BW IP (Flecknell, 1996) Rat 1000 mg/kg BW IP (Flecknell, 1987) Rabbit 1000 mg/kg BW IV, IP (Flecknell, 1987) Reptile Turtles: 2.8 g/kg PO (Marcus, 1981) 2.4 g/kg IV (Marcus, 1981) 1.7 g/kg IC (Marcus, 1981) 2.8 g/kg IP (Marcus, 1981)

183

Analgesics and Sedatives

Acepromazine Cat 0.1-0.2 mg/kg BW IM, SC (Kinsell, 1986) 0.5-1.0 mg/lb BW PO prn (Kinsell, 1986) Chinchilla 0.5 mg/kg BW IM (Johnson-Delaney, 1996) Dog 0.1-0.5 mg/kg BW IV, IM, SC (Kinsell, 1986) 0.25-1.0 mg/lb BW PO prn (Kinsell, 1986) Ferret 0.2 mg/kg BW IM (Flecknell, 1987) 0.2-0.5 mg/kg BW IM, SC (Morrisey et al., 1996) Gerbil May precipitate seizures (Harkness and Wagner, 1983) Goat 0.05-0.5 mg/kg BW IM (Swindle and Adams, 1988) 0.55 mg/kg BW IV (Swindle and Adams, 1988) 0.05-0.1 mg/kg BW IM (NCSU, 1987) Mouse 1-2 mg/kg BW IM (Harkness and Wagner, 1983) 2-5 mg/kg BW IP (Flecknell, 1987) NHP 0.5-1.0 mg/kg BW IM, SC (Melby and Altman, 1976) 0.2 mg/kg BW IM (Flecknell, 1987) Rat 1-2 mg/kg BW IM (Harkness and Wagner, 1983) Rabbit 1-2 mg/kg BW IM (Harkness and Wagner, 1983) 5 mg/kg BW IM (Flecknell, 1987) 2 mg/kg BW IM (Bauck, 1989) Raccoon 2-2.5 mg/kg BW (Evans and Evans, 1986) Reptile 0.125-0.5 mg/kg BWIM (Frye, 1981) Sheep 0.05-0.5 mg/kg BW IM (Swindle and Adams, 1988) 0.55 mg/kg BW IV (Swindle and Adams, 1988) Swine 0.11-0.22 mg/kg BW SC, IM, IV (Swindle and Adams, 1988) 0.05-0.1 mg/kg BW IM (NCSU, 1987) 0.03-0.22 mg/kg BW IM not to exceed 15 mg total (NCSU, 1987) Acepromazine and buprenorphine (respectively) Dog 0.07 mg/kg BW IM and 0.009 mg/kg BW IM (Flecknell, 1996)

Acetaminophen Cat Dog Mouse Toxic 15 mg/kg BW PO q8h (Jenkins, 1987) 300 mg/kg BW PO (Jenkins, 1987)

184

NHP Rat

5-10 mg/kg BW PO (Johnson et al, 1981) 110-300 mg/kg BW PO (Jenkins, 1987) 100-300 mg/kg BW PO q4h (Flecknell, 1991)

Acetaminophen/codeine Rabbit 1 ml elixer/100 ml drinking water (Wixson, 1994)

Alphaxalone/alphadolone Cat 9 mg/kg BW IM (Flecknell, 1987) Guineapig 40 mg/kg BW IM (Flecknell, 1987) NHP 12-18 mg/kg BW IM (Flecknell, 1987) Rat 9-12 mg/kg BW IP (Flecknell, 1987) Rabbit 9-12 mg/kg BW IM (Flecknell, 1987) Swine 6 mg/kg BW IM (Flecknell, 1987) Aminopyrine Dog 265 mg total PO (Borchard et al., 1990) Guineapig 130 mg/kg BW PO (Jenkins, 1987) Hamster 130 mg/kg BW PO (Jenkins, 1987) Mouse 150 mg/kg BW IP (Borchard et al., 1990) 300 mg/kg BW PO (Borchard et al., 1990) Rat 200 mg/kg BW SC (Borchard et al., 1990) 650 mg total PO (Borchard et al., 1990) Rabbit 50 mg/kg BW PO (Jenkins, 1987) Antipyrine Cat Dog Mouse Rat Rabbit 100 mg/kg BW IM, IP, SC (Borchard et al., 1990) 500 mg/kg BW PO (Borchard et al., 1990) 1000 mg total PO (Borchard et al., 1990) 197 mg/kg BW IP (Borchard et al., 1990) 600 mg/kg BW SC (Borchard et al., 1990) 220 mg/kg BW SC (Borchard et al., 1990) 100 mg/kg BW PO (Jenkins, 1987) 100 mg/kg BW IM, IP, SC (Borchard et al., 1990) 500 mg/kg BW PO (Borchard et al., 1990)

185

Aspirin Bird Cat 5 mg/kg BW PO tid (Ritchie and Harrison, 1997) 10 mg/kg BW PO q48h (Jenkins, 1987) 1 children's aspirin (1.25 g) PO q36h (Kinsell, 1986) Chinchilla 100-200 mg/kg BW PO q6-8h (Johnson-Delaney, 1996) Dog 10-20 mg/kg BW PO q12h (Jenkins, 1987) Note: Use buffered tabs: analgesic dosage 10 mg/kg BW PO q12h (Kinsell, 1986) Antirheumatic maximum dosage 40 mg/kg BW q18h (Kinsell, 1986) Ferret 10-20 mg/kg BW PO sid (Johnson-Delaney, 1996) Goat 10-20 mg/kg BW PO (Swindle and Adams, 1988) Guineapig 270 mg/kg BW IP sid (CCAC, 1984) 86 mg/kg BW PO, try q4h (Flecknell, 1987) Hamster 240 mg/kg BW IP sid (CCAC, 1984) Mouse 120-300 mg/kg BW PO (Jenkins, 1987) 120 mg/kg BW PO q4h (Flecknell, 1987) 400 mg/kg BW SC sid (CCAC, 1984) 25 mg/kg BW IP (Borchard et al., 1990) NHP 100 mg/kg BW PO sid (CCAC, 1984) 20 mg/kg BW PO q6-8h (Flecknell, 1987) Rat 100 mg/kg BW PO q4h (Flecknell, 1987; Jenkins, 1987) 400 mg/kg BW SC, PO (Harkness and Wagner, 1983) Rabbit 400 mg/kg BW SC, PO sid (Harkness and Wagner, 1983) 100 mg/kg BW PO, try q4h (Flecknell, 1991) 20 mg/kg BW PO sid (equivalent to 600 mg dose in humans) (Marangos et al., 1994) Sheep 10-20 mg/kg BW PO (Swindle and Adams, 1988) Swine 10-20 mg/kg BW PO q4h (Swindle and Adams, 1988) Bupivacaine Dog 1 ml/4.5 kg BW of 0.25% or 0.5% solution given epidurally (Carroll, 1996)

Buprenorphine Bird Cat Dog 0.01-0.05 mg/kg BW IM (Bennett, 1997) 0.005-0.01 mg/kg BW SC, IM q12h (Flecknell, 1985; Jenkins, 1987) 0.005-0.01 mg/kg BW IV, SC q8-12h (Flecknell, 1996) 0.01-0.02 mg/kg BW SC q12h (Flecknell, 1985; Jenkins, 1987) 0.003-0.005 mg/kg of preservative-free solution (in 0.9% saline) given epidurally; give 0.3 ml/kg BW not to exceed 6 ml (Carroll, 1996) 186

0.005-0.02 mg/kg BW IM, IV, SC q6-12h (Flecknell, 1996) Ferret 0.01-0.03 mg/kg BW IM, IV SC q8-12h (Flecknell, 1996) 0.01-0.5 mg/kg BW IV, SC q8-12h (Johnson-Delaney, 1996) Gerbil 0.1-0.2 mg/kg BW SC q8h (Flecknell, 1987) Guineapig 0.05 mg/kg BW SC q8-12h (Flecknell, 1985; Jenkins, 1987) 0.05 mg/kg BW SC q6-12h (Flecknell, 1991) Hamster 0.05 mg/kg BW SC q8-12h (Jenkins, 1987) 0.5 mg/kg BW SC q8h (Flecknell, 1987) Mouse 2 mg/kg BW SC q12h (Flecknell, 1985; Jenkins, 1987) 2.5 mg/kg BW IP q6-8h (Jenkins, 1987) 0.05-0.1 mg/kg BW SC q6-12h (Flecknell, 1991) 0.05-0.1 mg/kg BW SC bid (Flecknell, 1996) NHP 0.01 mg/kg BW IM, IV q12h (Flecknell, 1985; Jenkins, 1987) 0.005-0.01 mg/kg BW IM, IV q6-12h (Flecknell, 1996) Rat 0.1-0.5 mg/kg BW SC, IV q12h (Jenkins, 1987; Flecknell, 1985; Flecknell, 1987) 0.006 mg/ml drinking water (Deeb et al., 1989) 0.01-0.05 mg/kg BW IV, SC q8-12h (Flecknell, 1996) 0.1-0.25 mg/kg BW PO q8-12h (Flecknell, 1996) Rabbit 0.02-0.05 mg/kg BW SC, IM, IV q8-12h (Flecknell, 1985; Jenkins, 1987) 0.02-0.1 mg/kg BW IV, SC q12h (Carpenter et al., 1995) 0.01-0.05 mg/kg BW SC, IV q6-12h (Flecknell, 1991) Sheep 0.005-0.01 mg/kg BW IM q4-6h (Flecknell, 1989) Swine 0.005-0.01 mg/kg BW IM, IV (Swindle and Adams, 1988) 0.005-0.02 mg/kg BW IM, IV q6-12h (Flecknell, 1996) Up to 0.1 mg/kg BW can be used for major surgical procedures (Farris, 1990) Butorphanol Bird Cat 1-4 mg/kg BW IV, PO prn not to exceed q4h (Ritchie and Harrison, 1997) 0.4 mg/kg BW SC q6h (Jenkins, 1987) 0.22 mg/kg BW IM (Short, 1997) 0.4-1.5 mg/kg BW PO q4-8h (Hansen, 1996) 0.4 mg/kg BW SC q3-4h (Flecknell, 1996) 0.2-0.4 mg/kg BW SC, IM, IV q2-5h (Jenkins, 1987) 0.2-0.4 mg/kg BW IM, SC q3-4h (Flecknell, 1996) 1-3 mg/kg BW PO (Raffe, 1995) 0.4 mg/kg BW IM q4-6h (Flecknell, 1996) 0.05-0.1 mg/kg BW SC q8-12h (Johnson-Delaney, 1996) 0.05-5.0 mg/kg BW SC q4h (Jenkins, 1987)

Dog

Ferret Mouse

187

NHP Rat Rabbit Sheep Swine

5.4 mg/kg BW SC (Wright et al., 1985) 1-5 mg/kg BW SC q4h (Flecknell, 1991) 0.01 mg/kg BW IV q3-4h(?) (Flecknell, 1996) 0.05-2.0 mg/kg BW SC q4h (Jenkins, 1987) 2 mg/kg BW SC q4h (Flecknell, 1991) 0.1-0.5 mg/kg BW IV q4h (Flecknell, 1989) 0.1-0.5 mg/kg BW IM, IV, SC q4h (Carpenter et al., 1995) 0.5 mg/kg BW SC q2-3h (Flecknell, 1989) 0.1-0.3 mg/kg BW IM (Swindle and Adams, 1988)

Butorphanol and acepromazine (respectively) Cat Dog Rabbit 0.1-0.4 mg/kg BW IM, IV and 0.02-0.05 mg/kg BW IM, IV (Raffe, 1995) 0.2-0.4 mg/kg BW IM, IV and 0.02-0.05 mg/kg BW IM, IV (Raffe, 1995) 1 mg/kg BW IM and 1 mg/kg BW IM (Flecknell, 1996)

Butorphanol and diazepam (respectively) Dog 0.05-0.25 mg/lb BW IM and 0.1-0.2 mg/lb (maximum 10 mg) BW IM for induction (Ko et al., 1994)

Carprofen Cat Dog 4 mg/kg BW IV, SC (Flecknell, 1996) 2.2 mg/kg BW PO bid (Michels and Carr, 1997) 4 mg/kg BW IV, SC sid (Flecknell, 1996) 1-2 mg/kg BW PO bid for 7 days (Flecknell, 1996) Rat 5 mg/kg BW SC (Flecknell, 1996) Rabbit 1.5 mg/kg BW PO bid (Flecknell, 1996) Swine 2-4 mg/kg BW IV, SC sid (Flecknell, 1996) Chlorpromazine Cat 1-2 mg/kg BW IV, IM q12h (Kinsell, 1986) Dog 0.55-4.4 mg/kg BW IV q6-24h (Kinsell, 1986) 1.1-6.6 mg/kg BW IM q6-24h (Kinsell, 1986) Guineapig 0.2 mg/kg BW SC (Lumb and Jones, 1984) Hamster 0.5 mg/kg BW IM (Hofing, 1989) Mouse 5-10 mg/kg BW SC (Taber and Irwin, 1969) 25-50 mg/kg BW IM (Dolowy et al., 1960) NHP 3-6 mg/kg BW IM (Cramiet and Jones, 1976) Rat 1-2 mg/kg BW IM (Clifford, 1984) Rabbit 25 mg/kg BW IM (produces myositis) (CCAC, 1984)

188

Codeine Dog Mouse 2.2 mg/kg BW SC (Jenkins, 1987) 20 mg/kg BW SC (Jenkins, 1987) 60-90 mg/kg BW PO (Jenkins, 1987) 20 mg/kg BW SC q4h (Flecknell, 1987) 25-60 mg/kg BW SC q4h (Jenkins, 1987) 60-90 mg/kg BW SC q4h (Flecknell, 1991)

Rat Diazepam Bird

0.5-1 mg/kg BW IM, IV q8-12h (Ritchie and Harrison, 1997) 1-1.5 mg/kg IV, IM (McDonald, 1989) 2.5-4 mg/kg BW PO prn (Ritchie and Harrison, 1997) 2-5 mg/kg BW IM (Cooper, 1984) Cat 1 mg/kg BW IV to a maximum of 5 mg (Kinell, 1986) Chinchilla 2.5 mg/kg BW IP (Green, 1982) Dog 1 mg/kg BW IV to a maximum of 20 mg (Kinell, 1986) Ferret 2 mg/kg BW IM (CCAC, 1884; Flecknell, 1987) Gerbil 5 mg/kg BW IP (CCAC, 1884; Flecknell, 1987) Goat 0.5-1.5 mg/kg BW IM, IV (Swindle and Adams, 1988) 15 mg/kg BW PO mixed in feed (NCSU, 1987) Guineapig 5 mg/kg BW IP (Flecknell, 1987) 2.5 mg/kg BW IP, IM (Green, 1982) Hamster 5 mg/kg BW IP (CCAC, 1884; Flecknell, 1987) Mouse 5 mg/kg BW IP (Flecknell, 1987) NHP 1 mg/kg BW IM (Flecknell, 1987) 1 mg/kg BW IV (Green, 1982) Rat 2 mg/kg BW IV (Flecknell, 1987) 4 mg/kg BW IM, IP (Flecknell, 1987) 2.5 mg/kg BW IM, IP (Weihe, 1987) Rabbit 2 mg/kg BW IV (Flecknell, 1987) 4 mg/kg BW IM, IP (Flecknell, 1987) 5-10 mg/kg BW IM (Harkness and Wagner, 1983) 5-10 mg/kg BW IM, IP (Green, 1982) Raccoon 66-110 mg/kg BW PO (Balser, 1965) Sheep 0.5-1.5 mg/kg BW IM, IV (Swindle and Adams, 1988) 15 mg/kg BW PO mixed in feed (NCSU, 1987) Swine 0.5-10 mg/kg BW IM (Swindle and Adams, 1988) 0.5-1.5 mg/kg BW IV (Swindle and Adams, 1988)

189

Diazepam and xylazine (respectively) Rabbit 1 mg/kg BW IV and 3 mg/kg BW IV as a bolus for induction (Hatch and Wilson, 1988)

Diazepam, xylazine, and atropine (respectively) Dog 1 mg/kg BW IV, 1.1 mg/kg BW IV, and 0.05 mg/kg BW IV as a bolus for induction (Hatch and Wilson, 1988)

Diclofenac Guineapig 2.1 mg/kg BW PO (Albengres, 1988) Mouse 8 mg/kg BW PO (Liles and Flecknell, 1992) Rat 10 mg/kg BW PO (Liles and Flecknell, 1992) Fenoprofen Dog Fentanyl Cat Dog 25-g patch for cats >7 lb (Hansen, 1996) 0.04-0.08 mg/kg BW SC, IM, IV q1-2h (Jenkins, 1987) 0.001-0.003 mg/lb BW IM or slow IV (Kinsell, 1986) 25-g patch for dogs <15 lb; 50-g patch for dogs 15-40 lb; 75-g patch for dogs 40-60 lb; and 50-g patch for dogs >60 lb (Hansen, 1996) 0.05-0.1 mg/kg BW SC, IM (Jenkins, 1987) 0.02-0.05 mg/kg BW IM, IV (Swindle and Adams, 1988) 0.5-1 mg/kg BW PO q24h (Jenkins, 1987)

NHP Swine

Fentanyl/droperidol (Innovar-Vet) (a preanesthetic dose of atropine may be necessary) 1 ml/7-10 kg BW IM (Kinsell, 1986) 1 ml/12-30 kg BW IV (Kinsell, 1986) Ferret 0.15 ml/kg BW IM (Flecknell, 1987) Guineapig 0.5-1.0 ml/kg BW IM (CCAC, 1984) 0.08-0.66 ml/kg BW IM (Hughes, 1981) 0.22 ml/kg BW IM (Sander, 1992) Hamster 0.01 ml/kg BW IP (CCAC, 1984) (central nervous system stimulation may occur) (Hughes, 1981) Mouse 0.005 ml/kg BW IM (Jenkins, 1987) 0.02-0.03 ml/g BW IM (Hughes, 1981) Dog

190

NHP Rat Rabbit Swine

0.5 ml/kg BW IM (Flecknell, 1996) 0.1-0.2 ml/kg BW IM (CCAC, 1984) 0.3 ml/kg BW IM (Flecknell, 1987) 0.13 ml/kg BW IM (Jenkins, 1987) 0.5 ml/kg BW IM (Flecknell, 1996) 0.17 ml/kg BW IM (CCAC, 1984) 0.15-0.17 ml/kg BW IM (Lewis and Jennings, 1972) 0.07 ml/kg BW IM (Swindle and Adams, 1988)

Fentanyl/fluanisone (Hypnorm) Ferret 0.5 ml/kg BW IM (Flecknell, 1987) Gerbil 1 ml/kg BW IM, IP (Jenkins, 1987) Guineapig 1 ml/kg BW IM (Flecknell, 1987; Jenkins, 1987) Hamster 1 ml/kg BW IM, IP (Jenkins, 1987) Mouse 0.01 ml/30 g BW IP (Jenkins, 1987) 0.1-0.3 ml/kg BW IP (Flecknell, 1996) NHP 0.3 ml/kg BW IM (Flecknell, 1996) Rat 0.4 ml/kg BW IM, IP (Jenkins, 1987) 0.2-0.5 ml/kg BW IM or 0.3-0.6 mg/kg BW IP (Flecknell, 1987) 0.3-0.6 ml/kg BW IP (Flecknell, 1996) Rabbit Rb 0.5 ml/kg BW IM (Jenkins, 1987) Flunixin Bird 1-10 mg/kg IM; can be repeated (Harrison and Harrison, 1986) 1-10 mg/kg BW IM, IV (Ritchie and Harrison, 1997) Cat 1 mg/kg BW PO, IV q24h (Haskins, 1987) 0.3 mg/kg BW IM (Kinsell, 1986) Dog 0.5-2.2 mg/kg BW IM, IV; no repeat (Jenkins, 1987) 1 mg/kg BW PO, IV q24h (Haskins, 1987) 1 mg/kg BW IV sid for 3 days maximum (Boulay et al., 1995) Ferret 0.03 mg/kg BW IM tid prn (Johnson-Delaney, 1996) 0.3 mg/kg BW PO, SC sid (Johnson-Delaney; 1996) Mouse 2.5 mg/kg BW SC, IM, try q12h (Flecknell, 1991) NHP 0.5 mg/kg BW IM sid (Feeser and White, 1992) 1 mg/kg BW IV bid (Fraser, 1991) Prosimians: 0.5 mg/kg BW IM sid (Feeser and White, 1992) 10 mg/kg BW IM (Borchard et al., 1990) Rat 1.1 mg/kg BW SC, IM q12h (Flecknell, 1991) 2.5 mg/kg BW SC, IM (Liles and Flecknell, 1992) Rabbit 1.1 mg/kg BW SC, IM, try q12h (Liles and Flecknell, 1992) Swine 2-2.2 mg/kg BW IV, SC up to bid (Laval, 1992)

191

Haloperidol Rabbit Ibuprofen Cat Dog 5 mg/kg BW PO q24h (Haskins, 1987) 10 mg/kg BW PO q24-48h (Jenkins, 1987) 5 mg/kg BW PO q24h (Haskins, 1987) Guineapig 10 mg/kg BW IM, try q4h (Flecknell, 1991) Mouse 7.5 mg/kg BW PO (Jenkins, 1987) 7.5 mg/kg BW PO, try q4h (Flecknell, 1991) 30 mg/kg BW PO (Liles and Flecknell, 1992) Rat 10-30 mg/kg BW PO (Jenkins, 1987) 10-30 mg/kg BW PO, try q4h (Flecknell, 1991) 15 mg/kg BW PO (Flecknell, 1996) Rabbit 10-20 mg/kg BW IV, try q4h (Flecknell, 1991) Indomethacin Guineapig 8.8 mg/kg BW PO (Albengres et al., 1988) Mouse 1 mg/kg BW PO (Liles and Flecknell, 1992) Rat 2 mg/kg BW PO (Liles and Flecknell, 1992) Rabbit 12.5 mg/kg BW PO (Keller et al., 1988) Ketamine See under Anesthetics 10-30 mg/kg BW IM, IV (Kinsell, 1986) 10-20 mg/kg BW IM (Morrisey et al., 1996) 20-30 mg/kg BW IM (Flecknell, 1996) Guineapig 25-30 mg/kg BW IM (Bauck, 1989) 22-64 mg/kg BW IP (Sander, 1992) Hamster 60 mg/kg BW IM (Bauck, 1989) NHP 5-40 mg/kg BW IM (Holmes, 1984) Rabbit 30 mg/kg BW IM (Bauck, 1989) Ketoprofen Cat 1-2 mg/kg BW IM, IV, SC sid (Hellyer and Gaynor, 1998) 1 mg/kg BW PO after first 24 h following injection (Hellyer and Gaynor, 1998) Bird Cat Ferret 0.2-0.4 mg/kg BW IM bid (Iglauer et al., 1995)

192

Dog 2 mg/kg BW IM (Pibarot et al., 1997) Guineapig 1 mg/kg BW IM (Perrin et al., 1990) 3 mg/kg BW IM (Flecknell, 1996) Ketoprofen and oxymorphone (respectively) Dog 2 mg/kg BW IM and 0.05 mg/kg BW IM (Pibarot et al., 1997)

Meclofenamic acid Cat Dog 2.2 mg/kg BW PO q24h (Haskins, 1987) 0.5-1 mg/kg BW PO sid in food, then qod for maintenance (Boulay et al., 1995) 2.2 mg/kg BW PO q24h (Haskins, 1987) Note: Test dosage-0.5 mg/lb sid for 5 days. If therapeutic results achieved, wait till signs exacerbate. Then drop dosage to 0.5 mg/lb qod till achieve signs of remission. Then drop to 0.5 mg/lb every third day for 1 week. If signs still remissed, drop dosage to 0.5 mg/lb every fourth day. If signs still remissed, drop dosage to 0.5 mg/lb every fifth day. When signs show exacerbation, back up one step and maintain that dosage level (Kinsell, 1986).

Medetomidine Cat Dog 10-40 g/kg BW W (Ko et al., 1997) 40-80 g/kg BW IM (Ko et al., 1997) 10-20 g/kg BW IV (Ko et al., 1997) 30-40 g/kg BW IM (Ko et al., 1997) 0.1-0.8 mg/kg BW IM, IV, SC (Flecknell, 1996) 80 g/kg BW IM (Ko et al., 1997) 25 g/kg BW IM (Flecknell, 1996) 30-100 g/kg BW SC (Flecknell, 1996) 30-100 g/kg BW IP, SC (Flecknell, 1996) 0.1-0.5 mg/kg BW IM, SC (Flecknell, 1996) 0.3-0.5 mg/kg BW SC (Aeschbacher, 1995) 0.25 mg/kg BW IM (Ko et al., 1992) 25 g/kg BW IM (Flecknell, 1996)

Ferret Goat Mouse Rat Rabbit

Sheep

Meperidine Cat 2-10 mg/kg BW SC, IM q2h (Jenkins, 1987) 2-4 mg/kg BW IM, SC (Kinsell, 1986) Chinchilla 1-2 mg/kg BW IM, SC (Johnson-Delaney, 1996)

193

Dog

2-10 mg/kg BW SC, IM q2-3h (Jenkins, 1987) 6-10 mg/kg BW IM, SC (Kinsell, 1986) Ferret 5-10 mg/kg BW IM, SC q2-4h (Flecknell, 1996) Goat 2-10 mg/kg BW SC, IM (Swindle and Adams, 1988) Guineapig 20 mg/kg BW SC, IM q2-3h (Jenkins, 1987) 10-20 mg/kg BW SC, IM q2-3h (Flecknell, 1991) Hamster 20 mg/kg BW SC, IM q2-3h (Jenkins, 1987) Mouse 20 mg/kg BW SC, IM q2-3h (Jenkins, 1987) 10-20 mg/kg BW SC, IM q2-3h (Flecknell, 1991) 20-40 mg/kg BW IP (Clifford, 1984) 60 mg/kg BW IM (Hughes, 1981) NHP 2-4 mg/kg BW IM q3-4h (Jenkins, 1987) 11 mg/kg BW IM (CCAC, 1984) Rat 20 mg/kg BW SC, IM q2-3h (Jenkins, 1987) 10-20 mg/kg BW SC, IM q2-3h (Flecknell, 1991) Rabbit 10 mg/kg BW SC, IM q2-3h (Jenkins, 1987) 10-20 mg/kg BW SC, IM q2-3h (Flecknell, 1991) Sheep 2-10 mg/kg BW SC, IM (Swindle and Adams, 1988) 2 mg/kg BW IM, IV q2-4h (Flecknell, 1996) Swine 2 mg/kg BW IM, IV q2-4h (Flecknell, 1996) 4-10 mg/kg BW IM (Swindle and Adams, 1988) Methadone Guineapig 3-6 mg/kg BW SC (Jenkins, 1987) Hamster 3-6 mg/kg BW SC (Jenkins, 1987) Midazolam Bird Goat Mouse Rat Quail: 6 mg/kg BW IM (Day and Boge, 1996) 0.5 mg/kg BW IV (Flecknell, 1996) 5 mg/kg BW IM, IP (Flecknell, 1996) 2 mg/kg BW IV (Flecknell, 1987) 4 mg/kg BW IM, IP (Flecknell, 1987) 5 mg/kg BW IP (Flecknell, 1996) 2 mg/kg BW IV (Flecknell, 1987) 2 mg/kg BW intranasally (Robertson and Eberhart, 1994) 4 mg/kg BW IM, IP (Flecknell, 1987) 0.5-2 mg/kg BW IM, IP, IV (Flecknell, 1996)

Rabbit

194

Midazolam and ketamine (respectively) Cat 5-10 mg/kg BW IM and 0.2 mg/kg BW IM (Mama, 1998)

Midazolam and oxymorphone (respectively) Dog Morphine Cat 0.1 mg/kg BW SC, IM q4-6h (Flecknell, 1985; Jenkins, 1987) 0.1 mg/kg BW IM, SC q6-7h; use with caution (Kinsell, 1986) Dog 0.25-5.0 mg/kg BW SC, IM q4-6h (Flecknell, 1985; Jenkins, 1987) 0.1 mg/kg BW of preservative-free solution (in 0.9% saline) given epidurally; give 0.3 ml/kg BW not to exceed 6 ml (Carroll, 1996) Ferret 0.5-5 mg/kg BW IM, SC qid (Flecknell, 1996) Guineapig 10 mg/kg BW SC, IM q2-4h (Flecknell, 1985; Jenkins, 1987) 2-5 mg/kg BW SC, IM q4h (Flecknell, 1991) Hamster 10 mg/kg BW SC, IM q2-4h (Jenkins, 1987) Mouse 10 mg/kg BW SC q2-4h (Flecknell, 1985; Jenkins, 1987) 2-5 mg/kg BW SC, hourly (Flecknell, 1991) NHP 1-2 mg/kg BW SC q4h (Flecknell, 1985; Jenkins, 1987) 3 mg/kg BW SC (Domino et al., 1969) Rat 10 mg/kg BW SC q2-4h (Flecknell, 1985; Jenkins, 1987) 2-5 mg/kg BW SC, hourly (Flecknell, 1991) Rabbit 5 mg/kg BW SC, IM q2-4h (Flecknell, 1985; Jenkins, 1987) 2-5 mg/kg BW SC, IM q2-4h (Flecknell, 1991) Sheep 0.2-0.5 mg/kg BW IM q4h (Flecknell, 1996) Swine 0.2-0.9 mg/kg BW SC (Swindle and Adams, 1988) Morphine and acepromazine (respectively) Cat Dog 0.2-0.5 mg/kg BW IM and 0.02-0.05 mg/kg BW IM, IV (Raffe, 1995) 0.05-1 mg/lb BWIM and 0.025-0.1 mg/lb (maximum 3 mg) BW IM for induction (Ko et al., 1994) 0.5-1.5 mg/kg BW IM and 0.02-0.1 mg/kg BW IM, IV (Raffe, 1995) Nalbuphine Cat 1.5-3 mg/kg BW IV q3h (Flecknell, 1996) Dog 0.5-2.0 mg/kg BW SC, IM, IV q3-8h (Jenkins, 1987) Guineapig 1-2 mg/kg BW IM, IP, IV (Flecknell, 1996) 195 0.05 mg/lb BW IM and 0.025-0.1 mg/lb BW IM for induction (Ko et al., 1994)

Mouse Rat Rabbit Sheep Naproxen Dog

4-8 mg/kg BW IM q4h (Flecknell, 1989) 2-5 mg/kg BW IM q4h (Flecknell, 1989) 1-2 mg/kg BW IM q3h (Flecknell, 1991) 1-2 mg/kg BW IV q4-5h (Flecknell, 1989) 1 mg/kg SC q2-3h (Flecknell, 1989)

5 mg/kg BW loading dose, then 1.2-2.8 mg/kg BW PO q24h (Jenkins, 1987) 5 mg/kg BW PO sid, then 2 mg/kg BW PO qod are common but not recommended (high ulcerogenic potential and narrow margin of safety) (Bouiay et al., 1995) Guineapig 14.9 mg/kg BW PO (Albengres et al., 1988) NHP 10 mg/kg BW PO q12h Gunge et al., 1992) Rat 14.5 mg/kg BW PO (Borchard et al., 1990) Oxymorphone Cat 0.4-1.5 mg/kg BW SC, IM, IV (Jenkins, 1987) 0.2 mg/kg BW IM, IV, SC (Short, 1997) Dog 0.22 mg/kg BW SC, IM, IV (Jenkins, 1987) 0.1 mg/kg of preservative-free solution (in 0.9% saline) given epidurally; give 0.3 ml/kg BW not to exceed 6 ml (Carroll, 1996) Gerbil 0.15 mg/kg BW IM (Trim et al., 1987) Hamster 0.15 mg/kg BW IM (Trim et al., 1987) Mouse 0.15 mg/kg BW IM (Trim et al., 1987) NHP 0.15 mg/kg BW SC, IM, IV in Old World monkeys (Rosenberg, 1991) 0.075 mg/kg BW SC, IM, IV in New World monkeys (Rosenberg, 1991) Rat 0.15 mg/kg BW IM (Trim et al., 1987) Swine 0.15 mg/kg BW IM (Swindle and Adams, 1988) Oxymorphone and acepromazine (respectively) Cat Dog 0.05-0.15 mg/kg BW IM, IV and 0.02-0.05 mg/kg BW IM, IV (Raffe, 1995) 0.1-0.2 mg/kg BW IM, IV and 0.02-0.1 mg/kg BW IM, (Raffe, 1995)

196

Pentazocine Cat 2-3 mg/kg BW SC, IM, IV q4h (Jenkins, 1987) 8 mg/kg BW IP q4h (Flecknell, 1985) 1-3 mg/kg BW SC, IM, IV; IV duration 2-4 h (Kinsell, 1986) 2-3 mg/kg BW IM q4h (Flecknell, 1985; Jenkins, 1987) 15 mg/kg BW PO q8h (Jenkins, 1987) 1-3 mg/kg BW SC, IM, IV; IV duration 2-4 h (Kinsell, 1986) 10 mg/kg BW SC q3-4h (Flecknell, 1985; Jenkins, 1987) 10 mg/kg BW SC, hourly (Flecknell, 1991) 2-5 mg/kg BW IM q4h (Flecknell, 1985; Jenkins, 1987) 10 mg/kg BW SC q4h (Flecknell, 1985; Jenkins, 1987) 10 mg/kg BW SC, hourly (Flecknell, 1991) 10-20 mg/kg BW SC, IM q4h (Flecknell, 1985; Jenkins, 1987) 5 mg/kg BW IV q2-4h (Flecknell, 1991) 2-5 mg/kg BW IM q4h (Swindle and Adams, 1988)

Dog

Mouse NHP Rat Rabbit Swine

Pentobarbital sodium Cat Dog Pethidine Guineapig 20 mg/kg BW SC, IM q2-3h (Flecknell, 1987) Mouse 20 mg/kg BW SC, IM q2-3h (Flecknell, 1987) NHP 2-4 mg/kg BW IM q3-4h (Flecknell, 1987) Rat 20 mg/kg BW SC, IM q2-3h (Flecknell, 1987) Rabbit 10 mg/kg BW SC, IM q2-3h (Flecknell, 1987) Phenacetin Mouse Rat 200 mg/kg BW PO q4h (Flecknell, 1987) 100 mg/kg BW PO q4h (Flecknell, 1987) 2-4 mg/kg BW IV for sedation (Kinsell, 1986) 2-4 mg/kg BW IV for sedation (Kinsell, 1986)

Phenylbutazone Cat Dog 15 mg/kg BW IV q8h (Haskins, 1987) 10-14 mg/kg BW PO q12h (Kinsell, 1986) 15 mg/kg BW IV q8h (Haskins, 1987) 22 mg/kg BW PO q8h (Haskins, 1987) 6-7 mg/lb BW PO q8h with a maximum dosage of 800 mg per day, regardless of weight (Kinsell, 1986) 197

Guineapig 40 mg/kg BW PO (Wilhelmi, 1974) Mouse 30 mg/kg BW PO (Liles and Flecknell, 1992) Rat 20 mg/kg BW PO (Liles and Flecknell, 1992) Piroxicam Dog 0.3 mg/kg BW PO sid in food, then qod for maintenance (Boulay et al., 1995) Guineapig 5.7 mg/kg BW PO Albenges et al., 1988) Mouse 3 mg/kg BW PO (Liles and Flecknell, 1992) Rat 3 mg/kg BW PO (Liles and Flecknell, 1992) Rabbit 0.3 mg/kg BW PO q48h (Flecknell, 1996) Tiletamine/zolazepam (Telazol) Note: We recommend that users obtain the reference by Schobert, 1987, for the use of Telazol 12 mg/kg BW IM (Morrisey et al., 1996) Not recommended

Ferret Rabbit

Tiletamine/zolazepam and xylazine (respectively) Hamster 20 mg/kg BW IP and 10 mg/kg BW IP (Forsythe et al 1992) Xylazine Bird Cat Used in combination with ketamine 0.5 mg/lb BW IV (Kinsell, 1986) 1 mg/lb BW IM, SC (Kinsell, 1986) Dog 0.5 mg/lb BW IV (Kinsell, 1986) 1 mg/lb BW IM, SC (Kinsell, 1986) Goat 0.05-1 mg/kg BW IM (Swindle and Adams, 1988); however this is considered unpredictable when given IM 0.01 mg/kg BW IV (NCSU, 1987) Guineapig 3-5 mg/kg BW IM (Harkness and Wagner, 1983) Hamster 4 mg/kg BW IM (Bauck, 1989) Mouse 4-8 mg/kg BW IM (Harkness and Wagner, 1983) 10 mg/kg BW IP (Flecknell, 1987) NHP 1-2 mg/kg BW IM (Green, 1982; CCAC, 1984) Rat 4-8 mg/kg BW IM (Harkness and Wagner, 1983) 1-3 mg/kg BW IM (Flecknell, 1987) Rabbit 3-5 mg/kg BW IM (Harkness and Wagner, 1983) 198

Sheep Swine

5 mg/kg BW IM (Hughes, 1981) 1-3 mg/kg BW IM (Flecknell, 1987) 0.05-1 mg/kg BW IM (Swindle and Adams, 1988) 0.1-0.15 mg/kg BW slow IV (NCSU, 1987) 10 mg/kg BW IM (Swindle and Adams, 1988)

Xylazine and butorphanol (respectively) Dog 0.25-0.5 mg/lb BW IM and 0.05-0.25 mg/lb BW IM for induction (Ko et al., 1994)

Xylazine and morphine (respectively) Dog 0.25-0.5 mg/lb BW IM and 0.05-1 mg/lb BW IM for induction (Ko et al., 1994)

Xylazine and oxymorphone (respectively) Dog 0.25-0.5 mg/lb BW IM and 0.025-0.1 mg/lb BW IM for induction (Ko et al., 1994)

199

Anti-Infectives
Acyclovir Bird 80 mg/kg BW IM, IV, PO tid (Ritchie and Harrison, 1997) 20 mg/kg BW PO bid for 7 days (Ritchie and Harrison, 1997)

Amantadine Ferret Amikacin Bird 40 mg/kg BW IM sid or bid (Burke, 1986) 22 mg/kg BW q12h (Schultz, 1989) 10-15 mg/kg BW IM, IV, SC q8-12h (Ritchie and Harrison, 1997) Cockatiels: 15-20 mg/kg BW IM, IV, SC q8-12h (Ritchie and Harrison, 1997) Psittacines: 30 mg/kg BW total daily dose (Van der Heyden, 1994) Pigeons: 15-20 mg/kg BW IM, IV bid (Johnson-Delaney, 1996) Ratites: 10 mg/kg BW PO bid (Welsh et al., 1997) Cat 5-7 mg/kg BW IM, IV bid (Boothe, 1996) 15 mg/kg BW IM, IV sid (Boothe, 1996) Chinchilla 2 mg/kg BW IM, IV, SC tid (Jenkins, 1992) Dog 7-10 mg/kg BW IM, IV bid (Boothe, 1996) 20 mg/kg BW IM, IV sid (Boothe, 1996) NHP 2.3 mg/kg BW IM sid (Wissman and Parsons, 1992) Rabbit 10 mg/kg BW IM, SC q8-12h (Carpenter et al., 1995) Reptile Tortoises: 5 mg/kg BW IM q48h for 7-14 days (Page and Mautino, 1990) Amoxicillin Bird 150 mg/kg BW IM q6-8h (Ritchie and Harrison, 1997) Canaries: 300-500 mg/kg BW PO in soft food (Ritchie and Harrison, 1997) Ratites: 20 mg/kg BW PO bid (Welsh et al., 1997) 10 mg/kg BW PO q8-12h (Schultz, 1989) 3-5 mg/lb BW IM, SC sid (Kinsell, 1986) 400 mg/100 lb BW PO bid (Sundlofet al., 1991) 62.5 mg (contents of one prepackaged syringe) into each affected quarter q12h for a maximum of 3 treatments (Sundlofet al., 1991) 5-10 mg/lb BW PO q12h (Kinsell, 1986) 200 6 mg/kg BW as an aerosol bid (Cross, 1995)

Bovine

Cat

5 mg/lb BW IM, SC sid (Kinsell, 1986) 11-22 mg/kg BW IM, PO, SC q8-12h (Boothe, 1996) 7 mg/kg BW SC sid (Flecknell, 1996) Dog 5 mg/lb BW PO q12h (Kinsell, 1986) 5 mg/lb BW SC, IM sid (Kinsell, 1986) 20 mg/kg BW PO bid (Carr, 1997) 7 mg/kg BW SC sid (Flecknell, 1996) Ferret 11-22 mg/kg BW PO, SC (Messonnier, 1996) 7 mg/kg BW SC sid (Flecknell, 1996) 25-35 mg/kg BW PO bid (Johnson-Delaney, 1996) Guineapig Toxic (Flecknell, 1987) Hamster Toxic (Flecknell, 1987) Mouse 100 mg/kg BW SC, IM bid (Flecknell, 1987) 50 mg/kg BW/day in water for 14 days (Russell et al., 1995) NHP 7 mg/kg BW SC (Flecknell, 1987) 10 mg/kg BW PO (Flecknell, 1987) 11 mg/kg BW PO bid (Fraser, 1991) 11 mg/kg BW SC, IM sid (Fraser, 1991) Rat 150 mg/kg BW SC, IM bid (Flecknell, 1987) Sheep 7 mg/kg BW SC sid (Flecknell, 1996) Swine 7 mg/kg BW SC sid (Flecknell, 1996) Amoxicillin/clavulanate Bird Cat Dog Ferret 125 mg/kg BW PO bid (Ritchie and Harrison, 1997) Ratites: 10 mg/kg BW PO bid (Welsh et al., 1997) 13.75-20 mg/kg BW PO bid, tid (Boothe, 1996) 13.75-20 mg/kg BW PO bid, tid (Boothe, 1996) 12.5 mg/kg BW PO bid for 10-14 days Johnson-Delaney; 1996)

Amphotericin B Bird 1.5 mg/kg BW IV q8-12h for 3-7 days (Ritchie and Harrison, 1997) 1 mg/ml in sterile water to nebulize 15 min bid (Ritchie and Harrison, 1997) 0.25-0.5 mg/kg BW 2-3 times/week on alternate days, slow IV, IP with 5% dextrose and water (Kinsell, 1986) 0.25-0.5 mg/kg BW 2-3 times/week on alternate days, slow IV, IP with 5% dextrose and water (Kinsell, 1986) 0.25-1.0 mg/kg BW IV sid (Johnson et al., 1981) 0.25-1.0 mg/kg BW IV sid (Johnson et al., 1981)

Cat Dog

NHP

201

Ampicillin 250 mg/8 oz drinking water (change daily) (Burke, 1986) 100-200 mg/kg BW IM, PO q6-8h (Ritchie and Harrison, 1997) Emus: 15-20 mg/kg BW IM, PO tid (Ritchie and Harrison, 1997) Ratites: 5 mg/kg BW IM tid (Welsh et al., 1997) Bovine Ampicillin trihydrare: 5-10 mg/lb BW IM q8h for up to 7 days (Kinsell, 1986) Cat Ampicillin sodium: 3 mg/lb BW IV, IM q8-12h (Kinsell, 1986) Ampicillin trihydrate: 3-8 mg/lb BW IM, SC q8-12h or 10-30 mg/lb BW PO q8-12h (Kinsell, 1986) 22 mg/kg BW IV, PO, SC tid (Hawkins, 1996) 5-10 mg/kg BW IM, IV, SC tid (Boothe, 1996) 10-50 mg/kg BW PO tid (Boothe, 1996) Dog Ampicillin sodium: 3 mg/lb BW IV, IM q8-12h (Kinsell, 1986) Ampicillin trihydrate: 3-8 mg/lb BW IM, SC q8-12h or 5-10 mg/lb BW PO q6-8h (Kinsell, 1986) 20 mg/kg BW PO tid (Carr, 1997) 5-10 mg/kg BW IM, IV, SC tid (Boothe, 1996) 10-50 mg/kg BW PO tid (Boothe, 1996) 22 mg/kg BW IV, PO, SC tid (Hawkins, 1996) Ferret 5 mg/kg BW SC sid (McKellar, 1989) 10-30 mg/kg BW SC bid (Johnson-Delaney, 1996) Guineapig May cause enterocolitis (Bartlett et al., 1978) 6 mg/kg BW SC tid for 5 days (Young et al., 1987) Hamster Toxic (Flecknell, 1987) Mouse 2-10 mg/100 g BW PO bid (Russell et al., 1981) 50-150 mg/kg BW SC bid (Flecknell, 1987) NHP 30 mg/kg BW IM sid for 5 days (Welshman, 1985) 5 mg/kg BW IM bid (Flecknell, 1987) 20 mg/kg BW IM, IV, PO tid (Johnson et al., 1981) Rat 50-150 mg/kg BW SC bid (Flecknell, 1987) 50 mg/adult rat IP sid for 10 days (Rettig et al., 1989) Rabbit 22-44 mg/kg BW PO in divided doses (Bowman and Lang, 1986) 10-25 mg/kg BW IM sid for 5-7 days (Bowman and Lang, 1986) Reptile 3-6 mg/kg BW IM, SC sid until 48 h beyond recovery (Marcus, 1981) 20 mg/kg BW IC bid for 7-9 days (Snipes, 1984) Tortoises: 20 mg/kg BW IM sid for 7-14 days (Page and Mautino, 1990) Bird

202

Amprolium Bird Bovine Dog 2-4 ml/gal water of 9.6% solution for 5 days (Ritchie and Harrison, 1997) 10 mg/kg BW daily in feed for 5 days (Schultz, 1989) 100-200 mg/kg BW/day PO in food or water for 7-10 days (Kinsell, 1986)

Apramycin Swine 150 g/ton of food; use for 14 days (Sundlofet al., 1991) 12.5 mg/kg BW PO sid for 7 days (Mortensen et al., 1996)

Carbenicillin Bird 200 mg/kg BW PO bid (Burke, 1986) 100-200 mg/kg BW IM, IV q6-12h (Ritchie and Harrison, 1997) 200 mg/kg BW PO bid (Ritchie and Harrison, 1997) 10-15 mg/lb BW PO q8h or 5-10 mg/lb BW IV q8h (Kinsell, 1986) 100 mg/kg BW initially, then 75 mg/kg IM sid or IV bid (Frye, 1981) Tortoises: 200-400 mg/kg BW IM q48h for 7-14 days (Page and Mautino, 1990)

Dog Reptile

Carnidazole Bird 30-50 mg/kg BW once; may repeat in 10-14 days (Ritchie and Harrison, 1997)

Cefadroxil Bird Cefazolin Bird 25-50 mg/kg BW IM, IV bid (Ritchie and Harrison, 1997) Cat 15-25 mg/kg BW IM, IV, SC q4-8h (Boothe, 1996) Dog 15-25 mg/kg BW IM, IV, SC q4-8h (Boothe, 1996) Guineapig 100 mg/kg BW IM bid (Fritz et al., 1987) NHP 25 mg/kg BW IM, IV bid for 7-10 days (Univ. of Washington, 1987) Ratites: 20 mg/kg BW PO bid (Welsh et al., 1997)

203

Cefotaxime Bird Cat Dog NHP Reptile Cefoxitin Bird Cat Dog 50-100 mg/kg BW IM, IV bid, tid (Ritchie and Harrison, 1997) 10-30 mg/kg BW IM, IV, SC qid (Boothe, 1996) 10-30 mg/kg BW IM, IV, SC qid (Boothe, 1996) 75-100 mg/kg BW IM, IV q4-8h (Ritchie and Harrison, 1997) 50-100 mg/kg BW IM, IV tid (Ritchie and Harrison, 1997) 20-80 mg/kg BW IM, IV qid (Boothe, 1996) 20-80 mg/kg BW IM, IV qid (Boothe, 1996) 100-200 mg/kg BW IM tid-qid (Pernikoff and Orkin, 1991) Tortoises: 20-40 mg/kg BW IM sid for 7-14 days (Page and Mautino, 1990)

Ceftazidime NHP Reptile Ceftiofur Bird Bovine Dog Ratites: 20 mg/kg BW IM bid (Welsh et al., 1997) 1.1 mg/kg BW IM sid for up to 5 days (Schultz, 1989) 2.2-4.4 mg/kg BW SC bid (Hoskins, 1997) Propithecus: 50 mg/kg BW IM, IV tid (Feeser and White, 1992) 50 mg/kg BW IM tid (Feeser and White, 1992) 20 mg/kg BW q72h (Lawrence et al., 1984)

Ceftizoxime NHP 75-100 mg/kg BW IM bid for 7 days (Univ. of Washington, 1987)

Cephalexin Bird 50 mg/kg BW PO qid (Burke, 1986) Psittacines: 50-100 mg/kg BW PO tid (Ritchie and Harrison, 1997) Emus: 35-50 mg/kg BW PO qid (Ritchie and Harrison, 1997) Quail and ducks: 35-50 mg/kg BW PO q2-3h (Ritchie and Harrison, 1997) 35 mg/kg BW PO q12h (Kinsell, 1986) 20-40 mg/kg BW PO tid (Hawkins, 1996) 10-30 mg/kg BW PO q6-8h (Boothe, 1996) 10 mg/kg BW SC sid (Flecknell, 1996) 204

Cat

Dog

35 mg/kg BW PO q12h (Kinsell, 1986) 20-40 mg/kg BW PO tid (Carr, 1997) 10-30 mg/kg BW PO q6-8h (Boothe, 1996) 10 mg/kg BW SC sid (Flecknell, 1996) Ferret 10 mg/kg BW SC sid (Flecknell, 1996) 10-15 mg/kg BW PO bid for 10 days (Johnson-Delaney, 1996) Gerbil 25 mg/kg BW SC sid (Flecknell, 1996) Guineapig 50 mg/kg BW IM sid for 14 days (Richardson, 1992) 15 mg/kg BW SC sid (Flecknell, 1996) Mouse 60 mg/kg BW PO bid (Flecknell, 1987) 15 mg/kg BW IM bid (Flecknell, 1996) NHP 20 mg/kg BW PO bid (Flecknell, 1987) Rat 60 mg/kg BW PO bid (Flecknell, 1987) 15 mg/kg BW SC bid (Flecknell, 1996) Rabbit 15-20 mg/kg BW PO bid (Flecknell, 1987) 15 mg/kg BW SC bid (Flecknell, 1996) Sheep 10 mg/kg BW SC sid (Flecknell, 1996) Swine 10 mg/kg BW SC sid (Flecknell, 1996) Cephaloridine Ferret 15 mg/kg BW IM sid (McKellar, 1989) Gerbil 30 mg/kg BW IM bid (Flecknell, 1987) Guineapig 10-25 mg/kg BW IM sid for 5-7 days (Harkness and Wagner, 1977) 15-25 mg/kg BW SC sid (Bauck, 1989) 12.5 mg/kg BW IM sid for 14 days (Dixon, 1986) Hamster May cause enterocolitis (Bartlett et al., 1978) 10 mg/kg BW IM bid (Holmes, 1984) 30 mg/kg BW IM bid (Flecknell, 1987) Mouse 30 mg/kg BW IM bid (Flecknell, 1987) NHP 11 mg/kg BW IM bid (Melby and Altman, 1976) 20 mg/kg BW IM bid (Flecknell, 1987) Rat 30 mg/kg BW IM bid (Flecknell, 1987) Rabbit 10-25 mg/kg BW IM, SC sid for 5 days (Bowman and Lang, 1986) Reptile 10 mg/kg BW IM, SC bid (Frye, 1981)

205

Cephalothin Bird 100 mg/kg BW IM qid (Burke, 1986) 100 mg/kg BW IM, IV, PO qid (Ritchie and Harrison, 1997) Quail and ducks: 100 mg/kg BW IM, IV, PO q2-3h (Ritchie and Harrison, 1997) 40-80 mg/kg BW/day IM, IV q8-12h (Kinsell, 1986) 20-40 mg/kg BW IM, IV, SC tid (Hawkins, 1996) 15-35 mg/kg BW IM, IV, SC q6-8h (Boothe, 1996) 40-80 mg/kg BW/day IM, IV q8-12h (Kinsell, 1986) 20-40 mg/kg BW IM, IV, SC tid (Hawkins, 1996) 15-35 mg/kg BW IM, IV, SC q6-8h (Boothe, 1996) 13 mg/kg BW IM qid for 6 days (Bowman and Lang, 1986) 20-40 mg/kg BW IM bid (Frye, 1981)

Cat

Dog

Rabbit Reptile

Chloramphenicol palmitate (not for use in food animals) Bird Cat 30-50 mg/kg BW PO tid, qid (Ritchie and Harrison, 1997) 15-20 mg/lb BW PO q8-12h (Kinsell, 1986) 25-50 mg/kg BW PO bid (Carr, 1997) 50 mg/cat PO q4-6h (Booffie, 1996) Chinchilla 30-50 mg/kg BW PO bid (Jenkins, 1992) Dog 20-25 mg/lb BW PO q6-8h (Kinsell, 1986) 25-50 mg/kg BW PO tid (Carr, 1997) 50 mg/kg BW PO q4-6h (Boothe, 1996) Ferret 40 mg/kg BW PO tid for 14 days (Kiueger et al., 1989) 50 mg/kg BW PO bid for 10 days (Kiueger et al., 1989) Gerbil 50 mg/kg BW PO bid (Bauck, 1989) Guineapig 50 mg/kg BW PO bid (Bauck, 1989) 50 mg/kg BW PO tid (Russell et al., 1981) Hamster 20 mg/100 g BW PO tid (Russell et al., 1981) 50 mg/kg BW PO bid (Bauck, 1989) Mouse 20 mg/100 g BW PO tid (oral suspension) (Russell et al., 1981) 100 mg/200 ml drinking water for 3-5 days (Williams, 1976) 50 mg/kg BW PO bid (Bauck, 1989) NHP 50 mg/kg BW PO bid (Flecknell, 1987) Rat 20 mg/100 g BW PO tid (Russell et al., 1981) 50 mg/kg BW PO bid (Bauck, 1989) Rabbit 50 mg/kg BW PO sid for 5-7 days (Harkness and Wagner, 1983) 50 mg/kg BW PO bid (Bauck, 1989) 30-50 mg/kg BW PO bid for 5-7 days (Carpenter et al., 1995) Reptile Tortoises: 20 mg/kg BW PO bid for 7-14 days (Page and Mautino, 1990) 206

Chloramphenicol succinate (not for use in food animals) Bird 80 mg/kg BW IM bid or tid (Burke, 1986) 80 mg/kg BW IM, IV, SC bid, tid (Ritchie and Harrison, 1997) Cat 10 mg/kg BW IM, IV q12h (Kinsell, 1986) 50 mg/cat IM, IV, SC q4-6h (Boothe, 1996) Dog 10 mg/kg BW IM, IV q12h (Kinsell, 1986) 50 mg/kg BW IM, IV, SC q4-6h (Boothe, 1996) 50 mg/kg BW SC sid (Flecknell, 1996) Ferret 25 mg/kg BW SC sid (Flecknell, 1996) 30-50 mg/kg BW IM, IV bid (Johnson-Delaney, 1996) Fish 75 mg/kg BW PO sid in feed for 14 days (CCAC, 1984) Gerbil 30 mg/kg BW IM bid (Flecknell, 1987) 50 mg/60 ml drinking water for 2 weeks (Williams, 1976) 50 mg/kg BW SC bid (Bauck, 1989) 30 mg/kg BW SC bid (Flecknell, 1996) Guineapig 20 mg/kg BW IM bid (Flecknell, 1987) 50 mg/kg BW SC bid (Bauck, 1989) Hamster 30 mg/kg BM IM bid (Flecknell, 1987) 50 mg/kg BW SC bid (Bauck, 1989) 30 mg/kg BW SC bid (Flecknell, 1996) Mouse 50 mg/kg BW IM bid (Flecknell, 1987) 50 mg/kg BW SC bid (Bauck, 1989) NHP 25 mg/kg BW IV bid for 10 days (DaRif and Rush, 1983) 50 mg/kg BW IM bid for 10 days (DaRif and Rush, 1983) 110 mg/kg BW IM qid for 5-10 days for pneumococcal meningoencephalitis (Ialeggio, 1989) 20 mg/kg BW IM bid (Flecknell, 1996) Rat 50 mg/kg BW IM bid (Flecknell, 1987) 50 mg/kg BW SC bid (Bauck, 1989) 10 mg/kg BW IM bid (Flecknell, 1996) Rabbit 30 mg/kg BW IM sid for 5-7 days (Harkness and Wagner, 1983) 50 mg/kg BW SC bid (Bauck, 1989) 50 mg/kg BW SC, IM, IV tid (Russell et al., 1981) 30 mg/kg BW IM, IV tid for 5-7 days (Carpenter et al., 1995) 15 mg/kg BW IM bid (Flecknell, 1996) Reptile Toads: 5 mg/100 g BW initially, then 3 mg/100 g BW PO bid for 5 days (Marcus, 1981) Turtles: 40 mg/kg BW IM, IP bid for 7 days (Marcus, 1981) Tortoises: 20 mg/kg BW IM bid for 7-14 days (Page and Mautino, 1990) Swine 11 mg/kg BW IM sid (Flecknell, 1996)

207

Chlorhexidine Bird 10-25 ml of 2% solution/gal water PO; do not use in finches (Ritchie and Harrison, 1997) 10 ml of 2% solution/gal water PO for 10-14 days (Ritchie and Harrison, 1997) 5-10 mg/kg BW PO (Ritchie and Harrison, 1997)

Chlortetracycline Bird 5000 ppm in food for 30-45 days (Burke, 1986) Canaries: 1-1.5 g/l drinking water (Ritchie and Harrison, 1997) Ratites: 20 mg/kg BW PO tid (Welsh et al., 1997) Chinchilla 400 mg/gal drinking water for 4 days (Jenkins, 1992) Ciprofloxacin Bird Psittacines: 80 mg/kg BW total daily dose (Van der Heyden, 1994) Pigeons: 5-20 mg/kg BW PO bid for 5-7 days (Johnson-Delaney, 1996) Ratites: 5 mg/kg BW PO bid (Welsh et al., 1997) 20-40 mg/kg BW IV, PO bid (Ritchie and Harrison, 1997) 5.2 mg/kg BW PO bid (McKellar, 1996) 5-15 mg/kg BW IV, PO bid (Boothe, 1996) 5.2 mg/kg BW PO bid (McKellar, 1996) 5-15 mg/kg BW IV, PO bid (Boothe, 1996) 10-15 mg/kg BW PO bid (Johnson-Delaney, 1996) 16-20 mg/kg BW PO q12h in sterile water (Kelly et al., 1992) 50 mg/kg BW IM tid for 4 days (Strunk et al., 1985) 40 mg/kg BW IM tid for 28 days (Norden and Shinners, 1985) 40 mg/kg BW IM bid for 17 days (Bayer et al., 1985) 12-20 mg/kg BW PO (Gbel, 1996)

Cat Dog Ferret NHP Rabbit

Clindamycin Cat 11 mg/kg BW PO bid (Boothe, 1996) Dog 11 mg/kg BW PO bid (Boothe, 1996) Ferret 10 mg/kg BW PO bid (Johnson-Delaney, 1996) Guineapig May cause enterotoxic cecitis (Bartlett, 1979)

208

Clofazimine Bird Psittacines: 6 mg/kg BW total daily dose (Van der Heyden, 1994)

Clotrimazole Bird 30-45 min sid for 3 days of 1% solution, off 2 days; for up to 4 months (Ritchie and Harrison, 1997)

Danofloxacin Bird 50 ppm for 3 days (for day-old chicks) (Ritchie and Harrison, 1997)

Dimetridazole Hamster 500 mg/l drinking water (La Regina et al., 1980) Rabbit 0.025% solution prepared using 45 g active ingredient/50 gal drinking water (Williams, 1979) Doxycycline Bird 18-26 mg/kg BW oral syrup PO bid in psittacines (Burke, 1986) 22-44 mg/kg BW IV sid or bid (Burke, 1986) 25-50 mg/kg BW IV once; used to get peak dose in critical case (Ritchie and Harrison, 1997) Amazons, cockatoos, and African greys: 0.1% in diet (Ritchie and Harrison, 1997) Green-winged macaws, Amazons, and cockatiels: 25-50 mg/kg BW PO q24-48h (Ritchie and Harrison, 1997) African greys, Goffin cockatoos, blue and gold macaws, and pigeons: 25 mg/kg BW sid (Ritchie and Harrison, 1997) Senegal parrots: 25 mg/kg BW PO bid (Ritchie and Harrison, 1997) Canaries: 250 mg/l water; 1000 mg/kg in soft food (Ritchie and Harrison, 1997) Nectar eaters: 8 mg/kg BW PO q12-24h (Ritchie and Harrison, 1997) 5-10 mg/kg BW PO bid (Hawkins, 1996) 10 mg/kg BW PO bid (Carr, 1997) 5-10 mg/kg BW PO bid (Hawkins, 1996) 5 mg/kg BW PO divided bid day 1; 2.5 mg/kg BW the following days (Wolff, 1990) 2.5 mg/kg BW PO bid (Carpenter et al., 1995) 5-10 mg/kg BW PO sid for 10-45 days (Messonnier, 1996)

Cat Dog NHP Rabbit Reptile

209

Enrofloxacin Amphibia 1.5-10 mg/kg BW IM, SC sid (Gbel, 1996) Bird 7.5-15 mg/kg BW IM, PO bid (Ritchie and Harrison, 1997) 2.5-5 mg/kg BW IM bid (Rosskopf, 1989) Poultry: 50 ppm in water (MeKellar, 1996) Ratites: 1-2 mg/kg BW IM, PO bid (Welsh et al., 1997) Cat 2.5-5 mg/kg BW PO q12-24h (McKellar, 1996) 2.5-5 mg/kg BW IM, SC as a loading dose (McKellar, 1996) 5 mg/kg BW SC sid (Flecknell, 1996) 5 mg/kg BW IV bid (Hardie, 1995) Chinchilla 10 mg/kg BW IM, PO, SC bid (Jenkins, 1992) 2.5-5 mg/kg BW IM, SC, PO bid (Gbel, 1996) Dog 2.5-5 mg/kg BW PO q12-24h (McKellar, 1996) 2.5-5 mg/kg BW IM, SC as a loading dose (McKellar, 1996) 5 mg/kg BW SC sid (Flecknell, 1996) 5 mg/kg BW IV bid (Hardie, 1995) Ferret 2.5-5 mg/kg BW IM, PO, SC bid (Gbel, 1996) 5-10 mg/kg BW IM, PO, SC bid (Johnson-Delaney, 1996) Gerbil 2.5-5 mg/kg BW IM, PO, SC bid (Gbel, 1996) 10 mg/kg BW SC bid (Flecknell, 1996) Goat 2.5-5 mg/kg BW IM, SC sid (McKellar, 1996) Guineapig 5-10 mg/kg BW PO (Dorrestein, 1992) 2.5-5 mg/kg BW IM, PO, SC bid (Gbel, 1996) 5-10 mg/kg BW SC bid (Flecknell, 1996) 100 mg/l water (Dorrestein, 1992) Hamster 5-10 mg/kg BW PO (Dorrestein, 1992) 100 mg/l water (Dorrestein, 1992) 2.5-5 mg/kg BW IM, PO, SC bid (Gbel, 1996) 10 mg/kg BW SC bid (Flecknell, 1996) Mouse 2.5-5 mg/kg BW IM, PO, SC bid (Gbel, 1996) 85 mg/kg BW SC bid for 14 days (Goelz et al., 1994) 85 mg/(kg.d) PO in deionized water for 14 days (Goelz et al., 1994) NHP 5 mg/kg BW IM, PO q24h for 5 days (Line, 1993) 5 mg/kg BW by gastric intubation sid for 10 days (Line et al., 1992) 50 mg/kg BW SC bid (Flecknell, 1996) Rat 2.5-5 mg/kg BW IM, PO, SC bid (Gbel, 1996) 10 mg/kg BW SC bid (Flecknell, 1996) Rabbit 5-10 mg/kg BW IM, SC bid (repeated injections may lead to necrosis, abscesses) (Carpenter et al., 1995) 10 mg/kg BW bid (Mladinich, 1989) 5 mg/kg BW PO bid (Broome et al., 1991) 5-10 mg/kg BW PO (Dorrestein, 1992) 100 mg/l water (Dorrestein, 1992) 210

Reptile Sheep Swine

10 mg/kg BW IM, SC sid for 10-14 days (Messonnier, 1996) 2.5-5 mg/kg BW IM, PO bid for 10-14 days (Messonnier, 1996) 2.5-5 mg/kg BW IM, SC sid (McKellar, 1996) 2.5-5 mg/kg IM, PO sid (McKellar, 1996)

Erythromycin Bird 200 mg/10 ml saline for nebulization tid (15 min) (Ritchie and Harrison, 1997) Note: Do not inject IM; severe muscle necrosis. 45-90 mg/kg BW PO bid for 5-10 days (Ritchie and Harrison, 1997) Cat 5-10 mg/lb BW PO q8h (Kinsell, 1986) Dog 5-10 mg/lb BW PO q8h (Kinsell, 1986) Ferret 10-15 mg/kg BW PO qid (Johnson-Delaney, 1996) Fish 100 mg/kg BW in feed for 21 days (CCAC, 1984) Guineapig May cause enterocolitis (Bartlett et al., 1978) Hamster May cause enterocolitis (Bartlett et al., 1978) NHP 40 mg/kg BW IM sid (Welshman, 1985) 75 mg/kg BW PO bid for 10 days (Univ. of Washington, 1987) Ethambutol Bird NHP 15 mg/kg BW PO for up to 1 year (Rosskopf, 1989) Psittacines: 30 mg/kg BW total daily dose (Van der Heyden, 1994) 22.5 mg/kg BW PO sid in grape juice (reduce dose by a third after 6 weeks) (Wolf et al., 1988)

Fluconazole NHP 2-3 mg/kg BW PO (Graybill et al., 1990)

Flucytosine Bird Psittacines: 150-250 mg/kg BW PO bid for 2-4 weeks (Ritchie and Harrison, 1997) Psittacines: 50-250 mg/kg feed (Ritchie and Harrison, 1997) Furazolidone Bird 100-200 mg/l water (Ritchie and Harrison, 1997) 200 mg/kg soft food (Ritchie and Harrison, 1997) NHP 10-15 mg/kg BW PO sid (Melby and Altman, 1976) Reptile 25-40 mg/kg BW PO sid (Frye, 1981)

211

Gentamicin Bird Cockatiels: 5-10 mg/kg BW IM q8-12h (Ritchie and Harrison, 1997) Ratites: 1-2 mg/kg BW IM tid (Welsh et al., 1997) Most large: 5 mg/kg BW IM bid or tid (Burke, 1986) Most small: 10 mg/kg BW IM bid or tid (Burke, 1986) Raptors: 2.5 mg/kg BW IM tid (Burke, 1986) 40 mg/kg BW PO sid or bid (Burke, 1986) Cat 2 mg/lb BW IM, SC q12h the first day, then sid (Kinsell, 1986) 2.2 mg/kg BW SC tid (Senior, 1996) 6 mg/kg BW IV sid (Hardie, 1995) Dog 2 mg/lb BW IM, SC q12h the first day, then sid (Kinsell, 1986) 2.2 mg/kg BW SC tid (Senior, 1996) 6 mg/kg BW IV sid (Hardie, 1995) Ferret 5 mg/kg BW IM, SC sid for 5 days (Johnson-Delaney, 1996) Gerbil 0.5 mg/100 g BW IM sid (Russell et al., 1981) 5-8 mg/kg BW SC sid (Bauck, 1989) Guineapig 5-8 mg/kg BW SC sid (Bauck, 1989) Hamster May cause enterocolitis (Bartlett et al., 1978) 0.5 mg/100 g BW IM sid (Russell et al., 1981) 5-8 mg/kg BW SC sid (Bauck, 1989) Mouse 0.5 mg/100 g BW IM sid (Russell et al., 1981) 1.2 g/l drinking water for 3 days (Russell et al., 1981) 5-8 mg/kg BW SC sid (Bauck, 1989) NHP 2 mg/kg BW IM, IV bid for 10 days (DaRif and Rush, 1983) 2 mg/kg BW IM tid for 7-10 days (Ialeggio, 1989) Baboons: 3 mg/kg BW IM bid (Ralph et al., 1989) Rat 0.5 mg/100 g BWIM sid (Russell et al., 1981) 5-8 mg/kg BW SC sid (Bauck, 1989) Rabbit 4 mg/kg BW IM sid (Russell et al., 1981) 5-8 mg/kg BW SC sid (Bauck, 1989) 2.5 mg/kg BW IM, SC tid for 5 days (Carpenter et al., 1995) Reptile Nonchelonians: 2.5 mg/kg BW q72h supplemented with parenteral fluids (Frye, 1981) Chelonians: 10 mg/kg q48h supplemented with parenteral fluids (Frye, 1981) Chelonians: 10-20 mg/15 ml normal saline bid nebulized for 30 min (Snipes, 1984) Tortoises: 5 mg/kg BW IM q72h for 7-14 days (Page and Mautino, 1990)

212

Griseofulvin Cat 20 mg/kg BW/day PO sid for 6 weeks, or 140 mg/(kg.week) once each week for 6 weeks (see note) (Kinsell, 1986) Dog 20 mg/kg BW/day PO sid for 6 weeks, or 140 mg/(kg.week) once each week for 6 weeks (see note) (Kinsell, 1986) Note: For Cat and Dog, qualified individuals have found that the above dosages may not be adequate and suggest the dosage of 65 mg/(kg.day). One should consider treatment for at least 6 weeks' duration. The once-a-week treatment is to be discouraged (Kinsell, 1986). One should also consider immune deficiency diseases if treatment appears ineffective (Eds.). Ferret 25 mg/kg BW PO (Ryland and Gorham, 1978) Guineapig 75 mg/kg BW PO sid for 2 weeks (Harkness and Wagner, 1983) 1.5% in dimethyl sulfoxide applied topically bid for 14 days (Post and Saunders, 1979) Mouse 25 mg/100 g BWPO every 10 days (Russell et al., 1981) NHP 20 mg/kg BW PO sid (Johnson et al., 1981) 200 mg/kg BW PO once every 10 days (Johnson et al., 1981) Rat 25 mg/100 g BW PO every 10 days (Russell et al., 1981) Rabbit 25 mg/100 g BW PO every 10 days (Russell et al., 1981) 2.5 mg/100 g BW PO for 14 days (Russell et al., 1981) 12.5-25 mg/kg BW PO bid for 30 days (Carpenter et al., 1995) Hetacillin Cat Dog 25 mg/kg BW PO tid (Senior, 1996) 25 mg/kg BW PO tid (Senior, 1996)

Imipenem/cilastatin (Primaxin) Cat Dog Isoniazid Bird NHP Psittacines: 30 mg/kg BW total daily dose (Van der Heyden, 1994) 5 mg/kg BW PO in divided doses (Johnson et al., 1981) Chimpanzees: 15-25 mg/kg BW PO bid (Fineg et al., 1966) 25 mg/kg BW PO sid in grape juice (reduce dose by a third after 6weeks) (Wolfetal., 1988) 3-10 mg/kg BW IM, IV q6-8h (Boothe, 1996) 2-7.5 mg/kg BW IM, IV tid (Boothe, 1996) 3-10 mg/kg BW IM, IV q6-8h (Boothe, 1996) 2-7.5 mg/kg BW IM, IV tid (Boothe, 1996)

213

Kanamycin Bird Cat Dog NHP Reptile 10-20 mg/kg BW IM bid (Burke, 1986) 10-50 mg/l drinking water (change daily) for 3-5 days (Burke, 1986) 5-7.5 mg/kg BW IM, IV, SC tid (Boothe, 1996) 2.5 mg/lb BW SC q12h (Kinsell, 1986) 2.5 mg/lb BW SC q12h (Kinsell, 1986) 5-7.5 mg/kg BW IM, IV, SC tid (Boothe, 1996) 7.5 mg/kg BW IM bid (Johnson et al., 1981) 10-15 mg/(kg.d) in divided doses IV, IM, IP (Frye, 1981)

Ketoconazole Bird Cat Dog Reptile Psittacines: 30 mg/kg BW PO q12h (Ritchie and Harrison, 1997) 10-20 mg/kg BW PO q8-12h (Kinsell, 1986) 10-20 mg/kg BW PO q8-12h (Kinsell, 1986) Tortoises: 30 mg/kg BW PO sid for 2-4 weeks (Page and Mautino, 1990)

Lincomycin Bird Cat Raptors: 100 mg/kg BW PO sid (Burke, 1986) 100-200 mg/l water PO (Ritchie and Harrison, 1997) 10 mg/lb BW PO q12h or 7 mg/lb BW PO q8h (Kinsell, 1986) 10 mg/kg BW IM q12h (Kinsell, 1986) 5-10 mg/lb BW slow IV in 5% glucose or normal saline (Kinsell, 1986) Note: Do not continue therapy longer than 12 days; may cause pseudomembranous colitis. 10 mg/lb BW PO q12h or 7 mg/lb BW PO q8h (Kinsell, 1986) 10 mg/kg BW IM q12h (Kinsell, 1986) 5-10 mg/lb BW slow IV in 5% glucose or normal saline (Kinsell, 1986) Note: Do not continue therapy longer than 12 days; may cause pseudomembranous colitis. 5-10 mg/kg BW IM bid (Williams, 1976) 6 mg/kg BW IM bid, sid (Frye, 1981)

Dog

NHP Reptile

Marbofloxacin Cat Dog 2 mg/kg BW PO, SC sid (McKellar, 1996) 2 mg/kg BW PO, SC sid (McKellar, 1996)

214

Methicillin NHP 50 mg/kg BW IM bid for 7 days (Univ. of Washington, 1987)

Metronidazole Bird Pigeons: 50 mg/kg BW PO bid for 5 days (Johnson-Delaney; 1996) Pigeons: 200-250 mg/kg BW PO sid for 3-7 days (Johnson-Delaney, 1996) Pigeons: 10-20 mg/kg BW IM sid for 2 days (Johnson-Delaney, 1996) Pigeons: 4 g/gal drinking water for 3-7 days (Johnson-Delaney, 1996) Cat 10 mg/kg BW PO tid (Boothe, 1996) Dog 60 mg/kg BW PO sid for 5 days (Kinsell, 1986) 10 mg/kg BW PO tid (Boothe, 1996) Ferret 35 mg/kg BW PO sid for 5 days (Bell, 1994) Fish 50 mg/kg BW PO sid for 5 days (Harms, 1996) 5-10 ppm continuous bath (Harms, 1996) Guineapig 20 mg/kg BW PO, SC sid (Richardson, 1992) Mouse 2.5 mg/ml drinking water for 5 days (Roach et al., 1988) NHP 35-50 mg/(kg.day) BW PO bid for 10 days (Holmes, 1984) Rabbit 20 mg/kg BW PO bid (Carpenter et al., 1995) Reptile 125-275 mg/kg BW PO once; may be repeated at 7- to 10-day intervals for 1-2 more treatments (Frye, 1981) Tortoises: 250 mg/kg BW PO once; repeat in 2 weeks (Page and Mautino, 1990) Minocycline Cat Dog NHP Rabbit Neomycin Bird Cat Dog Ferret 10 mg/kg BW PO bid or tid (Burke, 1986) 80-100 mg/l drinking water (Ritchie and Harrison, 1997) 5-7 mg/lb BW PO q6-24h (Kinsell, 1986) 5-7 mg/lb BW PO q6-24h (Kinsell, 1986) 10-20 mg/kg BW PO (Ryland and Gorham, 1978) 10 mg/kg BW PO in divided doses (Flecknell, 1996) 5-12.5 mg/kg BW PO bid (Boothe, 1996) 5-12.5 mg/kg BW PO bid (Boothe, 1996) 4 mg/kg BW PO (Whitney et al., 1977) 15 mg/kg BW PO q12h for 7 days (Junge et al., 1992) 6 mg/kg BW IV q8h (Nicolau et al., 1993)

215

Gerbil

100 mg/kg BW PO sid (Flecknell, 1987) 10 g/gal drinking water for 5 days, then 5 g/gal for an additional 5 days (Russell et al., 1981) Guineapig 5 mg/300- to 400g-animal PO bid for 5 days (Farrar and Kent, 1965) 10 mg/kg BW PO sid (Flecknell, 1987; McKellar, 1989) 30 mg/kg SC (Flecknell, 1987) 5 mg/kg BW PO bid (Richardson, 1992) Hamster 5 ml Biosol/100 ml drinking water for 5 days, then give dose for an additional 5 days (Russell et al., 1981) 125 mg/l drinking water (La Regina et al., 1980) 10 mg in 0.25 ml water/40-g animal sid via intragastric administration (Sheffield and Beveridge, 1962) 10 mg/kg BW PO sid (Flecknell, 1987) Mouse 2 mg/ml drinking water for 14 days; prepare fresh daily (Barthold, 1980) 10 g/gal drinking water for 5 days, then 5 g/gal for an additional 5 days (Russell et al., 1981) 50 mg/kg BW SC sid (McKellar, 1989) NHP 10 mg/kg BW PO bid (Flecknell, 1987) Rat 50 mg/kg BW IM bid (Flecknell, 1987) 10 g/gal drinking water for 5 days, then 5 g/gal for an additional 5 days (Russell et al., 1981) 2 mg/ml drinking water (Flecknell, 1996) Rabbit 30 mg/kg BW PO bid for 5 days (Carpenter et al., 1995) 0.2-0.8 mg/ml drinking water (FleckneIl, 1996) Sheep 11 mg/kg BW PO bid (Flecknell, 1996) Swine 11 mg/kg BW PO bid (FlecknelI, 1996) Nitrofurantoin Cat 1-2 mg/lb BW PO q8h with food (Kinsell, 1986) Dog 1-2 mg/lb BW PO q8h with food (Kinsell, 1986) Guineapig 50 mg/kg BW sid for 3 days (Richardson, 1992) NHP 2-4 mg/kg BW IM, IV tid (Johnson et al., 1981) Rat 0.2% in feed for 6-8 weeks (Russell et al., 1981) Nitrofurazone Bird NHP Rabbit 1/8 to 1/4 tsp of 9.3% soluble powder/l of water (change daily) (Burke, 1986) 11 mg/kg BW PO sid (Melby and Altman, 1976) 11 mg/kg BW PO sid (Melby and Altman, 1976)

216

Norfloxacin Bird Cat Dog Mouse Nystatin Bird Psittacines: 300,000 IU/kg BW q8-12h for 7-14 days (Ritchie and Harrison, 1997) Passerines: 100 IU/l water (Ritchie and Harrison, 1997) 200,000 U PO qid until 2 days following recovery (Fraser, 1991) 100,000 IU/kg BW PO sid (Messonnier, 1996) Ratites: 3-5 mg/kg BW PO bid (Welsh et al., 1997) 22 mg/kg BW PO bid (McKellar, 1996) 22 mg/kg BW PO bid (McKellar, 1996) 200 mg/kg BW IM bid (our interpretation of Fromtling et al., 1985, Eds.)

NHP Reptile

Orbifloxacin Cat Dog Goat Sheep Swine 2.5-5 mg/kg BW IM sid (McKellar, 1996) 2.5-5 mg/kg BW IM sid (McKellar, 1996) 2.5-5 mg/kg BW IM sid (McKellar, 1996) 2.5-5 mg/kg BW IM sid (McKellar, 1996) 2.5-5 mg/kg BW IM sid (McKellar, 1996)

Oxytetracycline Bird 200 mg/kg BW IM sid (one dose) (Burke, 1986) Ratites: 5 mg/kg BW IM bid (Welsh et al., 1997) Bovine 7-11 mg/kg BW/day not to exceed 4 consecutive days (Schultz, 1989) Cat 20 mg/kg BW PO tid (Carr, 1997) Dog 20 mg/kg BW PO tid (Carr, 1997) Gerbil 800 mg/l drinking water (Williams, 1976) 20 mg/kg BW SC sid (McKellar, 1989) Hamster 20 mg/kg BW SC sid (McKellar, 1989) Mouse 400 mg/l drinking water given continuously (Williams, 1976) 100 mg/kg BW SC bid (Flecknell, 1987) NHP 10 mg/kg BW SC, IM (FleckneIl, 1987) Rat 60 mg/kg BW SC q72h of long-acting drug (Liquimycin LA-200) (Curl et al., 1988) Rabbit 30-100 mg/kg BW in divided doses PO (Bowman and Lang, 1986) 400-1000 mg/l drinking water (Bowman and Lang, 1986) 15 mg/kg BW SC, IM (FlecknelI, 1987) 15 mg/kg BW IM tid for 7 days (Carpenter et al., 1995) 217

Reptile Sheep Penicillin

6-10 mg/kg BW IV; IM sid (Frye, 1981) 7-11 mg/kg BW/day not to exceed 4 consecutive days (Schultz, 1989)

Penicillin G, benzathine: 100 mg/kg BW IM sid, qod (Ritchie and Harrison, 1997) Note: May cause death if given IV (Ritchie and Harrison, 1997). Penicillin G, procaine: 100 mg/kg BW IM q24-48h (Ritchie and Harrison, 1997) Note: Never use procaine in parrots or passerines (Ritchie and Harrison, 1997) Bovine Penicillin G, procaine: 20,000-40,000 U/kg BW IM q12h (Schultz, 1989) Penicillin G, procaine and penicillin G, benzathine: 20,000-40,000 U/kg BW SC q48h (Schultz, 1989) Cat Penicillin G, procaine: 40,000 U/kg BW IM q24h (Kinsell, 1986) Dog Penicillin G, potassium: 20,000 U/kg BW IM, IV (drip) q4-6h (Kinsell, 1986) Penicillin G, procaine: 40,000 U/kg BW IM sid (Kinsell, 1986) Penicillin G, procaine and penicillin G, benzathine: 1 ml/10-25 lb BW IM, SC repeat in 48 h (Kinsell, 1986) Guineapig May cause enterotoxic cecitis (Bartlett, 1979) Mouse Penicillin, potassium: 100,000 IU/kg BW IM bid (do not use procaine penicillin) (Russell et al., 1981) Penicillin, potassium: 60,000 U/mouse IM (Taber and Irwin, 1969) NHP Penicillin G, procaine: 20,000 U/kg BW IM bid (Johnson et al., 1981) Penicillin G, benzathine: 40,000 U/kg BW IM every 3 days (Johnson et al., 1981) Rat Penicillin, potassium: 100,000 IU/kg BW IM bid (Russell et al., 1981) Penicillin, oral: 15,000 IU/20 ml drinking water (Williams, 1976) Rabbit Penicillin G, procaine and penicillin G, benzathine: 42,000 or 84,000 IU/kg BW SC once each week for 3 weeks (Cunliffe-Beamer and Fox, 1981) Penicillin G, procaine and penicillin G, benzathine: "FloCillin"-2 ml/10 lb BW IM, SC qod (Russell et al., 1981) Penicillin G, procaine: 60,000 U/kg BW IM sid for 10 days (Jaslow et al., 1981; Welch et al., 1987) Penicillin G, procaine: 50,000 IU/kg BW sid (Bauck, 1989) Reptil Penicillin G, procaine and penicillin G, benzathine: 10,000 U total penicillin activity/kg BW IM at 24- to 72-h intervals (Frye, 1981) Penicillin G, potassium: 10,000-20,000 U/kg BW IM, SC tid or qid (Frye, 1981) Sheep Penicillin G, procaine and penicillin G, benzathine: 10,000 or 20,000

Bird

218

Swine

U/kg BW IM every 3 or 6 days, respectively (Schultz, 1989) Penicillin G, procaine and penicillin G, benzathine: 10,000-40,000 U/kg BW IM every 3 days (Schultz, 1989)

Piperacillin Bird NHP 100-200 mg/kg BW IM, IV q6-8h (Ritchie and Harrison, 1997) Budgerigars: 200 mg/kg BW IM, W q8h (Ritchie and Harrison, 1997) 100-150 mg/kg BW IM, IV bid for 7-10 days (Univ. of Washington, 1987) 80-100 mg/kg BW IM, IV tid for 7-10 days (Univ. ofWashington, 1987) 100-400 mg/kg BW IM sid (Messonnier, 1996)

Reptile

Polymyxin B Bird Rabbit Rifampin Bird NHP 10-20 mg/kg BW PO bid (Rosskopf, 1989) Psittacines: 45 mg/kg BW total daily dose (Van der Heyden, 1994) 22.5 mg/kg BW PO sid in grape juice (reduce by a third after 6 weeks) (Wolf et al., 1988) Canaries: 50,000 IU/l water (Ritchie and Harrison, 1997) 3 mg/300- to 400-g animal PO bid for 5 days (Farrar and Kent, 1965)

Spectinomycin Bird Dog Canaries: 200-400 mg/l water (Ritchie and Harrison, 1997) 2.5-5 mg/lb BW IM q12h (Kinsell, 1986)

Streptomycin sulfate Bird Not for use in psittacines or passerines (Ritchie and Harrison, 1997) 10-15 mg/kg BW IM bid (Burke, 1986) 10-30 mg/kg BW IM q8h (Ritchie and Harrison, 1997) 10-20 mg/kg BW IM bid for 7 days (Rosskopf, 1989) 30-40 mg/kg BW IP sid (CCAC, 1984) 4-5 mg/adult mouse SC sid (McDougall et al., 1967) 10 mg/kg BW IM q4h (CCAC, 1984) 10 mg/kg BW IM bid (Frye, 1981)

Fish Mouse Rabbit Reptile

219

Succinylsulfathiazole Guineapig 0.1% in drinking water (Williams, 1976) Sulfachlorpyrizidine Bird 0.25 tsp/l water for 5-10 days (Schultz, 1989) Canaries: 150-300 mg/l drinking water (Ritchie and Harrison, 1997)

Sulfadiazine and pyrimethamine (respectively) Mink Toxic

Sulfadimethoxine 20 mg/kg BW PO bid (Burke, 1986) 50 mg/kg BW PO sid for 5 days, off for 3 days, repeat for 5 days (Ritchie and Harrison, 1997) Ratites: 0.05% concentration in drinking water (Welsh et al., 1997) Cat 25 mg/lb BW IM, IP, PO, SC the first day, then 12.5 mg/lb BW q24h for 6 days (Kinsell, 1986) Chinchilla 12.5 mg/kg BW PO bid (Hoefer, 1994) Dog 25 mg/lb BW IM, IP, PO, SC the first day, then 12.5 mg/lb BW q24h for 6 days (Kinsell, 1986) Ferret 300 mg/kg BW daily in drinking water for 2 weeks (Bell, 1994) Mink Toxic Rabbit 75-100 mg/kg BW PO sid for 7 days (Rossoff, 1974) 12.5 mg/kg BW PO bid (Carpenter et al., 1995) Reptile 90 mg/kg BW IV, IM sid first day, then 45 mg/kg BW sid days 2-6 (Frye, 1981) Sulfamerazine Fish 240 mg/kg BW sid in feed for 14 days (CCAC, 1984) Guineapig 40 ml 12.5% solution/gal drinking water (Russell et al., 1981) Mouse 0.02% in drinking water (Flecknell, 1987) Mink Toxic Rat 0.02% in drinking water (Flecknell, 1987) Bird

220

Sulfamethazine Bird 30 mg/oz drinking water (Ritchie and Harrison, 1997) Chickens: for coccidia, 128-187 mg/kg BW sid for 2 days, then dose for 4 days (Ritchie and Harrison, 1997) 30 mg/oz solution PO full strength instead of drinking water for 5-7 days (Burke, 1986) Cat 50 mg/kg BW PO, IV q12h of 12.5% solution (Kinsell, 1986) Dog 50 mg/kg BW PO, IV q12h of 12.5% solution (Kinsell, 1986) Guineapig 12.5%: add 4 ml/500 ml drinking water for 1-2 weeks (Williams, 1976) 12.5%: add 1.33-4.14 ml/l drinking water (Melby and Altman, 1976) 166-517 mg/l drinking water (CCAC, 1984) Hamster 665-800 mg/l drinking water (CCAC, 1984) Mouse 12.5%: dilute 1 ml with 49 ml water and give 0.5 ml diluted solution to 30 g mouse bid (Russell et al., 1981) 12.5%: add 5 ml/pt in drinking water (100 mg/kg BW PO) (Russell et al., 1981) 450-1200 mg/l drinking water (CCAC, 1984) Mink Toxic NHP 66 mg/kg BW PO bid (CCAC, 1984) Rat 12.5%: add 5 ml/pt drinking water (100 mg/kg BW PO) (Russell et al., 1981) 665-950 mg/l drinking water (CCAC, 1984) Rabbit 12.5%: add 5 ml/pt drinking water (100 mg/kg BW PO) (Russell et al., 1981) 900-1350 mg/l drinking water (CCAC, 1984) Reptile 0.5 g/kg BW PO sid first day, then 0.25 g/kg BW days 2-4 (Frye, 1981) Sulfaquinoxaline Bird Poultry: 0.0125-0.025% in drinking water (Schultz, 1989) Bovine 10 g/100 lb BW PO daily for 3-5 days (Schultz, 1989) Guineapig 0.25-1.0 g/l drinking water for 30 days (Schuchman, 1977) Mink Toxic Rabbit 0.05% in drinking water (Patton, 1979) 6 mg/lb BW PO for 5-7 days (Russell et al., 1981) Reptile 0.04% in drinking water for 3-5 days (Frye, 1981) Sheep 10 g/100 lb BW PO daily for 3-5 days (Schultz, 1989) Swine 0.0125-0.025% in drinking water (Schultz, 1989)

221

Sulfasalazine NHP 30 mg/kg BW PO bid (Isaza et al., 1992)

Sulfisoxazole NHP 50 mg/kg BW PO sid (Johnson et al., 1981)

Tetracycline Amphibia 1 mg/6 g BW PO (stomach tube) bid for 7 days (mix in small volume of distilled water) (Marcus, 1981) Bird 250 mg/kg BW of oral suspension bid (Burke, 1986) 50 mg/kg BW PO tid (Ritchie and Harrison, 1997) Cat 10-25 mg/lb BW PO q8-12h (Kinsell, 1986) 22 mg/kg BW PO tid (Carr, 1997) Dog 10-25 mg/lb BW PO q8-12h (Kinsell, 1986) 22 mg/kg BW PO tid (Carr, 1997) Gerbil 250 mg/100 ml drinking water for 14 days (Williams, 1976) 2 mg/l00 g BW PO or IM (Clifford, 1973) 20 mg/kg BW PO bid (Bauck, 1989) Guineapig 112-350 mg/l drinking water (CCAC, 1984) 20 mg/kg BW PO bid (Bauck, 1989) 50 mg/kg BW PO by dropper divided into 3 doses (Richardson, 1992) 5 mg/kg BW IM bid (Richardson, 1992) Hamster 400 mg/l drinking water (La Regina et al., 1980) 20 mg/kg BW PO bid (Bauck, 1989) Mouse 3-5 mg/ml drinking water for 5-7 days (Harkness and Wagner, 1983) 1 mg/ml drinking water for 7 days (Barthold, 1980) 20 mg/kg BW PO bid (Bauck, 1989) 100 mg/kg BW SC sid (MeKellar, 1989) NHP 20-25 mg/kg BW PO bid to tid for 7-10 days (Johnson et al., 1981; Univ. of Washington, 1987) 25 mg/kg BW IM, IV bid (Univ. of Washington, 1987) Rat 450-643 mg/l drinking water (CCAC, 1984) 20 mg/kg BW PO bid (Bauck, 1989) 100 mg/kg BW SC (McKellar, 1989) Rabbit 30-100 mg/kg BW in divided doses PO (Bowman and Lang, 1986) 20 mg/kg BW PO bid (Bauck, 1989) 500-900 mg tetracycline powder in dextrose/l drinking water; fresh twice daily and protect from light (Bauck, 1989) Reptile 25-50 mg/kg BW PO bid until 48 h past recovery (Marcus, 1981)

222

Ticarcillin Bird Cat Dog 200 mg/kg BW IM, IV bid to qid (Burke, 1986) 75-100 mg/kg BW IV q6-8h (Boothe, 1996) 75-100 mg/kg BW IV q6-8h (Boothe, 1996)

Tilmicosin Rabbit 25 mg/kg BW SC once (McKay et al., 1996)

Tobramycin Bird 2.5-5 mg/kg BW IM bid (Ritchie and Harrison, 1997) Cat 2 mg/kg BW IM, IV SC tid (Boothe, 1996) Dog 2 mg/kg BW IM, IV SC tid (Boothe, 1996) Guineapig 30 mg/kg BW q24h (Kapusnik et al., 1988) Trimethoprim/sulfadiazine Cat 5 mg/lb BW sid (Kinsell, 1986) 15 mg/kg BW IM, PO bid (Hawkins, 1996) Chinchilla 30 mg/kg BW IM, PO, SC bid (Jenkins, 1992) Dog 15 mg/kg BW IM, PO bid (Hawkins, 1996) 30 mg/kg BW/day PO; in severe infections use daily dose q12h; administer 2-3 days after signs subside but not more than 14 consecutive days (Kinsell, 1986) 1 ml/5 lb BW of oral suspension (Kinsell, 1986) 1 ml/20 lb SC sid of 24% injectable (Kinsell, 1986) Ferret 30 mg/kg BW PO or oral suspension (Bell, 1994) Gerbil 30 mg/kg BW SC sid (Bauck, 1989) Guineapig 0.5 ml/kg BW SC of 240 mg/ml solution (Flecknell, 1987) 30 mg/kg BW SC sid (Bauck, 1989) Hamster 30 mg/kg BW SC sid (Bauck, 1989) Mouse 0.5 ml/kg BW SC of 240 mg/ml solution (Flecknell, 1987) NHP 0.2 ml/kg BW SC of 240 mg/ml solution (Flecknell, 1987) 0.1 ml/kg BW SC of 240 mg/ml solution for 7-10 days (Ialeggio, 1989) Prosimians: 25 mg/kg BW SC, IM sid (Feeser and White, 1992) Rat 0.5 ml/kg BW SC of 240 mg/ml solution (Flecknell, 1987) Rabbit 0.2 ml/kg BW SC bid of 240 mg/ml solution (Flecknell, 1987) 30 mg/kg BW SC sid (Bauck, 1989) Reptile Tortoises: 30 mg/kg BW IM, PO q48h for 7-14 days (Page and Mautino, 1990) 30 mg/kg BW IM, SC sid (Messonnier, 1996)

223

Trimethoprim and sulfamethoxazole (dosed on sulfa concentration) Bird 100 mg/kg BW PO bid (Burke, 1986) 25 mg/kg BW PO q12h (Ritchie and Harrison, 1997) 50 mg/kg BW PO sid (Ritchie and Harrison, 1997) Gerbil 15 mg/kg BW PO bid (Bauck, 1989) Guineapig 15 mg/kg BW PO bid (Bauck, 1989) Hamster 15 mg/kg BW PO bid (Bauck, 1989) NHP Lemur and Varecia: 50 mg/kg BW PO sid (Feeser and White, 1992) Rabbit 15 mg/kg BW PO bid (Bauck, 1989) Reptile Tortoises: 30 mg/kg BW IM, PO q48h for 7-14 days (Page and Mautino, 1990) Tylosin Bird Bovine Cat 10-40 mg/kg BW IM bid or tid (Burke, 1986) 17.6 mg/kg BW/day IM not to exceed 5 days (Schultz, 1989) 1-5 mg/lb BW IM q12-24h (do not mix with any other solution) (Kinsell, 1986) 10-20 mg/lb BW/day PO divided q6-8h (Kinsell, 1986) Dog 1-5 mg/lb BW IM q12-24h (do not mix with any other solution) (Kinsell, 1986) 10-20 mg/lb BW/day PO divided q6-8h (Kinsell, 1986) Gerbil 10 mg/100 g BW PO for 21 days (Russell etal., 1981) 10 mg/kg BW IM, SC sid (McKeliar, 1989) Hamster 100 mg/kg BW PO sid (Flecknell, 1987) 10 mg/100 g BW PO for 21 days (Russell et al., 1981) 10 mg/kg BW IM, SC sid (McKeliar, 1989) Mouse 0.2-0.8 mg/100 g BW IM bid (Russell et al., 1981) 10 mg/kg BW SC bid (Flecknell, 1987) 10 mg/100 g BW PO for 21 days (Russell et al., 1981) NHP 10 mg/kg BW IM bid (Weishman, 1985) Rat 10 mg/kg BW SC sid (Flecknell, 1996) 5 g/l in drinking water mixed with dextrose; give 100 ml treated water to each rat daily (Carter et al., 1987) 10 mg/kg BW SC bid (Flecknell, 1987) 10 mg/100 g BW PO for 21 days (Russell et al., 1981) Rabbit 10 mg/kg BW IM, SC, PO bid (Carpenter et al., 1995) Reptile 25 mg/kg BW IM, PO sid for 7 days (Marcus, 1981) Swine 8.8 mg/kg BW IM q12h not to exceed 3 days (Schultz, 1989) 2-10 mg/kg BW IM sid (Flecknell, 1996)

224

Vancomycin Hamster 20 mg/kg BW PO by gavage (Boss et al., 1994) Rabbit 50 mg/kg BW IV q8h (Nicoiau et al., 1993)

225

Miscellaneous Drugs
Acetylcysteine Cat Dog Mouse Rat 140 mg/kg BW IV once, then repeat q6h with 70 mg/kg BW IV or PO for 7 treatments (Kore, 1997) 140 mg/kg BW IV once, then repeat q6h with 70 mg/kg BW IV or PO for 7 treatments (Kore, 1997) 653 mg/kg PO IP (Borchard et al., 1990) 1200 mg/kg BW PO (Borchard et al., 1990) 400 mg/kg BW IP (Borchard et al., 1990)

Alcuronium Cat Dog Swine 0.1 mg/kg BW IV (Flecknell, 1996) 0.1 mg/kg BW IV (Flecknell, 1996) 0.25 mg/kg BW IV (Flecknell, 1996)

Allopurinol Bird Dog Alloxan Cat 1 ml 10% solution in citrate-phosphate buffer (pH 3.5-4.0) given IA at a rate of 0.5 ml/min (Reiser et al., 1987) 750 mg/kg BW PO (Borchard et al., 1990) 75 mg/kg BW IV (Borchard et al., 1990) 40 mg/kg BW IV (Borchard et al., 1990) 200 mg/kg BW IP, SC (Borchard et al., 1990) Budgerigars: 100 mg in 10 ml water, then dilute 1 ml of solution in 30 ml water; give fresh several times daily (Ritchie and Harrison, 1997) 10 mg/kg BW PO q8h, then reduce to 10 mg/kg BW PO sid (Kinsell, 1986)

Mouse Rat

Alprazolam Cat 0.1 mg/kg BW tid or prn (Dodman, 1995)

226

Aminophylline Bird Cat Dog NHP Reptile 10 mg/kg BW IV q3h; after initial response give PO (Ritchie and Harrison, 1997) 10 mg/kg BW IM, IV q8-12h: for IV use, dilute in 10-20 ml normal saline or 5% dextrose in water and inject slowly (Kinsell, 1986) 10 mg/kg BW IM, IV q8-12h: for IV use, dilute in 10-20 ml normal saline or 5% dextrose in water and inject slowly (Kinsell, 1986) 25-100 mg/animal PO bid (Johnson et al., 1981) Lemur: 10 mg/kg BW IV (Feeser and White, 1992) Re 2-4 mg/kg BW IM as needed (Frye, 1981)

Amitriptyline Cat 5-10 mg total dose PO (Borchard et al., 1990) 2-4 mg/kg BW sid-tid (Dodman, 1995) 0.5-1 mg/kg BW PO sid, bid (Shanley and Overall, 1995) 1-2 mg/kg BW PO (Borchard et al., 1990) 1-2 mg/kg BW PO bid to start (Shanley and Overall, 1995) 1 mg/kg BW IP, PO (Borchard et al., 1990) 20 mg/kg BW IP (Borchard et al., 1990) 10 mg/kg BW SC (Borchard et al., 1990) 30 mg/kg BW PO (Borchard et al., 1990)

Dog Mouse Rat

Amphetamine Mouse Atenolol Cat Dog Ferret 6.25-12.5 mg/kg BW PO q12-24h (Anonymous, 1994) 1 mg/kg BW PO sid (Jacobs, 1996) 6.25 mg/kg BW PO sid (Johnson-Delaney, 1996) 5 mg/kg BW IP (Taber and Irwin, 1969)

Atipamezole Cat Dog Gerbil Hamster Mouse 0.3-0.5 mg/kg BW IV, SC (Flecknell, 1996) 50-400 g/kg BW IM, IV (Flecknell, 1996) 1 mg/kg BW IP, SC (Flecknell, 1996) 1 mg/kg BW SC (Flecknell, 1996) 1-2.5 mg/kg BW IP (Cruz et al., 1998) 1 mg/kg BW IM, IP, SC, IV (Flecknell, 1993)

227

Rat Rabbit

1 mg/kg BW IP, SC (Flecknell, 1996) 0.2 mg/kg BW IV (Flecknell, 1996) 1 mg/kg BW IV, SC (Flecknell, 1996)

Atracuronium Bird Cat Chickens: 0.25-0.46 mg/kg BW IV (Lukasik, 1995) 0.2 mg/kg BW IV (Flecknell, 1996) 0.2-0.25 mg/kg BW IV initial bolus; 0.1-0.15 mg/kg BW IV repeat boluses (Lukasik, 1995) 0.25 mg/kg BW IV loading dose followed by 3-8 g/kg BW/min IV infusion (Lukasik, 1995) 0.5 mg/kg BW IV (Flecknell, 1996) 0.2-0.25 mg/kg BW IV initial bolus; 0.1-0.15 mg/kg BW IV repeat boluses (Lukasik, 1995) 0.25 mg/kg BW IV loading dose followed by 3-8 g/kg BW/min IV infusion (Lukasik, 1995)

Dog

Atropine Bird 0.01-0.04 mg/kg BW IM, SC (Ritchie and Harrison, 1997) 0.01-0.04 mg/kg BW IM, SC (Harrison and Harrison, 1986) Organophosphate toxicity: 0.1-0.5 mg/kg BW IM, SC repeated as needed (Ritchie and Harrison, 1997) Bovine 0.6-0.12 mg/kg BW IV (Schultz, 1989) For organophosphate poisoning: 0.5-1.0 mg/kg BW IV, may repeat in 1-2h (Schultz, 1989) Cat 0.05 mg/kg BW IM, IV, SC q6h (Kinsell, 1986) Chinchilla 0.15 mg SC, IM, IV (Rossoff, 1974) Dog 0.05 mg/kg BW IM, IV, SC q6h (Kinsell, 1986) Ferret 0.05 mg/kg BW IM, SC (Andrews and Illman, 1987) Gerbil 0.02-0.05 mg/kg BW SC, IM, IV (CCAC, 1984) Goat 0.04-0.80 mg/kg BW IM (Swindle and Adams, 1988) 0.13 mg/kg BW IV (Swindle and Adams, 1988) Guineapig 0.02-0.05 mg/kg SC, IM, IV (CCAC, 1984) Hamster 0.02-0.05 mg/kg BW SC, IM, IV (CCAC, 1984) Mouse 0.05 mg/kg BW IM, SC, IV (Green, 1982) 0.02-0.05 mg/kg BW SC, IM, IV (CCAC, 1984) NHP 0.10 mg/kg BW SC (Domino et al., 1969) 0.05 mg/kg BW SC, IM, IV (CCAC, 1984) Rat 0.04 mg/kg BW IM (Weisbroth and Fudens, 1972) 0.02-0.05 mg/kg BW SC, IM, IV (CCAC, 1984) Rabbit 0.20 mg/kg BW IM, IV SC (Green, 1982) 228

Reptile Sheep Swine Benazepril Dog

For organophosphate overdose: 10 mg/kg BW SC every 20 min (Harkness and Wagner, 1983) 1-3 mg/kg BW IM, SC 30 min before surgery (Green, 1982) 0.04 mg/kg BW IM, IV, SC, PO as needed (Frye, 1981) 0.04-0.80 mg/kg BW IM (Swindle and Adams, 1988) 0.13 mg/kg BW IV (Swindle and Adams, 1988) 0.05-0.5 mg/kg BW SC (Swindle and Adams, 1988) 0.044-0.4 mg/kg BW IM (Swindle and Adams, 1988)

0.25 mg/kg BW PO sid (Martin, 1996)

Betamethasone Guineapig 0.1-0.2 ml IM, SC (Richardson, 1992) Bretylium Cat Dog Mouse NHP Rat Rabbit Swine 15 mg/kg BW IV (Borchard et al., 1990) 5 mg/kg BW IV (Borchard et al., 1990) 12.5 mg/kg BW IV (Borchard et al., 1990) 200 mg/kg BW PO (Borchard et al., 1990) 5 mg/kg BW IV (Borchard et al., 1990) 400 mg/kg BW PO (Borchard et al., 1990) 10 mg/kg BW IV (Borchard et al., 1990) 5 mg/kg BW IV (Schumann et al., 1993)

Bromhexine Bird Buspirone Cat Dog 2-4 mg/kg BW PO bid (Dodman, 1995) 0.5-1 mg/kg BW PO sid (Shanley and Overall, 1995) 1 mg/kg BW PO sid (Shanley and Overall, 1995) 0.15 mg/100 g BW IM bid, sid (Harrison and Harrison, 1986)

Calcitonin-See Neo-Calglucon Reptile 50 IU/kg BW IM; use in conjunction with oral calcium supplementation (Messonnier, 1996)

229

Calcium EDTA Bird Bovine 35 mg/kg BW bid for 5 days; repeat in 3-4 days if necessary (Ritchie and Harrison, 1997) 110 mg/kg BW IP, IM in 1-2% solution in 5% glucose; skip 2 days and repeat for 2 days for up to 10-14 days (Schultz, 1989)

Calcium gluconate Bird Reptile 5 ml/30 ml water PO (Ritchie and Harrison, 1997) 50-500 mg/kg BW IV slowly to effect (Ritchie and Harrison, 1997) 500 mg/kg BW once each week for 4-6 weeks (Messonnier, 1996)

Calcium gluconate/calcium lactate Bird 5-10 mg/kg BW IM bid prn (Ritchie and Harrison, 1997)

Calcium glycerophosphate (Calphosan) Bird Captopril Cat Dog 0.5-2 mg/kg BW PO tid (Anonymous, 1994) 0.5-2 mg/kg BW PO tid (Jacobs, 1996) 0.5-1 ml/kg BW IM once; may repeat weekly (Harrison and Harrison, 1986)

Chloroquine phosphate NHP 150 mg/adult rhesus monkey PO days 1 and 3 (Schofield et al., 1985)

Chlorpheniramine Guineapig 5 mg/kg BW SC (Borchard et al., 1990) Mouse 1 mg/kg BW IP (Borchard et al., 1990) NHP 0.5 mg/kg BW/day PO in divided doses (Johnson et al., 1981) Chlorpromazine Cat Dog 1-2 mg/kg BW IV, IM q12h (Kinsell, 1986) 0.5 mg/kg BW IM tid (Hoskins, 1997) 230

1.1-6.6 mg/kg BW IM q6-24h (Kinsell, 1986) 0.55-4.4 mg/kg BW IV q6-12h (Kinsell, 1986) Gerbil 0.5 mg/kg BW IM (CCAC, 1984) Goat 2.2 mg/kg BW PO (Swindle and Adams, 1988) 1.0-4.4 mg/kg BW IM (Swindle and Adams, 1988) 0.22-1.10 mg/kg BW IV (Swindle and Adams, 1988) Guineapig 0.5 mg/kg BW IM (CCAC, 1984) Hamster 0.5 mg/kg BW IM (Melby and Altman, 1976) Mouse 3-5 mg/kg BW IV or 3-35 mg/kg BW IM (Harkness and Wagner, 1983) NHP 1-3 mg/kg BW IM (Melby and Altman, 1976) 2-5 mg/kg BW PO (CCAC, 1984) Rat 3-5 mg/kg BW IV or 3-35 mg/kg BW IM (Harkness and Wagner, 1983) Rabbit 1-10 mg/kg BW IM (Carpenter et al., 1995) Sheep 2.2 mg/kg BW PO (Swindle and Adams, 1988) 1-4.4 mg/kg BW IM (Swindle and Adams, 1988) 0.22-1.10 mg/kg BW IV (Swindle and Adams, 1988) Swine 0.5-4.0 mg/kg BW IM (Swindle and Adams, 1988) 0.55-3.3 mg/kg BW IV (Swindle and Adams, 1988) Cholestyramine (for reversal of antibiotic-induced enterocolitis) Rabbit Cholestyramine (2 g active ingredient, which is equivalent to 4 g Questran) in 20 ml drinking water for 21 days (Lipman et al., 1989)

Cimetidine Bird Dog Ferret Rabbit Cisapride Bird Cat Dog 0.5-1.5 mg/kg BW PO tid (Ritchie and Harrison, 1997) 0.1-1 mg/kg BW PO bid, tid (Washabau and Hall, 1997) 0.1-1 mg/kg BW PO bid, tid (Washabau and Hall, 1997) 2.5-5 mg/kg BW IV q6-12h slow injection over 30-40 min (Ritchie and Harrison, 1997) 5-10 mg/kg BW IM, IV bid, tid (Hoskins, 1997) 5-10 mg/kg BW IV, PO tid, qid (Washabau and Hall, 1997) 10 mg/kg BW IV, PO tid (Harrenstien, 1994) 5-10 mg/kg BW q6-12h (Carpenter et al., 1995)

231

Clomipramine Cat Dog 1-1.5 mg/kg BW PO sid (Dodman, 1995) 0.5 mg/kg BW PO sid (Shanley and Overall, 1995) 1 mg/kg BW PO bid for 2 weeks, then 2 mg/kg BW PO bid for 2 weeks, then 3 mg/kg BW PO bid for 4 weeks (maintenance) (Shanley and Overall, 1995)

Cortisone Rat 0.25-1.25 mg/day SC, IM, PO (Rossoff, 1974)

Cyclosporine Rat 100 mg/kg BW/day SC (Thuveris et al., 1991) 25 mg/kg BW/day IP (Thuveris et al., 1991) 15 mg/kg BW/day SC (Sonnino et al., 1990)

Cyproterone Dog 1.25-2.5 mg/kg BW/day for 10 days (Cotard, 1996)

Delmadinone acetate Dog 3 mg/kg BW SC once (Cotard, 1996)

Deoxycorticosterone pivalate Dog 2.2 mg/kg BW IM every 25 days (Sullivan and Graziani, 1996)

Dexamethasone Bird Bovine Cat Dog 0.5-2 mg/kg BW IM, IV sid (Ritchie and Harrison, 1997) 5-20 mg IV IM, PO (Schultz, 1989) 0.125-0.5 mg sid or divided doses IV, IM, PO (Kinsell, 1986) 0.25-1.25 mg sid or divided bid PO (Kinsell, 1986) 0.25-1.0 mg sid IM, IV (Kinsell, 1986) Ferret 0.5-1 mg/kg BW IM, SC (Johnson-Delaney, 1996) 2-4 mg/kg BW IM, IV once (Johnson-Delaney, 1996) Guineapig 0.1 ml SC (Richardson, 1992) NHP 0.25-1.0 mg/kg BW PO, IM total dose (Melby and Altman, 1976) Reptile 0.125-0.625 mg/kg BW IV, IM as needed (Frye, 1981)

232

Dexamethasone sodium phosphate Bovine Cat Dog Sheep 1-2 mg/kg BW slow IV (Schultz, 1989) 1-5 mg/kg BW slow IV (Schultz, 1989) 1-5 mg/kg BW slow IV (Schultz, 1989) 1-2 mg/kg BW slow IV (Schultz, 1989)

Dextrose Bird 50-100 mg/kg BW slow IV (Ritchie and Harrison, 1997)

Diethylstilbestrol Bird 0.03-0.1 ml of 0.25 mg/ml stock/30 g BW IM (Harrison and Harrison, 1986) 1 drop of 0.25 mg/ml stock/30 ml drinking water (Harrison and Harrison, 1986) 0.05-0.1 mg/day PO (Kinsell, 1986) 0.1-1 mg/day PO (Kinsell, 1986)

Cat Dog Digoxin Dog Diltiazem Cat Dog Ferret

0.006-0.009 mg/kg BW PO bid to achieve 1-2 ng/ml serum concentration (Jacobs, 1996)

7.5 mg/kg BW PO tid (Anonymous, 1994) 0.5-1.5 mg/kg BW PO tid (Jacobs, 1996) 3.75-7.5 mg/animal PO bid (Johnson-Delaney, 1996)

Dimethyl sulfoxide Bird Dog 1 ml/kg BW topically every 4-5 days or weekly (Ritchie and Harrison, 1997) Apply topically; do not exceed 20 ml/day for 14 days (Kin-sell, 1986)

Diphenhydramine Bird Cat 2-4 mg/kg BW q12h IM, IV, PO (Ritchie and Harrison, 1997) 4 mg/kg BW PO q8h (Kinsell, 1986) 233

0.5 mg/lb BW IV (considered a high dose by Kinsell, 1986) Dog 4 mg/kg BW PO q8h (Kinsell, 1986) 0.5 mg/lb BW IV (considered a high dose by, 1986) Ferret 0.5-2 mg/kg BW IM, IV, PO bid or tid prn (Johnson-Delaney, 1996) Guineapig 5 mg/kg BW SC (Melby and Altman, 1976) 12.5 mg/kg BW IP (Borchard et al., 1990) NHP Lemur: 5 mg/kg BW IM (Feeser and White, 1992) Rat 10 mg/kg BW SC (Borchard et al., 1990)

Diphenoxylate/atropine sulfate NHP 1 ml/animal PO tid (Holmes, 1984)

Doxapram 5-10 mg/kg BW IV, IM once (Harrison and Harrison, 1986) 5-10 mg/kg BW IV; may repeat in 15-20 min (Kinsell, 1986) 5-10 mg/kg BW IV; may repeat in 15-20 min (Kinsell, 1986) 5-11 mg/kg BW IV (Johnson-Delaney, 1996) 1-2 mg/kg BW IV (Flecknell, 1987) Gerbil 5-10 mg/kg BW IV (Flecknell, 1987) Goat 2-10 mg/kg BW IV (Swindle and Adams, 1988) Guineapig 5 mg/kg BW IV (Flecknell, 1987) 10-15 mg/kg BW IM, SC (Richardson, 1992) Hamster 5-10 mg/kg BW IV (Flecknell, 1987) Mouse 5-10 mg/kg BW IV (Flecknell, 1987) NHP 2 mg/kg BW IV (Flecknell, 1987) Rat 5-10 mg/kg BW IV (Flecknell, 1987) Rabbit 2-5 mg/kg BW IV (Flecknell, 1987) Sheep 2-10 mg/kg BW IV (Swindle and Adams, 1988) Swine 2-10 mg/kg BW IV (Swindle and Adams, 1988) Doxepin Bird Dog 0.5-1 mg/kg BW PO bid (Ritchie and Harrison, 1997) 3-5 mg/kg BW PO bid (Shanley and Overall, 1995) Bird Cat Dog Ferret

234

Edrophonium Cat Dog Enalapril Dog Ferret Esmolol Cat Dog 0.25-0.5 mg/kg BW IV slow bolus; 50-200 g/(kg.min) infusion (Anonymous, 1994) 0.25-0.5 mg/kg BW IV slow bolus; 50-200 g/(kg.min) infusion (Anonymous, 1994) 0.5 mg/kg BW PO sid, bid (Jacobs, 1996) 0.5 mg/kg BW PO sid (package insert) 0.5 mg/kg BW PO q48h (Johnson-Delaney, 1996) 0.5 mg/kg BW IV (Lukasik, 1995) 0.5 mg/kg BW IV (Lukasik, 1995)

Flumazenil Bird Quail: 0.1 mg/kg BW IM (Day and Boge, 1996)

Fluoxetine Bird Cat Dog Flutamide Dog 5 mg/kg BW/day PO for 7 days (Cotard, 1996) 2.3-3 mg/kg BW PO sid (Dodman, 1997) 0.5 mg/kg BW PO sid (Shanley and Overall, 1995) 1 mg/kg BW PO sid (Shanley and Overall, 1995)

Furosemide Bird Cat Dog NHP Reptile 0.15-2 mg/kg BW IM, IV q12-24h (Ritchie and Harrison, 1997) 0.05 mg/300 g BW IM bid (Harrison and Harrison, 1986) 2 mg/kg BW IV q12h to a maximum total dose of 5 mg (Kinsell, 1986) 2-4 mg/kg PO q8-12h (Kinsell, 1986) 2 mg/kg BW IV q12h to a maximum total dose of 40 mg (Kinsell, 1986) 2-4 mg/kg PO q8-12h (Kinsell, 1986) 2 mg/kg BW PO (Johnson et al., 1981) 5 mg/kg BW IM, IV sid or bid (Frye, 1981)

235

Gallamine Amphibia 6 mg/kg BW in ventral lymph sac (Lumb and Jones, 1984) Cat 1 mg/kg BW IV (Flecknell, 1996) Dog 1 mg/kg BW IV (Flecknell, 1996) Goat 4 mg/kg BW IV (Flecknell, 1996) Guineapig 0.1-0.2 mg/kg BW IV (Flecknell, 1996) Mouse 1.2 mg/kg BW IV (Lumb and Jones, 1984) Rat 1 mg/kg BW IV (Flecknell, 1996) 0.01 mg/kg BW IV(Borchard et al., 1990) Rabbit 1 mg/kg BW IV (Flecknell, 1996) 0.2-0.3 mg/kg BW IV (Lumb and Jones, 1984) Sheep 1 mg/kg BW IV (Flecknell, 1996) Swine 2 mg/kg BW IV (Flecknell, 1996) Flycopyrrolate Cat Dog 5 g/lb or 0.25 ml/10 lb BW IM (package insert) 0.01 mg/kg BW IM (Ko et al., 1997) 0.01 mg/kg BW IV (Flecknell, 1996) Ferret 0.01 mg/kg BW IM, SC (Mason, 1997) 0.01-0.02 mg/kg BW IM, SC (Mason, 1997) Gerbil 0.01-0.02 mg/kg BW IM, SC (Mason, 1997) Guineapig 0.01-0.02 mg/kg BW IM, SC (Mason, 1997) NHP 13-17 g/kg IM (Sanders et al., 1991) Rat 0.5 mg/kg BW IM (Flecknell, 1996) 0.01-0.02 mg/kg BW IM, SC (Mason, 1997) Rabbit 0.1 mg/kg BW IM, SC (Fieckneil, 1996) 0.011 mg/kg BW IV (Aeschbacher, 1995) 0.01 mg/kg BW IV (Flecknell, 1996) Gonadotropin-releasing hormone Ferret Heparin Cat 1 mg/kg BW IV (Kinsell, 1986) Dog 1 mg/kg BW IV (Kinsell, 1986) Guineapig 5 mg/kg BW IV (Melby and Altman, 1976) Mouse 10 mg/kg BW IV (Melby and Altman, 1976) 20 g IM; repeat in 12 days if necessary (Kolmstetter et al., 1996)

236

NHP Rat Rabbit

2 mg/kg BW IV (Meiby and Altman, 1976) 10 mg/kg BW IV (Borchard et al., 1990) 5 mg/kg BW IV (Melby and Altman, 1976)

Human chorionic gonadotropin (hCG) Ferret 100 IU IM; repeat in 12 days if necessary (Kolmstetter et al., 1996) 100 IU IM, SC; may repeat in 2 weeks (Johnson-Delaney, 1996)

Hydralazine Dog 0.5-2 mg/kg BW PO bid (Jacobs, 1996)

Indapamide Rat Insulin NHP Start NPH insulin at 0.25-0.5 U/kg BW/day SC (Schultz, 1989) 3 mg/kg BW IP (Delbarre and Delbarre, 1988)

Iodine (Lugol's) Bird 2 ml/30 ml water stock; dose at 1 drop in each 250 ml water given daily for goiter (Harrison and Harrison, 1986)

Iron dextran Bird Kaolin Guineapig 0.2 ml given 3-4 times daily (Kaopectate V) (Richardson, 1992) Kaolin/pectin NHP 0.5-1 ml/kg BW PO q2-6h (Johnson et al., 1981) 10 mg/kg BW IM; repeat weekly (Harrison and Harrison, 1986)

Levallorphan Any species give 1 mg levallorphan (up to a maximum of 0.5 mg/kg BW) for every 50 mg of morphine that was given (Green, 1982)

237

Levonorgestrel NHP 1 mg/kg BW PO q24h (Mann et al., 1986)

Levothyroxine Bird 20 g/kg BW PO q12-24h (Ritchie and Harrison, 1997)

Loperamide Dog Rabbit 0.08 mg/kg BW PO qid (Chiapella, 1988) 0.1 mg/kg BW PO tid for 3 days, then sid for 2 days (Banerjee et al., 1987)

Medroxyprogesterone acetate Bird 5-25 mg/kg BW IM, SC q4-6h (Ritchie and Harrison, 1997)

Megestrol acetate Dog Ferret 0.55 mg/kg PO for 4 weeks (Cotard, 1996) Not recommended (Koimstetter et al., 1996)

Meprobamate Guineapig 100 mg/kg BW IM (Melby and Altman, 1976) Hamster 100 mg/kg BW IM (Melby and Altman, 1976) Mouse 100 mg/kg BW IM (Melby and Altman, 1976) NHP 100-400 mg/kg BW PO (Melby and Altman, 1976) Rat 150 mg/kg BW IM (Melby and Altman, 1976) Rabbit 50-150 mg/kg BW IM (Melby and Altman, 1976) Methylprednisolone Cat Dog 1 mg/kg BW IM/week (Kinsell, 1986) 20 mg or less intrasynovially (Kinsell, 1986) 1 mg/kg BW IM/week (Kinsell, 1986) Guineapig 2 mg/kg BW IM every 30 days (Bauck, 1989)

238

Metoclopramide Cat 0.2-0.5 mg/kg BW PO tid (Washabau and Hall, 1997) Chinchilla 0.5 mg/kg BW SC tid (Johnson-Delaney, 1996) Dog 0.2-0.4 mg/kg BW SC tid (Hoskins, 1997) 0.2-0.5 mg/kg BW PO tid (Washabau and Hall, 1997) 1-2 mg/kg BW/day IV over 24 h (Hoskins, 1997) Rabbit 0.2-0.5 mg/kg BW PO, SC (Carpenter et al., 1995) 0.2-0.4 mg/kg BW SC sid-tid (Messonnier, 1996) Metocurine Amphibia Mouse Rat Rabbit 0.94 mg/kg BW in ventral lymph sac (Lumb and Jones, 1984) 0.08-0.1 mg/kg BW IV (Lumb and Jones, 1984) 0.009 mg/kg BW IV (Lumb and Jones, 1984) 0.01-0.015 mg/kg BW IV (Lumb and Jones, 1984)

Mineral oil Bird Cat Dog 1-3 drops/30 g BW PO once (Harrison and Harrison, 1986) 5 ml/kg BW PO once (Harrison and Harrison, 1986) 2-6 ml PO (Kinsell, 1986) 5-30 ml PO (Kinsell, 1986)

Misoprostol Cat Dog Not recommended (Kore, 1997) 2-5 g/kg BW PO tid (Kore, 1997)

Nalbuphine Gerbil 4 mg/kg BW IP, SC (Flecknell, 1996) Guineapig 1 mg/kg BW IP, SC (Flecknell, 1996) Hamster 2 mg/kg BW SC (Flecknell, 1996) Mouse 4 mg/kg BW IP, SC (Flecknell, 1996) Rat 0.1 mg/kg BW IV (Flecknell, 1996) 1 mg/kg BW IP, SC (Flecknell, 1996) rabbit 1 mg/kg BW IP, SC (Flecknell, 1996) 0.1 mg/kg BW IV (Flecknell, 1996)

239

Nalorphine Any species Cat Dog Mouse Rat Rabbit Naloxone Cat Dog 0.04 mg/kg BW IM, IV, SC (Short, 1997) 0.04 mg/kg BW IM, IV, SC (Short, 1997) Dose to effect, usually 0.2-0.4 mg total dose IM, SC, IV (Kinsell, 1986) Gerbil 0.01-0.1 mg/kg BW IP, IV (Flecknell, 1987) Guineapig 0.01-0.1 mg/kg BW IP, IV (Flecknell, 1987) Hamster 0.01-0.1 mg/kg BW IP, IV (Flecknell, 1987) Mouse 0.05-0.1 mg/kg BW IM, IP, IV (Flecknell, 1993) 0.01-0.1 mg/kg BW IP, IV (Flecknell, 1987) NHP 0.01-0.05 mg/kg BW IM, IV (Flecknell, 1987) 2-3 ml SC, IM, IV (Rosenberg, 1991) Rat 0.01-0.1 mg/kg BW IP, IV (Flecknell, 1987) Rabbit 0.01-0.1 mg/kg BW IM, IV (Flecknell, 1987) Naltrexone Cat 2-4 mg/kg BW sid (Dodman, 1995) give 1 mg nalorphine (up to a maximum of 2 mg/kg BW) for every 10 mg of morphine that was given (Green, 1982) 1 mg/kg BW IM, IV, SC; no more than 5 mg per dose (Kinsell, 1986) 5 mg/kg BW IM, IV, SC; no more than 5 mg per dose (Kinsell, 1986) 2 mg/kg BW IV (Harkness and Wagner, 1983) 2 mg/kg BW IV (Harkness and Wagner, 1983) 2 mg/kg BW IV (Harkness and Wagner, 1983)

Neo-Calglucon Reptile 1 ml/kg BW PO bid, prn (used with calcitonin) (Messonnier, 1996)

Neostigmine Cat Dog 40-60 g/kgBW IV (Lukasik, 1995) 40-60 g/kgBW IV (Lukasik, 1995)

240

Omeprazole Cat Dog Oxytocin Bird 5 U/kg BW IM, IV, SC once (Ritchie and Harrison, 1997) Bovine 75-100 U IM, IV (Schultz, 1989) Cat 5-10 U IM, IV, SC (Kinsell, 1986) Dog 5-30 U IM, IV, SC (Kinsell, 1986) Guineapig 0.2-0.3 U/kg BW IM (Harrenstien, 1994) 1-2 U IM (Richardson, 1992) NHP 5-20 U IM, IV total dose (Melby and Altman, 1976) Rat 1 U SC, IM total dose (Rossoff, 1974) Rabbit 1-2 U IM, SC total dose (Melby and Altman, 1976) Sheep 30-50 U IM, IV SC (Kinsell, 1986) Swine 30-50 U IM, IV, SC (Kinsell, 1986) Pancuronium Cat 0.06 mg/kg BW IV (Flecknell, 1996) 0.03-0.1 mg/kg BW IV initial bolus; 0.015-0.05 mg/kg BW IV repeat boluses (Lukasik, 1995) 0.1 mg/kg BW IV (Borchard et al., 1990) Dog 0.06 mg/kg BW IV (Flecknell, 1996) 0.03-0.1 mg/kg BW IV initial bolus; 0.015-0.05 mg/kg BW IV repeat boluses (Lukasik, 1995) 0.1 mg/kg BW IV (Borchard et al., 1990) Goat 0.06 mg/kg BW IV (Flecknell, 1996) Guineapig 0.06 mg/kg BW IV (Flecknell, 1996) Mouse 0.03 mg/kg BW IV (Lumb and Jones, 1984) Rat 2 mg/kg BW IV (Flecknell, 1996) Rabbit 0.1 mg/kg BW IV (Flecknell, 1996) 0.008 mg/kg BW IV (Lumb and Jones, 1984) Sheep 0.06 mg/kg BW IV (Flecknell, 1996) Swine 0.06 mg/kg BW IV (Flecknell, 1996) 0.7 mg/kg BW PO sid (Washabau and Hall, 1997) Not recommended (Kore, 1997) 0.7 mg/kg BW PO sid (Washabau and Hall, 1997)

241

Parachloramphetamine Rat Pindolol Dog 0.125-0.25 mg/kg BW PO bid (Dodman and Shuster, 1994) 2 mg/kg BW IP once (Saito et al., 1996) Note: Used for chemically induced ejaculation in rats.

Prednisolone Cat For prolonged use, 2-4 mg/kg BW PO qod (Kinsell, 1986) For immune suppression, 3 mg/kg BW IM, PO q12h (Kinsell, 1986) For allergy; 1 mg/kg BW IM, PO q12h (Kinsell, 1986) For prolonged use, 0.5-2 mg/kg BW PO qod (Kinsell, 1986) For immune suppression, 2 mg/kg BW IM, PO q12h (Kinsell, 1986) For allergy, 0.5 mg/kg BW IM, PO q12h (Kinsell, 1986)

Dog

Prednisolone sodium succinate Bird Dog NHP 10-20 mg/kg BW IV, IM every 15 mm to effect (Harrison and Harrison, 1986) 5.5-11 mg/kg BW IV, then repeat at 1, 3, 6, or 10 h prn (Kinsell, 1986) 1-15 mg/kg BW PO total dose (Melby and Altman, 1976) 1-5 mg/kg BW/day PO (Rosenberg et al., 1987) 10 mg/kg BW IV (Feeser and White, 1992) Lemur: 10 mg/kg BW IV (Feeser and White, 1992) 5-10 mg/kg BW IM, IV as needed (Frye, 1981)

Reptile

Prednisone NHP 0.5-1 mg/kg BW PO bid for 3-5 days, then sid for 3-5 days, then q48h for 10 days, then dose q48h (Isaza et al., 1992)

Prednisone and azathioprine (respectively) Dog 2-4 mg/kg BW IV IM, PO for 2-3 weeks (then reduce) and 50 mg/m2 PO sid for 2-6 weeks (then reduce) (Michels and Carr, 1997)

Prednisone and chlorambucil (respectively) Dog 2-4 mg/kg BW IV, IM, PO for 2-3 weeks (then reduce) and 2 mg/m2 PO sid or qod (use lowest effective dose for maintenance) (Michels and Carr, 1997) 242

Prednisone and cyclophosphamide (respectively) Dog 2-4 mg/kg BW IV, IM, PO for 2-3 weeks (then reduce) and 50 mg/m2 PO qod for 1 week, or sid for 4 days then skip 3 days; repeat cycle for 3-4 weeks (Michels and Carr, 1997)

Prochlorperazine Dog 0.1 mg/kg BW IM tid, qid (Hoskins, 1997)

Propranolol Cat Dog 0.5-1 mg/kg BW PO tid (Jacobs, 1996) 0.5-1 mg/kg BW PO tid (Jacobs, 1996)

Ranitidine Cat 1-2 mg/kg BW IV, PO bid, tid (Washabau and Hall, 1997) 1-2 mg/kg BW IM, PO bid, tid (Hall and Washabau, 1997) 2.5 mg/kg BW IV bid (Kore, 1997) 3.5 mg/kg BW PO bid (Kore, 1997) 2-4 mg/kg BW IV SC bid, tid (Hoskins, 1997) 1-2 mg/kg BW IV, PO bid, tid (Washabau and Hall, 1997) 1-2 mg/kg BW IM, PO bid, tid (Hall and Washabau, 1997)

Dog

Scopolamine NHP 0.01 mg/kg BW SC (Domino et al., 1969)

Streptokinase Dog Rabbit 20,000-500,000 U/h diluted in saline, continuous central vein infusion over 4-5 h (Dennis, 1993) 4000 U/kg BW/h IV (Agnelli et al., 1985)

Streptozotocin Mouse NHP Rat 200 mg/kg BW IV once (Fromtling et al., 1985) 45-55 mg/kg BW IV once (Takimoto et al., 1988) 55 mg/kg BW IV (Borchard et al., 1990) 60 mg/kg BW IP (Borchard et al., 1990) 22 mg/kg BW IM (Borchard et al., 1990) 50 mg/kg BW IP (Alder et al., 1992)

243

Succinylcholine Amphibia Cat Dog Mouse NHP Rabbit Reptile Sheep Swine Sucralfate Cat Dog Ferret 250 mg/animal PO bid, tid (Kore, 1997) 500-1000 mg/animal PO bid, tid (Kore, 1997) 125 mg/animal PO qid (Harrenstien, 1994) 2.5 mg/kg BW in ventral lymph sac (Lumb and Jones, 1984) 0.06 mg/kg BW via continuous IV infusion (Kinsell, 1986) 0.07 mg/kg BW via continuous IV infusion (Kinsell, 1986) 0.05-0.1 mg/kg BW IV (Lumb and Jones, 1984) 2 mg/kg BW IV (Cramlet and Jones, 1976) 0.5 mg/kg BW IV (Green, 1982) Chelonians: 0.25-1.5 mg/kg BW IM (Page, 1993) 0.02 mg/kg BW via continuous IV infusion (Kinsell, 1986) 0.12-0.18 mg/kg BW via continuous IV infusion (Kinsell, 1986)

Suxamethonium Cat Dog Rabbit Sheep Swine 0.2 mg/kg BW IV (Flecknell, 1996) 0.4 mg/kg BW IV (Flecknell, 1996) 0.5 mg/kg BW IV (Flecknell, 1996) 0.02 mg/kg BW IV (Flecknell, 1996) 2 mg/kg BW IV (Flecknell, 1996)

Testosterone Bird 8 mg/kg BW IM, PO once, then weekly as needed (Ritchie and Harrison, 1997)

Tissue plasminogen activator Dog 1 mg/kg BW IV over 15-90 min (Dennis, 1993) 1 mg/kg BW IV bolus every hour for 10 doses (Clare and Kraje, 1998) Tolazoline Bird 15 mg/kg BW IV (Sinn, 1997) Bovine 0.2 mg/kg BW IV (Schultz, 1989) 0.5 mg/kg BW SC (Schultz, 1989) Goat 2-5 mg/kg BW IV slowly over 1 min (NCSU, 1987) Sheep 2-5 mg/kg BW IV slowly over 1 min (NCSU, 1987)

244

Tripelennamine Guineapig 5 mg/kg BW PO, IM (Melby and Altman, 1976) Tubocurarine Amphibia 1.4-7.5 mg/kg BW in ventral lymph sac (Lumb and Jones, 1984) Cat 0.4 mg/kg BW IV (Flecknell, 1996) Dog 0.4 mg/kg BW IV (Flecknell, 1996) Goat 0.3 mg/kg BW IV (Flecknell, 1996) Guineapig 0.1-0.2 mg/kg BW IV (Flecknell, 1996) Mouse 1 mg/kg BW IV (Flecknell, 1996) 0.06-0.09 mg/kg BW IV (Lumb and Jones, 1984) NHP 0.09 mg/kg BW IV (Cramlet and Jones, 1976) Rat 0.4 mg/kg BW IV (Flecknell, 1996) 0.04-0.06 mg/kg BW IV (Lumb and Jones, 1984) Rabbit 0.4 mg/kg BW IV (Flecknell, 1996) 0.09-0.15 mg/kg BW IV (Lumb and Jones, 1984) Sheep 0.4 mg/kg BW IV (Flecknell, 1996) Vecuronium Cat 0.1 mg/kg BW IV (Flecknell, 1996) 0.01-0.1 mg/kg BW IV initial bolus; 0.005-0.04 mg/kg BW IV repeat boluses (Lukasik, 1995) 0.1 mg/kg BW IV (Flecknell, 1996) 0.01-0.1 mg/kg BW IV initial bolus; 0.005-0.04 mg/kg BW IV repeat boluses (Lukasik, 1995) 0.1 mg/kg BW IV initial bolus followed by 1.6-1.7 g/kg BW/min IV infusion (Lukasik, 1995) 0.15 mg/kg BW IV (Flecknell, 1996) 0.05 mg/kg BW IV (Flecknell, 1996) 0.15 mg/kg BW IV (Flecknell, 1996)

Dog

Goat Sheep Swine

Verapamil Dog 0.05 mg/kg BW IV slowly over 2-3 min; repeat to total dose of 0.15 mg/kg over 10-15 mm (Anonymous, 1994)

245

Vitamin A Reptile 50,000 IU every 2 weeks IM (Snipes, 1984) Tortoises: 11,000 IU/kg BW IM once (Page and Mautino, 1990)

Vitamin B complex Bird 10-30 mg/kg thiamine IM every 7 days (Ritchie and Harrison, 1997) 1-2 g/kg food (Ritchie and Harrison, 1997) Raptors, cranes, and penguins: 1-2 mg/kg sid (Ritchie and Harrison, 1997) 1-2 ml IM, IV, 1-2 times/week prn (Kinsell, 1986) 1-2 ml IM, IV, 1-2 times/week prn (Kinsell, 1986)

Cat Dog

Vitamin B12 Bird Vitamin C Bird Cat 20-40 mg/kg BW IM daily to weekly (Ritchie and Harrison, 1997) 100 mg/day PO (Kinsell, 1986) 25-75 mg IM, IV, SC (Kinsell, 1986) 100 mg PO q8h as urinary acidifier (Kinsell, 1986) Dog 100-500 mg/day PO (Kinsell, 1986) 25-75 mg IM, IV, SC (Kinsell, 1986) 100-500 mg PO q8h as urinary acidifier (Kinsell, 1986) Guineapig 10-30 mg/kg BW IM, PO sid (Harrenstien, 1994) 50 mg/day PO or parenterally (Williams, 1976) 200 mg/l drinking water (Harkness and Wagner, 1977) 10 mg/kg BW IM followed by oral supplementation (Bauck, 1989) Reptile 100-250 mg/kg BW IM sid (Messonnier, 1996) Tortoises: 10-20 mg/kg BW IM sid (Page and Mautino, 1990) Vitamin D3 Dog NHP Reptile 1-2 rounded tsp/10 lb BW PO sid; mix with feed or water (as a drench) (Kinsell, 1986) 2000 IU/kg BW in diet (Whitney et al., 1973) 7500 IU every 2 weeks IM (Snipes, 1984) Tortoises: 1650 IU/kg BW IM once (Page and Mautino, 1990) 200-500 g/kg BW IM every 7 days (Ritchie and Harrison, 1997)

246

Vitamin E/selenium (1 mg Se and 50 mg vitamin E/ml) Bird 0.05-0.1 ml/kg BW IM, SC every 14 days (Ritchie and Harrison, 1997)

Vitamin K1 Bird 0.2-2.5 mg/kg BW IM prn (Ritchie and Harrison, 1997) 0.2-2.5 mg/kg BW IM for 1-2 injections (Harrison and Harrison, 1986) Warfarin poisoning: 0.2-2.5 mg/kg BW IM bid for 7 days (Ritchie and Harrison, 1997)

Winstrol-V (stanozolol) Bird Cat Dog 0.5-1 mg/kg BW IM every 3-7 days (Ritchie and Harrison, 1997) 0.5-1 mg/kg BW IM (Harrison and Harrison, 1986) 10-25 mg IM weekly (Kinsell, 1986) 10-50 mg IM weekly (Kinsell, 1986)

Yohimbine Bird 0.1 mg/kg BW IV (Sinn, 1997) Chinchilla 2.1 mg/kg BW IP (Hargett et al., 1989) Goat 0.2 mg/kg BW IV slowly over 1 min (NCSU, 1987) Guineapig 1.0 mg/kg BW IP (Strother and Stokes, 1989) Mouse 2.1 mg/kg BW IP (Flecknell, 1993) Rat 2.1 mg/kg BW IP (Hsu et al., 1986) Rabbit 0.2 mg/kg BW IV (Keller et al., 1988) Sheep 0.2 mg/kg BW IV slowly over 1 min (NCSU, 1987)

247

Parasiticides
Acetic acid Fish 1-2 g/l water for 1-10 min (Kiesius and Rogers, 1995) 500 ppm 30-s dip (protozoa, crustacea) (Harms, 1996)

Albendazole Dog NHP 25 mg/kg BW PO q12h for 4 days (Barr et al., 1993) 25 mg/kg BW PO for 5 days (Wolff, 1990)

Amprolium Bird Bovine Dog Ferret Fish Rabbit 2-4 ml of 9.6% solution/gal water for 5 days (Ritchie and Harrison, 1997) 5 mg/kg BW daily in feed for 21 days prophylaxis (Schultz, 1989) 10 mg/kg BW daily in feed for 5 days for treatment (Schultz, 1989) 100-200 mg/kg BW PO sid in food or water for 7-10 days (Kinsell, 1986) 19 mg/kg BW daily PO sid or in drinking water (Bell, 1994) 10 ppm bath for 7-10 days (Harms, 1996) 9.6% solution: 1 ml/15 lb BW PO for 5 days (Williams, 1979) 1 ml/7 kg BW of 9.6% solution sid for 5 days (Carpenter et al., 1995) 5 ml/gal of 9.6% solution in drinking water for 5 days (Carpenter et al., 1995)

Bunamidine Cat Dog NHP Reptile 25-50 mg/kg BW PO; single dose given on an empty stomach (after 3to 4-h fast) (Kinsell, 1986) 25-50 mg/kg BW PO; single dose given on an empty stomach (after 3to 4-h fast) (Kinsell, 1986) 25 mg/kg BW PO (Williams, 1976) 25-50 mg/kg BW PO, not more often than once every 2-3 weeks (Frye, 1981)

Carbaryl Bird Dust lightly with 5% powder or add to nest box; remove after 24 h (Ritchie and Harrison, 1997) Mouse Dust with 5% powder or dilute 1:1 with talc (Harkness and Wagner, 1983) 248

Rat Rabbit

Dust with 5% powder or dilute 1:1 with talc (Harkness and Wagner, 1983) Dust with 5% powder or dilute 1:1 with talc (Harkness and Wagner, 1983)

Carnidazole Bird Clazuril Bird Pigeons: 2.5 mg/kg BW PO once (Coussement et al., 1988) 30-50 mg/kg BW PO once, repeat in 10-14 days if necessary (Ritchie and Harrison, 1997)

Copper sulfate Fish Alkalinity of water divided by 100 = mg/l dose (Kiesius and Rogers, 1995)

Decoquinate Ferret 0.5 mg/kg BW daily mixed in moist food (Bell, 1994)

Dichiorvos-See Vapona pest strip (DDVP) Cat Dog 5 mg/lb BW PO (Kinsell, 1986) 12-15 mg/lb BW PO in adults (Kinsell, 1986) 5 mg/lb BW PO in puppies (Kinsell, 1986) Fish 0.2 ppm continuous in water, repeated weekly for 4 weeks (Harms, 1996) Mouse 500 mg/kg food for 24 h; repeat in 12 and 24 days (Wagner, 1970) NHP 10-15 mg/kg BW PO for 2-3 days (Russell et al., 1981) 30 mg/kg BW PO once (Melby and Altman, 1976) Rat 0.5 mg/g food for 1 day (Wagner, 1970) Raccoon 30 mg/kg BW PO (Evans and Evans, 1986) Reptile 12.5 mg/kg BW PO daily for 2 doses (Frye, 1981) Diethylcarbamazine Cat Dog 25-50 mg/lb BW PO once, repeat in 10-20 days for ascarids (Kinsell, 1986) 3-5 mg/lb BW PO sid daily for heartworm prevention (Kinsell, 1986) 25-50 mg/lb BW PO once; repeat in 10-20 days for ascarids (Kinsell, 249

NHP

1986) 50 mg/kg sid for 10 days in orange juice (Eberhard, 1982)

Diiodohydroxyquin NHP 20 mg/kg BW PO bid for 3 weeks (Russell et al., 1981) 30 mg/kg BW PO for 10 days (Cummins et al., 1973) 630 mg/chimpanzee PO tid for 3 weeks (Van Riper et al., 1966) 650 mg daily/animal PO for 10-20 days (Ialeggio, 1989)

Dimetridazole (no longer available) Hamster 1 g/l drinking water for 2 weeks (La Regina et al., 1980) Mouse 1 g/l drinking water for 2 weeks (Frost, 1977) 10 mg/ml drinking water for 5 days (Roach et al., 1988) Dithiazanine iodide Mouse NHP 0.1 mg/g food for 7 days (Williams, 1976) 10-20 mg/kg BW PO sid for 3-10 days (Russell et al., 1981) 100 mg/12-20 lb BW bid for 2 weeks (maple syrup acts as vehicle) (Van Riper et al., 1966) 20 mg/kg BW PO sid for 10 days (Frye, 1981)

reptile

Emetine hydrochloride Reptile 0.5 mg/kg BW/day IM, SC sid, bid for 10 days (Frye, 1981)

Fenbendazole Amphibia Bird Bovine Cat Dog Fish 10 mg/kg BW PO (Cooper, 1985) Low margin of safety; see Ritchie and Harrison, 1997, for doses 7.5 mg/kg BW PO (Schultz, 1989) 33 mg/kg BW PO sid for 5-7 days (Kinsell, 1986) 50 mg/kg BW PO sid for 3 days (Kinsell, 1986) 11 mg/kg BW PO sid for 2 treatments (Harms, 1996) 20 mg/kg BW PO once; repeat in 7 days (Harms, 1996) 2.5 g/kg feed daily for 3 days; repeat in 14-21 days (Harms, 1996) 5 mg/kg BW PO (Schultz, 1989) 100 ppm in food for 14 days (Reiss et al., 1987) 20 mg/kg BW PO for 5 days (McKellar, 1989) Lemur, Varecia: 50 mg/kg BW PO sid for 3 days (Feeser and White,

Goat Mouse NHP

250

1992) Rat 8-12 mg/kg BW/day in feed daily (150 ppm) on alternating weeks (Coghlan et al., 1993) 20 mg/kg BW PO for 5 days (McKellar, 1989) Rabbit 50 ppm in food for 5 days (Duwel and Brech, 1981) 20 mg/kg BW PO for 5 days (McKellar, 1989) Raccoon 50 mg/kg BW PO sid for 3 days (Evans and Evans, 1986) Reptile Tortoises: 50-100 mg/kg BW PO once; repeat in 2 weeks (Page and Mautino, 1990) Sheep 5 mg/kg BW PO (Schultz, 1989) Swine 5 mg/kg BW PO (Schultz, 1989) Formalin Fish 25 mg/l water in ponds; <250 mg/l water for 1 h in tanks and raceways (Kiesius and Rogers, 1995) 10 ppm in bath indefinitely (hybrid striped bass and other sensitive species) (Harms, 1996) 15-25 ppm in bath indefinitely or repeated every 3 days with 70-90% water changes (Harms, 1996) 250 ppm in 5-10 mm dip (Harms, 1996) 400 ppm in soft water up to 1-h bath every 3 days for 3 treatments (Harms, 1996) 500 ppm in hard water up to 1-h bath every 3 days for 3 treatments (Harms, 1996)

Hydrogen peroxide (3%) Fish 17.5 ml/l water for 4- to 10-min dip once (Harms, 1996)

Ivermectin Amphibia Rana pipiens: 2 mg/kg BW SC (Letcher and Glade, 1992) Bird 200-400 g/kg BW PO or topically in birds <500 g (Clyde, 1996a) 200-400 g/kg BW IM, SC, PO in birds >500 g (Clyde, 1996a) Bovine 0.2 mg/kg BW SC (Schultz, 1989) Cat 400 g/kg BW SC (Clyde, 1996a) Chinchilla 200 g/kg BW PO, SC every 1-2 weeks prn (Hoefer, 1994) Ferret 1 mg/kg BW SC total dose (Egerton et al., 1980) 200-400 g/kg BW SC, PO (Messonnier, 1994) 1:20 dilution with propylene glycol for topical treatment of ear mites; repeat in 14 days (Clyde, 1996a) Guineapig 500 g/kg BW SC (McKellar et al., 1992)

251

Mouse

NHP

Rat

Rabbit

Reptile

Swine

400 g/kg BW SC; repeat in 14 days (Clyde, 1996a) 2 mg/kg BW by gavage; repeat in 10 days (Huerkamp, 1990) 1 part 1% ivermectin with 10 parts tap water; mist 1-2 ml over entire cage (Le Blanc et al., 1993) 200 g/kg BW IM; repeat in 10 days (Battles et al., 1988) 200 g/kg BW SC (Ialeggio, 1989) 200 g/kg BW PO (Feeser and White, 1992) 200 g/kg BW sid for 5 days by gastric intubation (Battles et al., 1987) 200 g/kg BW SC once (Findon and Miller, 1987) 3 mg/kg BW PO once (Summa et al., 1992) 2 mg/kg BW PO for 3 treatments at 7- to 9-day intervals (Huerkamp, 1993) 2 mg/kg BW topical as a spot method every 14 days for 3 treatments (Kondo et al., 1998) 200-400 g/kg BW SC, PO (Messonnier, 1994) 200-400 g/kg BW SC, repeat in 10-14 days (Carpenter et al., 1995) 400 g/kg BW SC (McKellar et al., 1992) Snakes: 200 g/kg BW SC, IM, PO; repeat in 14 days (Messonnier, 1994) Snakes and lizards: 200-400 g/kg BW IM, SC (Clyde, 1996a) Turtles and tortoises: TOXIC-Do Not Use (Clyde, 1996a) 0.3 mg/kg BW SC (Schultz, 1989)

Levamisole Amphibia 10 mg/kg BW IM (Cooper, 1985) Xenopus: 12 mg/l water with no more than 1 frog/5 l water (60 mg drug/animal minimum, up to 75 mg/frog) (Iglauer et al., 1997) Bird Australian parakeets: 15 mg/kg BW by gavage; repeat in 10 days (Ritchie and Harrison, 1997) Anseriformes: 20-50 mg/kg BW by gavage (Ritchie and Harrison, 1997) Ratites: 30 mg/kg BW by gavage; repeat in 10 days (Ritchie and Harrison, 1997) Immune modulators: 2 mg/kg BW IM q14 days for 3 treatments (Ritchie and Harrison, 1997) 4-8 mg/kg BW IM once; repeat in 10-14 days (Harrison and Harrison, 1986) Bovine 8 mg/kg BW SC, PO (Schultz, 1989) Fish 10 mg/kg BW PO once every 7 days for 3 treatments (Harms, 1996) 11 mg/kg BW IM once every 7 days for 2 treatments (Harms, 1996) 50 ppm in 2-h bath for external trematodes (Harms, 1996) NHP 7.5 mg/kg BW SC; repeat in 2 weeks (Welshman, 1985) Raccoon 4-10 mg/kg BW PO (Evans and Evans, 1986)

252

Reptile Sheep Swine

5 mg/kg BW intracoelomic once; may be repeated in 2-3 weeks (Frye, 1981) 8 mg/kg BW SC, PO (Schultz, 1989) 8 mg/kg BW SC, PO (Schultz, 1989)

Lime sulfur Guineapig 1:40 sponged over body weekly for 6 weeks (Russell et al., 1981) Lindane Guineapig 1% used as dip (Zajac et al., 1980) Malachite green Fish Malathion Guineapig 0.5% used as dip (Russell et al., 1981) Mouse 5 ml of 1% suspension in bedding (Russell et al., 1981) Rat 5 ml of 1% suspension in bedding (Russell et al., 1981) Rabbit 0.5% sponged twice weekly (Russell et al., 1981) Mebendazole Bird Dog 25 mg/kg BW bid for 5 days (Harrison and Harrison, 1986) 10 mg active ingredient/lb BW PO sid sprinkled on food for 5 days; may repeat in 3 weeks (Kinsell, 1986) Fish 50 mg/kg BW PO once every 3 weeks for 3 treatments (nematodes) (Harms, 1996) 100 ppm in 10-mm to 2-h dip (monogenean trematodes) (Harms, 1996) Gerbil 2.2 mg/ml tap water/animal sid for 5 days, by gavage (Smith and Snider, 1988) Mouse 40 mg/kg BW as a drench; repeat in 7 days (Russell et al., 1981) NHP 3-5 mg/kg BW PO (Russell et al., 1981) 15 mg/kg BW PO for 3 days (Wolff, 1990) Rat 10 mg/kg BW PO for 5 days (McKellar, 1989) Rabbit 10 mg/kg BW PO for 5 days (McKellar, 1989) Raccoon 25-40 mg/kg BW PO sid for 3-5 days (Evans and Evans, 1986) 0.1 ppm in continuous bath (Harms, 1996) 2 ppm in 30-min bath (Harms, 1996)

253

Methyridine Rat 125 mg/kg BW SC once (Weisbroth and Scher, 1971) 125 mg/kg BW IP once (Weisbroth and Scher, 1971) 200 mg/kg BW IP once (Peardon et al., 1966)

Metronidazole Bird Pigeons: 50 mg/kg BW PO bid for 5 days (Johnson-Delaney, 1996) Pigeons: 200-250 mg/kg BW PO sid for 3-7 days (Johnson-Delaney, 1996) Pigeons: 10-20 mg/kg BW IM sid for 2 days (Johnson-Delaney, 1996) Pigeons: 4 g/gal drinking water for 3-7 days (Johnson-Delaney, 1996) Cat 10 mg/kg BW PO tid (Boothe, 1996) Dog 60 mg/kg BW PO sid for 5 days (Kinsell, 1986) 10 mg/kg BW PO tid (Boothe, 1996) Ferret 35 mg/kg BW PO sid for 5 days (Bell, 1994) Fish 50 mg/kg BW PO sid for 5 days (Harms, 1996) 5-10 ppm in continuous bath (Harms, 1996) Guineapig 20 mg/kg BW PO, SC sid (Richardson, 1992) Mouse 2.5 mg/ml drinking water for 5 days (Roach et al., 1988) NHP 35-50 mg/(kg.day) BW PO bid for 10 days (Holmes, 1984) Rabbit 20 mg/kg BW PO bid (Carpenter et al., 1995) Reptile 125-275 mg/kg BW PO once, may be repeated at 7- to 10-day intervals for 1-2 more treatments (Frye, 1981) Tortoises: 250 mg/kg BW PO once; repeat in 2 weeks (Page and Mautino, 1990) Niclosamide Bird 220 mg/kg BW PO once; repeat in 10-14 days (Harrison and Harrison, 1986) Finches: 500 mg/kg BW PO once a week for 4 weeks (Harrison and Harrison, 1986) Gerbil 1 mg/10 g BW PO (Burke, 1979) Hamster 500 mg in 150 g food (Burke, 1979) 10 mg/100 g BW PO as a drench, repeat in 2 weeks (Russell et al., 1981) Mouse 100 mg/kg BW once PO (Harkness and Wagner, 1983) 500 mg/150 g ground feed for 1 week (Williams, 1976) NHP 30 mg/kg BW PO; repeat in 2-3 weeks (Russell et al., 1981) 140 mg/kg BW PO (Williams, 1976) Rat 100 mg/kg BW once PO (Harkness and Wagner, 1983)

254

Rabbit Reptile

10 mg/100 g BW as a drench; repeat in 2 weeks (Russell et al., 1981) 1 mg/g feed for 2 weeks separated by 1 week (Russell et al., 1981) 150 mg/kg BW PO (Williams, 1976) 150 mg/kg BW PO; not more often than once each month (Frye, 1981)

Nitrofurantoin Rat 0.2% in feed for 6-8 weeks (Russell et al., 1981)

Nitrofurazone Fish 75-100 mg/kg BW PO sid for 5-15 days (Harms, 1996)

Paromomycin NHP 50 mg/kg BW PO in 3 divided doses sid for 10 days (Williams, 1976)

Phenothiazine Rabbit 1 g/50 g molasses-treated feed (Siegmund, 1979)

Piperazine (adipate and citrate) Bird 100-500 mg/kg BW PO once; repeat in 10-14 days (Ritchie and Harrison, 1997) Psittacines: not effective (Ritchie and Harrison, 1997) Bovine 110 mg/kg BW PO (Schultz, 1989) Cat 0.86 g/lb BW PO; repeat in 10-21 days (Kinsell, 1986) Dog 0.86 g/lb BW PO; repeat in 10-21 days (Kinsell, 1986) Gerbil 20-60 mg/100 g BW PO (Russell et al., 1981) 3-5 mg/ml drinking water for 7 days, off 7 days, repeat for 7 days (Russell et al., 1981) Goat 110 mg/kg BW PO (Schultz, 1989) Guineapig Piperazine adipate: 4-7 mg/ml drinking water (Williams, 1976) Hamster 3-5 mg/ml drinking water for 7 days, off 7 days, repeat for 7 days (Russell et al., 1981) Piperazine citrate: 10 mg/ml drinking water for 7 days, off 5 days, repeat for 7 days (Unay and Davis, 1980) Piperazine citrate: 2 ml of 10 mg/ml given once by gavage (Unay and Davis, 1980) Mouse 500 mg/100 ml drinking water for 14 days (Reiss et al., 1987) 255

Piperazine adipate: 4-7 mg/ml drinking water for 3-10 days (Williams, 1976) Piperazine citrate: 200 mg/kg BW daily in drinking water for 7 days, off 7 days, repeat for 7 days (Hoag, 1961) NHP 65 mg/kg BW PO sid for 10 days (Russell et al., 1981) 100 mg/kg BW PO (Ialeggio, 1989) Rat 200 mg/100 ml drinking water (Rossoff, 1974) Piperazine adipate: 250 mg/50-60 g BW in drinking water for 3 days (Habermann and Williams, 1957) Rabbit Piperazine adipate: 0.5 mg/kg BW PO for 2 days (Brooks, 1979) Piperazine citrate: 100 mg/ml drinking water for 1 day (USDA, 1976) Piperazine powder: 200 mg/kg BW PO (Harkness and Wagner, 1983) Raccoon 75-150 mg/kg PO (Evans and Evans, 1986) Reptile Piperazine citrate: 40-60 mg/kg BW PO; not more often than once every 2 weeks (Frye, 1981) Sheep 110 mg/kg BW PO (Schultz, 1989) Swine 110 mg/kg BW PO (Schultz, 1989) Potassium permanganate Fish 2 mg/l water in ponds for an indefinite period; 10 mg/l water for 10 min (Kiesius and Rogers, 1995) 1 ppt for 30- to 40-s dip (Harms, 1996) 20 ppm for 1-h bath (Harms, 1996) 2-5 ppm for indefinite bath (Harms, 1996)

Praziquantel Bird Toxic in finches (Ritchie and Harrison, 1997) 10-20 mg/kg BW PO; repeat in 10 days (Ritchie and Harrison, 1997) Toucans for flukes: 10 mg/kg BW PO sid for 14 days, then 6 mg/kg BW PO sid for 14 days (Ritchie and Harrison, 1997) For flukes: 9 mg/kg BW IM sid for 3 days, then PO for 11 days (Ritchie and Harrison, 1997) For tapeworms: 9 mg/kg BW IM once; repeat in 10 days (Ritchie and Harrison, 1997) 2 ppm in 24-h bath (Harms, 1996) 1 ppm for >90-h bath or 2 ppm for 4-h bath (Diplostomum eye flukes) (Harms, 1996) 330 mg/kg BW PO once (Diplostomum eye flukes) (Harms, 1996) 500 mg/kg BW PO once (internal cestodes Bothriocephalus sp.) (Harms, 1996) 50 mg/kg BW PO once (internal cestodes Eubothrium sp.) (Harms, 1996)

Fish

256

5 mg/kg BW IP once; repeat in 14-21 days (Harms, 1996) Mouse 5 mg/kg BW SC or 10 mg/kg BW PO (McKellar, 1989) NHP 0.1 ml/kg BW IM (Droncit injectable) (Welshman, 1985) 40 mg/kg BW PO, IM once (Wolff, 1990) Rat 5 mg/kg BW SC or 10 mg/kg BW PO (McKellar, 1989) Rabbit 5-10 mg/kg BW IM, SC, PO once; repeat in 10 days (Carpenter et al., 1995) 5 mg/kg BW SC or 10 mg/kg BW PO (McKellar, 1989) Raccoon 5-10 mg/kg BW IM, PO (Evans and Evans, 1986) 10-15 mg/kg BW SC; up to 100 mg/kg BW for some trematodes (Evans and Evans, 1986) Reptile 8-20 mg/kg BW IM, PO once; repeat in 14 days (Messonnier, 1996) 10 mg/kg BW IM, PO; up to 30 mg/kg BW PO for trematodes (Clyde, 1996b) Pyrantel pamoate Bird 4.5 mg/kg BW PO once; repeat in 10-14 days (Ritchie and Harrison, 1997) Dog 1 ml/5-20 lb BW PO (Kinsell, 1986) NHP Lemur: 6 mg/kg BW PO (Feeser and White, 1992) Raccoon 10-20 mg/kg BW PO (Evans and Evans, 1986) Pyrethrin Rabbit 0.5% applied as a dust (Russell et al., 1981)

Pyrivinium pamoate Hamster 0.8 mg/l drinking water for 30 days (Frost, 1977) Mouse 0.8 mg/l drinking water for 28 days (Russell et al., 1981) NHP 5 mg/kg BW PO every 6 months (more often if needed) (Cummins et al., 1973) Rat 0.003% in drinking water for 30 days (Blair and Thompson, 1969) 0.012% in food for 30 days (Blair and Thompson, 1969) Quinacrine hydrochloride Bird 5-10 mg/kg BW PO sid for 7 days (Harrison and Harrison, 1986) NHP 10 mg/kg BW PO tid every 10 days (Russell et al., 1981) Rat 75 mg/kg BW PO total dose (Balazs et al., 1962)

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Ronnel NHP Rotenone NHP Rabbit One part rotenone in 3 parts mineral oil applied topically once a week for 2 weeks (Bowman and Griffith, 1987) Mix with mineral oil and apply in ear for 3 days off and on for 3 weeks (Russell et al., 1981) 55 mg/kg BW PO qod for 4 treatments, then once weekly for 3 months; a total of 16 treatments (Finegold et al., 1968)

Sodium chloride Fish 0.5-1% in water for indefinite period; 3% in water for 30 s to 10 min (dip); 1% for 10 min to 2 h (dip) (Kiesius and Rogers, 1995)

Tetrachlorethylene Reptile 0.2 ml/kg BW PO; not more often than once each month (Frye, 1981)

Thiabendazole Bird 250-500 mg/kg BW PO once; repeat in 10-14 days for ascarids (Ritchie and Harrison, 1997) 100 mg/kg BW PO sid for 7-10 days (Ritchie and Harrison, 1997) 66 mg/kg BW PO; 110 mg/kg BW PO for severe parasitism and Cooperia (Schultz, 1989) 100-200 mg/kg BW PO (Harkness and Wagner, 1983) 50-100 mg/kg BW PO; repeat in 2 weeks (Van Riper et al., 1966) 100 mg/kg BW PO; repeat in 2 weeks, then once every 6 months (Cummins et al., 1973; Ialeggio, 1989) 100 mg/kg BW PO sid for 3 days (Weishman, 1985) 200 mg/kg BW PO for 5 days (Rossoff, 1974) 0.1% in feed (Harkness and Wagner, 1983) 50 mg/kg BW PO; repeat in 3 weeks (Carpenter et al., 1995) 25 mg/kg BW PO (Williams, 1976) 100 mg/kg BW PO for 5 days (McKellar, 1989) 50 mg/kg BW PO as a drench; use as often as necessary (Frye, 1981) 75 mg/kg BW PO (Schultz, 1989)

Bovine Mouse NHP

Rat Rabbit

Reptile Swine

258

Thiabendazole and piperazine hydrate (respectively) Hamster 0.1% in diet for 6 weeks, and 0.6% in drinking water starting 2 weeks before the thiabendazole (Taylor, 1992) Tinidazole Mouse 2.5 mg/ml drinking water for 5 days (Roach et al., 1988)

Trichlorfon Fish 0.25-0.5 ppm in 1-h bath for 5 days (Harms, 1996) 2 ppm in 1-h bath once (Harms, 1996) 5 ppm in 30-min bath once (Harms, 1996) 1.75 g/l drinking water with 1 g sugar, for 14 days, assuming a mouse consumes 2.2-3.2 ml water daily (Simmons et al., 1965) 175 mg/100 ml drinking water for 14 days (Reiss et al., 1987)

Mouse

Vapona pest strip (DDVP) Mouse Reptile Place a 1 x 1 in. strip on each cage (for 24 h) on each cage-change day for four changings (our interpretation of French, 1987, Eds.) 1 strip/1000 cu ft room space; use continuously (Frye, 1981)

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