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Anthrax is an infection cause by Bacillus anthracis that occurs primarily in herbivores. Aerosolized spores of B. anthracis have the potential for use in biological warfare or bioterrorism.

Bacillus anthracis

a. It is a large, aerobic, spore-forming, Gram (+), rod-shaped microorganism that is capsulated and non-motile. This microorganism grows in chains. b. Spores of B. anthracis can survive for years in dry soil but can be destroyed by boiling for ten minutes. c. Treatment is done by oxidizing agents such as KMnO4 hydrogen peroxide, or diluted formaldehyde. d. Most strains of the agent are susceptible to penicillin. Anthrax occurs worldwide and is most prevalent among domestic herbivores ( including cattle, sheep, horses, and goats) and wild herbivores. Grazing animals become infected when they forage for food in areas contaminated with the spores. Terminally ill animals with overwhelming bacteremic infections often bleed at the nose, mouth, and bowel, thereby contaminating soil or water with vegetative anthracis that can sporulate and persist in the environment. The carcasses of infected animals provide additional potential foci of contamination. Humans are more resistant to anthrax than herbivores animals. Human cases are classified as: 1. Agricultural cases, which result most often with animals that are infected (e.g., during skinning, butchering, or dissecting), from bites or contaminated or infected flies, and from consumption of contaminated meat. 2. Industrial cases, which are associated with exposure to contaminated hides, goat hair, wool, or bones.

MODE OF TRANSMISSION a. Direct through contact with infected animals or contaminated animal products b. Indirect through animal bites and ingestion of contaminated meat c. Airborne through inhalation of contaminated or polluted air

1. Cutaneous anthrax

a. The incubation period ranges from nine hours to two weeks (2 to 7days). b. Two to three days after the entrance of the microorganism, a small pimple or macule appears. c. On the 4th day, a ring of vesicles develops around the papule. Vesicular fluid may exude. d. Marked edema starts to develop. Unless there is secondary infection, there is no pus and lesion is not painful, although painful lymph adenitis may occur in the inguinal area. e. On the 5th to 7th days, the original papules ulcerate to form the characteristic eschar. f. Edema extends to some distance from the lesion. g. Clinical symptoms may be severe if the lesions are located on the face, neck or chest. h. In more severe forms, clinical findings are high fever, toxemia, regional painful lymphadenopathy, and extensive edema. Shock and death may also ensue.

2. Inhalational anthrax (woolsorters disease)

a. Presenting symptoms resemble those of severe viral respiratory diseases. b. After the one-to-three-day acute phase, increasing fever, dyspnea, stridor, hypoxia, and hypotension occur, usually leading to death within 24 hours. c. Clinical findings showed that the organisms are directly deposited into the alveoli or into the alveolar ducts, producing hemorrhagic necrosis of the nodes associated with hemorrhagic mediastinitis.

3. Gastrointestinal anthrax results from ingestion of inadequatelycooked meat from animals with anthrax. a. Primary infection is initiated in the intestines where lesions are formed accompanied by hemorrhagic lymphadenitis. b. Symptoms include fever, nausea and vomiting, abdominal pain, bloody diarrhea, and sometimes rapidly developing ascites.

Approximately 95% of human cases of anthrax are of the cutaneous form and 5% are of the inhalation form. Gastrointestinal anthrax is very rare. B. anthracis bacteremia occurs in almost all cases of anthrax and progress to a fatal outcome. 3

COMPLICATIONS 1. Anthrax meningitis is the intense inflammation of the meninges of the brain and spinal cord. a. This is marked by elevated CSF pressure with bloody CSF, followed by rapid loss of consciousness and death. b. Fatality rate is almost 100 percent. 2. Anthrax sepsis develops after the lymphohematogenous spread of B. anthracis from the primary lesion.Clinical features are high fever, toxemia and shock, with death following in a short time.

TREATMENT 1. Parenteral penicillin G- 2 million units every six hours, until edema subsides, with subsequent administration of oral penicillin for a sevento-ten-day-course. 2. Patients who are sensitive to penicillin can be treated with erythromycin, tetracycline, or chloramphenicol. NURSING MANAGEMENT 1. 2. 3. 4. 5. Careful history taking Thorough physical examination Skin care, psychological ,and emotional support Supportive measures are geared toward type of anthrax exposure Any type of anthrax, either in livestock or humans, should be reported to health authorities.

CANDIDIASIS (Moniliasis/Candidosis)
An infection ranges from a mild superficial fungal infection, to systemic and potentially life-threatening disease. Most often, candidiasis infects the nails (onychomymosis), the sin(diaper rash), and mucous membranes, particularly those of the oropharynx (thrush), vagina (monillasis), esophagus, and the GIT.

INFECTIOUS AGENT Candida albicans 1. These organisms are part of the normal flora of the GIT, mouth vagina, and skin. 2. They cause infection when: a. There is rise blood glucose, as in diabetes mellitus; b. The persons resistance is lowered, especially when due to cancer; c. The person is taking an immunosuppressive drug, exposed to radiation, aging or when infected with the human immunodeficiency virus (HIV); d. The level of estrogen rises in pregnant women; e. They may introduced systematically by intravenous or urinary catheters, drug abuse, hyperalimentation, or surgery; f. Broad-spectrum antibiotics are used, as these depress normal flora and allow candida microbes to proliferate. 5

SIGNS/SYMPTOMS 1. The skin is scaly, erythematous, and popular rash is present, sometimes covered with exudates appearing below the breasts, between the fingers, and the axillae, groin, and umbilicus. 2. Nails are red and swollen; then nailbeds are darkened; there is occasional purulent discharge; and the separation of pruritic nails from nailbeds is evident. 3. Oropharyngeal mucosa (thrush)-cream-colored or bluish white patches exude on the tongue, mouth, or pharynx and reveal bloody engorgement when scrapped. They may swell and cause respiratory distress in infants. 4. The patient feels retrosternal pain and regurgitation. 5. Vaginal mucosa- white or yellow discharge with pruritus and local excoriation; white or gray raised patches on vaginal walls with local inflammation. 6. Renal system- fever, flank pain, dysuria, hematuria, pyuria 7. Pulmonary- hemoptysis, fever, cough 8. Brain- headache, nuchal rigidity, seizures 9. Endocardium systolic or diastolic, orbital or periorbital pain DIAGNOSIS 1. Stool culture 2. Gram staining of skin,, vaginal discharge, or scrapings

NURSING MANAGEMENT 1. Avoid sharing utensils 2. Meticulous mouth care 3. Proper disposal of oral secretions TREATMENT 1. Nystatin, for oral thrush 2. Clitrimazole, fluconazole, ketoconazole, for mucous membrane and vaginal infection 3. Fluconazole or amphotericin for systemic infection PREVENTION 1. Check high-risk patient daily for patchy areas of irritation, sore throat, and gum bleeding. 2. Check vaginal discharge and note the color, odor, and amounts.

CHICKENPOX (Varicella)
Chickenpox is an acute and highly contagious disease of viral etiology that is characterized by vesicular eruptions on the skin and mucous membrane with mild constitutional symptoms.

INFECTIOUS AGENT Herpesvirus varicellea a DNA- containing virus 1. Human beings are the only source of infection. 2. This is closely related or identical to herpes zoster virus. INCUBATION PERIOD The incubation period is 10 to 21 days or may be prolonged after passive immunization against chickenpox. MODE OF TRANSMISSION 1. Direct contact with a patient who sheds the virus from the vesicles 2. Indirect contact, through linens or fomites 3. Airborne, or spread by aerosolized droplets from the nasopharynx of ill individuals 4. High viral titers are found in the vesicles of chickenpox; thus, viral transmission may also occur through direct contact with these vesicles, although the risk is lower. 5. Following primary infection there is usually lifelong protective immunity from further episodes of chickenpox. PERIOD OF COMMUNICABILITY The patient is capable of transmitting the disease about a day before the eruption of the first lesion up to about five days after appearance of the last crop. CLINICAL MANIFESTATION 1. Preeruptive manifestations are mild fever and malaise. 2. Eruptive stage 7

a. Rash starts on the trunk (unexposed area), then spreads to other parts of the body. b. Initial lesions are distinctively red papules whose contents become milky and pus-like within four days. c. An adults and bigger children, the lesions are more widespread and more severe. d. There is rapid progression so that transition is completed in six to eight hours. e. Vesicular lesions are very pruritic. f. All stages are presents simultaneously before all are covered with scabs, leading to the appearance known as celestial map. g. The stages are characterized as follows: Macule is a lesion that is not elevated above the skin surface Papule is a lesion that is elevated above the skin surface with a diameter of about 3mm Vesicle is a pop-like eruption filled with fluid. The thin-walled vesicle easily burst and dries up in three to five days. Pustule is a vesicle that is infected or filled with pus. If the lesion becomes infected the scar may be big and wide. Crust is a scab or eschar. This is a secondary lesion caused by secretion of vesicle drying on the skin. The scars are superficial, depigmented and take time to fade out.

DIAGNOSTIC TEST 1. Determination of the V-Z virus through the complement fixation test 2. Determination of the V-Z virus through electron microscope examination of vesicular fluid COMPLICATIONS 1. Chickenpox is rarely fatal, although it is generally more severe in adults than in children. 2. Pregnant women and those with a suppressed immune system are the highest risk of serious complications.

3. The most common late complication of chickenpox is shingles, caused by reactivation of the varicella zoster virus decades after the initial episode of chickenpox. 4. Secondary infection of the lesion furuncles, cellulitis, skin abscess, erysipelas. 5. Meningoencephalitis 6. Pneumonia 7. Sepsis TREATMENT MODALITIES 1. 2. 3. 4. 5. 6. Oral acyclovir 800mg3x a day for five days must also be given. Oral antihistamine can be taken to symptomatic pruritus Calamine lotion eases itchiness. Salicylates must not be given. Antipyretic might be given for fever. Antihistamine must be given.

NURSING MANAGEMENT 1. Respiratory isolation is a must until all vesicles have crusted. 2. Prevent secondary infection of the skin lesions through hygienic care of the patient 3. Attention should be given to nasopharyngeal secretions and discharge. Linens must be disinfected under the sunlight or through boiling. 4. Cut fingernails short and wash hands more often to minimize bacterial infections that may be introduced by scratching. 5. A child must wear mittens. 6. Provide activities to keep children occupied to lessen pruritus. 7. Observe oral and nasal care as rashes may appear in the buccal cavity. PREVENTIVE MEASURES 1. Active immunization with live, attenuated varicella vaccine is necessary. 2. Avoid exposure as much as possible to infected persons. 3. Patient must be isolated to avoid transmission of organism to other members of the family.

( Elephantiasis) Filariasis is a parasitic caused by the microscopic, threadlike African eye worm. The adult worm can live only in the human lymphatic system. The disease is an extremely debilitating and stigmatizing and affects men, women, and children. It affects the poor in the rural and urban areas. The disease is rarely fatal; however, it causes extensive disability, gross disfigurement, and untold suffering in millions of men, women, children. 9

CAUSATIVE ORGANISM Wuchereria bancrofti is the causative agent of filariasis. It is a thread worm four to five centimeters long affects the lymph nodes and lymph vessels of the legs, arms, vulva, and breasts. Brugia malayi shows manifestations resembling that of the bancroftian, but swelling of the extremities is confined to the areas below the knees and below the elbows. Brugia timori rarely affects the genitals. Loa loa is another filarial parasite in humans transmitted by the deer fly.

MODE OF TRANSMISSION The disease is transferred from person to person by mosquito bites. Persons having circulating microfilariae are outwardly healthy but transmit the infection to others through mosquito bites. 10

Persons with chronic filarial swellings suffer severely from the disease but no longer transmit the infection. In India, 99.4% of cases are caused by the species Wuchereria bancrofti, whereas Brugia malayi is responsible for 0.6% of the problem. PATHOLOGY/PATHOGENESIS 1. When a mosquito bites a person with lymphatic filariasis, microscopic worms circulating in the persons enter and infect the mosquito. 2. The microscopic worms pass from the mosquito through human skin and travels to the lymph vessels where they grow into adults. 3. An adult worm lives for seven years in the lymph vessels, they mate and release into the bloodstream millions of microscopic worms known as microfilaria. 4. Once person has the worms in his or her blood, these are picked up by the biting mosquito when it feels and the disease is transmitted to another person via the larvae. 5. The larvae migrate to the lymph nodes, reach sexual maturity, and cycle is completed. 6. A person needs to get many mosquito bites over several months to several years to get filariasis. 7. At first, most people do not know they have filariasis. They usually do not feel any symptoms until after adult worms die. 8. The disease damages the kidneys and the lymph system; fluid collects and causes swelling in the arms, breast, legs, and for men, the genital area. 9. The entire legs, arms, and genital area may swell to several times their normal sizes. The swelling and decreased function of the lymphatic system make it difficult for the body to fight the infection. 10. A person with this disease tends to have more bacterial infections in the skin; thus, skin hardens and thickens. This is called elephantiasis. 11.In advanced stages, the worms can actually obstruct the vessels, causing the surrounding tissues to enlarge. In Bancroftian filariasis, the thighs, legs and genitals are mostly involved, while the Malayan variety affects the legs below the knees. 12.In conjunctival filariasis, larvae migrate to the eyes and can sometimes be seen beneath the conjunctiva. 13.Untreated conjunctival filariasis can cause a type of blindness known as onchocerciasis. SYMPTOMS 1. Symptoms vary, depending on the type of parasitic worm involved, but all infections usually begin with on-and-off chills, headache, and fever thats lasts between three months and one year after insects bite. 2. There may also be swelling , redness, and pain in the arms, legs or scrotum. 3. Areas of abscesses may appear as a result of dying worms or a secondary bacterial infection.


DIAGNOSTIC PROCEDURES 1. The circulating filarial antigen (CFA) test is performed on a finger-prick blood droplet taken anytime of the day. Results are available in a few minutes. 2. The larvae can also be found in the blood, but mosquitoes which spread the disease are active at night. Larvae are usually found between about 10:00pm to 2:00am. 3. The patients history must be taken and the pattern of inflammation and signs of lymphatic obstruction must be observed. MODALITIES OF TREATMENT 1. Ivermectin, albendazole, or diethylcarbamize (DEC) are used in treatment and act by: a. Eliminating the larvae, b. Impairing the adult worms ability to reproduce, and c. Actually killing the adult worms. The above medications are started at low doses to prevent immunologic reactions triggered by the large number of dying parasites. 2. Surgery may be performed to remove surplus tissue and provide a way to drain the fluid around the damaged lymphatic vessels. Surgery may also be used to minimize massive enlargement of the scrotum. 3. Elephantiasis of the legs can also be eased by elevating the legs and providing support with elastic bandages. 4. DEC- fortified salt is helpful. NURSING MANAGEMENT 1. Health education and information dissemination as to the mode of transmission must be carried out. 2. Environmental sanitation and the destruction of breeding places of mosquitoes must be emphasized. 3. Psychological and emotional support to client and the family are necessary. 4. Personal hygiene must be encouraged. 5. The course of the disease must be explained to the client and his/her family. PREVENTION AND CONTROL Mosquitoes that carry the microscopic worms usually bite between the hours of dusk and dawn. It is therefore advised that people living in an area with filariasis should: 1. sleep under mosquito net, 2. use mosquito repellant in the hours between duck and dawn, and 3. take a yearly dose of medicine that kills the worms circulating in the blood.


Fungi can be harmful or beneficial. Mushrooms are one type of fungus, but the term can also refer to microorganisms that live on us. These microorganisms are harmless most of the time, but they sometimes can cause a problem called fungal infection. Sometimes people get fungal infections, but they are usually easy to treat because they seldom spread below the skin. Some of these fungal infections are:

TINEA FLAVA ( Tinea alba/ Tinea versicolor) It is a common , benign, superficial, cutaneous fungal infection, characterized by hypo- or hyperpigmentation on the skin, usually on the back or chest.

ETIOLOGIC AGENT The causative organism of Tinea flava is a lipophilic fungus Malassezia furfur.

INCIDENCE 1. The disease affects young people in the puberty age, probably due to hormonal changes and the increase sebum secretion. 2. Males and females can be equally affected. 3. Tropical areas can have a prevalence of as high as 40%. PATHOLOGY 1. M.furfur is a member of the normal human flora and is found in 18% of infants and in 90 to 100% of adults. 13

2. The organism can be found in both the spore stages and filamentous (hyphal) form. 3. Even though M. furfur is a component of normal flora, it can also be an opportunities pathogen. 4. The organism is considered to be a factor in other cutaneous diseases, including Pityrosporum folliculitis, confluent and reticulate papillomatosis, seborrheic dermatitis, and someforms of atopic dermatitis. CLINICAL MANIFESTATION 1. Most individuals with tinea versicolor complain of cosmetically disturbing abnormal pigmentation. 2. The involved skin regions are usually the trunk, back, abdomen, proximal extremities, and face. 3. The color of each lesion varies from almost white to reddish brown fawn. 4. A fine, dust-like scale covers the lesions. 5. Patient complains of mild pruritus. TREATMENT MODALITIES Therapeutic options include topical agents and oral medications. Topical applications are cheaper and safer. Topical agents include: Micoconazole Ciclopirox colamine Propylene glycol lotion Topical terbinafine Benzoyl peroxide

NURSING MANAGEMENT 1. Instruct patient to use a clean towel and washcloth daily. 2. All skin area and skin folds that retain moisture must be dried thoroughly. 3. Clean cotton clothing should be worn next to the skin. TINEA BARBAE( Barbers Itch) This is a colonization of the bearded areas of the face and neck and is restricted to adult males only.


ETIOLOGIC AGENT The most common causes are Trichophyton mentagrophytes (originating from cattle) and Trichophyton verrucosum(originating from horses). MODE OF TRANSMISSION 1. The organism is acquired from contact with cattle, dogs, and other animals; therefore, the disease is common among dairy farmers and cattle ranchers. 2. Person-to-person transmission can occur through shavers used on infected persons in barber shops. CLINICAL MANIFESTATION Lesions of three types: 1. Mild superficial form, which causes erythema and perifollicular papules and pustules. Hair of the area maybe affected with endothrix, which causes brittleness and lusterless hair. 2. Inflammatory or deep, pustular, kerion crusting around the hair. unilateral involvement of the neck, chin, or maxillary area, sparing the upper lip. Nodular lesions covered with crust and seropurulent materials ending up in an abscess-like appearance Hair becomes loose and brittle Permanent alopecia and scarring may be the final consequence 3. Circinate variety has a spreading vesiculo-pustular border with central scaling. TREATMENT MODALITIES 1. Tinea barbae should be treated with sysytemic anit-fungal agents such as griseofulvin, ketoconazole, fluconazole, itraconazole, and terbinafine. 2. These drugs are given as regular doses for two to three weeks until clinical resolution is achieved. 3. Systemic antibiotics may be beneficial.

TRICHOPHYTOSIS (Ringworm) This is used to designate a group of disease caused by vegetable fungi, affecting various portions of the body in different ways. There are two types of ringworm, the dry and the moist. 1. The dry type is characterized by the presence of rounded macular areas of reddish or yellowish-brown color of varying size (may be as large as a coin). Sometimes these areas are slightly elevated above the surrounding skin. The center tends to be paler than the periphery of the lesion. 2. The moist is less frequently seen. This may arise from the dry lesion and rapidly becomes pustular in the presence of secondary infection. 15

PREVENTION AND CONTROL 1. Avoid contact with infected animals. 2. Avoid sharing combs and razors with infected individuals. 3. Observe personal hygiene. ATHLETES FOOT An infection that usually appears between the toes characterized by red, dry, cracked, and itchy skin between the toes and can also affect toenails. Some people manifest red, scaly bumps filled with pus on the planter area and the sides of the feet.

PREVENTION OF ATHLETES FOOT Wash feet every day. Dry feet completely, especially the areas between the toes. Wear sandals or shower shoes when walking around in locker rooms, public pools, and public showers. Wear clean socks. If they get wet or damp, be sure to change them as soon as you can. Use medicated powder on your feet to help reduce perspiration.

JOCK ITCH Infection of the groin and upper thighs. Both men and women can be infested with disease. 16

The rash is itchy and oftentimes feels like burning.

PREVENTION OF JOCK ITCH Avoid contact with infected animals. Avoid sharing comb, razors, shoes, and undergarments with infected individuals. Observe personal hygiene. Keep the groin always clean and dry. Wear clean, cotton underwear and loose-fitting pants.

(Rubella/Three-Day Measles)
An acute contagious disease characterized by mild constitutional symptoms and a rose-colored macular eruption which sometimes resemble measles and at other times, scarlet fever. It causes mild, feverish illness associated with rashes and aches in joints. It has a teratogenic effect on the fetus. Rubella can affect anyone of any age and is generally a mild disease,rare in infants or those over the age of 40. The older the person is the severe the symptoms are likely to be. Up to one-third of older the girls or women experience joint pain or arthritis type symptoms with rubella.


INFECTIOUS AGENT Rubella virus (Family-Togaviridae; Genus- Rubivirus) INCUBATION PERIOD From exposure to the appearance of the rash, the incubation period is usually 14 to 21 days. PERIOD OF COMMUNICABILITY The virus is communicable approximately one week before and four days after the onset of the rash, but is at its worst when the rash is its peak. Highly communicable infants with congenital rubella may shed virus for months after birth. MODE OF TRANSMISSION 1. 2. 3. 4. Direct contact with nasopharyngeal secretions Air droplets Transplacental transmission in congenital rubella Infants with congenital rubella shed large quantities of the virus through their pharyngeal secretions and urine, which serve as sources of infection to other contacts.

CLINICAL MANIFESTATIONS 1. Prodromal Period a. Low grade fever b. Headache c. Malaise d. Mild coryza e. Conjuctivitis f. Post-auricular, sub-occipital, and posterior cervical lymphadenopathy which occurs on the 3rd to the 5th days after onset 2. Eruptive Period a. A pinkish rash on the soft palate (Forchheeimers spot) an exanthematous rash that appears first on the face, spreading to the neck, the arms, trunk and legs. b. Eruption appears after the onset of adenopathy c. Children usually present less or no constitutional symptoms. d. The rash may last for one to five days and leaves nopigmentations nor desquamation. e. Testicular pain in young adults f. Transient polyarthralgia and polyarthritis may occur in adults and occasionally in children. MODALITIES OF TREATMENT Very little treatment is necessary; treatment is essentially symptomatic.


COMPLICATIONS 1. Encephalitis 2. Neuritis 3. Arthritis 4. Arthralgias 5. Rubella syndrome, manifested by: Microcephaly Mental retardation Cataract Deaf-mutism Heart disease RISK CONGENITAL MAFORMATION 1. 100%- when maternal infection occurs on the first trimester of pregnancy of first month of gestation 2. 4% - in the second and third trimester of pregnancy 3. 90% of congenital rubella cases excrete the virus at birth and are therefore infectious 4. 10% - the virus remains contagious until the first year of age the infected child.



(Congenital Rubella) 1. Classic congenital rubella syndrome a. Intrauterine growth retardation; infant has low birth weight b. All manifestations of congenital rubella syndrome c. Thrombocytopenia purpura known as blueberry muffin skin d. Lethargy and hypothermia 2. Intrauterine infection a. may result in spontaneous abortion b. birth of a live child who may have one or multiple birth anomalies such as: cleft palate, hare lip, talipes, and eruption of teeth cardiac defects (patient ductus arterious, atrial septal defect) eye defects (glaucoma, retinopathy, micropthalmia, unequalsized eyeballs) 19

eye defects(deafness usually bilateral, abnormally-shaped ears) neurologic (microcephaly, mental retardation, psychomotor retardation, behavioral disturbances, vasomotor instability)

NURSING MANAGEMENT 1. 2. 3. 4. 5. The patient should be isolated. The patient should be advised to rest in bed until fever subsides. The patients room must be darkened to avoid photopobia. The patient must take a mild liquid but nourishing diet. The patients eyes should be irritated with warm normal saline to relieve irritation. 6. The ears must be taken care of. Do not apply heat or cold compress unless ordered. 7. Good ventilation is necessary. 8. The spread of infection must be prevented. 9. The occurrence of complications must also be prevented. 10.Encourage increased fluid intake. PREVENTION 1. Administration of live attenuated vaccine(MMR) 2. Pregnant women should avoid exposure to patients infected with rubella virus. 3. Administration of immune serum globulin one week after exposure to rubella 4. Prevent spread of infection by minimizing contact with visitors

Herpes simplex is a viral disease characterized by the appearance of sores and blisters anywhere on the skin. These sores usually occurs either around the mouth and nose, or on the genitals and buttocks 9thus the nickname virus of love). Herpes simplex is related to the viruses that cause infectious mononucleosis (Epstein- Barr virus), chickenpox and shingles ETIOLOGIC AGENT Herpes simplex virus (HSV) TYPE 1 VIRUS 1. This virus can cause cold sores that usually infect during infancy and childhood. 2. The sore is characterized by tiny, clear, fluid-filled blisters.


3. The sore most commonly affects the lips, mouth, nose, chin or cheeks and occurs shortly after exposure. It may also develop on wound on the skin. 4. Patients may barely notice the symptoms or need medical attention for relief of pain. 5. The disease can be transmitted by kissing and sharing kitchens utensils and towels. 6. Patients usually catch the infection appears two to twenty days after contact with an infected person and usually last from seven to ten days.

PATHOGENESIS 1. Before the blister appears, the skin may itch or become very sensitive. 2. Lesions are limited to the epidermisor superficial mucous membrane. 3. The blister may break as a result of injury, allowing the fluid of the blister to ooze and crust. 4. The crust falls off, leaving slightly red, healing skin; however, the virus remains in the body. It then infects nerve cells, where it remains in a resting state. 5. Then infection may recur in either the same location or in a nearby site. The infection may recur every few weeks or less frequently. 6. Subsequent infections tend to be milder than the primary infection. This can be set off by a variety of factors, including fever, sun expose and the menstrual period. For many, the recurrence is unpredictable and has no recognizable cause. TYPE 2 VIRUS 1. This type genitals ores, affecting the buttocks, penis, vagina or cervix, and lasts two to twenty days. 2. Most people get the infection from sexual contact with an infected person. 3. The virus affects about 20% of sexually active individuals 4. The virus can also be spread by touching and unaffected part of the body after touching the herpes lesion. 5. Manifestations include minor rash or itching and painful sores, fever, muscular pain and burning sensation during urination.


CLINCAL MANIFESTATION The clinical manifestation of herpes simplex virus infection ranges from mild to fatal disease, depending on the age and other characteristics of the host, the organs involved and the nature of the infection. I. Mild to Moderate 1. Oral Herpes. Gingivostomatitis in young children is the most common clinical manifestation of the initial infection with HSV. Vesicular and ulcerative lesions occur in the buccal mucosa and may involve the tongue. Inflammation of the gums cervical adonopathy and fever are present. Excessive salivation results from pain on swallowing in infants and young children. Feeding is painful and fluid intake is poor.

2. Labial herpes. The lips may occasionally be involved in the primary infection; in such cases, it is commonly known as cold sores or fever blisters. The lesions then crust and heal within three to ten days. Subsequent recurrences are usually close to the original site.


3. Ocular herpes. Herpetic keratitis is a major medical problem that potentially leads to loss of vision. Primary keratitis may be accompanied by conjunctivitis and preauricular lymphadenopathy. Conjunctivitis alone may also be a manifestation of primary infection Recurrent keratitis is usually unilateral, but 2% to 6% of cases may be bilateral. More serious disease may occur if the stoma is involved or if iridocyclitis occurs.

4. Cutaneous herpes. HSV may affect the skin on many part of the body. The primary cutaneous infection may be accompanied by deep, burning pain, fever, skin edema, ascending lymphangitis and regional lymphadenopathy. Majority of samples isolated from above the waistline is type 1 and those isolated from below the waistline is type 2.

5. Erythema multiforme. This allergic reaction of the skin is sometimes a complication of HSV infections. HSV lesions sometimes appear as a zosteriform distribution that mimics herpes zoster. 6. Genital herpes. Is considered one of the most common sexually transmitted diseases.


II. SEVERE TO FATAL DISEASE 1. Newborns. Neonatal herpetic infection is usually acquired from maternal infection at the time of delivery. 2. Eczema varicelliforn eruption occurs most commonly in individuals with atopic dermatitis. this occasionally occurs in patients with other skin disorders, such as seborrheic dermatitis and diaper rash. Fatality rate range from 5 -10%. Death is usually due to disseminated viremia to the brain and visceral organs or a superimposed bacterial infection. 3. Encephalitis is considered as one of the most non-epidemic forms of herpes infection in the United States and other country. This form may observed in infected patients of any age, even among those who already have circulating HSV in the blood.

MODALITIES OF TREATMENT/MANAGEMENT 1. 2. 3. 4. Oral anti-viral drugs such as acyclovir, famciclovir or valacyclovir Personal hygiene Restoration of fluid and electrolyte balance Isolation of clients, especially those with eczema herpeticum or neonatal herpes 5. Practice of universal precaution and through hand washing.

(Shingles/Acute Posterior Ganglionitis) Herpes zoster, commonly known as shingles, is caused by the same virus responsible for chickenpox, the varicella-zoster virus. After the initial exposure, herpes zoster lies dormant in certain nerve fibers. It may become active as a result of many factors such as aging stress, suppression of the immune system and certain medications. 24

ETIOLOGIC AGENT Varicella-zoster(V-Z) virus 1. This agent has been found to cause two diseases, varicella and herpes zoster. 2. The virus occurs in partially immune individuals due to previous varicella infection. INCUBATION PERIOD The incubation period of herpes zoster is unknown, but is believed to be 13 to 17 days. PERIOD OF COMMUNICABILITY Herpes zoster is communicable a day before the appearance of the first rash until five to six after the last crust disappears.

MODE OF TRANSMISSION 1. Herpes zoster can be transmitted through direct contact, specifically, through droplet infection and airborne spread. 2. It can also be transmitted through indirect contact, e.g., articles freshly soiled by secretions and discharges from an infected person. PATHOGENESIS The virus is identical with the causative agent of chickenpox. After the primary infection, the varicella zoster virus may persist in a dormant state in the dorsal nerve root ganglia. The virus may later emerge from the site, either spontaneously or in association with immunosuppression, to cause herpes zoster. It produces localized vesicular skin lesions confined to a dermatone and severe neurologic


pain in the peripheral areas innervated by the nerves arising in the inflamed root ganglion. This infection usually occurs in adults.

CLINICAL MANIFESTATIONS Any part of the trunk may be infected, but the thoracic segment is commonly involved. Other areas that may be affected are the extremities and branches of the 5th and 7th cranial nerves. The virus affects the ganglion of the posterior nerve roots or the extramedullary cranial nerve ganglion. 1. The erythematous base of the skin lesion appears first. It is followed by the appearance of the vesicles within 24 hours. A cluster of vesicles appears to form patches, which coalesce to form an irregular, band-like distribution along the course of involved dermatones. Eruptions are unilateral and never cross the midline of the body. The vesicles become pustular, break down, and form crusts. Lesions may last for one to two weeks. 2. Pain of varying intensity is a presenting symptom in a about two-thirds of patients. Pain occurs from one to five days prior to the development of rash and is neuralgic and paroxysmal in type. The pain may be described as burning or stabbing. Patient may complain of pruritus. The pain is usually worse at night and is intensity by movement. 3. Fever, malaise, anorexia, and headache occur for one or more days. 4. Regional lymph nodes are involved in the early stage of the disease. 5. When the ophthalmic (5th cranial) nerve is affected, corneal anesthesia may occur, and the condition is known as Gasserian ganlionitis. 6. Paralysis of the facial nerve and vesicles in the external auditory canal affects the 7th cranial nerve. The condition is called Ramsay-Hunt Syndrome.


DIAGNOSTIC EXAM 1. The characteristic skin rash may be diagnostic. 2. Tissue culture technique- the virus may be isolated from fluid taken from newly developing vesicles. 3. Smear of vesicle fluid 4. Microscopy COMPLICATIONS 1. Encephalitis 2. Paralytic ileus, bladder paralysis 3. Ophthalmic herpes, which may lead to blindness MODALITIES OF TREATMENT 1. 2. 3. 4. Symptomatic Antiviral drugs Analgesics to control pain Anti-inflammatory

NURSING MANAGEMENT 1. 2. 3. 4. 5. Keep the patient comfortable. Maintain meticulous hygiene. Keep the patient in strict isolation. Apply cool, wet dressings with NSS to pruritic lesions. Efforts should be made to prevent secondary infection. Prevent entrance of microorganism into the lesions, especially if they are broken. 6. Assess the degree of pain. To avoid neuralgic pain, do not delay the administration of pain relievers as prescribed. 7. Encourage sufficient bed rest and provide supportive care to promote proper healing of lesions. 8. Provide the patient with a diversionary activity ttotake his mind off the pain and the pruritus. PREVENTION Immunization against chickenpox Avoid exposure to a patient suffering from either varicella or herpes zoster Increase the patients immune resistance

(Hansens Disease/Hansenosis) Leprosy is a chronic systemic infection characterized by progressive cutaneous lesions.



ETIOLOGIC AGENT Mycobacterium leprae is an acid-fast bacillus that attacks cutaneous tissues and peripheral nerves, producing skin lesions, anesthesia, infection and deformities. Contrary to popular belief, leprosy is not higly contagious and actually has low infectivity. INCUBATION PERIOD The incubation period of leprosy ranges from five-and-a-half months to eight years. MODE OF TRANSMISSION 1. The disease can be transmitted through respiratory droplets. 2. Inoculation through the skin break and mucous membrane may also be a mode of transmission. Leprosy occurs in three distinct forms: 1. LEPROMATOUS LEPROSY(multibacillary) a. This is most serious type and is considered to be the most infectious. b. It causes damage to the respiratory tract, eyes and testes, as well as the nerve and the skin. c. Lepromin test is negative but the skin lesion contains large amount of Hansens bacillus. 28

d. There is gradual thickening of the sin with development of granulomatous condition. e. The lesions frequently appear as macules and become nodular in character (leproma). f. There is slow involvement of the peripheral nerves, with some degree of anesthesia and loss of sensation and gradual destruction of the nerves. g. There is atrophy of the skin and muscles and eventual melting or absorption of small bones, primarily those of the hands and feet. h. There is ulceration of the mucous membrane of the nose. i. Because of the melting or absorption of small bones and ulcerations, natural amputations may occur.

2. TUBERCULOID LEPROSY a. It affects the peripheral nerves and sometimes the surrounding skin, especially on the face, eyes and testes as well as the nerves and the skin. b. Lepromin test is positive, but the organism is rarely isolated from the lesions. c. Macules are elevated, with clearing aat the center, and are more clearly defined than in the lepromatous form. d. Anesthesia is present, and involvement of the peripheral nerves occurs more rapidly than in lepromatous form.


3.BORDERLINE (dimorphous) leprosy has the characteristics of both lepromatous and tuberculoid leprosy. Skon lesions of this type of leprosy are diffused and poorly defined.

PATHOLOGY 1. M.leprae attacks the peripheral nerves, especially the ulnar, radial, posterior-popliteal, anterior-tibial and facial nerves. 2. When the bacilli damage the skins fine nerves, they cause anesthesia and pain, anhidrosis and dryness. 3. If they attack a large nerve trunk, motor nerve damage, weakness and pain occur, followed by peripheral anesthesia, muscle paralysis and atrophy. CLINICAL MANIFESTATION 1. Neural involvement The earliest manifestations of the disease in most cases are the result of nerve damage, as characterized by; a. Atrophy of the muscles of the hands which extends to the thenar, the hypothenar, and the forearm muscles, resulting in clawhand. b. Nerves often involved are the ulnar, median, radial, lateral popliteal and facial. c. Paralysis and peripheral anesthesia can occur either independent or concurrently. d. Secondary consequences of nerve involvement include malperforant, clawhand and ocular complications incident to corneal insensitivity or paralysis of the eyelids. 2. Skin Lepromatous and tuberculoid leprosy differ greatly in their cutaneous manifestations: a. In lepromatous disease, early lesions are multiple, symmetrical and erythematous, sometimes appearing as macules or papules with smooth surfaces. b. Later, these lesions enlarge and form plaques or nodules on the earlobes, nose, eyebrows and forehead, giving the patient a leonine appearance. c. Eventually, there is the loss of eyebrows and eyelashes. 30

d. The loss of function of the sweat and sebaceous glands makes affected skin appear dry and hairless. e. Tuberculoid leprosy may be purely neural or may simultaneously affect the skin. f. Raised, large erythematous plaques appear on the skin with clearly defined boarders. As they grow, they become rough, hairless and hypo-pigmented, leaving an anesthetic scar. 3. Eye a. Specific ocular manifestations are found only in lepromatous and borderline leprosy. b. The conjunctiva, sclera, cornea and iris are affected, sparing the retina and optic nerve. c. Photophobia, conjunctivitis and iridocyelitis frequently occur. Opacity of the cornea, insensitivity and ulceration can lead to blindness. 4. Upper respiratory tract a. The nose, mouth, pharynx, larynx, trachea and esophagus are often involved in lepromatous leprosy. b. Epistaxis, ulceration of the uvula and tonsils, septal perforation and nasal collapse are also present. 5. Visceral leprosy Apart from the skin and nerves, the heaviest concentration of lesions is in the organs representing the reticulo-endothelial system, the lymph system and the liver. Testicular damage occurs in almost all moderately advanced cease of lepromatous leprosy. DIAGNOSTIC PROCEDURES 1. 2. 3. 4. Identifications of the signs and symptoms Tissue biopsy Tissue smear Blood test show increased RBC and ESR; and decreased serum calcium, albumin and cholesterol levels.

MODALITIES OF TREATMENT 1. Sulfone therapy 2. Rehabilitation, recreational and occupational therapy 3. Multiple drug therapy(MDT) a. The drugs used in MDT are combinations of rifampicin, clofazimine and dapsone for multibacillary leprosy, and rifampicin and dapsone for the pausibacillary type. b. Among these, rifampicin is the most important anti-leprosy drug and is therefore included in the treatment of both types of leprosy. c. Treatment of leprosy with only one anti-leprosy drug will always result in the development of drug resistance. d. Treatment of leprosy with dapsone or any anti-leprosy drug uses as monotherapy should be considered as an unethical practice.


e. For multibacillary leprosy, rifamppicin 600 mg is given once a month; dapsone 100mgdaily; and clofazimine 50mg daily for a 12-month duration. f. For paucibacillary lepros, give rifampicin 600 mg once a month, dapsone once daily; duration of treatment is 6 months. g. Clofazimine causes brownish black discoloration and dryness of the skin. However, this disappears within a few months after stopping treatment. This should be explained to patients starting the MDT regimen for MB leprosy. h. MB and PB patients should have fixed-duration treatment, which means: for MB patients- after taking 12 monthly doses MDT, the person is considered cured and should be removed from the register; for PB patients- after taking 6 monthly doses MDT, the person considered cured and should be discharged. NURSING MANAGEMENT 1. If the patient is admitted to the hospital isolation and medial asepsis should be carried out. 2. Moral support and encouragement are necessary. 3. Diet should be full, wholesome and nutritious. 4. Special attention should be given to personal hygiene. 5. Terminal disinfection should be carried out. PREVENTION 1. Report all cases and suspects of leprosy 2. Newborn infants should be separated from leprous mother. 3. BCG vaccine may be protective if given during the first 6 months of life. 4. Health education should be given, with particular focus on the mode of transmission.

MEASLES (Rubeola/Morbilli)
Measles is an acute, contagious and exanthematous disease that usually affects children who are susceptible to upper respiratory tract infection (URTI).This may be one of the most common and most serious of all childhood disease.


ETIOLOGIC AGENT A filterable virus which belongs to the genus Morbilivirus of the family paramyxoviridae is the agent of measles. The measles virus is rapidly inactivated by heat, ultraviolet light and extreme degrees of acidity and alkalinity. INCUBATION PERIOD 1. The incubation period is form ten to twelve days (longest is 20 days and the shortest is eight days.) 2. A single attack conveys lifelong immunity. PERIOD OF COMMUNICABILITY 1. Measles usually lasts about nine to ten days, measured from the beginning of the prodromal symptoms to the fading of the rash. 2. The disease is communicable four days before and five days after the appearance of rashes. 3. The disease is most communicable at the height of the rash. SOURCES OF INFECTION The virus has been found in patients blood, as well as in the secretions from the eyes, nose and throat. MODE OF TRANSMISSION 1. The disease is transmitted through direct contact with droplets spread through coughing or sneezing. 2. It can also be transmitted indirectly through articles or fomites freshly contaminated with respiratory secretions of infected patients.

PATHOGNOMINIC SIGN Kopliks spots are pathognomonic of measles. These are inflammatory lesions of the buccal mucous gland with superficial necrosis 1. They appear on the mucosa of the inner cheek opposite to the second molars, or near the junction of the gum and the inner cheek. 2. They usually appear one to two days before the measles rash.


CLINICAL MANIFESTATION Clinical manifestations come in three stages: 1. Pre-eruptive stage a. Fever b. Catarrhal symptoms (rhinitis, conjunctivitis, photophobia, coryza) c. Respiratory symptoms start from common colds to persistent coughing. d. Enanthem sign (Kopliks spot, Stimsons line) 2. Eruptive stage a. A maculo-papular rash usually starts to appear late on the 4th day. b. The maculo-papular rash appears first on the cheeks, bridge of the nose, temples, earlobes, or along the hairline. c. The rash is fully developed by the end of the second day all symptoms are at their most severe at this time. d. High-grade fever comes on and off. e. Anorexia and irritability. f. Abdominal tympanism, pruritus and lethargy g. The throat is red and often extremely sore. h. As fever subsides, coughing may diminish, but more often it hangs on for a week or two and becomes looser and less metallic. 3. Stage of convalescence a. Rashes fade away in the same manner as they erupted. b. The fever subsides are rashes start to fade. c. When the rashes have faded, desquamation begins. d. Symptoms subside and appetite is restored. DIAGNOSTIC PROCEDURES 1. 2. 3. 4. Nose and throat swab Urinalysis Blood exams (CBC, leukopenia, leukocytosis) Complement fixation or hemogglutinin test

MODALITIES OF TREAMENT 1. Anti-viral drugs(Isoprinosine) 2. Antibiotics if with complication 3. Supportive therapy (oxygen inhalation, IV fluids) COMPLICATIONS 1. 2. 3. 4. 5. 6. Bronchopneumonia Otitis media Pneumonia/bronchitis Nephritis Encephalitis; encephalomyelitis Blindness(seldom)


UNFAVORABLES SIGNALS 1. 2. 3. 4. 5. Violent onset high-grade fever Fading eruption with rising fever Hemorrhagic or black measles Persistence of fever for ten days or more Slight eruptions accompanied by severe symptoms, especially those of encephalitis.

NURSING MANAGEMENT 1. Isolation of the patient is necessary (the room must be quiet, wellventilated and must have subdued light). 2. Control patients high temperature with warm or tepid sponges. 3. Skin care is utmost importance. The patient should have a daily cleansing bed bath. The water should be comfortably warm. 4. Oral and nasal hygiene is very important aspect of the nursing care of a patient with measles. 5. Care of the eyes is necessary. The patient is sensitive to light. Therefore, position the patient in such a way that direct glare of light is avoided. Keep eyes free of secretions. 6. Care of the ears is also important. It is the responsibility of the nurse to be on the alert for any signs of early mastoid infection. 7. Daily elimination is important. This can be accomplished with a mild laxative, as prescribed by the physician. 8. During the febrile stage, limit the diet to fruit juices, milk and water. If the patient is vomiting , give frequent, small servings of iced juices. 9. The patients position should be changed every three to four hours. 10.Penicillin or other prescribed medications, are usually given in cases where there is complication. PREVENTIVE MEASURES 1. Immunization with anti-measles at age of 9months, as a single dose. The first dose of the measles-mumps-rubella (MMR) vaccine is given at 15 months old, with 2nd dose at 11 to 12 years. The measles vaccine should not be given to pregnant women or to persons with active tuberculosis, leukemia or lymphoma, or those with depressed immune systems. 2. Avoid overcrowded place to lessen the chances of contracting the virus.


Scabies is an age-old skin infection caused by an itch mite, which penetrates the skin, forming burrows. (Burrows are tiny thread-like projections ranging from 2-6mm long that appear as thin gray, brown lines in affected areas.)


The disease is caused by a mite, Sarcoptes scabiei. 1. The mite is yellowish-white and can barely be seen by the unaided eye. 2. The female parasite burrows beneath the epidermis to lay her eggs. This causes intense irritation. 3. The male are smaller and reside on the surface of the skin. 4. Scabies occurs worldwide and is predisposed by overcrowding and poor hygiene. 5. The parasite does not survive more than 3-4 days away from the skin.



The itch mite may burrow under the skin and lay ova within 24 hours of the original contact.

This disease is communicable for the entire period that the host is infected.

1. Transmission is direct-through an infected individual. 2. The disease is also acquired through sleeping on an infested bed or wearing infested clothing. 3. Anyone may become infected or re-infected. 4. Infestation with mites may also result from contact with dogs, cats and other small animals. 5. Scabies on dogs is called mange. When canine or feline mites land on human skin, they fail to thrive and produce only a mild itch that eventually disappears. 6. On the other hand, human scabies gets worse and worse unless the condition is treated.


a. The female mite burrows into the skin to lay her eggs, from which larvae emerge to copulate and re-burrow under the skin. b. While any part of the body may be infected, the itch mite is commonly found in the inter digital spaces of the fingers or in warm folds in the skin. c. Areas of friction, such as the crotch, axillae, the belt line, around the nipple in women and the peri-umbilical region are sites of predilection. d. The external genitalia are most frequently involved in adult males. e. The lesions are slightly elevated, straight or twitching burrows, threadlike and are either brown or black in color. They measure 5 to 6mm in length. f. Severe inflammation, with the development of papules, blisters, pustules and crust, may occur as a result of infection from scratching. g. In infants, burrows may appear on the head and neck. h. The disease may become fully developed in two weeks; the eggs hatch in about six days and the parasite grows very rapidly. It may persist for months or even years if not recognized or properly treated.

1. The disease is invariably accompanied by itching, characteristically more pronounced at night, when the patient has retired, since the increased warmth of the skin has a stimulating effect on the parasite. 2. For the first week the itch is subtle. It gradually becomes more intense that after a month or two, sleep becomes almost impossible.


3. Secondary lesions like vesicles, papules, pustules, excoriations and crust may be found on the affected site. 4. Bacterial superinfection may result from constant excoriation of burrows and papules.


A drop of mineral oil placed over the burrow, followed by superficial scraping and examination of expressed material under a low-power microscope, may reveal mites, ova or mite feces.

1. Treatment for scabies consist of application of pediculicide, such as permethrin cream or lindane lotion, as a thin layer over the entire skin surface, left on for ten to twelve (10to12) hours. 2. Crotamition cream is applied for five consecutive nights. 3. Neosporin ointment is rubbed onto the affected skin four or five times a day. 4. Eurax and Kwell lotion also prove effective in some patients. 5. Antihistamines, like diphenhydramine (Benadryl) can be useful in giving relief from the itch. 6. All clothes used before and during the treatment period should be disinfected by dry cleaning or boiling.


1. Instruct the patient to apply the cream at bedtime, from the neck down to the toes, covering the entire body. 2. Contaminated clothing or bedclothes should be dry-cleaned or boiled. 3. Advise the patient to report any skin irritation. 4. Suggests that family members and others close contacts of the patient be checked for possible symptoms and treated if necessary. 5. If the patient is hospitalized, practice good handwashing technique or use gloves while performing nursing procedure. 6. Terminal disinfection should be carried out after the discharge of the patient.

Good personal hygiene Avoid contact with infected persons All members of the household, including close contacts, should be treated. After treatment, bedding and clothing worn next to the skin should be properly laundered.



The word came from the Latin botulus,(sausage), a rare but serious paralytic illness caused by a potent neurotoxin produced by the bacterium Clostridium Botulinum, which processes the following characteristics: 1. Gram (+), spore-forming, anerobic organism whose natural habitat is the soil; 2. the spore can withstand boiling for several hours; and 3. botulinal toxin is the most potent toxin known to man. There are three human forms of botulism: 1. Foodborne (classical) botulism usually results from ingestion of inadequately cooked contaminated food, especially those with low acid content.

a. Wound botulism, also known as cutaneous botulism, is characterized by the formation of ulcers with sharply demarcated edges and a membranous base as a result of deposition of toxin in the area.


2. Infant botulism usually afflicts infants aged three to 20 weeks. The disease can produce hypotonic (floppy) infant syndrome, manifested by constipation, feeble cry, depressed gag reflex, and inability to suck. Toxins released by the organism can cause death of the infant by weakening or paralyzing the muscles of the tongue and pharynx, which are enervated by cranial nerves IX to XII.

PATHOGENESIS All the three forms disease via a final common pathway. The toxin is disseminated to peripheral cholinergic synapse and blocks acetylcholamine, causing impaired autonomic and voluntary neuromuscular transmission. CLINICAL MANIFESTATION 1. Regardless of the source of botulinal toxin, i.e., whether ingested from food or produced in a wound, or from infant gut, flaccid paralysis first affects and descends via the bulbar musculature. 2. The somatic musculature is the next part to be affected and the patient may have generalized weakness. Because the toxin is blood-borne, paralysis almost invariably displays symmetry as it descends. 3. Neurological symptoms are as follows: a. Diplopia and blurred vision, b. Ptosis, dry mouth, dysphagia, and dysarthria. 4. Classic symptoms of botulism include: a. Double vision, blurred vision, drooping eyelids b. Slurred speech, difficulty swallowing, and dry mouth c. Muscle weakness d. Infants with botulism appear lethargic, feed poorly, and are usually constipated e. Weak cry and poor muscle tone


f. If untreated, these symptoms may cause paralysis of the arms, legs, trunk, and respiratory muscles g. In foodborne botulism, symptoms usually begin 18 to 36 hours after eating contaminated food. h. The symptoms may contain to cause paralytic ileus with severe constipation and lead to body paralysis. i. Respiratory muscles are affected, which may cause death due to respiratory failure. COMPLICATIONS 1. 2. 3. 4. 5. Pneumonia Urinary tract infection Pulmonary embolism Decubitus ulcer Flexion contractures

TREATMENT/MANAGEMENT 1. Supportive care is needed, with particular attention to respiratory and nutritional needs. 2. In foodborne botulism, emetics and gastric lavage are recommended. 3. In wound botulism, exploration and debridement of the site need to be undertaken. PREVENTION AND CONTROL 1. Health education through instruction on proper preparation of food, especially on home canning is necessary. 2. Infant botulism can be prevented by not giving infants food with honey, as it is known contain Clostridium botulinum. 3. Promptly report suspected cases or an outbreak of foodborne botulism.

(Brain Fever) Encephalitis is an inflammatory disease involving part or all of the nervous system, resulting in abnormal functioning of the brain and spinal cord.

ETIOLOGIC AGENT It may be caused by a variety of pathologic agents, including bacteria, viruses, fungi, rickettsia, toxins, chemical substances, or trauma. 41

Arthropod-born encephalitis viruses belong to the group of arboviruses. The natural habitat of these viruses appears to be many species of wild birds and some domestic birds that live in a symbiotic relationship with several known species of mosquitoes, many of which belong to the Culex group. INCUBATION PERIOD The incubation period is typically 5 to 15 days, but may range from 4 to 21 days. MODE OF TRANSMISSION Encephalitis is transmitted to humans by the bite of an infected mosquito. The mosquito becomes infected by biting an infected bird. After incubating the virus in its own body for 5 to 7 days, the mosquito carries the virus to healthy birds, horses, pigs, and humans. Infection of man is the end of the cycle, since the infection is not transmitted from man to man. Mosquitoes do not carry the virus from humans. CLASSIFICATION 1. Primary encephalitis is an infection caused by direct invasion of the CNS by the virus, resulting in an inflammatory reaction. The arthropod-borne viruses are as follows: a. Eastern Equine Encephalitis (EEE) This is considered as a serious epidemic disease of horses. It principally affects children under five years of age. The virus can multiply in the Aedes sullicans mosquito. b. Western Equine encephalitis (WEE) is milder and usually affects adults. c. St. Louis Encephalitis The virus is transmitted by the bite of an infected mosquito. The organism is believed to gain entrance through the olfactory tract. d. Japanese Encephalitis This is a potentially severe viral disease that is spread by the bite of an infected mosquito, Culex triteaniorhynchus, which lives in rural rice-growing and pig-farming regions. The mosquito breeds in flooded rice fields and standing water around planted fields. Once the mosquito is infected, it carries the virus and is capable of transmitting the disease for life. It is a mosquito-borne viral disease that can affect the central nervous system and cause several complications and even death. JE can be a risk to travelers to rural areas where the disease is prevalent. This affects children five to ten years old, more in males than females with a ratio of 3:1. The case fatality rate is 30 to 35%. The peak season for JE is March to April and September to October. 42

There is not specific treatment for JE. 2. Secondary encephalitis a. Post-infection encephalitis is usually a complication or sequel to some viral disease like measles, chickenpox, and mumps. b. Post-vaccinal results after the client receives a vaccine, most commonly with the anti-rabies vaccine.

WHO ARE AT RISK FOR JAPANESE ENCEPHALITIS? Anyone can get Japanese encephalitis, but some people are at an increased risk: People living in rural areas where the disease is common Active-duty military deployed to areas where the disease is common Travelers to rural areas where the disease is common

CLINICAL MANIFESTATION 1. Japanese encephalitis a. Flu-like symptoms (fever, chills, headache, nausea, and vomiting) b. Stiff neck, confusion, and neurologic manifestation occur within 72 hours (drowsiness, seizures, bizarre, coma) c. Decreased IQ d. Serious brain damage 2. General manifestation a. During the prodromal period (1 to 4 days), the patient experiences fever, headache, dizziness, vomiting, and apathy. b. The patient may experience chills, sore throat, conjunctivitis, arthralgia, myalgia, and abdominal pain. c. Later, the patient shows encephalitic signs such as nuchal rigidity, ataxia, tremors, mental confusion, speech difficulties, stupor hyperexcitability, convulsions, coma, and death. d. Ocular palsy, ptosis, and flaccid paralysis e. The patient may feel disturbance in swallowing, mastication, phonation, respiration, and movements of the muscles of the eyes or face. f. The muscles of the different parts of the body contract uncontrollably and twitch.


DIAGNOSTIC EXAMS 1. 2. 3. 4. CSF analysis Serologic test 90% confirmatory, done on the 7th days of illness ELISA (IgM) Polymerase chain reaction

SEQUELAE 1. Motor Disturbances a. Persistent convulsions b. Parkinsonian syndrome or paralysis agitans c. Epilepsy 2. Mental Disturbances a. Mental dullness b. Mental deterioration c. Lethargy d. Mental depression e. Sleep disturbances 3. Endocrine Disturbances a. Patient may grow either fat or thin. b. Sexual interest or activity is lost. TREATMENT 1. 2. 3. 4. Treatment must be symptomatic and supportive. Convulsions must be controlled. Nose and throat secretions should be sanitarily disposed of. TSB or alcohol sponges may be given if the temperature is excessively high. 5. Unless patient is comatose, oral fluid should be encouraged. 6. Oral care should be done strictly, 7. A mouth gag and protective devices, such as bedrails, should be available in case convulsions occur. 8. Intake and output should be closely monitored. 9. Patients should be observed for neurologic signs involving speech, swallowing difficulty, twitching, eye movements, and indications of paralysis. 10.The beginning, duration, and frequency of all convulsion should be carefully observed and recorded. NURSING MANAGEMENT 1. Provide comfort. Keep the patient in a quiet, well-ventilated room. Stretch linens. Encourage or perform oral hygiene on the patient. Do bed bath if not contraindicated. 2. Prevent complications. Turn the patient to sides at least every 3-4 hours. Encourage high caloric intake. Moisten lips with mineral oil. Render TSN if febrile. 3. Monitor intake and output. 44

PREVENTION AND CONTROL 1. Preventive measures are directed toward the identification of mosquito vectors. 2. Prevention and control must be geared toward the elimination of breeding places destruction of larvae, screening of homes, and use of repellents. 3. A broad public education program about all phases of preventive program is important.

(Cerebrospinal Fever) Meningitis is the inflammation of the meninges of the brain and spinal cord as a result of viral or bacterial infection. Such inflammation may involve the three meningeal membranes-the dura matter, the arachnoid membrane and the pia matter.

ETIOLOGIC AGENT The disease can be causes by several kinds of organism, including Pneumococcus, Staphylococcus, Streptococcus and the tubercle bacillus. The species Neisseria Meningitides (meningococcus) is the organism causing most epidemics of meningitis. INCUBATION PERIOD Incubation period varies, the extreme limits being set from 1 to 10 days. MODE OF TRANSMISSION 1. Meningitis is transmitted by respiratory droplets through the nasopharyngeal mucosa. 2. This infection can also be transmitted by direct invasion through otitis media. 3. Meningitis may result after a skull fracture, a penetrating head wound, lumbar puncture or ventricular shunting procedures.


DIAGNOSTIC PROCEDURES 1. CSF analysis through lumbar puncture, the purposes of which are: a. Diagnostic purpose Obtaining the CSF specimen Taking x-rays of the spinal canal and cord b. Therapeutic purposes Reducing intracranial pressure Introducing serum and other medications Injecting an anesthesia agent 2. Gram-staining 3. Smear and blood culture 4. Smear from petechiae 5. Urine culture CLASSIFICATIONS 1. Acute meningococcemia a. Meningococci invade the bloodstream without involving the meninges. b. The onset is characterized nasopharyngitis, followed by a sudden attack oh high-grade fever with chills, nausea, vomiting, malaise and headache. c. Petechial, purpuric or ercchymotic hemorrhages scatter over the entire body and mucous membranes. d. Adrenal lesions start to bleed into the medulla, extending to the cortex. e. The combination of meningococcemia and adrenal medullary hemorrhage is known as Waterhouse-Friderichsen syndrome. f. Waterhouse-Friderichsen syndrome is the rapid development of petechiae that become purpuric and echymotic spots in association with shock. g. The condition runs a short course and is usually fatal. This frequenly occurs in the fulminant type.


Waterhouse-Friderichsen syndrome.

2. Aseptic meningitis a. It is a benign syndrome characterized by headache, fever, vomiting and meningeal symptoms. b. It begins suddenly with a fever of up to 40C, alterations in consciousness (drowsiness, confusion and stupor), and neck spine stiffness, which is slight first. c. Characteristic signs of meningeal irritation: stiff neck or nuchal rigidity opisthotonos (+)Brudzinskis sign (+) Kernigs sign Exaggerated and symmetrical deep tendon reflexes d. Sinus arrhythmia, irritability, photophobia, diplopia and other visual probles e. Delirium, deep stupor and coma f. Signs of intracranial pressure bulging fontanels in infants nausea and vomiting (projectile) severe frontal headache blurring of vision alteration in sensorium


COMPLICATIONS 1. 2. 3. 4. 5. 6. subdural effusion hydrocephalus deaf-mutism blindness of either one or both eyes otitis media and mastoiditis pneumonia or bronchitis

MODALITIES OF TREATMENT 1. If meningitis is left untreated it has a mortality rate of 70-100%. 2. Treatment includes appropriate antibiotic therapy and vigorous supportive care. 3. IV antibiotics are usually given for two weeks and are followed by oral antibiotics such as: ampicillin cephalosporin (ceftriaxone) aminoglycosides 4. Digitalis glycoside (digoxin)is administered to control arrhythmias. 5. Mannitol is given to decrease cerebral edema. 6. An anticonvulsant or sedative is needed to reduce restlessness and convulsions. 7. Acetaminophen is helpful in relieving headache and fever. NURSING MANAGEMENT 1. Assess neurologic signs often. Observe the patients level of consciousness and check for increased intracranial pressure (ICP) (signs include plucking at bedcovers, vomiting, seizures and changes in motor functions and vital signs). 2. Watch out for the deterioration of the patients condition, which may signal an impending crisis. 3. Monitor fluid balance. Maintain adequate fluid intake to avoid dehydration, but avoid fluid overload because of the danger of cerebral edema. Measure central venous pressure and intake and output. 4. Watch out for any adverse reaction to the antibiotics and/ or other drugs. Avoid infiltration and phlebitis. Position the patient carefully to prevent joint stiffness and neck pain. Turn the patient often to avoid pressure sores and respiratory complications. Assist with ROM. Maintain adequate and elimination. Ensure the patients comfort. Provide reassurance and support to the patient and the family. 48


6. 7. 8.

9. Follows strict aseptic technique when treating patients with head wounds or skull fractures. 10.Isolation is necessary, especially if nasal culture is positive. PREVENTION 1. Several vaccines are available to protect against certain types of meningitis. 2. Teach clients with chronic sinusitis or other chronic infections the importance of proper and prompt medical treatment. 3. Give rifampicin as prophylaxis, as ordered by the physician. 4. Implement the universal precaution.

(Infantile Paralysis/Heine-Medin Disease) Poliomyelitis is an acute infectious disease characterized by changes in the CNS which may result in pathologic reflexes, muscle spasm, and paresis or paralysis. It is a disease of the lower motor neurons. There is anterior horn involvement, such that it is named anterior poliomyelitis. ETIOLOGIC AGENT The disease is caused by filterable virus, the polio virus (Legio debilitans). There are three strains of this virus and so far, the disease has affected man alone. 1. Brunhilde 2. Lansing 3. Leon INCUBATION PERIOD The incubation period is 7 to 21 days for paralytic cases; with a repeated range of 3 to 35 days.


PERIOD OF COMMUNICABILITY The patient is capable of transmitting the disease during the first 3 days to 3 months of illness. The disease is most contagious during the first few days of active disease, and possibility from 3 to 4 days before the onset of symptoms.


MODE OF TRANSMISSION The virus is transmitted from person to person by: 1. direct contact with infected oropharyngeal secretions and feces; 2. person-to-person transmission through healthy carriers; and 3. indirectly, through flies and contaminated water, food, utensils and other articles. PREDISPOSING CAUSES OF POLIOMYELITIS 1. Age. About 60% of patients are under 10 years of age. 2. Sex. Males are more prone to the disease than females, with a ratio of 3:2. Deaths rate is proportionately higher in males. 3. Heredity. Poliomyelitis is not hereditary. 4. Environment and hygiene condition. The rich are more often spared than the poor. Excessive work, strain and marked overexertion are also factors causing the disease. TYPES OF POLIOMYELITIS 1. The abortive a. does not invade the central nervous system b. headache and sore throat c. slight or moderate fever d. occasional vomiting e. low lumbar pain f. The patient usually recovers within 72 hours. g. accounts for about 4 to 8% 2. Non-paralytic a. All the signs of the abortive type are observed. b. types and spasm of the muscles of the hamstring c. changes in deep and superficial reflexes d. pain in the neck, back, arms, legs and abdomen e. inability to place the head in between the knees f. positive Pandys test g. transient paresis occur h. usually lasts for about a week, with meningeal irritation persisting for about 2 weeks. 3. Paralytic a. The signs and symptoms listed under the abortive and nonparalytic types are observed are present. b. positive (+) Hoynes sign c. paralysis occurs d. less tendon reflexes e. positive (+) Kernig and Brudzinski tests f. weakness of the muscles g. hypersensitivity to touch h. there usually is urine retention, constipation and abdominal distension. Spinal paralytic Paralysis occurs in muscles innervated by the motor neurons of the spinal cord. 50

It is characterized by asymmetry and scattered flaccid paralysis on one or both lower extremities. There is automatic involvement manifested by excessive sweating. Bulbar This type of paralysis develops rapidly and is more serious. Motor neurons in the brainstem are attacked, affecting the medulla. This weakens the muscles supplied by the cranial nerves, especially th 9th (glossopharyngeal) and the 10th (vagus). Facial, pharyngeal and ocular muscles are paralyzed. There are cardiac irregularities and respiratory failure. There is hypothalamic dysfunction, as manifested by impaired temperature regulation. Encephalitic manifestations, such as facial weakness, dysphagia, difficulty in chewing, inability to swallow or expel saliva, regurgitation of food through the nasal passages and dyspnea, are observed in about 30% of patients. Bulbospinal There is an involvement of the neurons both in the brainstem and the spinal cord.

PATHOLOGY 1. The organism usually enters the body through the alimentary tract and multiples in the oropharyngeal and lower intestinal tract. 2. The organism spread to the regional lymph nodes and the blood.


3. In the spinal type, there is evidence of gross inflammation in the anterior horns of the gray matter in the cord that often extends into the arachnoid of the nerve roots. 4. In the cerebral type, the lesions are indistinguishable from other brain inflammations, although there seems to be predilection for the medulla and basal ganglia. 5. There seem to be subsequent congestion, edema and necrosis in the area. 6. The lesions are found mainly in the anterior horn cells at the following sites: a. spinal cord b. the vestibular nuclei of the medulla and the cranial nerves c. the roof and dermis of the cerebellum d. gray matter of the midbrain e. the motor cortex COMPLICATIONS 1. 2. 3. 4. 5. Respiratory failure Circulatory collapse Electrolyte imbalance Bacterial infection Urinary problems related to retention or paralysis of the urinary bladder 6. Abdominal distention DIAGNOSTIC PROCEDURES 1. Isolation of the virus from throat washings or swab early in the disease 2. Stool culture throughout the course of the disease 3. Culture from the cerebrospinal fluid (CSF) MODALITIEES OF TREATMENT 1. Analgesics are helpful in easing headaches, back pain, and leg spasms. Morphine is contraindicated because of the danger of additional respiratory suppression. 2. Moist heat application may reduce muscle spasm and pain. 3. Bed rest necessary. 4. Paralytic polio requires rehabilitation using physical therapy, braces, corrective shoes and, in some cases, orthopedic surgery. NURSING MANAGEMENT 1. Carry enteric isolation 2. Observe the patient closely for signs of paralysis and other neurologic damage. 3. Perform neurologic assessment at least once a day, but dont demand any vigorous muscular activity. 4. Check blood pressure regularly, especially in bulbar poliomyelitis.


5. Watch for signs of fecal impaction due to dehydration and immobility. To prevent this, give sufficient fluid to ensure adequate daily output. 6. Prevent the occurrence of pressure sores. Provide good skin care. Reposition the patient frequently and keep the bed dry. 7. To prevent the spread of the disease, wash hands after every contact with the patient. 8. Apply hot packs on the affected limb to relieve pain and muscle shortening. 9. Provide emotional support both to the patient and his/her family. 10.Maintain good personal hygiene, particularly oral care and skin care. PREVENTION AND CONTROL 1. 2. 3. 4. 5. Immunization: oral polio vaccine (OPV) Proper disposal of GIT secretions Isolation Implementation of standard precaution Sanitation of the premises and proper food handling should be strictly observed to avoid contamination by flies.

(Hydrophobia/Lyssa) Rabies is a specific, acute viral infection communicated to man by the saliva of an infected animal. ETIOLOGIC AGENT Rhabdovirus 1. It is a bullet-shaped filtrated virus with a strong affinity for the CNS. 2. The organism is sensitive to sunlight, ultraviolet light, ether, formalin, mercury and nitric acid. It is resistant to phenol, merthiolate and common antibacterial agents. INCUBATION PERIOD 1. One week to seven and-a-half months in dogs 2. Ten days fifteen years in human 3. Incubation period depends on the following factors: a. distance of the bite to the brain b. extensive of the bite c. species of the animal d. richness of the nerve supply in the area of the bite e. resistance of the host



PERIOD OF COMMUNICABILITY The patient is communicable from three to five days before the onset of symptoms until the entire course if illness. MODE OF TRANSMISSION An infected animal carries the rabies virus in its saliva and transmits it to humans by biting. In some cases, the virus spreads when the saliva comes in contact with the persons mucus membranes, such as those of the mouth and eyelids, or broken skin, like in cuts, scratches or open wounds. PATHOGENESIS 1. From the site of the bite, the organism proceeds to the CNS through the exoplasm of the peripheral nerves. 2. Experimental studies have shown that the virus stays for some time in the inoculation site and that the multiplication of the virus occurs in the myocytes. 3. It has been observed that the period between inoculation and nerve invasion is the only time when prophylactic vaccine is effective. 4. Once the virus infects the individual, the spread is both centripetal and centrifugal. 5. After infection of the CNS, the virus spreads through the peripheral nerves to the salivary glands and other organs, such as the lungs, adrenals, kidneys, bladder.

PATHOLOGY 1. The rabies virus causes widespread changes throughout the CNS. 2. Histologic findings include neural necrosis and mononuclear cellular infiltration, especially in the thalamus, hypothalamus, pons and medulla. 3. The cranial nerve nuclei are extensively damaged. 4. Neural changes are present in the spinal cord, especially in the posterior horn. 5. Negri bodies are most abundant in the hypocampus, basal ganglia, pons and medulla and are found in the degenerating neurons of the salivary glands (pathologic sign rabies).


Negri bodies

CLINICAL MANIFESTATION 1. Prodromal/Invasion phase a. The phase is characterized by fever, anorexia, malaise, sore throat, copious salivation,, lacrimation, perspiration, irritability, hyper excitability, apprehensiveness, restlessness, (drowsiness) sometimes, mental depression, melancholia and marked insomnia. b. There is pain at the original site of the bite. Headache and nausea may be present. c. The patient becomes sensitive to light, sound and temperature. d. There are pain and aches in different parts of the body. e. Anesthesia, numbness, and tingling, burning and cold sensation may be felt along the peripheral nerves involved and the site of the bite. f. Mild difficulty in swallowing. 2. Excitement or neurologic phase a. This phase is characterized by marked excitation and apprehension. Terror may even occur. b. This is delirium associated with nuchal rigidity, involuntary twitching or generalized convulsions c. The patient may exhibit maniacal behavior; eyes are fixed and glossy and the skin is cold and clammy. d. There are severe and painful spasm of the muscles of the mouth, pharynx and larynx on attempt to swallow water or food even at the mere sight of them. e. There is aerophobia or intense fear or dislike of air. f. There is profuse drooling. g. There are tonic or clonic contractions of the muscles. h. Death may occur during the episode of spasm or from cardiac/respiratory failure. i. If patient survives this phase, he/she deteriorates rapidly and enters the terminal phase. 3. Terminal/paralytic phase a. The patient becomes quiet and unconscious. b. There is loss of bowel and urinary control. 55

c. Spasms cease and there is progressive paralysis. d. There is tachycardia and labored irregular respiration. e. Death occurs due to respiratory paralysis, circulatory collapse or heart failure.

DIAGNOSTIC PROCEDURES 1. Virus isolation from the patients saliva or throat 2. Fluorescent rabies antibody (FRA) provides the most definitive diagnosis 3. Presence of Negri bodies in the dogs brain. MODALITIES OF TREATMENT 1. Thoroughly wash the wounds from bite and scratches with soap and running water for at least 3 minutes. 2. Check the patients immunization status. Give tetanus toxoid if needed. 3. Give antiserum infiltrated around the wound or intramuscularly after a negative skin test. 4. Give anti-rabies vaccines, both passive and active, depending on the site and size of the bite, as well as the health condition of the biting animal. NURSING MANAGEMENT 1. Isolate the patient. 2. Give emotional and spiritual support. 3. Provide optimum comfort and prevent injury, especially during hyperactive episodes. 4. Darken the room and provide a quiet environment. 5. The patient should not be bathed and there should be any running water in the room or within the hearing distance of the patient. 6. If IV has to be given, it should be wrapped. The needles should be securely anchored to the vein to avoid dislodging in times of restlessness. 7. Concurrent and terminal disinfection should be carried out.


PREVENTION AND CONTROL The eradication of rabies should be done on a global scale and should include measures to prevent and control the disease in animals. The primary preventive measure in rabies is the interruption of the mode of transmission. Specific steps include: vaccinations of all dogs; enforcement of regulations for the pick-up and destruction of stray dogs; ten-to-fourteen-day confinement of any dog that has bitten a person; availability of laboratory facilities for observation and diagnosis; and providing public education, especially to children, on the avoidance and reporting of all animals that appear sick.

(Meningococcal septicemia; Meningococcal blood poisoning; Meningococcal bacteremia) Meningococcemia is an acute and potentially life-threatening infection of the bloodstream. CAUSES, INCIDENCE, AND RISK FACTORS Meningococcemia is caused by bacteria called Neisseria meningitidis. The bacteria frequently live in a person's upper respiratory tract without causing visible signs of illness. The bacteria can be spread from person to person through respiratory droplets -- for example, you may become infected if you are around someone with the condition when they sneeze or cough. Family members and those closely exposed to someone with the condition are at increased risk. The infection occurs more frequently in winter and early spring.


SYMPTOMS There may be few symptoms at first. Some may include: Fever Headache Irritability Muscle pain Nausea Rash with red or purple spots (petechiae)

Later symptoms may include: Changing level of consciousness Large areas of bleeding under the skin (purpura) Shock

SIGNS AND TESTS Blood tests will be done to rule out other infections and help confirm meningococcemia. Such tests may include: Blood culture Complete blood count with differential Clotting studies (PT, PTT)

Other tests that may be done include: Lumbar puncture to get a sample of spinal fluid for CSF culture Skin biopsy and Gram stain Urinalysis


TREATMENT Meningococcemia is a medical emergency. Persons with this type of infection are often admitted to the intensive care unit of the hospital, where they are closely monitored. The person may be placed in respiratory isolation for the first 24 hours to help prevent the spread of the infection to others. Treatments may include: 1. Antibiotics given through a vein (IV), given immediately 2. Breathing support 3. Clotting factors or platelet replacement -- if bleeding disorders develop 4. Fluids through a vein (IV) 5. Medications to treat low blood pressure 6. Wound care for areas of skin with blood clots

COMPLICATIONS Arthritis Disseminated intravascular coagulopathy (DIC) Gangrene due to lack of blood supply Inflammation of blood vessels in the skin (cutaneous vasculitis) Myocarditis Pericarditis Shock Severe damage to adrenal glands that can lead to low blood pressure (Waterhouse-Friderichsen syndrome)

PREVENTION Preventive antibiotics for family members and contacts are often recommended. Speak with your health care provider about this option. A vaccine that covers some -- but not all -- strains of meningococcus is recommended for children age 11 or 12. A booster is given at age 16. Unvaccinated college students who live in dormitories should also consider receiving this vaccine. It should be given a few weeks before they first move into the dorm. Talk to your doctor about the appropriate use of this vaccine.


(Transmissible spongiform encephalopathy)

Creutzfeldt-Jakob disease

Creutzfeldt-Jakob disease (CJD) is a neurodegenerative disease that affects the brain. The progressive loss of mental capacity and impaired ability to perform a motor activity resulting in the death of the subject within six months. The disease was first described in 1920. Related forms of the disease were observed in subjects with fatal familial insomnia and customs of practicing cannibalism. The sporadic form of the disease (sCJD) is mainly transmitted to humans through brain transplants and corneas. The new form of the disease was discovered in 1996. This is a variant of the disease triggered by prions (infectious protein particles), which are absorbed through consumption of infected food. Young subjects may also be affected.

CAUSES, INCIDENCE, AND RISK FACTOR CJD is thought to be caused by a protein called a prion. A prion causes normal proteins to fold abnormally. This affects the other proteins' ability to function. There are several types of CJD. The disorder is very rare, occurring in about 1 out of 1 million people. It usually first appears between ages 20 and 70. Symptoms usually start in the late 50s. CJD can be grouped into two types: classic or new variant disease. The classic types of CJD are: Sporadic CJD makes up most cases. It occurs for no known reason. The average age at which it starts is 65. Familial CJD occurs when a person inherits the abnormal prion from a parent (inherited CJD is rare)

Classic CJD is not related to mad cow disease (bovine spongiform encephalitis). However, variant CJD (vCJD) is a form of the disease that is related to mad cow disease. The infection that causes the disease in cows is believed to be the same one that causes vCJD in humans. Variant CJD accounts for less than 1% of cases, and it tends to affect younger people. However, fewer than 200 people worldwide have had this disease.


Variant CJD can be caused by exposure to contaminated products. Other vCJD cases have occurred when people were given corneal transplants, other tissues, or blood transfusions from infected donors. It may also have been caused by contaminated electrodes used in brain surgery (before instruments started to be properly disinfected). CJD may be related to several other diseases caused by prions, including: Chronic wasting disease (found in deer) Kuru (seen in New Guinea women who ate the brains of dead relatives as part of a funeral ritual) Scrapie (found in sheep) Other rare human diseases, such as Gerstmann-StrausslerScheinker disease and fatal familial insomnia

SYMPTOMS Blurred vision (sometimes) Changes in gait (walking) Confusion, disorientation Dementia that occurs over a few weeks or months Hallucinations Lack of coordination (for example, stumbling and falling) Muscle stiffness Muscle twitching 61

Myoclonic jerks or seizures Nervous, jumpy feelings Personality changes Sleepiness Speech impairment

CJD is rarely confused with other types of dementia (such as Alzheimer's disease) because in CJD, the symptoms get worse much more quickly. Both forms of CJD are different than dementia because the symptoms progress quickly to disability and death.

SIGNS AND TESTS Early in the disease, a nervous system and mental examination will show memory problems and changes in other mental functions. Later in the disease, a motor system examination may show: 1. Abnormal reflexes or increased normal reflex responses 2. Increase in muscle tone 3. Muscle twitching and spasms 4. Strong startle response 5. Weakness and loss of muscle tissue (muscle wasting) There is loss of coordination and changes in the cerebellum, the area of the brain that controls coordination (cerebellar ataxia). An eye examination shows areas of blindness that the person may not notice. Tests used to diagnose this condition may include: Blood tests to rule out other forms of dementia and to look for markers that sometimes occur with the disease CT scan of the brain Electroencephalogram (EEG) MRI of the brain Spinal tap to test for a protein called 14-3-3

The disease can only be confirmed with a brain biopsy or autopsy. TREATMENT There is no known cure for this condition. Interleukins and other medications may help slow the disease. The person may need care early in the disease. Medications may be needed to control aggressive behaviors. Providing a safe environment, controlling aggressive or agitated behavior, and meeting the person's needs may require monitoring and assistance in the home or in a care facility. Family counseling may help the family cope with the changes needed for home care. Visiting nurses or aides, volunteer services, homemakers, adult protective services, and other community resources may help care for the person with CJD. People with this condition may need help controlling unacceptable or dangerous behaviors. This involves rewarding positive behaviors


and ignoring negative behaviors (when it is safe). They may also need help getting oriented to their surroundings. Getting legal help with advance directives, powers of attorney, and other legal actions early in the disorder can make it easier to make ethical decisions about the CJD patient's care.

PROGNOSIS The outcome of CJD is usually very poor. Within 6 months or less after symptoms begin, the person will be unable to care for himself or herself. The disorder is fatal in a short time, usually within 8 months. However, a few people survive for as long as 1 or 2 years. The cause of death is usually infection, heart failure, or respiratory failure.

COMPLICATION 1. Infection 2. Loss of ability to interact with others 3. Loss of ability to function or care for oneself 4. Death PREVENTION Medical equipment should be treated to remove the proteins that may cause the disease. People who have a history of CJD should not donate a cornea or tissue. Most countries now have strict guidelines for managing infected cows to avoid transmitting CJD to humans.

(Lockjaw) Tetanus is an infectious disease caused by Clostridium tetani, which produces a potent exotoxin with prominent systemic neuromascular effects such as generalized spasmodic contractions of the skeletal musculator. Tetanus is fatal in up to 60% of unimmunized person, with death occurring usually within 10 days of onset. When symptoms develop within three days, the prognosis is poor. INCUBATION PERIOD The incubation period is 3 days to 3 weeks in adults and 3 to 30 days in newborn (tetanus neonatorum)


ETIOLOGIC AGENT The causative organism of the disease is CI.tetani with the following characteristics: 1. Anerobic, Gram (+), with a tound terminal spore and a slender body, giving it a drumstick appearance. 2. The organism comes in two forms, spore-forming and vegetative. 3. The organism releases two types of toxin: a. tetanospasmin, which is responsible for muscle spasms; and b. tetanolysin, which is responsible for the destruction of RBCs SOURCE OF INFECTION 1. Animal and human feces ( The organisms are found in the intestinal wall of herbivorous animals, including man.) 2. Soil and dust 3. Plaster of Paris; unsterile sutures, pins, and scissors; and rusty materials MODE OF TRANSMISION Normally, the mode of transmission is through punctured wounds contaminated by dust, soil, or animal excreta containing CI.tetani. 1. Rugged, traumatic wounds and burns; 2. The umbilical stump of the newborn, especially if delivered at home and thus have faulty cord dressings; 3. Babies delivered to mothers without tetanus toxoid immunization; 4. Unrecognized wounds (cleaning of the ears with sharp materials) 5. Dental extraction. Circumcision and ear piercings.


PATHOGENESIS 1. When CI. tetani enters the body, it causes local infection and extensive tissue destruction. 2. Local multiplication of microorganism occurs more frequently when the wound has healed. While reproducing, CI. Tetani also release toxins that are absorbed by the bloodstream and lymphatics or directly by the peripheral motor nerves. These eventually spread into the central nervous system. 3. The toxins ( tetanospasmin) has a high affinity for central nervous system tissues and spinal motor ganglia. It induces hyper-excitability of the motor neurons by interfering with release of an inhibitory transmitter. 4. Other tissues exhibits effects of toxic degeneration, inanition and nonspecific complications.

CLINICAL MANIFESTATIONS 1. Neonate a. Newborn infants have feeding and sucking difficulties b. The infant may cry excessively; most of the time, however, the cry is short, mild and voiceless. c. An attempt to suck results in spasm and cyanosis. d. There is fever due to infection and dehydration. e. The jaw becomes so stiff that the baby cannot suck or swallow. f. Tonic or rigid muscular contractions, spasm or convulsions are provided by stimuli. g. Cyanosis and pallor develop. h. Severe cases may end flaccidity, exhaustion and family, death.

2. Older children and adult a. If tetanus remains localized, signs of onset are spasm and increased muscle tone near the wound. b. If it becomes systemic or generalized, signs include: 65

Grinning expression(risus sardonicus) considered pathognomonic of the disease Board-like abdomen/abdominal rigidity Opisthotonos Intermittent tonic convulsions lasting for several minutes which may result in cyanosis and sudden death due to asphyxiation In severe cases, laryngospasm is followed by the accumulation of secretions in the lower airways, resulting in respiratory distress due to the involvement of respiratory muscles. Fracture of the vertebrae may occur during severe spasm, yielding to coma and death. c. In mild cases, after a period of weeks, spasm gradually diminish in frequency and severity, with trimus being the last symptom to disappear. d. In fatal cases, death usually occurs during the first 10 days of the disease.

Hyper-tonicity, hyperactive deep tendon reflex, tachycardia, profuse sweating, low-grade fever and painful involuntary muscle contractions Neck and facial muscle rigidity( trismus)

COMPLICATIONS 1. Results of laryngospasm and involvement of the respiratory muscles: a. Hypostatic pneumonia b. Hypoxia due to laryngospasm and decreased oxygen c. Atelectasis and pneumothorax d. Traumatic glossitis and microglossia 2. Changes related to sympathetic nervous system: a. Transitory hallucinosis b. Hyper-salivation, diaphoresis, and unusual tachycardia, especially with the use of aerosolized bronchodilators. c. Cardiac standstill and bradycardia (high mortality) 3. Due to trauma 66

a. Laceration of the tongue and buccal mucosa b. Intramuscular hematoma c. Fracture of the spine and ribs 4. Septicemia MODALITIES OF TREATMENT 1. Specific a. Within 72 hours after a puncture wound, the patient should receive ATS, TAT or TIG, especially if the patient does not have any previous immunization. b. Tetanus toxoid, .5cc IM, given on standard schedule c. Pen G Na, to control infection d. Muscle relaxant to decrease rigidity and spasm 2. Non-specific a. Oxygen inhalation b. NGT feeding c. Tracheostomy d. Adequate fluid, electrolyte, and caloric intake e. Good nursing care: Maintain an adequate airway. Provide cardiac monitoring. Maintain an IV line for medication and emergency care if necessary. Carry out efficient wound care. Avoid stimulation; warn visitors not to upset or overly stimulate the patient. Prevent contractures and pressure sores. Watch out for urinary retention. Closely monitor vital signs and muscle tone. Provided optimum comfort measures. PROGNOSIS The highest fatality rates occur at the extremes of life (very young and very old) Local tetanus usually offers favorable prognosis, except in the dysphagia form of cephalic tetanus. Absence of convulsions favors the prognosis, especially in patients 20 years old and below. Apnea occurs after a prolonged spasm and is a critical factor in sudden death. Acute respiratory obstruction and over sedation may lead to early death. Response to anticonvulsant therapy is relevant to the prognosis. PREVENTION AND CONTROL 1. Active immunization with tetanus toxoid for adults and pregnant women (in the later, to prevent the occurrence of tetanus neonatorum) 2. DPT for babies and children


TETANUS NEONATORUM Tetanus affecting newborns, usually due to infection of the severed umbilical cord. 1. Feeding and sucking difficulty a. Sucking results in spasm and cyanosis b. Jaw becomes stiff, baby cannot suck or swallow properly 2. Excessive and voiceless crying 3. Muscle spasm or convulsions provoked by stimuli a. flaccidity, exhaustion, death Among older children and adults: 1. Increase muscle tone and spasm near the wound 2. Hyperactive DTR, tachycardia, profuse sweating, fever, painful involuntary contractions 3. Full blown rigidity of muscles Both extensor &flexor groups are affected Usually lasts 5 to 10 seconds Precipitated by the slightest stimuli such as bright lights,noise or movement of the patient Trismus first symptom to appear & last symptom to disappear Neck and jaw muscle rigidity Difficulty in opening the mouth Risus Sardonicus/ Sardonic grin Facial muscle spasm Grinning expression (grimace) Opisthotonus position Back muscle rigidity Arching of the trunk Board like abdomen/ abdominal rigidity Convulsions Cyanosis Asphyxiation/saphocation Laryngospasm Respiratory distress Vertebral fracture Causes of death usually during the first 10 days of the disease


COMPLICATIONS 1. Resulting from laryngospam and involvement of the muscles of respiration a. Pneumonia- respiration obstruction from secretions b. Hypoxia c. Atelectasis d. Pneumothorax 2. Due to trauma a. Laceration of the tongue b. Intramuscular hematomas c. Fractures of the spine & ribs may occur rarely 3.septicemia

TREATMENT 1. 2. 3. 4. 5. 6. 7. Anti tetanus serum/ ATS Tetanus Immune Globulin /TIG Tetanus toxoid Penicillin is the drug of choice Muscle relaxant (diazepam, phenobarbital Wound debridment If the patient is admitted : Oxygen NGT/ proper nutrition Tracheostomy

NURSING MANAGEMENT 1. 2. 3. 4. 5. Maintain adequate airway Cardiac monitoring Maintain IV line Wound care Avoid stimulation

PREVENTION AND CONTROL 1. Avoid contamination by the organism Aseptic handling of the neonatal umbilical stump and other wounds Tetanus toxoid to pregnant women during the last semester 2. Prevent multiplication and pthogenecity of the microorganism Tetanus toxoid among women of child bearing age and pregnant omen DPT among pedia Anti-tetanus serum Tetanus Immune Globulin Antibiotics (penicillin, erythromycin, tetracycline)



(Amoebic Dysentery) Amoebiasis protozoal infections of human begins initially involves the colon, but may spread to soft tissues, most commonly the liver and lungs, by contiguity or hematogenous or lympathic dissemination. ETIOLOGIC AGENT Entamoeba histolytica Prevalent in unsanitary areas Cammon in awrm climates Acquired by swallowing Cyst survives a few days outside of the body Cyst passes to the large intestine and hatches into a trophozite. It passes into the mesenteric veins, the portal vein, and finally to the liver, where it causes amoebic liver abscess.

Entamoeba histolytica has two developmental stages: 1. Trophozite/vegetative form Trophozite are facultative parasites that may invade the tissues or may be found in parasitized tissues and liquid colonic contents. 2. Cyst a. The cyst is passed out with formed or semi-formed stools and resistant to environmental conditions. b. The cyst is considered as the infected stage in the life cycle of E. histolytica PATHOLOGY When the cyst is swallowed, it passes through the stomach unharmed and shows no activity while in an acidic environment. When it reaches the alkaline medium of the intestine, the metacyst begins to move within the cyst wall, which rapidly weakens and tears. The quadrinucleate amoeba emerges and divides into amebulas that are swept down into the cecum. This is the first opportunity of the organism to colonize, and its success depends on one more metacystic tropozoites making contact with the mucosa. The mature cyst in the large intestines leaves the host in great numbers ( the host remains asymptomatic). The cyst can remain viable and infective in a moist and cool environment for about 12 days and in water for 30 days. The cyst are resistant to levels of chlorine normally used for water purification. They are rapidly killed by


prutrefaction, desiccation, and temperatures below 5 and above 40 degrees centigrade. SOURCE Human excreta INCUBATION PERIOD The incubation period in severe infection is three days. In sub-acute and chronic form it lasts for several months. In average cases the incubation period varies from 3 to 4 weeks. PERIOD OF COMMUNICABILITY The microorganism is communicable for the entire duration of the illness. MODE OF TRANSMISSION 1. The disease can be passed from one person to another through fecal-oral transmission. 2. The disease can be transmitted through direct contact, through sexual contact by orogenital, oroanal, and proctogenital sexual activity. 3. Through indirect contact, the disease can infect humans by ingestion of food especially uncooked leafy vegetables or foods contaminated with fecal material containing E. histolytica cysts. Food or drinks may be contaminated by cyst through pollution of water supply, exposure to flies, use of night soil for fertilizing vegetables, and through un-hygiene practices of food handlers. PATHOGENESIS 1. The metacyst trophozite or their progenies reach the cecum and those that come in contract with mucosa penetrate or invade the epithelium by lytic. 2. The trophozites burrow deeper, with tendency to spread laterally or continues the lysis of cells until they reach the submucosa, forming flask-shape ulcers. There may be several points of penetrations. 3. From the primary site of invasion, secondary lesions may be produced at the lower level of the large intestine. 4. Progenies of the original colony are squeeze out to the lower portion of the bowel and thus have the opportunity to invade and produce additional ulcers. Eventually, the whole colon maybe involved, 5. E. histolytica has been demonstrated in practically every soft organ of the body. 6. Trophozites which reach the muscularis mucosa frequently erode the lymphatics or walls of the mesenteric venules on the floor of the ulcers and are carried to the intrahepatic portal vein. 7. If thrombi occur in the small branches of the portal veins, the tophozites in thrombi cause lytic necrosis on the walls of the vessels and digest a pathway into the lobules. 8. The colony increases in size and develops into an abscess. A typical liver abscess develops and consist of: a. A central zone necrosis, b. A median zone of stoma only, and 71

c. An outer zone of normal tissue newly invaded by amoebae. Most amoebic abscess of the liver is in the right lobe. 9. Next to the liver, the organ which is the most frequent site extraintestinal amoebiasis is the lung. This commonly develops as an extension of the hepatic abscess.

CLINICAL MANIFESTATION 1. Acute amoebic dysentery a. Slight attack of diarrhea, altered with periods of constipation and often accompanied by tenesmus b. Diarrhea, watery, and foul-smelling stools often containing bloodstreaked mucus c. Colic and gaseous distension, of the lower abdomen d. Nausea, flatulence, abdominal distension, and tenderness in the right iliac region over the colon 2. Chronic amoebic dysentery a. Attack of dysentery thats last for several days, usually succeeded by constipation b. Tenesmus accompanied by the desire to defecate c. Anorexia, weight loss, and weakness d. The liver may be enlarged e. Stools at first are semifluid, but soon become watery, bloody, and mucoid. f. Vague abdominal distress, flatulence, constipation or irregularity of bowel movement g. Mild toxemia, constant fatigue, and lassitude h. The abdomen loses its elasticity when picked up between the fingers. i. On sigmoidoscopy, scattered ulceration, with yellowish and erythematous borders, is noted.


j. The gangrenous type (fatal) is characterized by the appearance of large sloughs of intestinal tissues in the stools, accompanied by hemorrhage. 3. Extraintestinal forms Hepatic a. Pain in the upper right quadrant with tenderness of the liver b. Jaundice c. Intermittent fever d. Loss of weight or anorexia e. Abscess may break through the lungs; patient coughs anchovysauce sputum

CLINICAL FEATUREES OF AMOEBIASIS 1. Onset is gradual. 2. Diarrhea increases and stools becomes bloody and mucoid. 3. In untreated cases: Fluid stool severe bloody-mucoid stool Hemorrhage intestinal perforation Peritonitis DEATH DIAGNOSTIC EXAMS 1. Stool exams (cyst; white and yellow pus with plenty of amoeba) 2. Blood exam (leukocytosis) 3. Protoscopy/sigmoidoscopy TREATMENT MODALITIES 1. 2. 3. 4. 5. Metronidazole (flagyl) 800 mg TID x 5days Tetracycline 250 mg every 6 hours Ampicillin ,quinolone, sulfadiazine Streptomycin SO4, chloramphenicol Lost fluids and electrolytes should be replaced.

NURSING MANAGEMENT 1. Observe isolation and enteric precaution. 2. Provide health education and instruct patient to: a. boil water for drinking or use purified water; b. avoid washing food with water from open drums or pails; c. cover leftover food; d. wash hands after defecation and before eating; and 73



5. 6.


e. avoid eating ground vegetables (lettuce, carrots and the like). Proper collection of stool specimen: Never give paraffin or any oil preparation for att least 48 hours prior to the collection of specimen. Instruct the patient to avoid mixing urine with stools. If whole stools cannot be sent to the laboratory, select as large portions containing blood and mucus as possible. Send the specimen immediately to the laboratory; stools that are not fresh are nearly useless for examination. Label the specimen properly. Skin care Cleanliness and freedom from wrinkles on the sheet will be helful with all the usual precautionary measure against pressure sores. Mouth care Provide optimum comfort The patient should be kept warm. Dysenteric patient should never be allowed to feel cold, even for a moment. Diet During the acute stage, fluids should be forced. In the beginning of an attack, cereals and strained meat broths without fat should be given. Chicken and fish may be added when convalescence is established. A bland diet without cellulose or bulk-producing foods should be maintained for a long time.

METHODS OF PREVENTION 1. 2. 3. 4. Health education Sanitary disposal of feces Protect, chlorinate, and purify drinking water Observe scrupulous cleanliness in food preparation and food handling 5. Detection and treatment of carriers 6. Fly control (they can serve as vectors)

(Roundworm infection) Ascariasis is an infection caused by a parasitic roundworm, Ascaris lumbricoides. ETILOGIC AGENT Ascaris lumbaricoides 1. They are elongated, cylindrical worms that are tapered at the oral portion and pointed at the anal end. 2. They appear creamy and pinkish yellow when fresh. 3. They can grow as thick as a pencil and live for 1 -2 years. 74


4. A female worm can produce up to 240,00 eggs per day, which are then discharged into the feces and incubated in the soil for weeks.

MODE OF TRANSMISSION 1. Acaris lumbricoides is transmitted through contaminated fingers put into the mouth. 2. Ingestion of food and drinks contaminated with embryonated eggs can transmit ascariasis. EPIDEMIOLOGY 1. Ascariasis occurs worldwide but is most common in tropical regions, especially in poorly sanitized areas and in farms where might soil is used as fertilizer. 2. It is known to have an infection rate of 70-90% in poor areas of the Philippines and it mostly affects children who are 4 to 12 years old. a. It is still considered as the most prevalent form of paratism in the Philippines. b. Children with nutritional status show a high incidence of positive ascaris in stool examinations. They get infected more easily because they usually put things into their mouth and children also have poorer hygiene than adults.


PATHOGENESIS Infection may start with ingestion of contaminated water or with eating raw vegetables, especially if night soil is used as fertilizer. After ingestion, Ascaris lumbricoides hatches and releases larvae, which penetrate the intestinal wall and reach the lungs through the bloodstream. After ten days in the pulmonary capillaries and alveoli, the larvae migrate to the bronchioles, the bronchi, trachea and epiglottis. They are then swallowed and returned to the intestine where they mature and mate.

DIAGNOSTIC TESTS 1. Stool for ova demonstration of fertilized or unfertilized eggs in the stools (Kato-Katz technique) 2. Abdominal x-ray densed shadow of adult ascaris which looks like strands of spaghetti ( dot sign) 3. Routine blood counts - significant eosinophilia


TREATMENT 1. Albendazole or mebendazole 15 cc as a single dose 2. Piperazine citrate 75mg/kg twice daily, orally 3. Pyrantel pamoate 1mg/kg as a single dose, orally

Infection with ascaris is not an emergency. Therefore, if a pregnant woman gets infected with ascaris, treatment is postponed until after deliver COMPLICATIONS 1. 2. 3. 4. Biliary tract obstruction; patient develops cholestatic jaundice Hepatic abscess and cholangitis Intestinal obstruction, perforation ,peritonitis Malnutrition due to damage of the intestinal mucosa, which impairs the absorption of nutrients

NURSING INTERVENTIONS 1. Isolation is not needed. 2. Preventive measures in each home and in the community should be enforced. 3. All members of the family must be taught on sanitary practices such as washing of hands before handling food, washing of all fruits and vegetables that are eaten raw, and effective sewage disposal. 4. Availability of toilet facilities must be ensured. 77

5. Importance of personal hygiene should be explained. 6. Proper disposal of diapers should be emphasized to mothers. PREVENTION 1. 2. 3. 4. Improved sanitation and hygienic practices Improved nutrition Deworming may be advised When travelling to areas where sanitation and hygiene are poor, avoid water or food that may be contaminated.

(Shigellaosis/Bloody Flux) Bacillary dysentery is an acute bacterial infection of the intestines characterized by diarrhea and fever is associated with the passing out of bloody-mucoid stools accompanied by tenesmus. ETIOLOGIC AGENT The causative agent is a bacterium of the shigella group, a short, non-motile, Gram-negative organism. There are four serologic groups: 1. 2. 3. 4. Shigella flexneri (Grioup B) common in the Philippines Shigella boydii Shigella connei Shigella dysenteriae a. Considered as the most infectious b. Their habitats its exclusively the GIT of man c. Like other Gram-negative bacilli, they develop resistance against antibiotics d. They rarely invade the blood stream


INCUBATION PERIOD The incubation period is seven hours to seven days, with an average of three to five days. PERIOD OF COMMUNICABILITY The patient is capable of transmitting the microorganism during the acute infection until the feces are negative of the organism. Some patients remain carriers for a year or two. MODE OF TRANSMISSION 1. The organism is transmitted through ingestion of contaminated food or water or milk. 2. It may be transmitted by flies or through other objects contaminated by the feces of the patient. 3. Fecal-oral transmission n is possible. PATHOGENESIS/PATHOLOGY 1. After the incubation period, the organism invades the intestinal mucosa and causes inflammation. 2. Dirty green, fibrinous sloughing areas or ulcers are formed. 3. Within a few days, the stools may contain pus, mucus, and blood.

CLINICAL MANIFESTATIONS 1. Fever, especially in children 2. Tenesmus, nausea, vomiting, and headache


3. Colicky or cramping abdominal pain associated with anorexia and body weakness 4. Diarrhea with bloody-mucoid stools that are watery at first 5. Rapid dehydration and loss of weight COMPLICATIONS 1. Rectal prolapse, particularly in undernourished children 2. Respiratory complications, such as cough and pneumonia 3. Non-supportive arthritis and peripheral neurophaty DIAGNOSTIC PROCEDURE 1. 2. 3. 4. 5. Fecalysis or microscopic examination of stools Isolation of the causative organism from rectal swab or culture Peripheral blood examination Blood culture Sheets of polymorphoneuclear leukocytes seen in staining with methylene blue

MODALITIES OF TREAMENT 1. Antibiotics are of question in the treatment of shigellosis; however, ampicillin, tetracycline, and contramoxazole may be useful in severe cases. 2. IV might be infused with normal saline (with electrolytes)to prevent dehydration. 3. Low-residua diet is recommended 4. Anti- diarrheal drugs are contraindicated because they delay fecal excretion that can lead to prolonged fever. NURSING MANAGEMENT 1. Maintain fluid and electrolyte balance to prevent profound dehydration. 2. Keep the patient warm and comfortable. 3. Restrict food until nausea and vomiting subsides. 4. Isolation can be carried out through medical aseptic technique. 5. Personal hygiene must be maintained. 6. Excreta must be properly disposed. 7. Concurrent to normal activities must be gradual because relapse as a result of fatigue. METHODS OF PREVENTION AND CONTROL 1. Sanitary disposal of human feces 2. Sanitary supervision of processing, preparation, and serving of food, particularly those eaten raw 3. Adequate provision of safe washing facilities 4. Fly control and protecting against fly contamination 5. Isolation of patient during acute stage 6. Protection and purification of public water supply 7. Persons known to be infected should be excluded from handling food forpublic consumption


(El Tor) Cholera is an acute bacterial enteric disease of the GIT characterized by profuse diarrhea, vomiting, massive loss of fluid and electrolytes, which could result in hypovolemic shock, acidosis, and death.

ETIOLOGIC AGENT Vibrio cholera/ Vibrio coma 1. The organism is a slightly curved rod (comma-shaped), Gram-negative and motile with a polar flagellum. 2. The organism survives well at ordinary temperatures and multiplies well in temperatures ranging from 22-40 degrees centigrade. 3. They survive longer in refrigerated foods. 4. An enterotoxin, choleragen, is elaborated by the organism as it grows in the intestinal tract.

PATHOGNOMONIC SIGN Rice-water stools INCUBATION PERIOD The incubation period ranges from a few hours to five days, usually one to three days. PERIOD OF COMMUNICABILITY The organisms are communicable during the stool-positive stage, usually a few days after recovery; however, occasionally the carrier may have the organism for several months. MODE OF TRANSMMISION 1. Fecal transmission passes via the oral route from contaminated water, milk, and other foods. 2. The organisms are transmitted through the ingestion of food or water contaminated with the stools or vomitus of a patient. 3. Flies, soiled hands, and utensils also serve to transmit the infection.


PATHOGENESIS 1. Fluid loss is attributed to the enterotoxin elaborated by the organism as it lies in opposition with the lining cells of the intestines. 2. The toxin stimulates adenylate cyclase, which results in the conversion of adenosine triphosphate (ATP) to cyclic adesine monophosphate (cAMP). 3. The mucosal cells are stimulated to increase the secretion of chloride. The increased secretion is associated with water and bicarbonate loss. 4. The toxin acts upon the intact epithelium on the vasculature of the bowel, thus resulting in the outpouring of intestinal fluids. 5. Fluid loss of 5 to 10% of the body weight results in dehydration and metabolic acidosis. 6. If treatment is delayed or inadequate, acute renal failure and hypokalemia become secondary problems. PRINCIPAL PATHOGENIC EVENTS IN CHOLERA 1. 2. 3. 4. The passage of Vibrio cholera into the small intestines The multiplication of the bacteria in the small intestines The production of enterotoxin by the bacteria Secretion of isotonic fluid by the intestinal epithelium in response to the production of enterotoxin


CLINICAL MANIFESTATIONS 1. There is an acute, profuse, watery diarrhea with no tenesmus or intestinal cramping. 2. Initially, the stool is brown and contains fecal material, but soon becomes pale gray and rice water-like in appearance, with no inoffensive, slightly fishy odor. 3. Vomiting often occurs after diarrhea has been established. 4. Diarrhea causes fluid loss amounting to 1 to 30 liters per day, owing to subsequent dehydration and electrolyte loss. 5. Tissue turgor is poor and eyes are sunken into the orbits. 6. The skin is cold; the fingers and toes are wrinkled, assuming the characteristics washerwomans hand. 7. Radial pulses become imperceptible and blood pressure unobtainable. 8. Cyanosis is present. 9. The voice becomes hoarse and then is lost, such that the patient speaks in whispers (aphonia). 10.Breathing is rapid and deep. 11.Despite marked diminished peripheral circulation, consciousness is present. 12.The patient develops oliguria and sometimes even anuria. 13.Temperature could be normal at the onset of the disease but becomes subnormal in later stages, especially if the patient is in shock. 14.When the patient is in deep shock, the passage of diarrhea stops. 15.Death may come as rapidly as four hours after onset, but usually on the first or the second day if not properly treated.

PRINCIPAL DEFICITS 1. Extracellular volume in the loss of intestinal fluid that can lead to: a. Severe dehydration with the appearance of washerwomans hand, restlessness, and excessive thirst, and b. Circulatory collapse or shock.


2. Metabolic acidosis is due to the loss of large volume of bicarbonaterich stools, which result in rapid respiration with intervals of apnea (Kussmaul respiration). 3. Hypokalemia is due to a massive loss of potassium through the stools. Patient may manifest abdominal distention that could be attributed to paralytic ileus. 4. Renal failure occurs as a consequence of prolonged, untreated shock or unrelieved hypokalemia. 5. Convulsions and tetany are probably caused by loss of magnesium. 6. Hypoglycemia may occur in untreated children who have been in stupor for several days. 7. Corneal scarring can occur in a stuporous patient who has lost th ewink reflex. 8. Acute pulmonary edema may follow hydration in cases of uncorrected metabolic acidosis DIAGNOSTIC EXAMS 1. Rectal swab 2. Dark field or phase microscopy 3. Stool exam MODALITIES OF TREATMENT Treatment of cholera consists of correcting the basic abnormalities without delay-restoring the circulating blood volume and blood electrolytes to normal levels. 1. Intravenous treatment is achieved by rapid intravenous infusion of an alkaline saline solution containing sodium, potassium, chloride, and bicarbonate ions in proportions comparable to that in waterstools. 2. Oral therapy rehydration can be completed by the oral route (ORESOL, HYDDRITES) unless contraindicated or if the patient is not vomiting. 3. Maintenance of the volume of fluid and electrolytes lost after rehydration. This is done by careful intake and output measurement. 4. Antibiotics a. Tetracycline 500mmg every 6 hours might be administered to adults; 125mg/kg body weight for children every 6 hours for 72 hours. b. Furazolidone 100 mg for adults and 125mg/kg for children might be given every 6 hours for 72 hours. c. Chloramphenicol may also be given 500 mg for adults and 18 mg/kg for children every 6 hours for 72 hours. d. Cotrimoxazole may also be administered 8mg/kg for 72 hours. NURSING MANAGEMENT 1. Medical aseptic protective care must be provided. Hand washing is imperative before any food item is handled. 2. Enteric isolation must be observed. 3. Vital sign must be recorded accurately. 84

4. Intake and output must be accurately measured. 5. A thorough and careful personal hygiene must be provided. 6. Excreta must be properly disposed of. 7. Concurrent disinfection must be applied. 8. Food must be properly prepared. 9. Environment sanitation must be observed. 10.Weighing the patient provides additional data that there is no deficit in fluid input. 11.Appropriate diet is given according to the stage of recovery. PREVENTION 1. Food and water supply must be protected from fecal contamination. 2. Water should be boiled or chlorinated. 3. Milk should be pasteurized. 4. Sanitary disposal of human excreta is a must. 5. Sanitary supervision is important.

Hepatitis is defined as inflammation of the liver, and is classified as either viral or non-viral. I.HEPATITIS A (Infection hepatitis/Catarrhal jaundice) Hepatitis A is a liver disease caused by the hepatitis A virus. This is an inflammation of the liver that is not really very severe and runs an acute course. This generally starts within 2 weeks after contact with the virus, and lasts no longer than 2 months. It is known as infectious hepatitis because it spreads relatively easy to individuals who have close contact with the infected. INCUBATION PERIOD The incubation period for hepatitis A range from 15 to 60 days, or three to five weeks, with a mean incubation period of 30 days. PERIOD OF COMMUNICABILITY The infected patient is capable of transmitting the organism from a week before until a week after the appearance of symptoms. MODE OF TRANSMISSION The virus is transmitted through the fecal-oral pathway: 1. ingestion of contaminated drinking water rice, uncooked fruits and vegetables, and fruits and vegetables grown in or washed with contaminated water; and 2. contamination of food/drinks by infected food handlers.


GROUPS AT RISK FOR HAV 1. Children in day care centers can transmit the infection through diapers and toys. 2. Troops living in crowded conditions at military camps or in the field are at great risk. 3. Homosexual men are at an increased at risk of HAV infection from oral-anal sexual contact. 4. People who live in areas with a breakdown of sanitary conditions, such as after a flood or other natural disasters.

PATHOLOGY/PATHOGENESIS 1. Following ingestion, HAV enters bloodstream through the epithelium of the oropharynx or intestines.


2. The blood carries the virus to its target, the liver, where it lives and multiplies within the hepatocytes and Kupffer cells (i.e., liver macrophages). 3. Virions are secreted into the bile and released in stools. HAV is excreted in large quantities approximately 11 days prior to the appearance of symptoms or anti-HAV IgM antibodies in the blood. CLINICAL MANIFESTATIONS 1. 2. 3. 4. 5. 6. Flu-like illness with chills and high fever Diarrhea, fatigue and abdominal pain Loss of appetite Nausea, diarrhea and fever Jaundice and dark-colored urine The infection in young children is often mild and asymptomatic. 7. Hepatitis A does not have a chronic stage and does not cause permanent liver damage. 8. Flowing infection, the immune system makes antibodies against the hepatitis A virus that confer immunity against future infection. The disease can be prevented by hepatitis A vaccine.

COMPLICATIONS 1. Progressive encephalopathy characterized by drowsiness and cerebral edema 2. GIT bleeding progressing to stupor and later coma. Bleeding is not responsive to parenteral vitamin K administration. 3. Clonus and hyper-reflexia are later replaced by loss of deep tendon reflex. 4. Edema and ascites 5. Aplastic anemia 6. In the late course of the disease, loss of corneal and papillary reflexes, elevated arterial blood, respiratory failure, and cerebrovascular collapse may be present. DIAGNOSTIC PROCEDURES 1. HAV and HIV complement fixation rate 2. Liver function test - to determine the presence and extent of liver damage and check the progress of the liver 3. Bile examination of stool and urine samples 4. SGOT serum glutamic oxaloacetic transaminase SGPT serum glutamic pyruvic transaminase ALT serum alanine transaminase 5. IgM level


TREATMENT MODALITIES 1. There is no specific treatment, although bed rest is essential. 2. Diet must be high in carbohydrates, low in fat and low in protein. 3. Patient must take vitamin supplements, especially B complex group. 4. Intravenous therapy is occasionally necessary. 5. Isoprinosine (methisoprenol) may enhance the cell-mediated immunity of the T-lymphocytes. 6. Alkalies, belladonna, and anti-emetics should be administered to control dyspepsia and malaise. NURSING MANAGEMENT 1. The patient must be isolated (enteric isolation). 2. Patient should be encouraged to rest during the acute or symptomatic phase. 3. The patients nutritional status must be improved. 4. Appropriate measure to minimized spread of the disease must be taken. 5. Observe the patient for melena and check stools for the presence of blood. 6. Provide optimum skin and oral care. 7. Increase the ability to carry out activities. a. Encourage the patient to limit activity when fatigued. b. Assist the client in planning periods of rest and activity. c. Encourage gradual resumption of activities and mild exercise during recovery. II. HEPATITIS B (Serum hepatitis) Hepatitis B is the inflammation of the liver caused by hepatitis B virus. This is considered to be more serious than hepatitis A due to the possibility of severe complications such as massive damage and hepatocarcinoma of the liver. It was once thought to be transmitted only through direct exchange of contaminated blood. Hepa B is now known to be transmitted also by contact with human secretions and stools. Recipient of plasm-derived product and hemodialysis clients are particularly at risk. ETIOLOGIC AGENT The 1. 2. 3. disease is caused by the hepatitis B virus. This virus has very limited tissue tropism. HBV infects the liver and possibly the pancreas. HBsAg appears in the blood 30 to 60 days after exposure and persist for variable periods of time.

INCUBATION PERIOD The incubation period is 50 to 180 days or 2 to 5 months with a mean equal to 90 days. 88

PERIOD OF COMMUNICABILITY The patient is capable of transmitting the virus during the latter part of the incubation period and during the acute phase. The virus may persist of the blood for many years.

MODE OF TRANSMISSION 1. Hepatitis B can be directly transmitted by person-to-person contact via infected body fluids. 2. It can be transmitted through contaminated needles and syringes. 3. Transmission can occur through infected blood or body fluids introduced at birth. 4. It can also be transmitted through sexual contact. HBV transmission does not occur via: 1. The fecal-oral route 2. Foodborne or waterborne transmission 3. Arthropod (mosquito)transmission

PATHOGENESIS 1. Hepatitis B virus primarily interferes with the functions of the liver by replicating in liver cells, known as hepatocytes. 2. During HBV infection, the host immune response causes both hepatocellular damage and viral clearance. 3. The virus replicates and large amounts of HBsAg are released into the blood, in addition to virions.


4. Initiation of virus replication may be as soon as 3 days from acquisition, but symptoms may not be observed until after 45days or much longer. 5. Replication of the virus is not cytopathic and proceeds for relatively lonf periods without causing liver damage. 6. During the acute phase of infection, the liver parenchyma shows degenerative changes consisting of cellular swelling and necrosis, especially in hepatocytes.

CLINICAL MANIFESTATIONS 1. Prodromal period a. Fever, malaise, and anorexia b. Nausea, vomiting abdominal discomfort, fever and chills c. Jaundice, dark urine and pale stools d. Recovery is indicated by a decline of fever and improved appetite. 2. Fulminant hepatitis may be fatal and manifested by severe symptoms like ascites and bleeding. DIAGNOSTIC PROCEDURES 1. 2. 3. 4. 5. 6. 7. Compliment fixation test Radio-immunoassay-hemaglutinin test Liver function test Bile examination in blood and urine Blood count Serum transaminase SGOT,SGPT,ALT HBsAg

PREVENTION 1. Blood donors must be screened to exclude carriers. 2. Caution must be observed in giving care to patient infected with HBV. 90

3. Hands and other skin areas must be washed immediately and thoroughly after contact with body fluids. 4. Avoid injury with sharp objector instruments. 5. Use disposable needles and syringes only once and discard properly. 6. Avoid sharing toothbrushes, razors and other instruments that may be contaminated with blood. 7. Practice safe sex. 8. Get adequate rest, sleep, and exercise, and eat nutritious foods. 9. Hepatitis B vaccine is recommended for pre-exposure. 10.Hepatitis immune globulin (HBIg) should be administered within 72 hours to those exposed directly to hepatitis B virus by either ingestion, prick or inoculation. III.HEPATITIS C Is a blood-borne infectious disease caused by the hepatitis C virus (HCV), originally known as non-A, non-B hepatitis The infection is often asymptomatic, but once established, can cause scarring of the liver (fibrosis) and eventually, cirrhosis (advance scarring). The hepa C virus is associated with a high rate of chronic liver diseases (chronic hepatitis, cirrhosis, and an increased risk for hepatocellular carcinoma). Clients with chronic hepatitis C are considered infectious. No vaccine is available for hepatitis C.


IV.HEPATITIS D Hepatitis D virus (also called delta virus) is a small, circular RNA virus. Hepatitis D virus is replication-defective and therefore cannot propagate in the absence of another virus. In humans, hepatitis D virus infection occurs only in the presence of hepatitis B infection. Hepatitis D virus infection is transmitted by blood and blood products. The risk factors for infection are similar to those in hepatitis B virus infections. A patient can acquire hepatitis D virus infections at the same time that he/she is infected with the hepatitis B virus. This is called coinfection. A patient can also be infected with hepatitis D virus at any time during acute hepatitis B virus infection. This is called superinfection. Found only in patients with an acute episode of or chronic hepatis B and requires the presence of HbsAg. This virus on the double-shelled type B to replicate. For this reason, type D infection does not outlast type B infection. Type D is rare in the United States, except among drugs users.

V. HEPATITIS E Transmitted enterically (fecal-oral and waterborne routes), like hepatitis A. Hepatitis E virus is inconsistently shed in stools; therefore, detection is difficult.


The hepatitis E virus (HEV) is a common cause of hepatitis that is transmitted via the intestinal tract. Spread is most often by drinking contaminated water. Hepatitis E never becomes a chronic (long lasting) illness, but on rare occasions the acute illness damages and destroys so many liver cells that the live can no longer function. This is called fulminant liver failure and may cause death. Pregnant women are at a much higher risk of dying from fulminant liver failure The great majority of patients who recover from acute infection do not continue to carry HEV and cannot pass the infection to others.

SIGNS AND SYMPTOMS Assessment findings are similar for the different types of hepatitis. Signs and symptoms progress in three stages: Prodromal stage Patient complains of easy fatigue, anorexia, body malaise, headache, arthralgia, myalgia, photophobia and nausea with vomiting. There are changes in the patients senses of smell and taste. There is moderate grade fever ranging from 37.8 -38.9C. As the prodromal stage draws to a close, urine may become darkcolored and stools are clay-colored.

Clinical jaundice stage Patient manifest with pruritus, abdominal pain or tenderness and indigestion. There is yellowish discoloration of the sclerae, mucuos membrane and the skin, which can last for one to two weeks. 93

On inspection of the skin, rashes, erythematous patches and urticaria may be seen, especially if the client is suffering from hepatitis B or C. Pain, tenderness of the RUQ, an enlarged and tender liver, splenomegaly and cervical adenopathy are present.

Recovery stage During this stage, most of the patients symptoms decrease or subside. Recovery stage commonly lasts for 2-12 weeks.

DIAGNOSIS 1. Hepatitis A: detection of antibodies to hepatitis A confirms the diagnosis. 2. Hepatitis B: the presence of HbsAg and hepatitis B antibiotics confirms the diagnosis 3. Hepatitis C: the diagnosis depends on serologic testing for the specific antibody one or more months after the onset acute hepatitis. 4. Hepatitis D: Detection of intrahepatic delta or immunoglobulin M (IgM) establishes the diagnosis. 5. Hepatitis E: detection of hepatitis E antigen supports the diagnosis. Following are additional findings from liver function tests that support the diagnosis: 1. Serum aspartate aminotransferase levels and serum alanine aminotransferase are increase in the prodromal stage of acute viral hepatitis. 2. Serum alkaline phosphatase levels are slightly increased. 3. Serum bilirubin levels are elevated and may continue to rise in severe cases. 4. Prolonged prothrombin time (PT) (more than 3 seconds) indicates severe liver damage. 5. WBC reveals transient neutropenia and lymphopenia followed by lymphocytosis. 6. Liver biopsy is performed only if diagnosis is questionable.

GENERAL NURSING MANAGEMENT 1. Suggest that a large meal be eaten in the morning because nausea trends to intensify as the day progresses. 2. Provide diversional activities to relieve boredom and anxiety. 3. Encourage anorexic patients to take juices with occasional ice chips to maintain hydration without inducing vomiting. 4. Monitor the patients weight daily. Record intake and output. 5. Observe stools for color, consistency and amount. Record the frequency of bowel movement. 6. Before the patient is discharge, discuss restrictions and how to prevent recurrence of hepatitis.


NON VIRAL HEPATITIS Non-viral is classified as either toxic or drug-induced (idiocyncratic) hepatitis. Most of the patients recover from this type of hepatitis, although a few develop fulminant hepatitis or cirrhosis. CAUSES 1. Alcohol overuse follows heavy alcohol consumption 2. Direct hepatotoxicity - hepatocellular damage and necrosis usually caused by toxins; it is a dose-dependent and occurs primarily in acetaminophen overdose. 3. Idiosyncratic hepatotoxicity follows a sensitization period of several weeks caused by the hosts hypersensitivity to medication, such as, INH, methyldopalovastatin and halothane. 4. Cholestatic reactions caused by a lack of bile excretion; direct hepatotoxicity from hormonal contraceptives or anabolic steroids; and hypersensitivity to antibiotics, thyroid medications, antidiabetics and cytotoxic drugs. 5. Metabolic and autoimmune disorders acute exacerbations of sub-clinical liver disease.

(Ancylostomiasis/Miners Disease/ Egyptian Chlorosis) Hookworm disease is an intestinal parasite of humans that usually causes diarrhea or cramps. Hookworm infection occurs mostly in tropical and subtropical countries. ETIOLOGIC AGENT 1. Ancylostoma duodenale is the agent which is most prevalent in Europe and Asia. 2. Necato americans is distributed in Central and South America and West Africa. a. Both species are pathogenic to man and have similar life cycles. b. They have slight differences in the structure of the mouth, though they both have hooks or piercing mechanism, by which they attach themselves to the intestinal mucosa. c. The source of infection is soil contaminated with feces that contains hookworm ova. d. The female hookworm may produce as many as 10,000 to 20,000 eggs per day. e. Eggs deposited in moist and oxygen-rich soil will develop into embryos within 24 to 72 hours. f. The rhabditiform(young) larvae take about six weeks to develop into filariform (mature) larvae which cause human infection. The larvae remain alive in the soil for several weeks under favorable conditions. 95

g. They remain in the infective stage for several days or weeks and enter the body by penetrating the skin when brought in contact the skin surface. h. The feet are the usual site of penetration, especially if the client goes barefoot. i. After penetrating the skin by way of the sweat glands, hair follicles or abrasions, the larvae enter the venous circulation and lodge in the lung capillaries. j. They break through the capillary walls into the alveoli, from which they are carried by the mucus to the trachea and larynx. k. The larvae are swallowed and pass through the stomach to the large intestine, where they mature. It is also here where the female lays eggs that pass out in the feces. l. The worms life span is form a few to 10 years. INCUBATION PERIOD 1. Hookworm ova appear in the stools about 4 to 6 weeks after the larvae penetrate the skin. 2. The incubation period is 40 to 100 days, or 2 to 8 weeks. PERIOD OF COMMUNICABILITY Persons remain spreaders of infection as long as they are infected. MODE OF TRANSMISSION 1. Transmission is usually accomplished directly through the skin of the foot (ground itch). 2. Transmission is also possible through the ingestion of contaminated drinking water or food. PATHOLOGY 1. The larvae penetrate the unbroken skin of the feet and legs of the host, entering through the suboriferous glands and hair follicles. 2. The larvae penetrate the blood and lymph vessels, damaging them in the process, after which they enter the inferior vena cava and the right atrium, then proceed to the lungs where they pierce the capillary walls and pass into the alveoli. 3. Some may be coughed out and expectorated, while some are swallowed and reach the small intestine where maturation occurs and egg production takes place. 4. The adult worm survives by attaching itself to the duodenal and jejunal mucosa, from where it continuously sucks blood. 5. Hemorrhagic spots in the intestinal mucus membrane mark the site of previous worm attachments. 6. Death may result from severe anemia and cachexia.


INCIDENCE 1. The incidence varies, but hookworm disease is still considered as the most important helminth infection of man. 2. All persons, regardless of age, race and sex are susceptible to hookworm disease. 3. The greatest incidence of infection is found among the persons 15 to 25 years of age. 4. The disease is prevalent in rural areas where sanitary disposal of human excreta is inadequate. 5. The disease is widespread in tropical and subtropical countries, where the climate is warm and humid and where people often walk barefoot. These conditions provide an ideal environment for the infection to flourish. SYMPTOMS 1. The type severity of the symptoms of hookworm disease depends on the number of worms present in the intestine. 2. The worms engulf small bits of tissue from the intestinal mucosa, causing the development of small lesions. 3. They feed on the hosts blood and may consume as much as 50 ml daily. The gradual loss of blood results in iron deficiency anemia. 4. Other symptoms include abdominal pain, diarrhea and allergic reactions like urticaria. 5. Children infected with worms are often mentally and physically underdeveloped. They have protruding abdomens and are lethargic. 6. Infected children tend to be malnourished and undersized. 7. Infected children are lazy, have no energy and lack ambition 8. The pupils of the patients eyes are more or less dilated. 9. Many of the infected children have perverted appetites. 10.Pedal edema and edema in other portion of the body may be present.


DIAGNOSTIC PROCEDURES 1. Microscopic examination of feces for the eggs 2. Blood exam reveals eosinophilia. MODALITIES OF TREATMENT 1. Pyrantel embonate (Quantrel) 2. Tetrachloroethylene 3. Carbon tetrachloride NURSING MANAGEMENT 1. Isolation is not necessary. 2. Diet should be high in calories, vitamins and minerals. 3. Personal hygiene should be maintained. PREVENTION 1. Health education on the proper disposal of excreta is necessary. 2. Regulations to prevent the pollution of stream and lakes with human excreta should be adopted. 3. In areas where hookworm is endemic, all persons should be avoid walking barefoot. 4. Good hygiene is extremely important. 5. Animals should not be allowed to defecate on the streets or beaches where people most likely linger. 6. Purified or boiled water must be used for drinking. 7. Vegetables should not be eaten raw. 8. Night soil and sewage effluent are dangerous to use as fertilizer.


(Weils Disease/Canicola Fever/Hemorrhagic Jaundice/Mud Fever/Swine herd Disease) Leptospirosis is a zoonotic infectious bacterial disease carried by animals, both domestic and wild. Infected urine contaminates water or food, which causes disease when ingested or inoculated through the skin. ETIOLOGIC AGENT A spirochete of the genus Leptospira (Leptospira interrogans) 1. These are chiefly saprophytic organisms which are found in river and lake waters, sewage, and in the sea. 2. There are 150 serotypes divided among 18 serogroups; some species are pathogenic to man and animals. 3. Wells disease is specifically caused by the serovar icterohaemorrhagiae. INCUBATION PERIOD The incubation period varies from six to fifteen days. PERIOD OF COMMUNICABILITY Leptospira is found in the urine between 10 to 20 days after disease onset. SOURCE OF INFECTION Infection comes from contaminated food and water and infected wildlife and domestic animals, especially rodents. 1. Rats (L.icterochaemorrhagiae) are the source of Weils disease frequently observed among mine, sewer and abattoir workers. Rats (L.bataviae) are also the source of infection that attacks riefields workers. 2. Dogs (L.canicola) can also be the source of infection among veterinarians, breeders and owners of dogs. 3. Mice (L.grippotyphosa) may also be a source of infection that affects farmers and flax workers. CLINICAL MANIFESTATIONS 1. The symptoms range in severity from asymptomatic to fatal. 2. Clinical course is generally biphasic and the majority of the cases are unicteric. 3. Three septic stages can be recognized: a. Septic stage this stage is marked by febrile lasting from four to seven days. There is an abrupt onset of remittent fever, chills, headache, anorexia, abdominal pain and severe prostration. There is also respiratory distress. Fever subsides with lysis.


b. Immune or toxic stage this stage can be with or without jaundice, and lasts for 4 to 30 days. Iritis, headache, meningeal manifestations like disorientation, and convulsion with CSF findings of aseptic meningitis Oliguria and anuria with progressive renal failure Shock, coma, and congestion heart failure are also seen in severe cases. Death may occur between the 9th and 16th days. c. Convalescence At this stage, relapse may occur during the 4th to 5th weeks.

LABORATORY DIAGNOSIS 1. Blood urea-nitrogen and creatinine 2. Enzyme-linked immunosorbent assay (ELISA) 3. Liver function tests usually are slightly to moderately elevated: Aspartate aminotransferase (AST) Alanine aminotransferase (ALT) Gamma-glutamyltransferase (GGT) 4. Leptospira antigen-antibody test (LAAT) 5. Leptospira antibody test (LAT) ORGANS OF THE BODY INVADED BY ORGANISM 1. After the organism gains entrance into the body, it multiplies in the bloodstream and invades the liver, resulting in jaundice. 2. In the kidneys, the presence of the organism causes inflammation of the nephrons and tubular necrosis, resulting in renal failure. 3. Leptospira may affect the muscles, resulting in pain and sometimes edema. 4. The organism also invades the eyes, resulting in conjunctivitis. In addition, due to liver involvement, the patient becomes icteric, thereby giving an orange-colored sclera. 100

COMPLICATIONS 1. Meningitis 2. Respiratory distress 3. Renal intestinal tubular necrosis that results in renal failure (Weils disease 4. Cardiovascular problems MANAGEMENT 1. Medical. Treatment of leptospirosis is geared toward: A. Suppressing the causative agent B. Fighting possible complications Aetiotropic drugs penicillin, doxycycline, ampicillin, amoxicillin For prophylaxis, doxycycline 100 mg p.o every 12 hours for 1 week Peritoneal dialysis Administration of fluid and electrolytes an dblood, as indicated

2. Nursing a. Isolate the patient; urine must be properly disposed of. b. Darken the patients room because light is irritating to the patients eyes. c. Observe meticulous skin care to ease pruritus. d. Keep clients under close surveillance. e. Keep homes clean. Regularly replace water in pools, vases, aquaria, etc. to prevent stagnation. f. Eradicate rats and rodents. g. Provide health education on the modes of transmission of the disease. h. Encourage oral fluid intake.

PREVENTION AND CONTROL 1. Sanitation in homes, workplaces and farms is a must. 2. There is a need for proper drainage system and control of rodents (40-60% infected) 3. Animals (cattle, dogs, cats, and pigs) must be vaccinated. 4. Infected humans and pets should treated. 5. Information dissemination campaign must be conducted effectively.


Red tide is caused by a population explosion of toxic, naturally occurring microscopic phytoplanktons, specifically subgroup known as dinoflagellates. ETIOLOGIC AGENT The marine red tide organisms used to be referred to as Gonyaulax, Protogonyaulax and gessnerium. 1. Alexandrium tsmsrense is found along the Atlantic coast. 2. Alexandrium catenelle is found along the Pacific West Cost. 3. Ptychodiscus brevis is present in the gulf of Mexico along the West Florida coast. Explosions or blooms are coastal phenomena caused by environmental conditions which promote the explosive growth of microorganisms. Factors which are favorable for growth are: 1. 2. 3. 4. Warm surface temperature; High-nutrient content; Low salinity and calm seas; and Rainy days followed by sunny weather.

SEAFOODS THAT ARE UNSAFE TO EAT FROM INFECTED WATERS Only certain kinds of seafood accumulated red tide toxins. Shellfish are particularly prone to contamination as they feed by filtering microscopic food out of the water. If toxic planktonic organisms are present, they are filtered from the water, along with their non-toxic food. Such shellfish include: 1. 2. 3. 4. 5. 6. quahogs soft shell clamps oysters mussels scallops moon snails

There are four syndromes of shellfish poisoning: 1. 2. 3. 4. Paralytic shellfish poisoning Diarrheal shellfish poisoning Amnestic shellfish poisoning Neurologic shellfish poisoning

All four syndromes share some common features and are primarily associated with bivalve mollusks, such as mussels, clams, oysters, and scallops. These shellfish are filter feeders and, therefore, 102

accumulate toxins produced by microscopic algae in the form of dinoflagellates and diatoms. Lobster, crabs, shrimps and fish do not accumulate toxins and are safe to eat even if they are from affected waters.

PATHOPHYSIOLOGY Eating toxic shellfish can cause paralytic shellfish poisoning (PSP) in humans. PSP is caused by saxitoxin, which is produced by A. catenella and is one of the most potent toxins known. Saxitoxin acts by blocking sodium movement in muscle tissue. Conduction block primarily occurs in the neurons and muscles. The toxins responsible for shellfish poisoning are water-soluble, heat-and acid-stable, and are not inactivated by ordinary cooking. After ingestion, the toxin immediately affects the nervous system, with symptoms usually appearing within 30 minutes. Severity depends on the amount of toxin consumed. Toxic shellfish taste and appear no different from non-toxic shellfish, and cooking does not destroy the organism.

CLINCAL MANIFESTATIONS 1. The initial sign is tingling of the lips and tongue which spreads to the face, neck, fingertips and toes. 2. Headache, dizziness and nausea follows, symptoms which may be mistaken as being due to a drunken condition. 3. Such symptoms are aggravated by alcohol consumption. 4. In severe cases, muscular paralysis and breathing difficulty may occur in five to twelve hours due to paralysis of the diaphragm; the victim can survive only with the aid of a respirator. 5. Fatalities from respiratory arrest have been reported.


MODALITIES OF TREATMENT 1. The patient is induced to vomit. 2. Charcoal hemoperfusion is a process done by pumping the arterial blood through an activated charcoal filter remove the toxin. 3. Alkaline fluids, such as sodium bicarbonate, are thought to be helpful because the toxin is unstable in alkaline condition. 4. Artificial respiration is required if the patient exhibits respiratory stress. PREVENTION AND CONTROL 1. All shellfish-producing areas should have a monitoring program to test water, sediments, and shellfish for contamination. 2. The Department of Environmental Quality Engineering (DEQE) is responsible for year-round testing of shellfish-growing areas. 3. When blooms subside, shellfish has purified themselves of the toxin and when testing indicates a return to safe levels, the areas are reopened. 4. If accidentally ingestion of toxic shellfish is suspected, seek medical attention immediately. 5. Recreational shellfish gatherers should look for posted warnings and pay close attention to local media announcements.

(Bilharziasis/Snail Fever) This is a slowly, progressive disease cause by blood flukes of class Trematoda. It is a chronic wasting disease common farmer and their families in certain parts of the Philippines. This is not a public health concern but also a socio-economic problem cause by causing ill health, it reduces agricultural productivity. ETIOLOGIC AGENT The cause of the disease is a parasitic worm, Schistosoma japonicum. There are three major types of the organism: 1. Schistosoma japonicum a. This is agent infects the intestinal tract (Katayama disease). b. It is found to be the only that is endemic in the Philippines. c. This is also known as oriental schistosomiasis. 104

2. Schistosoma mansoni a. It also affects the intestinal tract. b. It is common in some parts of Africa. 3. Schistosoma haematobium a. It affects the urinary tract. b. It can be found in some of the Middle east, like Iraq and Iran. INCUBATION PERIOD The incubation period is at least two months. SOURCE OF INFECTION 1. Feces if infected persons 2. Dogs, pigs, carabaos, cows, monkeys and wild rats have been found to be infected and, therefore, also serve as hosts. MODE OF TRANSMISSION 1. The disease is transmitted through the infestion of contaminated water. 2. The disease is transmitted through skin pores. 3. The disease is transmitted through an intermediary host, a tiny snail called Oncomelania quadrasi. CHARACTERISTICS OF ONCOMELANIA QUADRASI 1. The snail thrives best along riverbanks freshwater stream, creeks, canals and swamps. 2. It can be found clinging to water hyacinths, grasses, decaying leaves and pieces of rotting wood, bamboo, and coconut husks. 3. It also loves to stay in areas with sandy-loamy soil. 4. The adult snail if greenish-brown in color and is just as big as the smallest grain of palay. PATHOGENESIS/PATHOLOGY 1. The larvae (cercariae) penetrate the skin or mucous membranes and eventually work their way to livers venous portal circulation. 2. In the portal vessels, they mature within one to three months. 3. The mature worms live in copula in the portal vessels surrounding the large intestine or bladder. 4. The female cercaria lays eggs in the blood vessels surrounding the large intestine or bladder. 5. Ulceration in the mucosa occurs and the eggs are able to escape into the lumen of the large intestine and are excreted with feces. 6. Some of eggs are carried by the portal circulation and filtered in the liver, where small lesions or granulomas are formed. 7. These granulomas are resolved and are replaced by fibrous tissue. 8. Likewise, the ulcerations in the intestines are healed and scar formation occurs. 9. As the disease progress, the liver enlarges due to increasing fibrosis. 10.The flow of blood is interrupted in the intrahepatic portion, thereby resulting in portal hypertension. 105

11. Fluid accumulates in the patients belly, making it bulge.

CLINICAL MANIFESTATIONS The signs and symptoms of the disease depend on the site of infection; however, the following can be observed: 1. A pruritic rash, known as swimmers itch, develops at the site of penetration. 2. There is low-grade fever, myalgia, and cough. 3. There is abdominal discomfort due to hepatomegaly, splenomegaly and lymphadenopathy. 4. There are bloody-mucoid stools, similar to those in dysentery, that comes on and off for weeks. 5. The patient becomes icteric and jaundice. 6. Later, the patients belly becomes big because of an inflamed liver, resulting from the accumulation of eggs in the organ. 7. After some years of suffering from this chronic disease, the patient becomes weak and pale and there is marked muscle wasting. 8. When the parasites reach the brain, the victim experience severe headaches, dizziness and convulsions.



COMPLICATIONS 1. 2. 3. 4. 5. 6. 7. Liver cirrhosis and portal hypertension Cor plumonale and pulmonary hypertension Heart failure Ascitis Hematemesis as a result from rupture of esophageal varices Renal failure Cerebral schistosomiasis

Cerebral schistosomiasis is caused by the hosts reaction to schistosoma eggs. The mechanism of egg deposition in unknown, but the presence of the eggs suggests that they may cross the blood-brain barrier or that some worm pairs may reach the venous side of the cerebral circulation. Patients with cerebral schistosomiasis usually have clinical manifestation of increased intracaranial pressure associated with focal neurologic signs. Several aspects of the pathogenesis of cerebral schistosomiasis are unknown, although available evidence suggests that: It starts with cercariae penetrating the human skin and entering the venous circulation. Schistosomiasis migrate to the lungs and the liver. They then mature into mating pairs, and settle in the mesenteric veins. The eggs may reach the brain through the valveness venous plexus of Batson, which joints the deep iliac veins and the inferior vena cava with the veins of the spinal cord and the brain. Alternately, the eggs may migrate to the brain via the pulmonary arteriovenosus or the portal- pulmonary arteriovenosus shunts. Once, the worms have entered the cerebral veins they lay eggs directly at the ectopic sites, which could be the cerebrum, cerebellum, meninges or the brainstem. DIAGNOSTIC PROCEDURES 1. 2. 3. 4. 5. Fecalysis or direct stool exam Kato-katz technique Liver and rectal biopsy Enzyme-linked immunosorbent assay (ELISA) Circumoval precipitin test (COPT) confirmatory diagnostic test

MODALITIES OF TREATMENT Treatment is effective only when given early in the course of the disease. 1. Praziquantel tablet for 6 months; 1 tab x a day for three months, then 1 tab a day for another three months. 2. Faudin injection given either IM or IV. The patient should consume 360 mg for the entire treatment.


3. If the patient continues to live in the endemic area, he frequently gets reinfected and has to be retreated.

PREVENTION AND CONTROL To prevent schistosomiasis, one must have through knowledge of how the disease spreads. The basic principle of its prevention and control is interrupting the life cycle of the worm and protecting people from infection. This can be achieved through the following measure: 1. Have a stool examination. 2. Reduce snail density by: a. Clearing vegetation, thus exposing the snails to sunshine; b. Constructing a drainage system (canals) to dry areas where the snails thrive; and c. Improve farming through proper irrigation and drainage, crop rotation and removal of weeds thus disturbing the living conditions of the snail. 3. Diminish infection rate through: a. Proper waste disposal; b. Control of stray animals; c. The prohibition of people, especially children, from bathing in infested streams; d. The construction of footbridges over snail-infested streams; and e. The provision of an adequate water supply for bathing and laundering and safe water for drinking. f. Providing health on the disease process, mode of transmission and prevention.

Typhoid fever is a bacterial infection transmitted by contaminated water, milk shellfish and other foods. It is a n infections of the GIT affecting the lymphoid tissues of the small intestines called Peyers patches. ETIOLOGIC AGENT The disease is caused by the organism Salmonella typhosa/typhi. 1. Gram-negative, motile and non-dpore-forming 2. Pathogenic only to man 3. It is hardy organism and easily survives in naturals habitats like water or inorganic materials.


INCUBATION PERIOD The incubation period is from 5 to 40 days, with a mean of 10 to 20 days. PERIOD OF COMMUNICABILITY The period of communicability is variable. As long as the patient is excreting the microorganism, he is capable of infecting others. SOURCES OF INFECTION 1. Person who has just recovered from the disease or has recently taken care of a patient with typhoid and was infected is considered a potential carrier. 2. Ingestion of shellfish (Oysters) taken from waters contaminated with sewage disposal can be a source of infection. 3. The stools and vomits of an infected individual are sources of infection. MODE OF TRANSMISSION 1. The disease can be passed from one person to another through fecal-oral transmission. 2. The organism can be transmitted through the 5 Fs. 3. The disease can be transmitted through the ingestion of contaminated food, water and milk.

PATHOGENENESIS 1. The organism gains access to the bloodstream through the bowels, principally through infected Peyers patches in the lymphoid tissues.


2. During the first week these lymph nodes are swollen. Necrosis of the lymph nodes follows, caused by progressive edema and eventual vascular obstruction from the center to the periphery of the node, resulting in an oval ulcer along the long axis of the small intestine. 3. During the second week, they form sloughs which are often bilecolored. 4. During the third weeks, the sloughs separated and leave an ulcerated surface. 5. Hemorrhage and perforation may occur due to the growth of the lesion and the continuous erosion of the epithelial lining of the small intestines. 6. Since toxin is absorbed into the bloodstream, almost all organs of the body are affected, but most commonly the heart, liver and spleen. The mesenteric lymph glands are red and swollen.

CLINICAL MANIFESTATION 1. Onset a. Headache, chilly sensation and aching all over the body b. Nausea, vomiting and diarrhea c. During the 4th and 5th days, all symptoms are at their worst. d. Fever is higher in the morning than in the afternoon. e. Breathing is accelerated, the tongue furred, the skin dry and hot, and the abdomen distended and tender. f. Rose spots appear on the abdominal wall on the 7th to the 9th days. g. On the second week, symptoms become more aggravated. Temperature becomes stable. Rose spots become more prominent. 2. Typhoid State a. Symptoms decline in severity. b. The tongue protrudes, becoming dry and brown. c. Teeth and lips accumulate a dirty-brown collection of dried mucus and bacteria known as sordes (preventable by good nursing care) d. Patient seems to be staring blankly (coma vigil). e. Twitching of the tendons sets in especially those of the wrist (subsultus tendinum).


f. Patient mutters deliriously and picks up aimlessly at bedclothes with his fingers in a continuous fashion (carphologia). g. There is a constant tendency for the patient to slip dwon to the foot apart of the bed. h. In severe cases rambling delirium sets in, often ending in death.

COMPLICATIONS 1. 2. 3. 4. 5. 6. 7. 8. 9. Hemorrhage or perforation the two most dreaded complications Peritonitis Bronchitis and pneumonia Meteorism or excessive distention of the bowels (tympanties) Thrombosis and embolism Early heart failure typhoid spine or neuritis Septicemia Reiters syndrome joint pain, eye irritation and painful urination that can lead to chronic arthritis

DIAGNOSTIC PROCEDURE 1. 2. 3. 4. Typhidot confirmatory ELISA Widal test Rectal swab

MODALITIES OF TREATMENT 1. 2. 3. 4. 5. Chloramphenicol (drug of choice) Ampicillin Co-trimoxazole Ciprofloxacin or ceftriaxone If the patient does not respond to chloramphenicol, 3rd and 4th generation drugs are administered.

NURSING MANAGEMENT 1. Isolation by the medical aseptic technique 2. Maintain or restore fluid and electrolyte balance by giving nourishing fluids in small quantities at frequent intervals. 3. Monitor the patients vital signs. 4. Prevent further injury (such as falls) of patient with typhoid psychosis. 5. Maintain good personal hygiene and mouth care. 6. Cooling measures are necessary during the febrile state. 7. Watch out for signs of intestinal bleeding. 8. Terminal and concurrent disinfection. PREVENTION AND CONTROL 1. Sanitary and proper disposal of excreta 2. Proper supervision of food handlers 3. Enteric isolation 112

4. 5. 6. 7.

Provision of adequate amounts of safe drinking water supply Reporting of cases to health authorities Detection and monitoring of typhoid carriers Education of the general public on the mode of transmission

Campylobacteriosis is food poisoning caused by the campylobacter bacterium. It is one of the most common causes of diarrhea in the United States, affecting more than 2.4 million people every year. Campylobacteriosis occurs much more often in the summer months than in the winter months. Infants, young adults, and males are most likely to get the condition.

CAUSES Campylobacteriosis is usually caused by handling poultry (such as chicken or turkey) that is contaminated with the campylobacter bacterium and is raw or undercooked. For example, you can be infected by cutting poultry meat on a cutting board and then using the unwashed cutting board or utensil to prepare vegetables or other raw or lightly cooked foods. Drinking contaminated milk or water from contaminated lakes or streams can also result in infection. Campylobacteriosis usually is not spread from person to person. But this can happen if you have the condition and do not properly wash your hands. Some people have become infected through contact with the infected stool of a dog or cat.


SYMPTOMS The symptoms of campylobacteriosis include diarrhea, cramping, stomach pain, and fever within 2 to 5 days after exposure to the bacteria. Your diarrhea may be bloody, and you may feel sick to your stomach and vomit. The illness usually lasts 1 week. Some people don't have any symptoms at all. In people with impaired immune systems, campylobacteriosis can be life-threatening.

DIAGNOSIS PROCEDURE Your doctor will do a medical history and a physical exam and ask you questions about your symptoms, foods you have recently eaten, and your work and home environments. A stool culture can confirm the diagnosis. TREATMENT You treat campylobacteriosis by managing any complications until it passes.Dehydration caused by diarrhea and vomiting is the most common complication. Do not use medicines, including antibiotics and other treatments, unless your doctor recommends them. Most people recover completely within a week after symptoms begin, although sometimes recovery can take up to 10 days.


To prevent dehydration, take frequent sips of a rehydration drink (such as Pedialyte). Try to drink a cup of water or rehydration drink for each large, loose stool you have. Soda and fruit juices have too much sugar and not enough of the important electrolytes that are lost during diarrhea, and they should not be used to rehydrate. Try to stay with your normal diet as much as possible. Eating your usual diet will help you to get enough nutrition. Doctors believe that eating a normal diet will also help you feel better faster. But try to avoid foods that are high in fat and sugar. Also avoid spicy foods, alcohol, and coffee for 2 days after all symptoms have disappeared.


Diphtheria is an acute bacterial disease can infect the body in two areas: the throat (respiratory diphtheria and the skin (skin diphtheria). ETIOLOGIC AGENT Corynebacterium diphtheria (Klebs- Leopffler bacillus) 1. It is a toxin-producing organism that manufactures an exotoxin which is responsible for major pathologic changes. 2. It is Gram (+), non-sporulating, and generally aerobic. 3. The bacilli invade the superficial tissues with very limited extension beyond the mucous membrane, but soluble toxin is capable of producing severe fatal sequel. 4. It is unstable and easily destroyed by light, heat, and aging. 5. It is capable of damaging muscle and especially the kidneys, liver, cardiac nerves, and other tissues. 6. It has 3 strains of organisms: a. Gravis (severe) is the strain that produces the most severe and greatest number of fatal cases in Europe. b. Mitis (mild) is the strain that produces lesions extending to the larynx and lungs but is rarely a cause of death. c. Intermedius (intermediate)is related to garvis but results in a tendency to bleed.

INCUBATION PERIOD After being exposed to the bacterium, it usually takes 2 to 5 days for symptoms to develop. PERIOD OF COMMUNICABILITY The period of communicability varies. It is more than 2 to 4 weeks in untreated patients and 1 to 2 days in treated patients.


SOURCE OF INFECTION Infection can come from discharges of the nose, pharynx, and eyes, or lesions on other parts of the body of infected persons. MODE OF TRANSMISSION Diphtheria is transmitted through contact with person or a carrier, or with articles soiled with discharge of infected persons. PREDISPOSING FACTORS 1. 2. 3. 4. An operation in an area of the nose and throat Economic status Lack of proper nutrition Overcrowding

PATHOGENESIS/ PATHOLOGY 1. The toxin is absorbed into the mucous membranes and causes destruction of the epithelium and superficial inflammatory response takes place. 2. Necrotic epithelium becomes embedded in exuding fibrin so that a grayish pseudomembrane is formed by leukocytes, fibrin, and necrotic tissues. Microorganisms that adhere to the underlying tissues leave a raw bleeding when detached. The size of the pseudommembrane reflects the amount of toxin produced. (The larger the pseudomembrane, the more toxins are present in the blood stream and in the tissues.) 3. The microorganism are commonly seen over the tonsils, pharynx or larynx, so that any attempt to remove the pseudomemebrane, exposes and tears the capillaries and results in bleeding. 4. The bacilli within the pseudomembrane continue to actively produce toxins that result in distinct damage, particularly parenchymatous degeneration, fatty infiltration, and necrosis in the muscles of the heart and in the liver, kidney and adrenals, sometimes accompanied by gross hemorrhage. 5. The toxin also produces nerve damage, resulting in paralysis of the soft palate, eye muscles, or extremities. TYPES 1. Nasal with foul-smelling serosanguinous secretions from the nose. 2. Tonsilar, which has a low fatality rate. The lesion are confined to the tonsils, but tend to spread over the pillars and into the soft and uvula. 3. Facial Nasopharyngeal (the more severe type) a. Cervical lymph nodes are swollen. b. Neck tissues are edematous, resulting in the appearance of a bulls neck. c. It has a marked degree of toxemia. 117

d. Breath is usually fetid. 4. Laryngeal This is most commonly found in children ages 2 to 5 years old. It is considered as most the severe and more fatal type due to the narrowing of the air passages. There is moderate hoarseness, the voice is diminished until it is finally absent. 5. Wound or cutaneous diphtheria affects the mucous membrane and any break on the skin

CLINICAL MANIFESTATIONS 1. The onset of the disease is insidious, marked by a feeling of fatigue, malaise,slight sore throat, and elevation of temperature usually not exceeding 38C. 2. Inflammatory reaction is initiated by the body. Exudates consisting of leukocytes, RBC, and necrotic tissues begin to form. 3. The exudates forming the membrane are grayish in appearance as they begin to form. As they thicken, the become dull white. 4. Cervical adenitis with tenderness of the glands occurs. 5. There is the presence of body malaise, weakness, and apathy, with a rapid pulse rate that becomes disproportionate to the low-grade fever.


6. In severe cases, the entire neck becomes swollen, with edema extending to the chest. 7. The swelling of the neck was given the name bulls neck form. 8. After administration of the antitoxin, the membrane begins to curl at the edges, separate, and flake off in large pieces. Other common symptoms of respiratory diphtheria include: Breathing difficulty Husky voice Increased heart rate Stridor (a shrill breathing sound heard on inspiration) Nasal drainage/secretions (serosanguinous with a foul smell) Swelling of the palate Low-grade fever

Symptoms of skin or cutaneous diphtheria are usually milder and may include yellow spots or sores (similar to impetigo)on the skin. COMPLICATIONS 1. Myocarditis caused by the action of diphtheria toxin on the heart muscles 2. Polyneuritis that includes paralysis of the soft palate, the ciliary muscles of the eye, pharynx larynx, or extremities 3. Airway obstruction may lead to death through asphyxiation. 4. Cervical adenitis 5. Otitis media 6. Bronchopneumonia DIAGNOSTIC PROCEDURE 1. 2. 3. 4. 5. Swab from nose and throat or other suspected lesions Virulence test Schick test Molony test Leoffler slant

TREATMENT MODALITIES Specific treatment of diphtheria is determined by the physician based on: 1. Overall health and medical history 2. Extent of the condition, and 3. Tolerance for specific medications, procedures and therapies. a. Penicillin is usually effective in treating respiratory diphtheria before it releases toxins in the blood. b. Antitoxin can be in combination with penicillin Skin testing is necessary before the administration of anti-toxin Fractional doses are given in positive (+) cases, with the following schedule: 0.05 ml (1:20 dilution) subcutaneously 0.05 ml (1:10 dilution) subcutaneously 0.10 ml undiluted subcutaneously 119

0.20 ml undiluted subcutaneously 0.50 ml undiluted subcutaneously 0.10 ml undiluted subcutaneously The above doses given at 15-minutes intervals if no reaction is noted. If there is any, the remaining dose is given after an hour. c. Erythromycin, 40mg/kg bw in 4 doses for x 7to 10 days. d. Supportive therapy Maintenance of adequate nutrition Maintenance of adequate fluid and electrolytes Bed rest Oxygen inhalation In the presence of laryngeal obstruction, tracheostomy is usually done. NURSING MANAGEMENT 1. Patient must be advised to take full bed rest for at least two weeks. Patient must not be permitted to bathe by himself. The patient must avoid exertion during defecation in order to conserve energy and decrease cardiac workload. 2. Soft diet recommended. Small, frequent feedings are advised. 3. Patient must be encouraged to drink fruit juices rich in vitamin C to maintain the alkalinity of the blood and increase his/her resistance. 4. Ice collar must be applied to the neck. 5. Nose and throat must be taken care of. PREVENTION 1. Cases of diphtheria must be mandatorily reported. 2. Patients should be isolated for a minimum of fourteen days from the onset of the disease until three cultures from the nose and throat are reported negative. 3. Patient should avoid contact with children and refrain from handling food until bacteriologic examination of cultures is reported negative. 4. Children under five years should be given booster doses of diphtheria tetanus vaccine. 5. DPT immunization of babies is mandatory.


(La Grippe) Influenza is an acute viral infectious disease affecting the respiratory system. ETIOLOGIC AGENT The agents that cause influenza are the RNA- containing myxoviruses, types A, A-prime, B, and C. INCUBATION PERIOD The usual incubation period is usually from 42 to 48 hours. PERIOD OF COMMUNICABILITY The disease is communicable until the 5th day of illness (up to the 7th day in children). MODE OF TRANSMISSION 1. The disease is transmitted through airborne spread among crowded populations. 2. The disease can also be transmitted through direct contact with the infected droplet. 3. The influenza virus persists for hours in dried mucus.

PAHTOLOGY/PATHOGENESIS Influenza virus is airborne and invades the respiratory mucosa first, specially the nasal, tracheal and bronchial mucosa, where rapid inflammation damages the ciliated epithelium of the tracheobronchial tree, rendering the patient vulnerable to secondary infection by pneumococci or staphylococci, and other organism. Severe reactions produce edema of the respiratory passages with serosanguinous discharge.


CLINICAL MANIFESTATION 1. Onset is sudden and is marked by chilly sensation, hyperpyrexia, malaise, sore throat, coryza, rhinorrhea, myalagia and headache. 2. Severe ahces and pain, usually at the back, associated with severe sweating may manifest. 3. Sometimes there are gastrointestinal symptoms and vomiting. 4. The worst symptoms usually last from 3 to 5 days before the condition begins to improve. 5. Influenza may occasionally cause severe disease, but most people recover. COMPLICATIONS 1. Directly to primarily viral infection a. Hemorrhagic pneumonia b. Encephalitis and other neurologic syndromes c. Reyes syndrome, which is an acute encephalopathy and fatty degeneration of the liver associated with epidemic influenza B infection d. Myocarditis, which may lead to cardiac failure e. Sudden infant death syndrome f. Myoglobinuria 2. Superimposed bacterial infections due to Streptococcus pneumonia, Haemophilus influenza, Streptococcus pyogenes and Staphylococcus aureus. a. Otitis media b. Sinusitis c. Pneumonia DIAGNOSTIC PROCEDURE 1. Blood examination is usually normal but leukopenia may be noted 2. The virus may be cultured from oropharyngeal washings or swabs during the first few days of illness 3. Viral serology a. Complement fixation test b. Hemo-agglutination test c. Neutralization test MANAGEMENT Until recently there has been specific treatment for influenza. Advice the client to: 1. stay at home; 2. drink plenty of fluids; 3. take the following to relieve fever and headache: a. paracetamol b. aspirin, unless contraindicated (should not to be given to children below 16 years old of age) or c. ibuprofen or other anti- inflammatory drugs; 122

4. sponge down with tepid water. Also, you must make sure to: 1. isolate the patient to decreases the risk of infecting others (respiratory isolation); 2. limit strenuous activity specially in children ; and 3. watch for complications, especially among people at risk.

PREVENTIVE MEASURES 1. Immunization 2. Avoidance of crowded places 3. Educate the public and health care personnel regarding the basic personal hygiene 4. It is advised that people belonging to the following categories should receive the vaccine annually: a. The elderly b. People who have poor immunity and c. Those with conditions such as diabetes and lung, kidney, heart or liver disease.

(Bird Flu) Avian influenza (also known as bird flu) is a type of influenza that was first identified in Italy in the early 1900s and is now known to exist worldwide. Human deaths from avian influenza were unknown until 1997, when sis people in Hong Kong died from the particularly virulent H5N1 strain. In January 2004, a new major outbreak of H5N1 avian influenza surfaced in Vietnams and Thailands poultry industries, and within weeks, spread to ten countries in Asia, including Indonesia, South Korea, Japan and China. Intensive efforts were undertaken to slaughter chickens (over 40 million chickens alone were slaughtered in high-infection areas) and the outbreak was contained by March. The total human death toll in Vietnam and Thailand was 23 people. It is feared that if the avian influenza virus undergoes antigenic shift with a human influenza virus, the new subtype created could be both highly contagious and lethal in humans. Such as subtype can cause a global influenza pandemic similar to Spanish flu, which killed over 20 million people in 1918. In February 2004, the avian influenza virus was detected in pigs in Vietnam, increasing fears of the emergence of new variant strains.


Fresh outbreaks in poultry were confirmed in the Ayutthaya and Pathumthani provinces of Thailand, and in Chaohu City in Anhui, China in July 2004. In North America, the presence of avian influenza was confirmed in several poultry farms British Columbia in February 2004. As of April 2004, 18 farms had been quarantined to halt the spread of the virus. Two case of humans with avian influenza. In August 2004, avian flu was confirmed in Kampung Paris, Kelantan, Malaysia. Two chickens were confirmed to be carrying H5N1. As a result, Singapore imposed a ban on the importation of chickens and poultry products. A cull of all poultry has been ordered by the government within a 10kilometer radius of the location of the outbreaks.

ETIOLOGIC AGENT The causative agent is the avian influenza (AI) virus. All AI viruses belong to Influenzavirus A, a genus of the Orthomyxoviridae family, and are negative-stranded and segmented.

MODE OF TRANSMISSION 1. Avian influenza in the air and in manure. Wild fowl often act as resistant carriers, spreading it to more susceptible domestic stocks.


2. It can also be transmitted through contaminated feeds, water, equipment and clothing; however, there is no evidence that the virus can survive in well-cooked meat. 3. Cats are also thought to be possible infection vectors for H5N1 strains of avian flu.

AVIAN INFLEUNZA IN HUMAN While avian influenza spreads rapidly among birds, it does not infect humans easily, and there is no confirmed evidence of human-to-human transmission. Of the 15 subtypes known to be capable of crossing the species barrier.

INCUBATION PERIOD The incubation period is 3 to 5 days.

SIGNS AND SYMPTOMS 1. Symptoms in animals vary, but virulent strains can cause death within few days. 2. The symptoms of avian influenza in human are akin to those of human influenza, i.e., fever, sore throat, cough and, in severe cases, pneumonia. PREVENTION AND TREATMENT Avian influenza in humans can be detected reliability with standard influenza tests. Antiviral drugs are clinically effective in both preventint and treating the disease. Vaccines, however, take at least four months to produce and must be prepared for each subtype.


(Glandular Fever) Glandular fever is an acute self-limiting disease of the lymphatic system caused by the Epstein-Barr virus, (EBV), a member of the herpes group. The disease is often called mono.) INCUBATION PERIOD The incubation period ranges from 30 to 50 days in young adults, averaging about 6 weeks

MODE OF TRANSMISSION Close personal contacts, probably via the oral route in children and kissing in young adults, hence the synonym kissing disease. Generally, organisms are found in the saliva, blood and genital secretions. Contagiousness is low, even among individuals who are susceptible or have been exposed. High and lasting immunity usually develops.

CLINICAL MANIFESTATION 1. Prodromal symptoms are fatigue, anorexia, inability to concentrate, chilly sensation and headache. 2. There is fever that usually lasts for 5 days , sore throat and enlarged lymphnodes. 3. Sore throat is usually accompanied by exudative tonsillitis characterized by whitish, pasty exudates and a foul-smelling and spreading greenish-gray membrane, often leaving an ulceration. 4. Dyspahagia is severe and gum bleeding may occur. 5. Palatine petechial are seen in the first week. 6. There are retro-orbital headache, photophobia and puffy eyelids. 7. Splenomegaly, hepatomegaly and jaundice sometimes appear in about 10-15%of cases.


LABORATORY FINDINGS 1. 2. 3. 4. Lymphocytes Positive for cephalin-cholesterol flocculation test Increase in transaminase 4 levels, especially SGOT,SGPT and LDH Increase in total IgM levels

TREATMENT 1. Treatment is purely symptomatic and non-specific 2. Use of antibiotics is no help. 3. Steroids are beneficial in the presence of certain complication like airway obstruction and CNS involvement. 4. Bed rest and sufficient fluids are necessary. COMPLICATIONS 1.Pneumonia or pneumonitis (primary atypical pneumonia) 2.Neurological manifestations such as meningitis ,encephalitis and Guillain-Barre Syndrome (GBS) 3.Hematological manifestations NURSING MANAGEMENT 1. Oral secretions should be properly disposed of. 2. Clients should be cautioned to avoid straining or to refrain from any strenuous activity. 3. Cooling measures should be taken for febrile patients. 4. Encourage soft diet and increase fluid intake.


(Infectious Parotitis/Epidemic Parotitis) Mumps is an acute viral disease manifested by the swelling of one or both parotid glands, with occasional involvement or other glandular structures, particularly the testes in males. ETIOLOGIC AGENT The causative organism is a filterable virus of the Paramyxovirus group, usually found in the saliva of an infected person. Man is the only natural reservoir.

INCUBATION PERIOD The dincubation period ranges from 14 to 25 days (the average is 18 days). PERIOD OF COMMUNICABILITY The disease is communicable six days before and nine days after the onset of parotid gland swelling; 48-hours period immediately preceding the onset of swelling is considered the time of highest communicability. PATHOLOGY 1. Mumps is a generalized disease that affects glandular structures, as well as renal and nervous tissues. 2. The virus gains entry into the system through droplet infection and multiplies in the upper respiratory tract and localizes in the salivary glands. 3. The glands become edematous and the ducts are obstructed because of the swelling of the epithelial lining. 4. On some occasions, necrosis may occur in the acinar cells. CLINICAL MANIFESTATIONS 1. The first symptoms of mumps may be a sudden headache, earache, loss of appetite, fever and swelling of the parotid glands, which are located in front of the below the ears. 2. Pain is related to the extent of swelling of the gland, which usually reaches its peak in about two days and continues for seven to ten days. 128

3. Temperatures usually remains moderately elevated, but may reach 40C during the acute stage of the disease. 4. One gland may be affected at first. One to three days later, the other side may become involved.

COMPLICATIONS 1. The most notorious complication of mumps is orchitis. Testicular involvement usually occurs several days after the onset of parotid swelling. Orchitis is often accompanied by elevation of temperature. Pain is often excruciating and is aggravated by movement. The testes are swollen and are tender to palpation. 2. In females, oophoritis may occur and manifests as pain and tenderness of the abdomen. 3. Mastitis has also been reported to accompany mumps. 4. Central nervous system involvement has been reported to complicate mumps, as manifested by headache, elevation of cerebrospinal protein concentration and cell count changes. 5. Nuchal rigidity, associated with lethargy, headache, convulsions or delirium 6. Deafness as a result of mumps has been reviewed and studied. 7. Menigoencephalitis is also a common complication of mumps. 8. Pancreatitis manifests asepigastric pain, vomiting, chills and prostration. 9. Rare complications of mumps include transverse myelitis, ataxia, thrombocytopenia, myocarditis, arthritis and nephritis. DIAGNOSTIC PROCEDURES 1. Compliment fixation test shows a presumptive evidence of infection. 2. The hemoagglutination inhibition test is used to determine immune status. 3. The neutralization test determines immunity to mumps.


4. A viral culture or the isolation of virus from the pharynx a few days before and at least five days after parotid swelling is done. 5. Serum amylase determination is the most useful test in making an early presumptive diagnosis for mumps.

TREATMENT MODALITIES 1. Anti-viral drugs 2. Relief of pain from parotid swelling can be afforded by the application of a hot or cold pack, whichever is preferred the patient. NURSING MANAGEMENT 1. Medical aseptic protective care a. Patient should be for in a single-occupancy room. b. Susceptible individuals must use masks and must was hands regularly. c. Terminal disinfection is desirable. d. Oral care and overall personal hygiene are a must. 2. General management of the disease a. Bed rest is encouraged by some physician to avoid complications. b. Diversion activities are recommended for the less ill patient. 3. Diet a. No restriction of food is necessary, except during the acute stage, when the patient may find it very difficult foods and painful to chew and swallow. b. Acidic foods, like fruits juices, may increase discomfort. PREVENTION AND CONTROL 1. Active immunization (MMR) 2. Reporting of cases to health authorities 3. Isolation of patient

(Whooping Cough) Whooping cough is an infectious disease characterized by repeated attacks of spasmodic coughing which consists of a series of explosive expirations, typically ending in a long-drawn forced inspiration which produces a crowning sound, the whoop, and is usually followed by vomiting. CAUSATIVE AGENT Pertussis is a bacterial infection caused by Bordetella pertussis, an infection that is more serious when it occurs in infants. The organism is a non-motile, gram-negative bacillus that is easily destroyed by light, heat and drying. 130


INCUBATION PERIOD The incubation period is seven to fourteen days. PERIOD OF COMMUNICABILITY The period of communicability starts from 7 days after exposure to 3 weeks after typical paroxysms. MODE OF TRANSMISSION 1. Pertussis is primarily spread by direct contact and droplet. 2. It may also be spread indirectly through soiled linens and other articles contaminated by respiratory secretions. SOURCES OF INFECTION The secretions from the nose and throat of infected persons contain the causative organism. It extremely contagious in non-immune cases. INCIDENCE 1. Infants are highly susceptible. 2. One attack usually produces lifetime immunity. 3. Second attack may be due to other microorganism causing whooping cough syndrome. PATHOLOGY 1. After the incubation period, large numbers of B. pertussis are confined to the tracheobronchial mucosa, entangled in the cilia where it produces progressively tenacious mucus. 2. This mucus is irritating to the mucosa and initiates coughing. Cough is spasmodic because the tenacious material is not readily expelled. 3. Whooping cough follows a classic sis-day course of three stages, each of which lasts about two weeks. 4. It is believed that coughing is initiated by the direct toxic effect of the organism on the central nervous system. CLINICAL MANIFESTATIONS The signs and symptoms are characterized by three distinct stages: 131

1. Catarrhal stage a. This stage characterized by non-specific symptomatology where there is mucoid rhinoria, sneezing, lacrimation and dry bronchial cough. b. Cough becomes irritating, hacking, nocturnal and more severe. c. It is during this stage that the disease is most communicable. d. This stage lasts for about one to two weeks. 2. Paroxysmal stage a. This stage occurs on the 7th to the 14th day. b. Cough becomes spasmodic and recurrent with excessive, explosive outbursts in a rapid series of five to ten rapid coughs in one expiration. c. Each cough characteristically ends in a loud, crowing inspiratory whoop, and choking on mucus that causes vomiting. d. Paroxysmal coughing may induce nosebleeding, increased venous pressure, periorbital edema, conjunctival hemorrhage and hemorrhage of the anterior chamber of the eye. e. During a paroxysm, the face becomes cyanotic, veins on the face and neck become distended, the eyes appear to bulge or pop out of the eyeballs, and the tongue protrudes. f. Violent coughing is usually accompanied by profuse sweating, involuntary urination, lethargy and exhaustion. g. The cough is usually provoked by crying, eating drinking or physical exertion. h. Convulsions may occur as a result of intracranial hemorrhage. i. Between paroxysms, the child appears well and no physical signs can be observed. j. This stage lasts from four to six weeks. 3. Convalescnet stage a. This stage is marked by a gradual decrease in the paroxysms of coughing in both in frequency and severity. At this stage, vomiting ceases. b. After about six weeks from the onset, the attack subsides.

COMPLICATIONS 1. Tissues around the bronchioles become inflamed and interstitial pneumonia occurs.


2. Air passages become obstructed by mucus plugs. This results in atelectasis. 3. Convulsions due to lack of oxygen on the tissues. 4. Umbilical hernia 5. Otitis media 6. Bronchopneumonia, the most dangerous complication 7. Severe malnutrition and starvation, due to persistent vomiting sleep and rest. DIAGNOSTIC PROCEDURES 1. Nasopharyngeal swabs 2. Sputum culture 3. CBC (leukocytosis) MODALITIES OF TREATMENT 1. Supportive therapy a. Fluid and electrolyte replacement b. Adequate nutrition c. Oxygen therapy 2. Antibiotics, such as erythromycin and ampicillin, are helpful in eliminating infection and to shorten the period communicability. 3. Hyperimmune convalescent serum or gammaglobulin has been found effective. NUSRING MANAGEMENT The major objective of care is to prevent complications; therefore, the following nursing management could be beneficial: 1. Isolation and medical asepsis should be carried out. 2. During a paroxysm, the patient should not be left alone. Suctioning equipment should be ready at all times for emergency use to avoid obstruction of the airways. 3. Sunshine and fresh air are important, but the patient should be protected from drafts. 4. The child should be kept as still and quiet as possible since activity and excitement precipitate paroxysm. 5. Provide warm baths and keep the bed and free from soiled linens. 6. Intake and output should be closely monitored. PREVENTION 1. Any cause of pertussis should be reported at one. 2. Previously immunized children should be given reinforcing injection/immunization. 3. Patient should be isolated 4 to 6weeks from the onset of illness. 4. Effective control measures should include efforts to locate subclinical or unreported cases. 5. Public education for active for active immunization and early diagnosis, together with reporting of all cases, should be encouraged.


Pneumonia is an acute infectious disease caused by Pneumococcus and its associated with general toxemia and a consolidation of one or more lobes of either or both lungs. It is an inflammation of the lungs in which the air sacs are filled with pus or exudate so that air is excluded and the lungs become solid. CAUSATIVE AGENTS Streptococcus pneumoniae Staphylococcus aureus Haemphilus influenza Klebsiella pneumonia (Friedlanders bacilli) Pneumonia is not a single disease. It can have over 30 different causes, the five main once being: 1. 2. 3. 4. 5. Bacteria Viruses Mycoplasma Other infectious agents, such as fungi Various chemicals

INCUBATION PERIOD The incubation period ranges from one to three days with a sudden onset of shaking chills, rapidly rising fever and stabbing chest pains aggravated by coughing and respiration. MODE OF TRANSMISSION 1. The disease is transmitted through droplet infection. Droplets from the mouth and nose of an infected person via the nasopharynx carry the infectious disease and the disease is transmitted through intimate contact with carriers. 2. The disease can also be transmitted through indirect contact. Contaminated objects may possibly carry the infectious disease. Systemic is possible through inhalation of caustic or toxic chemicals and aspiration of food, fluid or vomitus. Pneumonia is sometimes classified according to where and how the client was exposed to the disease: 1. Community-acquired pneumonia acquired in the course of ones daily life- at work, at school or the gym. If a hospitalized patient develops pneumonia in less than 36 hours during his stay in the hospital, he is diagnosed as having community acquired pneumonia.


Streptococcus pneumoniae (pneumococcus) is the most common bacterial cause of community-acquired pneumonia, although Hemophillus influenza, and Legionella can also be the cause of community-acquired pneumonia. 2. Nosocomial pneumonia is a pneumonia that develops while the client is in the hospital. Such pneumonia reflects the kind of nursing car given to the client. 3. Aspirations pneumonia occurs when foreign matter is inhaled (aspirated) into the lungs, most commonly when gastric contents enter the lungs after vomiting. Clients prone to Aspiration Pneumonia a. decreased level of consciousness b. clients with poor gag reflex c. the elderly d. the very young 4. pneumocystic carinii pneumonia. Caused by opportunistic, this type of pneumonia strikes people with a compromised immune system. (Organisms that are not normally harmful for healthy people can be extremely dangerous to those with HIV/AIDS, sickle cell disease and other conditions that impair the immune system.) 5. Actinomycosis Caused by an anaerobic Gram-positive bacterial species that is present in the mouth, known as Actinomyces Israeli Usually associated with poor dental hygiene The organism cause pleural infection, resulting in a thickened pleura, empyma and a fistulous tract. ANATOMICAL CLASSIFICATION OF PNEUMONIA 1. Bronchopneumonia (lobular or catarrhal pneumonia)

a. This is most common type of pneumonia b. Infection usually starts from the bronchus and bronchioles and spreads to the alveoli in the periphery. c. The lobules are inflamed and consolidated. d. Sometimes these lobules are not inflamed but are collapsed due to mucopurulent plugging of the bronchioles which supply them. e. This pneumonia is caused by Pneumococcus, klebsiella pneumonia, and Haemophillus influenza. f. The onset of this type of pneumonia is slow and the fever is lower. g. The period of communicability remains unknown; however, it is believed that the disease remains infectious while the exciting agent is given off the discharge from the nose and throat. 2. Lobar pneumonia (Croupous oneumonia) a. This is consolidation of the entire lobe. b. It manifests as chills, chest pain on breathing and cough with bloodstreaked sputum (prune juice or rusty in appearance). c. As the disease progresses, the prune-juice color of the sputum may be replaced by a thinner or yellowish color. 135

d. In severe cases, the heart weakness and death occurs from heart failure, edema of the lungs or severe general exhaustion. 3. Primary atypical pneumonia (viral pneumonia) a. It is a solidification of the lungs that comes in patches. b. Cough is often delayed in appearing and greenish to whitish secretions are often expelled by coughing on the 3rd to the 5th days.

GENERAL CLASSIFIACTION OF PNEUMONIA 1. Primary pneumonia is produced as a direct result of inhalation or aspiration of pathogens or noxious substances. It includes some cases of pneumococcal pneumonia, mycoplasma pneumonia and pneumonia caused by tubercle bacilli. 2. Secondary pneumonia develops as a complication of the disease. There are three types of secondary pneumonia. a. Primary pulmonary infection, which is usually viral, is predisposed to super-infection with an unrelated organism.( Example: Staphylococcal pneumonia superimposed upon viral pneumonia caused by type A influenza virus.) b. Secondary bacterial infection may follow damage caused by an initial noxious chemical insult to the lungs, such as aspiration of gastric contents. c. Hematogenous spread of bacterial pathogens from a distant focus may result is secondary pneumonia. PATHOGENESIS 1. Properties of the host and the prospective parasite are important determinants in the pathogenesis of pneumonia. 2. The lungs and the tracheobronchial tree below the larynx are normally kept sterile by the continuous upward movement of the mucociliary system and the clearing activities of the alveolar macrophages. 3. From the ambient atmosphere, the microorganism passes through the tracheobronchial tree to the parynchyma of the lungs. 4. The number of bacteria, their virulence and the health status of the host determine whether infection will be established.


5. When the bacteria establish themselves in the alveoli, they multiply and spread to the adjacent alveoli via the pores of Kohn by enzymatic destruction of tissues 6. Inflammation may spread to the pleural surface and stimulate effusion, which, when invaded by bacteria, become empyema. 7. Organism may also enter the lymphatic system, empty into the bloodstream and establish bacteremic infections such as meningitis, endocarditis and arthritis. 8. The presence of bacteria and their toxins results in fever and other systemic signs of infection.

PATHOLOGY The course of symptomatic disease may be divided into four stages: 1. Stage of lung engorgement a. The lung is heavy. b. The lung is dark red in color. c. The lung pits upon pressure with the fingers. d. The lung exudes a bubbly, blood-tinged froth. 2. Red hepatization a. The lung is still heavy. b. It sinks in water. c. It looks like a piece of red granite. 3. Gray hepatization a. The red color changes to gray. b. It looks like ordinary granite c. It is softer and tears more easily. d. When pressed, it exudes a purulent fluid. 4. Stage of resolution The inflammatory exudate is either absorbed by the bloodstream or expectorated. CLINICAL MANIFESTATION The symptoms of pneumonia vary, depending on the etiologic agent. 1. There is a sudden onset of shills with fever. 2. There is stabbing chest pain aggravated by respirations and coughing. 137

3. There is paroxysmal or choking cough. 4. The sputum is rusty or prune juice in color. This is considered pathognomonic to pneumonia. 5. There is pain on the abdomen mistaken as appendicitis. 6. Herpes may appear on the lips. 7. Body malaise 8. There is respiratory grunting with marked tachypnea and flaring of the nares. 9. There is labored respiration. 10.The pulse is rapid and bounding. 11.Diaphoresis 12.There is convulsions and vomiting in children. DIAGNOSTIC PROCEDURES The physician diagnoses the type of pneumonia suffered by the patient. But usually the diagnosis depends upon the history of the patient, the course and the physical findings. 1. Physical findings for patient with lobar pneumonia a. The patient has malar paleness, a flushed face, dilated pupils, highgrade fever, tachypnea, and a relatively low pulse. b. The patients sputum is rusty and experiences hacking paroxysmal cough. c. Chest movement on the affected side is diminished; percussions is dull 2. Chest x-ray is necessary to confirm the diagnostic examination. 3. Sputum analysis, semar and culture is important. 4. The patient may be subjected to blood/serologic exam. MODALITIES AND TREATMENT 1. Antimicrobial therapy varies with each agent. Example: a. Streptococcus. Pneumonia caused by this agent can be treated with macrolides for 7 to 10 days. b. Klebsiella. Treatment of pneumonia caused by this agent includes aminoglycosides and cephalosporins. c. Streptococcus. The patient may be given nafcillin or oxacillin for 14 days. d. Pneumocystis carinii. Cotrimoxazole or pentamidine may be given to patients with pneumonia caused by this agent. 2. Supportive measures include: a. Humidified oxygen therapy for hypoxia b. Mechanical ventilation for respiratory failure c. High-calorie diet and adequate fluid intake, unless contraindicated d. Absolute bedrest 3. Bronchodilators aminophylline may be of some benefit 4. Expectorants 5. Pain reliever for pleuritic pain


NURSING MANAGEMENT 1. Maintain the patients airway and adequate oxygenation. 2. Teach the patient how to cough and perform deep- breathing exercises to clear secretions. Advise him/her to do this often. 3. Obtain sputum specimens as needed. Teach the correct collection of specimen. 4. Maintain adequate nutrition to offset high-calorie utilization. 5. Provide a calm environment as the patient needs rest. 6. Control the spread of infection by disposing secretions properly. 7. Control temperature by implementing cooling measures. 8. Monitor vital signs closely and watch for danger signs like: marked dyspnea, thread, small, irregular pulse, delirium with extreme restlessness, cold, moist skin, and cyanosis and exhaustion. PREVENTION AND CONTROL Since pneumonia usually follows an injury to the respiratory system, efforts should include: 1. preventing common cold, influenza and other upper respiratory infections; 2. immunization with pneumonia vaccine; and 3. addressing environmental factors, such as exposure to cold, pollution and physical conditions of fatigue or alcoholism (There are contributory factors in lowering ones resistance to pneumonia.



Leading scientist worldwide investigating the cause of severe acute respiratory syndrome (SARS) confirm that a novel coronavirus is the primary cause of the disease. SARS was first reported in China in November 2002, with over 8,300 cases and 812 deaths reported by the beginning of July 2003. CLINICAL CRITERIA 1. Asymptomatic or mild respiratory illness with a temperature of .>100.4F (>38C) 2. One or more clinical findings of respiratory illness (e.g., cough, shortness of breath, difficulty in breathing or hypoxia)


EPIDEMIOLOGIC CRITERIA 1. Travel (including transit in an airport) within 10 days of the onset of symptoms to an area with current or previously documented or suspected community transmission of SARS. 2. Close contact within 10 days of the most of symptoms with a person known or suspected to have SARS. MODE OF TRANSMISSION 1. The primary mode of transmission appears to be direct. Mucous membranes (especially those of the eye, nose, and mouths)are always involved. 2. Contact with infectious respiratory droplets and / or through exposure to fomites. 3. Transmission through casual and social contact occasionally occurs as a result of intense exposure to a case of SARS (in workplaces, in vehicles) or in high-risk transmission setting, such as healthcare and household settings. 4. Contamination of inanimate materials or objects by infectious respiratory secretions or body fluids (saliva, tears, urine, and stools) which have been found to contain the virus.


FOR HOW LONG WILL THE SARS VIRUS EXIST ON SURFACE? 1. The virus is stable in urine and feces at room temperature for at least 1 to 2 days and in stools from patients with diarrhea for up to 4 days. 2. It survives on paper, on a plastered wall after 36 hours, on a plastic surface or stainless steel after 72 hours and on a glass slide after 96 hours. 3. Hospital environmental samples from a number of sites , including walls and ventilation systems, have tested positives for SARS virus. 4. The virus loses its infectivity after exposure to different commonly-used disinfectants and fixatives. Heat at 56C rapidly kills the virus. 5. Other risk factors: households contact with a probable case of SARS increasing age male sex presence of co-morbidities

WHAT ARE THE SIGNS AND SYMPTOMS OF SARS? 1. Sudden onset of high-grade fever, usually greater than 38C 2. Headache and overall feeling of discomfort and body aches 3. Mild respiratory symptoms at the onset; 2 days, dry cough and respiratory difficulty TREATMENT No specific treatment recommendation can be made at this time. Empiric therapy should include coverage for organisms associated with any community-acquired pneumonia of unclear etiology, including agents which activity against both typical and atypical respiratory pathogens, treatment choices may be influenced by the severity of the illness. Consultation is recommended. CLINICAL COURSE AND MANAGEMENT OF SARS 1. It is difficult to decide on the appropriate time to discharge a SARS patient. 2. SARS appears to have lingering after-effects once the acute phase of the disease ends. 3. The psychosocial aspects of this illness should not be underestimated. PREVENTIVE MEASURES 1. Consult a doctor promptly if there are respiratory symptoms suchs as fever, malaise, chills, headache, joint pain, dizziness, rigors, cough sore throat and runny nose. Early treatment is the KEY. 2. Build up good body immunity. This means having a proper diet, getting regular exercise and adequate rest, reducing stress and avoiding smoking. 3. Practice good personal hygiene. Cover the nose and mouth when sneezing or coughing. 4. Wear a mask if you develop a runny nose, sore throat or cough.


5. Wear a protective mask in public areas, classrooms, computers rooms, public transport etc. 6. Wash hands properly and keep them clean, use liquid soap for hand washing and disposable towels for drying hands.

(Kochs Disease/Phthisis/Consumption Disease) Tuberculosis is a chronic, subacute or acute respiratory disease commonly affecting the lungs characterized by the formation of tubercles in the tissues which tent to undergo caseation, necrosis and calcification. ETIOLOGIC AGENT The causative agents are rod-shape organisms Mycobacterium tuberculosis and M.africanum in humans and M. bovis in cattle. INCUBATION PERIOD The incubation period is from 2 to 10 weeks. PERIOD OF COMMUNICABILITY The patient is capable of discharging the organism all through his/ her life if he /she remains untreated. The disease is highly communicable during its active phase. MODE OF TRANSMISSION The disease is transmitted by the deliberate inoculation of the microorganism respiratory droplets. 1. The disease is transmitted through the inhalation of organism directly in to the lungs from contaminated air. 2. It can also be transmitted through direct or indirect contact with affected persons, usually by discharges from respiratory tract by means of coughing, sneezing or kissing. 3. The disease is transmitted through contact with contaminated eating or drinking utensils. 4. Rarely is the disease transmitted through skin lesions.


SOURCE OF INFECTION Sputum, blood from hemoptysis, nasal discharge and saliva QUANTITATIVE CLASSIFICATION OF TUBERCULOSIS 1. Minimal characterized by small lesions without demonstrable excavation that are confined to a small part or both lungs. 2. Moderately advanced a. Once or both lungs may be involved. b. The volume affected should not extend to one lobe. c. The total diameter of the cavity should exceed 4cm. 3. Advanced characterized by lesions that are more extensive than moderate CLINCAL CLASSIFICATION 1. Inactive TB a. Symptoms of tuberculosis are absent. b. Sputum is negative for tubercle bacilli after repeated examinations. c. There is no evidence of cavities on chest x-ray. 2. Active a. The tuberculin test is positive. b. X-ray of the chest is generally progressive. c. Symptoms due to lesions are usually present. d. Sputum and gastric contents are positive for tubercle bacilli. 3. Activity not determined Activity has not been determined from a suitable period of observation or adequate laboratory and x-ray studies. CLINICAL MANIFESTATIONS 1. 2. 3. 4. 5. 6. 7. 8. Afternoon rise in temperature Night sweating Body malaise and weight loss Dry to productive cough Dyspnea and hoarseness of voice Hemoptysis (considered pathognomonic of the disease) Occasional chest pains Sputum positive for AFB 143

PATHOGENESIS/PATHOLOGY After gaining entry into the body, the organism penetrates the lining of the respiratory tract or the intestinal mucosa, is picked up by lymph or blood channels, and reaches the lungs or other organs where it lodges and produces the first lesion, the tubercle, from where the disease got its name. This formation of the tubercle is due to the structural changes in the tissues brought about by tubercle bacillus. Usually, the site is in the parenchyma of the lungs and is termed Ghons tubercle. Then, the bacilli will establish themselves in the alveoli of the lungs, the walls of the blood vessels, in the lymph channels or glands or in the walls of the bronchi. The bacteria replicate within the macrophages for 2 to 3 weeks before spreading throughout the body. Some bacteria are not completely killed and can remain dormant for years. Granulomas become dormant and are sealed off with scar tissue. If the bacilli survive, they may reactive years later. What triggers reactivation is not well understood. After 5 years or more, bacteria activate some immune cells to release substances that liquefy the bacteria-containing center of the granuloma. When a granuloma and the surrounding tissue erode, the liquefied material is discharged into the airway and a cavity forms in the lung. Oxygen and carbon dioxide the freely enter the spaces, and the bacilli replicate in great numbers. Bacilli spread through air passages from a cavity to other parts of the lungs and to the larynx. Swallowed with microorganisms may cause lesions in the alimentary tract.


DIAGNOSTIC PROCEDURES 1. Sputum analysis for AFB (confirmatory) 2. Chest x-ray 3. Tuberculin testing a. Mantaux test (PPD) b. Tine test (OT) c. Heaf test (LT) MODALITIES OF TREATMENT 1. Short-course chemotherapy consisting of isoniazid (INH, rifampicin, pyrazinamide (PZA), and ethambutol may be given for e period of 6 months. 2. Patients with drug resistance may be given second-line drugs such as capreomycin, streptomycin, cycloserine, amikacin and quinolone. 3. WHO recommends the directly observed treatment , short-course (DOTS) to prevent non-compliance. The health worker ensures that the patient takes his/her drugs. 4. If the medicine is taken incorrectly, the patient becomes resistant to anti-TB drugs. This is very dangerous because if the disease recurs it becomes hard to treat the second time around. 5. Relapsing patients usually become resistant to individual drugs (INH, rifampicin, ethambutol, and PZA). They are given a combination of the abovementioned drugs.


OTHER DISEASES/PROBLEMS ASSOCIATED WITH PTB 1. 2. 3. 4. 5. 6. Older age groups Diabetes mellitus Chronic alcoholism Psychiatric patient Hematologic disorder HIV infection

NURSING MANAGEMENT 1. Maintain respiratory isolation until the patient responds to treatment or until he/she is no longer contagious. 2. Administer medicines as ordered. 3. Always check the sputum for blood or purulent expectoration. 4. Encourage questions and conversation so that the patient can air his/her feelings. 5. Teach or educate the patient about PTB. 6. Encourage the patient to stop smoking. 7. Teach the patient to cough or sneeze onto tissue paper and dispose of secretions properly. 8. Advise the patient to get plenty of rest and eat balanced meals. 9. Be alert for signs of drugs reaction. 10.If the patient is receiving ethambutol, watch out for optic neuritis. If it develops discontinue the drug. 11.If the patient is receiving rifampicin, watch out for hepatitis and purpura. Observe the patient for other complications like hemoptysis. 12.Emphasize the importance of regular follow-up examinations and instruct the patient and his/her family about the signs and symptoms of recurring TB. PREVENTION AND CONTROL 1. 2. 3. 4. Submit all babies for BCG immunization. Avoid overcrowding. Improve nutritional and health status. Advise persons who have been exposed to infected persons to receive the tuberculin test and, if necessary, chest x-ray and prophylactic isoniazid.

Disseminated histoplasmosis is a fungal infection that occurs after inhaling the spores of the fungus Histoplasma capsulatum.


CAUSES, INCIDENCE, AND RISK FACTORS Histoplasmosis is caused by a fungus found in the central and eastern United States (Mississippi and Ohio River Valley), eastern Canada, Mexico, Central America, South America, Africa, and Southeast Asia. Most cases are mild or without symptoms. Acute pulmonary histoplasmosis may occur in epidemics after heavy exposure. Progressive or spreading (disseminated) and chronic disease can also occur. In disseminated disease, the infection has spread to other organs from the lungs through the bloodstream. The liver and spleen are usually enlarged, and any body organ may be involved. Ulcerations of the mouth or gastrointestinal tract may occur. Risk factors are travel to or residence within the central or eastern United States, and exposure to the droppings of birds and bats.


SYMPTOMS Chills Cough Fever Headache Joint pain Mental status changes Muscle aches and stiffness Nausea, vomiting Possible rash (erythema nodosum) Skin lesions Visual changes (chorioretinitis)

SIGNS AND TESTS A physical examination may show abnormalities throughout the body. Tests used to diagnose disseminated histoplasmosis may include:

Abdominal CT scan Abdominal ultrasound Biopsy or culture of affected organs, bone marrow, liver, lymph node, lung, or skin Blood cultures Chest x-ray Complete blood count (CBC) Histoplasma urinary antigen test MRI scan of the affected organs

TREATMENT Doctors prescribe antifungal medications to control the infection. Most patients should be treated for a year or more. Those who have suppressed immune systems (for example, from AIDS) may need lifelong treatment. PROGNOSIS The disease may progress rapidly and death can occur. COMPLICATIONS Multiple organs are affected. PREVENTION Avoiding travel to areas where this spore is found can prevent the disease, but this may not be practical. Avoid bird or bat droppings if you are in one of these areas, especially if you are immunosuppressed.


The common cold usually causes a runny nose, nasal congestion, and sneezing. You may also have a sore throat, cough, headache, or other symptoms.

CAUSES, INCIDENCE, AND RISK FACTORS It is called the common cold for good reason. There are over one billion colds in the United States each year. You and your children will probably have more colds than any other type of illness. Colds are the most common reason that children miss school and parents miss work. Parents often get colds from their children. Children can get many colds every year. They usually get them from other children. A cold can spread quickly through schools or daycares. Colds can occur at any time of the year, but they are most common in the winter or rainy seasons. A cold virus spreads through tiny, air droplets that are released when the sick person sneezes, coughs, or blows their nose. You can catch a cold if:

A person with a cold sneezes, coughs, or blows their nose near you You touch your nose, eyes, or mouth after you have touched something contamined by the virus, such as a toy or doorknob.

People are most contagious for the first 2 to 3 days of a cold. A cold is usually not contagious after the first week. 149

SYMPTOMS Cold symptoms usually start about 2 or 3 days after you came in contact with the virus, although it could take up to a week. Symptoms mostly affect the nose. The most common cold symptoms are:

Nasal congestion Runny nose Scratchy throat Sneezing

Adults and older children with colds generally have a low fever or no fever. Young children often run a fever around 100-102F. Depending on which virus caused your cold, you may also have:

Cough Decreased appetite Headache Muscle aches Postnasal drip Sore throat

TREATMENT Get plenty of rest and drink plenty of fluids. COLD MEDICINES Over-the-counter cold and cough medicines may help ease symptoms in adults and older children. They do not make your cold go away faster, but can help you feel better. Over-the-counter (OTC) cough and cold medicines are not recommended for children under age 6. Talk to your doctor before giving your child any type of over-the-counter or nonprescription cough medicine, even if the label says it is made for children. These medicines likely will not work for children, and may have serious side effects. 150

ANTIBIOTICS Antibiotics should not be used to treat a common cold. They will not help and may make the situation worse. Thick yellow or green nasal discharge normally occurs with a cold after a few days. If it does not get better within 10 to 14 days, then your doctor may prescribe antibiotics.

OTHER MEDICINES Newer antiviral drugs used to relieve flu symptoms do not help reduce cold symptoms. ALTERNATIVE TREATMENTS Alternative treatments that have been used for colds include:

Chicken soup Vitamin C Zinc Echinacea

Chicken soup has been used for treating common colds for centuries. It may really help. The heat, fluid, and salt may help you fight the infection. Vitamin C is a popular remedy for the common cold. Research shows it does not prevent colds in many adults, but people who take vitamin C regularly seem to have slightly shorter colds and milder symptoms. Taking vitamin C after your have a cold doesn't seem to be helpful. Zinc supplements taken for at least 5 days may reduce your risk of catching the common cold. Taking a zinc supplement within 24 hours of when you first feel sick may make your cold symptoms less severe and help them go away faster. Echinacea is a herb that has been promoted as a natural way for preventing colds and the flu, and for making symptoms less severe. However, high-quality studies have failed to show that this herb helps prevent or treat colds. Alternative treatments are safe for most people. However, some alternative treatments may cause side effects or allergic reactions. For example, some people are allergic to echinacea. Herbs and supplements may also change the way other medicines work. Talk to your doctor before trying an alternative treatment.

COMPLICATIONS Colds are the most common trigger of asthma symptoms in children with asthma. A cold may also lead to: Bronchitis Ear infection Pneumonia Sinusitis


PREVENTION Here are five proven ways to help lower your chances of getting sick: Always wash your hands: Children and adults should wash hands after nose-wiping, diapering, and using the bathroom, and before eating and preparing food. Disinfect: Clean commonly touched surfaces (such as sink handles, door knobs, and sleeping mats) with an EPA-approved disinfectant. Choose smaller daycare classes: Attending a day care where there are six or fewer children dramatically reduces the spread of germs. Use instant hand sanitizers: These products use alcohol to destroy germs. They are an antiseptic, not an antibiotic, so resistance can't develop. A little dab will kill 99.99% of germs without any water or towels. Use paper towels instead of sharing cloth towels.

The immune system helps your body fight off infection. Here are six ways to support the immune system: Avoid secondhand smoke: Keep as far away from secondhand smoke as possible. It is responsible for many health problems, including colds. Avoid unnecessary antibiotics: Using antibiotics too often leads to antibiotic resistance. The more you use antibiotics, the more likely the medicines may not work as well for you in the future. That means, you have a higher chance of getting sick with longer, more stubborn infections. Breastfeed: Breast milk is known to protect against respiratory tract infections in children, even years after you stop breastfeeding. Kids who are not breastfeed get about five times more ear infections than those who are. Drink water: Fluids help your immune system work properly. Eat yogurt: Certain yogurt contains "active cultures," or beneficial bacteria that helps prevent colds. Get enough sleep: Not getting enough sleep makes you more likely to get sick.


(Breakbone Fever/Hemorrhagic Fever/Dandy Fever/Infectious Thrombocytopenia Pupura) Dengue fever is an acute febrile disease caused by infection with one of the serotypes of dengue virus, which is transmitted by mosquito genus Aedes. It refers to a benign form of disease with systemic symptoms, fever, and often rash associated with pain and in the joints, bones, and behind the eyes. Dengue hemorrhagic fever is a severe, sometimes fatal manifestation of the dengue virus infection characterized by a bleeding diathesis and hypovolemic shock.

ETIOLOGIC AGENT 1. Flaviviruses 1,2,3,4, a familyof Togaviridae, are small viruses that contain single-stranded RNA. 2. Arboviruse group B MODE OF TRANSMISSION 1. Bite of an infected mosquito,principally the Aedes aegypti b. Aedes agypti is day biting mosquito (they appear two hours after sunrise and two hours before sunset). c. It breeds in areas of stagnant water. d. It has limited, low-flying movement. e. It has fine white dots at the base of the wings and white bands on the legs. 2. Aedes albopictus may contribute to the transmission of the dengue virus in rural areas. 3. other contributory mosquitoes: d. Aedes polymensis e. Aedes scutellaris simplex


INCUBATION PERIOD The incubation period is three to fourteen days; commonly 7 to 10days. PERIOD OF COMMUNICABILITY 1. Patients are usually infective to the mosquito from a day before the febrile period to the end of it. 2. The mosquito becomes infective from day 8 to 12 after the blood meal and remains infective throughout its life. SOURCES OF INFECTION 1. Infected persons the virus is present in the blood of patients during the acute phase of the disease and will become a reservoir of the virus, sucked by mosquitoes, which may then transmit the disease. 2. Standing water any stagnant water in the household and its premises are usual breeding places of these mosquitoes. INCIDENCE 1. Age- Dengue fever may occur at any age, but it is common among children and peaks between 4 to 9 years old. 2. Sex- both sexes can be affected. 3. Season it is more frequent during the rainy season. 4. Location dengue fever is more prevalent in urban communities. PATHOGENESIS 1. The infectious virus is deposited in the skin by the vector and initial replication occurs that at the site of infection and in local lymphatic tissues. 2. Within a few days, viremia occurs, lasting until the 4th or 5th day after the onset of symptoms. 3. Evidence indicates that macrophages are the principal site of replication. 4. At the site of petechial rash, non-specific changes are noted, which include endothelial swelling, perivascular edema, and extravasation of blood. 5. There is marked increase in vascular permeability, hypotension, hemoconcentration, thrombocytopenia with increased platelet agglutinability, and or moderate dessiminated intravascular coagulation. 6. The most serious pathophysiological abnormality is hypovolemic shock resulting from the increased permeability of the vascular endothelium and loss of plasma from the intravascular space. CLINICAL MANIFESTATIONS A. Dengue fever 1. Prodromal symptoms characterized by: 154

a. malaise and anorexia up to 12 hour b. fever and chills accompanied by severe frontal headache, ocular pain ,myalgia with sever backache, and arthralgia 2. Nausea and vomiting 3. Fever is non-remitting and persists for 3 to 7 days. 4. Rash is more prominent on the extremities and the trunk. It may involve the face in some isolated cases. 5. Petechial usually appears near the end of the febrile period and most the face in some isolated cases. B. Dengue Hemorrhagic Fever (DHF) This severe form of dengue virus infection is manifested by fever, hemorrhagic diathesis, hepatomegaly and hypovolemic shock. PHASES OF THE ILLNESS 1. b. c. d. e. f. g. Initial febrile phase lasting from two to three days fever(39-40C) accompanied by headache febrile convulsions may appear palms and sole are usually flushed positive tourniquet test anorexia, vomiting, myalgia maculopapular or petechial rash may be present and usually starts in the distal portion of the extremities (sparing the axilla and chest), the skin appears purple, with blanched areas of varying size (Hermans sign, considered pathognomonic to the disease). h. generalized or abdominal pain i. hemorrhagic manifestations like positive tourniquet test, purpura, epistaxis and gum bleeding may be present 2. Circulatory phase a. There is a fall of temperature accompanied by profound circulatory changes, usually on the 3rd to 5th days. b. Patient becomes restless, with cool, clammy skin. c. Cyanosis is present. d. Profound thrombocytopenia accompanies the onset of shock. e. Bleeding diathesis may become more severe and lead to GIT hemorrhage. f. Shock may occur due to loss of plasma from the intravascular spaces; hemoconcentration with markedly elevated hematocrit is present. g. Pulse is rapid and weak; pulse pressure becomes narrow and blood pressure may drop to an unobtainable level. h. Untreated shock may result in coma; metabolic acidosis and death may occur within two days. i. With effective therapy, recovery may follow in 2 to 3 days.


CLASSIFICATION ACCORDING TO SEVERITY (Halstead & Nimmanitya) Grade I There is fever accompanied with non-specific constitutional symptoms and the only hemorrhagic manifestation is positive (+) in the tourniquet test. Grade II All signs of Grade I, plus spontaneous bleeding from the nose, gums, and GIT, are present.

Grade III There is the pressure of circulatory failure, as manifested by a weak pulse, narrow pulse pressure, hypotension, cold, clammy skin, and restlessness. Grade IV There is profound shock, and undetectable blood pressure and pulse. COMPLICATIONS 1. Dengue fever a. Epistaxis; menorrhagia b. Gastrointestinal bleeding c. Concomitant gastrointestinal disorder (peptic ulcer) 2. DHF a. Metabolic acidosis b. Hyperkalemia c. Tissue anoxia d. Hemorrhage into the CNS or adrenal glands e. Uterine bleeding may occur f. Myocarditis 3. Severe manifestation Dengue encephalopathy is manifested by increasing restlessness, apprehension or anxiety, disturbed sensorium, convulsions spacity, and Hyporeflexia


DIAGNOSTIC TESTS 1. Tourniquet test- screening test, done by occluding the arm veins for about 5 minutes to detect capillary fragility. 2. Platelet count (decreased) confirmatory test 3. Hemoconcentration an increase of at least 20% in the hematocrit or s steady rise in the hematocrit 4. Occult blood 5. Hemoglobin determination TREATMENT MODALITIES There is no effective antiviral therapy for dengue fever. Treatment is entirely symptomatic. 1. Analgesic drugs other than aspirin may be required for relief from headache ocular pain, and myalgia. 2. Initial phase may require intravenous infusion to prevent dehydration and replacement of plasma. 3. Blood transfusion is indicated in patient with severe bleeding. 4. Oxygen therapy is indicated for all patients in shock. 5. Sedatives may be needed to allay anxiety and apprehension. NURSING MANAGEMENT 1. Patient should be kept in a mosquito-free environment to avoid further transmission of infection. 2. Keep patient at rest during bleeding episodes. 3. Vital signs must be promptly monitored. 4. In cases of nose bleeding, keep the patients trunk elevated; apply ice bag to the bridge of nose to the forehead. 5. Observe fours signs of shock, such as slow pulse, cold, clammy skin, prostration, and fall of blood pressure. 6. Restore blood volume by putting the patient in trendelenburg position to provide greater blood volume to the head part. 7. Patient with damage is not infectious; therefore, isolation is not required. PREVENTION AND CONTROL 1. Health education 2. Early detection and treatment of cases will not worsen the victims condition. 3. Treat mosquito nets with insecticides. 4. House spraying is advised. 5. Eliminating vector by: a. changing water and scrubbing sides of flower vases once a week, b. destroying the breeding places of mosquitoes by cleaning the surroundings, and c. keeping the water containers covered. 6. Avoid hanging too many clothes inside the house. 7. Case findings.


(Ague) Malaria is an acute and chronic parasitic disease transmitted by the bite of infected mosquitoes and is confined mainly to tropical and subtropical areas. This disease causes more disability and heavier economic burden than any other parasitic disease.

ETIOLOGIC AGENT Protozoa of genus plasmodia 1. The disease is caused by four species of protozoa: a. Plasmodium falciparum (malignant tertian) This is considered the most serious malarial infection because of the development of high parasitic densities in the blood (RBC). This type tends to cause agglutination, resulting in microembolus formation. This type is the most common in the Philippines. b. Plamosdium vivax (benign tertian) This is non-life threatening, except for the very young and the very old. It is manifested by chills every 48 hours on the 3rd day onward, especially if untreated. c. Plasmodium malariae (quartan) It is less frequency seen than the first two types. This species is non-life threatening. Fever and chills usually occur every 72 hours, usually on the 4th day after onset. d. Plasmodium ovale is the rare type of protozoan species. This type is rarely seen in the Philippines. 2. The primary vector of malaria is the female Anopheles mosquito which has the following characteristics: a. It breeds in clear, flowing and shaded streams, usually in the mountains. b. It is bigger in size than ordinary mosquitoes. c. It is brown in color d. It is a night-biting mosquito e. It usually does not bite a person in motion. f. It assumes a 36position when it alights on walls, trees, curtains and the like. INCUBATION PERIOD 1. 12 days for P. Falciparum 2. 14 days for P.vivax and ovale 3. 30 days for P. malariae 158

PERIOD OF COMMUNICABILITY An untreated or insufficiently treated patient may be the source of mosquito infection for more than three years in P. malariae, 1 to 2 years in P. vivax and not more than one year on P. falciparum. MODE OF TRANSMISSION 1. The disease is transmitted mechanically through the bite of an infected female Anopheles mosquito. 2. It can be transmitted parenterally through blood transfusion, 3. On rare occasions, it is transmitted from shared contaminated needles. 4. However, transplacental transmission of congenital malaria is a rare case.

CLINICAL MANIFESTATIONS 1. 2. 3. 4. 5. 6. 7. Paroxysms with shaking chills Rapidly rising fever with severe headache Profuse sweating Myalgia, with feeling of well-being in between Splenomegaly, hepatomegaly Orthostatic hypotension Paroxysms may last or 12 hours and may attack daily or every two days. 8. In children: a. Fever may be continuous; b. Convulsions and gastrointestinal symptoms are prominent; and c. Splenomegaly is present. 9. In cerebral malaria: a. There are severe headache, vomiting and changes in sensorium; and b. Jacksonian or grand mal seizure may occur. PATHOGENESIS 1. The parasite enters the mosquitos stomach through infected human blood obtained during a blood meal. 2. Within the stomach of the female mosquito, the female gametocyte matures into the female gamete and the male gametocyte divides into several male gametes. They undergo sexual conjugation and form a zygote. 3. The zygote matures into a motile form called the ookinete. 4. After a number of days, young parasites (sporozoites) are released and work their way into the salivary glands of the mosquito. The mosquito phase of the parasites life cycle lasts 8-35 days, depending on the species. 5. The organism is transmitted from the saliva into the victim when the mosquito bites. 159

6. The female alone plays the role of vector and definitive host in conveying the disease (sexual propagation). 7. In humans the organisms invade the RBC, where they grow and undergo asexual schizogony. 8. Erythrocytic merozoites are produced, leading to the rupture of RBCs upon the release of the tiny organisms. 9. Young merozoites invade a new batch of RBCs to start another schizonic cycle.


DIAGNOSTIC PROCEDURE 1. Malarial smear In this procedure, a film of blood is placed on a slide, stained and examined microscopically. 2. Rapid diagnostic test (RDT)- This is a blood test for malaria that can be conducted outside the laboratory and in the field. It gives results within 10 to 15 minutes. This is done to detect malarial parasite antigen in the blood.

MANAGEMENT 1. Medical a. Anti-malarial drugs Chloroquine (all species, except for P.malariae) Quinine Sulfadoxine for the resistant p.Falciparum Primaquine for relapses of P.vivax. and ovale b. Erythrocyte exchange transfusion for rapid production of high levels parasites in the blood. 2. Nursing management a. The patient must be closely monitored. b. Intake and output should be closely monitored to prevent pulmonary edema. Daily monitoring of patients serum bilirubin, BUN creatinine and parasitic count If the patient exhibits respiratory and renal symptoms, determine the arterial blood gas and plasma electrolyte. c. During the febrile stage, tepid sponges, alcohol rubs and an ice cap on the head help bring the temperature down. d. Application of external heat and hot drinks during the chilling stage are helpful. e. Provide comfort and psychological support. f. Encourage the patient to take plenty of fluids. g. As the temperature falls and sweating begins, warm sponge baths may be given. h. The bed and clothing should be kept dry. i. Watch for neurologic toxicity (from quinine infusion) like muscular twitching delirium, confusion, convulsion and coma. j. Evaluate the degree of anemia. k. Watch for any signs, especially abnormal bleeding. l. Consider severe malaria as medical emergency that requires close monitoring of vital PREVENTION AND CONTROL 1. All malaria cases should be reported. 2. Thorough screening of all infected persons from mosquitoes is important 3. Breeding places of mosquitoes must be destroyed. 4. Homes should be sprayed with effective insecticides that have residual actions on the walls. 161

5. Mosquito nets should be used, especially in infected areas. 6. Insect repellents must be applied to the exposed portion of the body. 7. People living in malaria infested areas should not donate blood for at least three years. 8. Blood donors should be properly screened.



(Soft Chancre/ Soft Sore/ Suicus Mole) Chancroid is a sexually-transmitted disease characterized by painful genital ulcers and inguinal adenitis. It affects males more than females.

INFECTIOUS AGENT Haemophilus discreyi, a Gram (-), non-spore-forming streptobacillus INCUBATION PERIOD The incubation period is one to fourteen days, with an average of three to five days. PATHOLOGY Lesions are usually confined to the genital sites most commonly traumatized during sexual contact. A lesion begins as a small papule surrounded by a zone of erythema and soon erodes to produces a sharply-circumscribed, non-endurated ulcer with a granulating base. Multiple lesions may develop rapidly by autoinoculation and supurative adenitis is evident. In a women the most common location for ulcers is the labia majora.Kissing ulcers may develop. These ulcers that occur on opposing surfaces of labia. Other areas, such as the labia minora, perineal area, and inner thighs, may also be involved. The most common symptoms in women are pain during urination and intercourse.


The initial ulcer may be mistaken as a hard chancre- the typical sore of primary syphilis as opposed to the soft chancre of chancroid. Approximately one-third of infected individuals develop enlargements of the inguinal lymph nodes, (nodes located in the folds between the legs and lower abdomen). Half of those who develop swelling of the inguinal lymph nodes progress to a point where nodes rupture through the skin, producing draining abscesses. The swollen lymph nodes and abscesses are often referred to as buboes. The lesions show three layers: 1. The shallow surface contains many polymorphonuclear cells, red blood cells, and debris. 2. The wide middle zone is edematous and shows endothelial proliferations of blood vessels but lacks fibroplastic repair. 3. In deep zone, there is a densed infiltration of plasma cells and lymphocytes. SIGNS AND SYMPTOMS 1. Small lesions appear at the groin or inner thigh. In males, it may appear on the penis and in females, on the vulva, vagina, and cervix. 2. Sometimes these lesions may erupt on the lips, tongue, breasts, or navel. 3. The papule rapidly ulcerates, becoming painful, soft and malodorous. 4. The papules bleed easily and produce pus. 5. Within two or three weeks, inguinal adenitis may develop, creating suppurated inflamed nodes that may rupture into large ulcer or buboes. 6. During the healing stage, phimosis may develop. DIAGNOSIS 1. Gram stain of ulcer exudate 2. Biopsy 3. Darkfield examination and serologic test TREATMENT 1. Azithromycin 500 mg, taken orally as a single dose 2. Erythromycin 500 mg , 1cap BID x 7 days 3. Ceftriaxone 250mg IM as a single dose NURSING MANAGEMENT 1. Standard precaution should be practiced. 2. Check for drug allergy. 3. Lotion, cream, or oil should be applied on lesions.


4. Instruct the patient to abstain from sexual contact until healing is complete(two weeks) 5. The patient should wash his/ her genitalia daily with soap and water. PREVENTION 1. Advice client to avoid sexual contact with infected persons. 2. Use condoms during sexual activity. 3. Wash the genitalia with soap and water after sexual activity.


Chlamydial is a sexual transmitted disease caused by the bacteria Chlamydia trachomatis. When transmitted through sexual contact, the bacteria can infect the urinary and reproductive organs. The term chlamydia typically refers to Chlamydial trachomatis, the STD. But two other types of this bacteria can lead to illness. 1. Chlamydia pneumonia, which can spread through coughing and sneezing, and 2. Chlamydia psittaci, which birds can pass to humans. Chlamydia can be treated with antibiotics. But in many cases, it causes no symptoms, so people can be infected without even knowing it. If chlamydial infections go untreated, they can lead to more serious health problems, such as infertility. So its important to take the precautions to prevent chlamydia, and if its suspected, to seek treatment as soon as possible. Untreated chlamydial infections can lead epididymitis, salphingitis, pelvic inflammatory disease, and eventually sterility. Some studies show that women infected with this organism may have spontaneous abortion and sometimes premature delivery.


MODE OF TRANSMISSION 1. The disease is transmitted through vaginal or rectal intercourse. 2. The disease is also transmitted through oral-genital contact with infected person. 3. Conjunctivitis, otitis media, and pneumonia may develop in children born to mothers with chlamydial infection passed through the birth canal. SIGNS AND SYMPTOMS Signs and symptoms vary according to the part affected. 1. Women with cervicitis may develop cervical erosion, mucopurulent discharge, pelvic pain, and dyspareunia. 2. Women with endometritis or salphingitis may experience signs of pelvic inflammatory disease, such as pain and tenderness of the abdomen, cervix, uterus, and lymph nodes; chills; fever; breakthrough bleeding; and bleeding after intercourse. 3. Women with urethral syndrome may experience dysuria, pyuria, and urinary frequency. 4. Men who have urethral syndrome may experience dysuria, erythema, tenderness of the urethral meatus, urinary frequency, pruritus, and urethral discharge. 5. Men with epididymitis may experience painful scrotal swelling and urethral discharge. 6. Some patients may have diarrhea, tenesmus, pruritus, bloody or mucopurulent discharge and diffuse or discrete ulceration in the rectosigmoid colon. 166

DIAGNOSIS 1. 2. 3. 4. Swab from the site of infection Culture of aspirated materials ELISA Direct fluorescent antibody test

TREATMENT 1. Doxycycline oral for seven days 2. Azithromycin in single dose NURSING MANAGEMENT 1. Practice universal precaution 2. Suggest that both partners should submit for HIV testing. 3. Check newborn for signs of chlamydial infection.

(Clap/Flores Blancas/Gleet) Gonorrhea is a sexually-transmitted bacterial disease involving the mucosal lining of the genitourinary tract, the rectum, and pharynx. INFECTIOUS AGENT Neiserria gonorrhoeae or gonococcus 1. 2. 3. 4. 5. This is a gram-negative coccus found in pairs. This occurs is non-spore former and non-motile. It is fragile and does not survive long outside the body. It is readily killed by drying, sunlight, and ultraviolet light. It may be killed ordinary disinfectants.


INCUBATION PERIOD The incubation period is from three to twenty-one days and averages from three to five days. PERIOD OF COMMUNICABILITY The period of communicability of the disease is varied. The infected person remains communicable as long as the organism are present in secretions and discharges. MODE OF TRANSMISSION 1. Bacteria are transmitted by contact with exudates from the mucous membranes of infected persons, usually as a result of a sexual activity.


2. Transmission may occur in utero upon the rupture of membranes, as observed in infants delivered by cesarean section after the membrane ruptures. 3. Bacteria are transmitted through direct contact with contaminated vaginal secretions of the mother as the baby comes out of the birth canal. 4. It may be acquired through sexual contact (orogenital, anogenital) between opposite sexes, as well as of the same sex. 5. Bacteria may also be transmitted through fomites. PATHOLOGY 1. After infection, gonococci become adherent to the urethral epithelium. 2. Penetration of the mucosa usually elicits an acute inflammatory response consisting mainly of polymorphonuclear leukocytes in the sub-mucosa. 3. Inflammatory edema of the gland ducts or plugs of debris obstruct drainage to form microabscesses that may coalesce to form large abscesses. 4. Infection tends to spread along mucosal surfaces and may involve the fallopian tubes and the endometrium and eventually enter the peritoneal cavity of women. 5. Scarring from this abscess formation or tubal involvement may lead to strictures and sterility. 6. A similar mechanism, epididymitis, and, therefore, possible sterility may occur in men.

CLINICAL MANIFESTATION 1. a. b. c. d. e. f. g. In Females Burning sensation and frequent urination Yellowish purulent vaginal discharge Redness and swelling of the genitals Burning sensation and itching of the vaginal area Urinary frequency and pain on urination Urethritis or cervicitis occurs initially a few days after exposure Endometritis salphingitis or pelvic peritonitis are symptom of uterine invasion which may lead to infertility. There is the presence of early signs of pelvic infection like fever, nausea and vomiting, and abdominal pain/ tenderness. h. Pregnant women with gonorrhea may infect the eye of her baby during the passage through the birth canal.


2. In Males After a three-to six-day incubation period, the following may be noted: a. Dysuria with purulent discharge (gleet) from the urethra two to seven days after exposure. b. Rectal infection is common in homosexuals. c. Inflammation of the urethra can cause strictures which can prevent the passage of urine. d. Prostatitis e. Urethritis f. Pelvic pain and fever

OTHER CLINICAL FEATURES VARY ACCORDING TO SITE INVOLVED 1. Urethra a. Dysuria b. Urinary frequency and incontinence c. Purulent discharge d. Itching e. Red and edematous meatus 2. Vulva a. Occasional itching b. Burning and pain due to exudates from the adjacent infected area c. Vulva symptoms are more severe before puberty and after menopause 3. Vagina a. Engorgement, redness, and swelling b. Profuse purulent discharge 4. Pelvis a. Severe pelvic and lower abdominal pain b. muscle rigidity, tenderness and abdominal distention 169

c. Tachycardia may develop in patients with PID and salphingitis 5. Liver a. RUQ pain 6. Other possible symptoms include pharyngitis, tonsillitis, rectal burning

COMPLICATIONS 1. 2. 3. 4. 5. 6. Sterility and pelvic inflammatory disease in women Epididymitis Arthritis Endocarditis Conjunctivitis Meningitis

DIAGNOSTIC EXAM 1. In females culture of specimen taken from the cervix and anal (inoculation of specimen on Thayer-Martin medium. The medium contains antibiotic that inhibits the growth of microorganism). 2. In males Gram stain TREATMENT MODALITIES 1. For uncomplicated gonorrhea in adults ceftriaxone 125-250 mg IM single dose; doxycycline 100mg orally BID x seven days. 2. For pregnant women- ceftriaxone, 125-250mg IM, single dose plus erythromycin, 500 mg orally for seven days. 3. Aqueous procaine penicillin 4 million units injected intramuscularly after a negative skin test. 170

4. Recommended initial regimen for disseminated gonococcal infection in adults and adolescents is 1 gram ceftriaxone IM or IV every 24 hours, or for patients allergic to beta-lactam antibiotics, 2 g spectinomycin IM every 12 hours. 5. All regimen should be continued for 24 to 48 hours after improvement begins, then therapy may be switched to the following regimens to complete one gull week of antimicrobial therapy: a. 400 mg cefixime p.o. twice a daily or 500mg ciprofloxacin p.o. 2x daily. Ciprofloxacin is contraindicated for children, adolescents, and pregnant and lactating women. b. Treatment for gonococcal conjunctivitis requires 1g single dose of ceftriaxone IM and irrigation of affected eye with normal saline solution. NURSING MANAGEMENT 1. Before treatment, ask the patient whether he/she has drug sensitivities watch closely for adverse effects during therapy. 2. Explain to the patient that until cultures prove negative, he/she is still infectious and can transmit gonococcal infection. 3. Practice standard precautions. 4. All information concerning the patient is considered confidential. There should be no discussion concerning the patient and the laboratory reports. 5. The patient should be isolated until he/she recovers from the disease. 6. For a patient with gonococcal arthritis, apply moist heat to relieve on the affected site. 7. Infants born to mothers positive for gonorrhea should instilled with one percent silver nitrate or any recommended ophthalmic prophylaxis onto both eyes at the time of birth. 8. Report all gonorrheal cases to health authorities, and for gonorrhea in children to Child Abuse Authorities. 9. Encourage patient to inform sexual contact so that they can seek treatment . Advise them to refrain from sexual intercourse until treatment is completed. SIGNS OF GONOCOCCAL OPTHALMIA NEONATOTUM Lid edema Bilateral conjunctival edema Abundant purulent discharge 2-3 days after birth Untreated gonococcal conjunctivitis can progress to corneal ulceration and blindness.


PREVENTION AND CONTROL 1. Sex education, not only in schools, but also in the community, must emphasize the mode of transmission and the source of the infection. 2. Case finding, contact tracing 3. Incidence of gonorrhea must be reported so that health authorities may be notified and contacts can be treated.

(Lues Venereal/ Morbus Gallicus) Syphilis is a chronic, infectious, sexually transmitted disease that usually begins in the mucous membranes and quickly becomes systemic. It is cause by spirochete and is acquired through sexual contact. It may also be congenital in nature. ETIOLOGIC AGENT The infection is caused by a spirochete, Treponema pallidum. 1. T. pallidum has no other host but a man. 2. From a fresh smear taken from a lesion, T.pallidum appears as a shiny, twirling thread twisting its way in a wave-like corkscrew motion through the debris in the smear. 3. It is believed that the spirochete can pass through the mucosa even though a crack on its surface may not be visible at the site of entry. 4. The organism is also able to pass through the placenta and infect the developing fetus within the body of a syphilitic mother. 5. The spirochete does not withstand drying, but withstands considerable temperature variation. 6. Based on studies, the organism has been found alive in a drinking glass a half-hour after the glass has been rinsed with cold water. SOURCES OF INFECTION 1. Discharge from obvious or concealed lesions of the skin or mucous membranes. 2. The semen, blood, tear and urine of infected persons. 3. Mucous discharges from the nose, eyes, genital tract or bowels 4. Surface lesions contain spirochetes in very high numbers. INCUBATION PERIOD The incubation period is from 10 to 90 days. The average is three weeks. 172

PERIOD OF COMMUNICABILITY The period of communicability is variable and indefinite. MODE OF TRANSMISSION 1. The disease can be transmitted through direct transmission, which occurs through any kind of intimate contact with an infected person. Mucus or glandular secretions from an infected individual is transmitted to the skin or mucous surface of any one with whom he comes in contact. 2. It can also be transmitted through indirect, e.g., articles freshly soiled with discharges or blood containing the organism. 3. It can also be transmitted through direct the placenta of a syphilitic mother. 4. Accidentally, the disease can be transmitted from a syphilitic baby to a wet nurse or to anyone carelessly handling diapers.

CLINICAL MANIFESTATIONS If the disease is untreated, it is characterized by the progression of the following stages 1. Primary syphilis a. Starts with one or more chancres that erupt in the genitalia, anus, nipples, tonsils or eyelids. b. These chancres, which are usually painless, start as papule and then erode. c. The chancres have endurated, raised edges and clear bases. d. Chancres disappear after three to six weeks even without treatment. e. These chancres are usually associated with lymphadenopathy that is either unilateral or bilateral. f. In women, chancres are often overlooked because they often develop on internal surfaces such as the cervix and the vaginal wall.


2. Secondary syphilis The development of mucocutaneous lesions and generalized lymphadenopathy signifies the onset of the secondary phase, which usually occurs from a few days to about eight weeks after the onset of the initial chancre. a. The rash of secondary syphilis can be macular, popular, pustule, or nodular. b. Lesions are of a uniform size, well-defined and generalized. c. Macules often erupt between rolls of fat on the trunk and on the arms, palms, soles, face, and scalp. d. In warm, moist areas of the body, such as the perineum, vulva and rolls of fats in the scrotum, the lesions enlarge and erode, producing highly contaminated pin or grayish-white lesions (condylomata lata). e. There are mild constitutional symptoms in the second stage. These include headache, anorexia, malaise, weight loss, nausea and vomiting, sore throat and possibly, slight fever. f. Alopecia may occur, but it is temporary. g. Nails become brittle and pitted.

3. Latent syphilis a. No clinical symptoms occur in latent syphilis, but a serologic test will prove reactive. b. Approximately two-thirds of patients remain asymptomatic until death.


4. Late syphilis a. Considered as a destructive but non-infectious stage b. Late syphilis has three subtypes: Late, benign syphilis Develops between 1 to 10 years after the infection. The typical lesion is the gumma, a chronic, superficial nodule, or a deep granulomtous lesion that is solitary, asymmetric, painless, and endurated. They may appear on the skin, bones, mucous membranes, upper respiratory tract, liver or stomach. Gummas can be found in any bone, particularly the long bones of the legs. The late syphilis It involves the liver. It can cause epigastric pain, tenderness, an enlarged spleen and anemia. If it affects the upper respiratory tract, it may cause perforation of the nasal septum or the palate. In severe cases, the disease causes the destruction of bones and other organs, which may lead to death. Cardiovascular syphilis develops about two years after the initial infection. The patient may appear asymptomatic but may fuffer from aortic regurgitation and aneurysm.


5. Congenital syphilis a. Once the treponema enters the fetal circulation, dissemination to all the tissues occur at once. The treponema multiplies and infects many organs. b. The fetus may be overwhelmed by the infection and die. The fetus will then be expelled by the uterus, leading to either miscarriage or stillbirth, depending on the stage of pregnancy. c. A syphilitic still born may have macerated appearance, with a collapsed skull and a protuberant abdomen. d. The skin is of a livid red color. On its surface may be seen a number of bullae filled with hemorrhagic fluid. e. On autopsy, the spleen and the liver are found to be enlarged, with intense pancreatitis and thickening of the intestines. f. If treponemal infection does not prove fatal, it may still how alterations in fetal development at various stages.

CLINICAL MANIFESTATIONS 1. Early Congenital Syphilis a. Lesions of the skin and mucous membranes: Bullous rash, sometimes called, syphilitic pemphigus, may be present at birth. The bullae are approximately three cm in diameter, rounded and contain serous to seropurulent fluid swarming with treponemes. Apart from rashes, loss of weight may produce wrinkling of the skin especially on the face, giving what has been called the old man look. Syphilitic papules may involve the skin at the base of the nails and extend to the nailbeds. The nails may be loosened and shed (syphiliticnonychia). Mucous patches may also be found on the lips, in the mouth, in the throat, and in the nasal passages. Nasal discharges may be slightly mucoid or abundant and mucopurulent or purulent. Sometimes they are blood-stained and contain large number of T.pallidum, rendering them highly infectious. 176

b. Liver and Spleen The infants abdomen is protuberant, owing to the enlargement of the liver and the spleen. The liver cells tend to be immature and imperfectly formed. Hepatic insufficiency results in the failure of protein metabolism. 2. Late Congenital Syphilis a. Interstitial keratitis is the commonest late lesion. It may begin at any age from four to thirty years or even later. It appears as circumcorneal vascularization of the sclera followed by vascular infiltration from the sclera into the deep layers of the cornea. It usually affects one eys at first and eventually affects the other eye from a few weeks to many years. Severe lesions are likely to cause corneal scarring, giving rise to opacities which may cause slight impairment of vision or even complete blindness. COMPLICATIONS 1. Severe damage to several organs and the nervous system 2. Heart disease, insanity and brain damage 3. Severe illness or death in newborn DIAGNOSTIC PROCEDURE 1. Dark field illumination test is most effective if moist lesions are present. 2. Fluorescent treponemal antibody absorption test, in which the specimen consists of exudates from a lesion. 3. VDRL slide test and rapid plasma reagent test 4. CSF analysis MODALITIES OF TREATMENT 1. For early syphilis, treatment consists of the administration of penicillin G benzathine IM (2.4 million units). 2. Syphilis of more than a years duration is treated with penicillin G benzathine, 2.4 million units/week for three weeks. 3. Non-pregnant patients who develop an allergy to penicillin may be treated with oral tetracycline or doxycycline for 15 days for early syphilis and for 30 days for late infections. Tetracycline is contraindicated in pregnant women. 4. Patients who are receiving treatment must abstain from sexual contact until the infection is completely healed.

NURSING MANAGEMENT 1. Stresses to the client the importance of completing the treatment even after the symptom subside. 2. Instruct infected individuals to inform their partner that they should be tested and if necessary treated. 3. Practice universal precaution. 177

4. In secondary syphilis, keep the lesions dry as much as possible. If they are draining, dispose of contaminated materials properly. 5. In cardiovascular syphilis, check for signs of decreased cardiac output (decreased sensorium and urine output and hypoxia)and pulmonary congestion. 6. In neurosyphiliis, regularly check the level of consciousness, mood and coherence. Watch for signs of ataxia. 7. Encourage the patient to undergo VDRL testing after 3, 6,12 and 24 months to detect any possible relapse. 8. Be sure to report all cases of syphilis to local public health authorities. Refers the patient and his/her sexual partners for HIV testing.

PREVENTION AND CONTROL 1. 2. 3. 4. Report cases to the Department of Health. Control prostitution. Requires sex works to have regular check-ups. Proper sex education should be given in early life at home, in schools and in the community. 5. Look for cases of syphilis infection. 6. Contact tracing

Gardnerella vaginitis is a vaginal infection that is commonly referred to as bacterial vaginosis. It is a common gynecological condition in women, but men can be infected with the bacteria, as well. While some bacterial vaginosis infections clear without medication, it is important to seek treatment to avoid serious complications.

CAUSE Gardnerella vaginitis bacteria are present in the bacterial flora of many women's vaginas. When the natural balance of the vagina becomes unbalanced, the Gardnerella vaginitis bacteria may overgrow and create an infection. It is often spread by sexual contact but also appears in women who are not sexually active. Use of antibiotics, contraceptive sponges, a diaphragm, an IUD or spermicide may all increase the risk of contracting the infection. Douching and tampon misuse are also felt to increase the odds of developing a Gardnnerella vaginitis infection.


SYMPTOMS Some women have a Gardnerella vaginitis infection without having any noticeable symptoms. A green or gray-white vaginal discharge may be present, according to the text, "Medical-Surgical Nursing." It may have a sticky, smooth or thin consistency. A fishy odor may be present; this is more likely to be noticeable after vaginal intercourse. Burning may be felt during urination. Vaginal intercourse may be painful.

DIAGNOSIS Diagnosis usually begins with a pelvic examination. At this time, a sample of vaginal fluid may be obtained. The fluid is mixed with a laboratory chemical to see if a characteristic odor is produced, signaling the presence of a Gardnerella vaginitis infection. The vaginal pH may also be checked; an elevated pH may be indicative of the infection. A sample of vaginal secretion may be allowed to grow for a few days in the lab to make a definitive diagnosis.

TREATMENT The infection is often treated with the oral antibiotics tinidazole, clindamycin or metronidazole. They are typically taken for a week or less. Alternatively, some physicians prescribe a vaginal cream or gel, explains the California State University, Northridge. Vaginal intercourse should be avoided or engaged in only with condom use. The woman's sexual partner may need to be treated. COMPLICATIONS The Centers for Disease Control and Prevention relates that a woman with bacterial vaginosis is at an increased risk of contracting human immunodeficiency virus, or HIV, the virus that causes acquired immunodeficiency syndrome, or AIDS, if she is exposed to the virus. It also raises a woman's risk of contracting other sexually transmitted diseases. The 179

infection can travel to the woman's uterus or fallopian tubes, increasing her chances of pelvic inflammatory disease or infertility. A pregnant woman who develops a Gardnerella vaginitis infection may have a baby who is born early or below a healthy weight.

(Trichomonas vaginitis) Trichomoniasis is a sexually transmitted infection caused by the parasite Trichomonas vaginalis. CAUSES, INCIDENCE, AND RISK FACTOR Trichomoniasis is found worldwide. In the United States, the highest number of cases are seen in women between age 16 and 35.Trichomonas vaginalis is spread through sexual contact with an infected partner. This include penis-to-vagina intercourse or vulva-tovulva contact. The parasite cannot survive in the mouth or rectum. The disease can affect both men and women, but the symptoms differ between the two groups. The infection usually does not cause symptoms in men and goes away on its own in a few weeks.



Discomfort with intercourse Itching of the inner thighs Vaginal discharge (thin, greenish-yellow, frothy or foamy) Vaginal itching Vulvar itching or swelling of the labia Vaginal odor (foul or strong smell)


Burning after urination or ejaculation Itching of urethra Slight discharge from urethra

Occasionally, some men with trichomoniasis may develop prostatitis or epididymitis from the infection. SIGNS AND TESTS In women, a pelvic examination shows red blotches on the vaginal wall or cervix. A wet prep (microscopic examination of discharge) may show signs of inflammation or infection-causing organisms in vaginal fluids. A pap smear may also diagnose the condition. The disease can be hard to diagnose in men. Men are treated if the infection is diagnosed in any of their sexual partners. Men may also be treated if they have ongoing symptoms of urethral burning or itching despite treatment for gonorrhea and chlamydia.

TREATMENT The antibiotic metronidazole is commonly used to cure the infection. A newer drug, called Tinidazole may be used. You should not drink alcohol while taking the medicine and for 48 hours afterwards. Doing so can cause severe nausea, abdominal pain, and vomiting. Avoid sexual intercourse until treatment has been completed. Sexual partners should be treated at the same time, even if they have no symptoms. If you have been diagnosed with a sexually transmitted infection, you should be screened for other ones. 181

COMPLICATIONS Long-term infection may cause changes in the tissue on the cervix. These changes may be seen on a routine Pap smear. In such cases, treatment should be started and the Pap smear repeated 3 to 6 months later. Treatment of trichomoniasis helps prevents the spread of the disease to sexual partners. Trichomoniasis is common among persons with HIV. This condition in pregnant women has been linked to premature birth. More research is needed.

PREVENTION A monogamous sexual relationship with a known healthy partner can help reduce the risk of sexually transmitted infections, including trichomoniasis. Other than total abstinence, condoms remain the best and most reliable protection against sexually transmitted infections. Condoms must be used consistently and correctly to be effective.

(HPV Infections) Genital warts are flesh-colored or gray growths found in the genital area and anal region in both men and women. Genital warts are sometimes referred to as condyloma acuminata or venereal warts. They represent the most common sexually-transmitted disease caused by a virus. The warts are caused by the human papillomavirus (HPV). Infection with genital warts may not be obvious. Genital warts affect both men and women and can occur at any age.

Most patients with genital warts are between the ages of 17-33 years. Genital warts are highly contagious. There is around a 60% risk of getting the infection from a single sexual contact with someone who has genital warts. In children younger than three years of age, genital warts are thought to be transmitted by nonsexual methods such as direct manual contact. Nevertheless, the presence of genital warts in children should raise the suspicion for sexual abuse. Up to 20% of people with genital warts will have other sexually transmitted diseases(STDs).


CAUSES Genital warts are caused by the human papillomavirus (HPV). Over 100 types of HPVs have been identified; about 40 of these types have the potential to infect the genital area. 1. About 90% of genital warts are caused by two specific types of the virus (HPV-6 and -11), and these HPV types are considered "low risk," meaning they have a low cancercausing potential. Other HPV types are known causes of premalignant changes and cervical cancers in women. HPV16, one of the "high-risk" types, is responsible for about 50% of cervical cancers. HPV types 16, 18, 31, and 45 are other known "high risk" virus types. High-risk HPV types are also referred to as oncogenic HPV types. HPV is believed to cause 100% of cases of cervical cancer. 2. Common warts are not the same as genital warts and are caused by different HPV types that infect the skin. The viral particles are able to penetrate the skin and mucosal surfaces through microscopic abrasions in the genital area, which occur during sexual activity. Once cells are invaded by HPV, a latency (quiet) period of months to years may occur, during which there is no evidence of infection. 1. Generally, about two-thirds of people who have sexual contact with a partner who has genital warts develop them within three months. 2. Genital warts are indirectly associated with use of birth control pills due to increased sexual contact without the use of barrier protection, multiple sex partners, and having sex at an early age. SYMPTOMS Although genital warts are painless, they may be bothersome because of their location, size, or due to itching.

The size may range from less than one millimeter (1 mm = 0.039 inches) across to several square centimeters (1 cm = 0.39 inches) when many warts join together. Men and women with genital warts will often complain of painless bumps, itching, and discharge. Rarely, bleeding or urinary obstruction may be the initial problem when the wart involves the urethral opening (the opening where urine exits the body.) Warts in more than one area are common. There may be a history of previous or concurrent sexually transmitted diseases(STDs). Specific descriptions

In men, genital warts can infect the urethra,penis, scrotum, and rectal area. The warts can appear as soft, raised masses with a 183

surface that can be smooth (on the penile shaft) or rough with many fingerlike projections (anal warts). Others may appear pearly, cauliflower-like, or rough with a slightly dark surface. Most lesions are raised, but some may be flat with only slight elevation above the skin surface. Sometimes lesions may be hidden by hair or in the inner aspect of the uncircumcised foreskin in males.

In women, genital warts have a similar appearance and usually occur in the moist areas of the labia minora and vaginal opening. Lesions visible on the outer genitals warrant a thorough examination of the vaginal canal, cervix, and anorectal area. Most vaginal warts occur without symptoms. Rarely, women may experience bleeding after sexual intercourse, itching, or vaginal discharge.


DIAGNOSIS Diagnosis is often based on findings from the history and appearance of the genital warts. 1. Sometimes, lesions are only visible with an enhancing technique called acetowhitening. This technique involves the application of 5% acetic acid solution to the area of suspicion for about 5-10 minutes. Infected areas will turn white. 2. Magnification of the area (colposcopy) using a scope may be necessary to see the lesions. In females, a colposcope may be used to look for lesions in the vaginal canal and on the cervix. 3. A routine Pap smear should always be done in order to look for evidence of HPV infection and abnormal cells on the cervix. 4. A biopsy can be performed if the lesion appears unusual or recurs after treatment. 5. Special laboratory tests can also be used to confirm the presence of HPV infection. TREATMENT Self-Care at Home Because genital warts essentially have no symptoms other than their appearance, there is little need for home treatment. It is important, however, to recognize that the warts exist. Take the necessary precautions to prevent trauma to the area, which can result in bleeding. Be careful to prevent transmission to a sexual partner. Because the warts themselves are infectious, avoid touching them. Do not pick or squeeze the warts. Medical Treatment There is no single effective cure for removal of genital warts. A number of treatment options exist; however, no treatment is 100% effective in eliminating warts and preventing them from coming back in all patients. It also is not possible to eliminate infection with human papillomavirus once it has occurred. Genital warts may go away on their own in about 10%-20% of people over a period of three to four months. Cryotherapy: This technique freezes the wart using liquid nitrogen or a "cryoprobe." It is an excellent first-line treatment because response rates are high with few side effects. Laser treatment: This treatment is used for extensive or recurrent genital warts. It may require local, regional, or general anesthesia. The laser physically destroys the HPV-induced lesion. Disadvantages include high cost, increased healing time, scarring, and potentially infectious viral particles in the air caused by the laser plume. Electrodesiccation: This technique uses an electric current to destroy the warts. It can be done in the office with local anesthesia. Of note, the resulting smoke plume may be infectious.


Medications Several medications exist for treating genital warts and can be used as an alternative to other treatments. 1. Podophyllum resin (Pod-Ben-25, Podofin) is topically applied by a health care practitioner. 2. Podofilox (Condylox) can be topically applied at home and has a highercure rate than podophyllum resin. Podofilox also is useful for prevention. 3. Trichloroacetic acid or bichloracetic acid is topically applied; however, the response is often incomplete and recurrence is higher and it may cause pain and burning. 4. 5-Fluorouracil (Efudex) is applied as a cream, has a long treatment time, can cause burning and irritation, and has many side effects. 5. Interferon alpha-n3 (Alferon N) is an injection used for warts that do not respond to other therapies; however, it has many side effects. 6. Imiquimod (Aldara) is applied as a cream and local skin irritation is a common side effect.

PREVENTION In 2006, an HPV vaccine (Gardasil) was approved by the FDA. It is currently recommended for both males and females aged 9 to 26 years. This vaccine has been shown to be safe and 100% effective in preventing infection with the four most common HPV types (6, 11, 16, and 18) in women who have had no previous exposure to the virus. However, it is less effective in those who have already been infected with HPV, and it does not protect against all types of HPV infection. Studies are underway to determine whether the vaccine is safe and effective in older women and in males. Another vaccine against HPV types 16 and 18, Cervarix, has been approved by the FDA for females aged 10 to 25 years. Because no treatment is 100% effective, it is important to prevent the spread of HPV, which causes genital warts and some cancers whenever possible. Transmission of genital warts can be decreased if condoms are used and the infected individual refrains from sexual activity until therapy is completed.


HIV (human immunodeficiency virus) is a virus that attacks the immune system, the body's natural defense system. Without a strong immune system, the body has trouble fighting off disease. Both the virus and the infection it causes are called HIV. White blood cells are an important part of the immune system. HIV invades and destroys certain white blood cells called CD4+ cells. If


too many CD4+ cells are destroyed, the body can no longer defend itself against infection. The last stage of HIV infection is AIDS (acquired immunodeficiency syndrome). People with AIDS have a low number of CD4+ cells and get infections or cancers that rarely occur in healthy people. These can be deadly. But having HIV does not mean you have AIDS. Even without treatment, it takes a long time for HIV to progress to AIDSusually 10 to 12 years. If HIV is diagnosed before it becomes AIDS, medicines can slow or stop the damage to the immune system. With treatment, many people with HIV are able to live long and active lives.

CAUSES HIV infection is caused by the human immunodeficiency virus. You can get HIV from contact with infected blood, semen, or vaginal fluids. 1. Most people get the virus by having unprotected sex with someone who has HIV. 2. Another common way of getting the virus is by sharing drug needles with someone who is infected with HIV. 3. The virus can also be passed from a mother to her baby during pregnancy, birth, or breast-feeding. HIV doesn't survive well outside the body. So it cannot be spread by casual contact such as kissing or sharing drinking glasses with an infected person. SYMPTOMS HIV may not cause symptoms early on. People who do have symptoms may mistake them for the flu or mono. Common early symptoms include: 187

Fever. Sore throat. Headache. Muscle aches and joint pain. Swollen glands (swollen lymph nodes). Skin rash.

Symptoms may appear from a few days to several weeks after a person is first infected. The early symptoms usually go away within 2 to 3 weeks. After the early symptoms go away, an infected person may not have symptoms again for many years. Without treatment, the virus continues to grow in the body and attack the immune system. After a certain point, symptoms reappear and then remain. These symptoms usually include: Swollen lymph nodes. Extreme tiredness. Weight loss. Fever. Night sweats.

A doctor may suspect HIV if these symptoms last and no other cause can be found. Treatment usually keeps the virus under control and helps the immune system stay healthy.

DIAGNOSIS The U.S. Food and Drug Administration (FDA) has approved tests that detect HIV antibodies in urine, fluid from the mouth (oral fluid), or blood. If a test on urine or oral fluid shows that you are infected with HIV, you will probably need a blood test to confirm the results. If you have been exposed to HIV, your immune system will make antibodies to try to destroy the virus. Blood tests can find these antibodies in your blood. 188

Most doctors use two blood tests, called the ELISA and the Western blot assay. If the first ELISA is positive (meaning that HIV antibodies are found), the blood sample is tested again. If the second test is positive, a Western blot will be done to be sure. It may take as long as 6 months for HIV antibodies to show up in a blood sample. If you think you have been exposed to HIV but you test negative for it: Get tested again. Tests at 6, 12, and 24 weeks can be done to be sure you are not infected. Meanwhile, take steps to prevent the spread of the virus. If you are infected, you can still pass HIV to another person during this time. Some people are afraid to be tested for HIV. But if there is any chance you could be infected, it is very important to find out. HIV can be treated. Getting early treatment can slow down the virus and help you stay healthy. And you need to know if you are infected so you can prevent spreading the infection to other people. You can get HIV testing in most doctors' offices, public health clinics, hospitals, and Planned Parenthood clinics. You can also buy a home HIV test kit in a drugstore or by mail order. But be very careful to choose only a test that has been approved by the U.S. Food and Drug Administration (FDA). If a home test is positive, see a doctor to have the result confirmed and to find out what to do next. TREATMENT The standard treatment for HIV is a combination of medicines called highly active antiretroviral therapy (HAART). Antiretroviral medicines slow the rate at which the virus multiplies. Taking these medicines can reduce the amount of virus in your body and help you stay healthy. It may not be easy to decide the best time to start treatment. There are pros and cons to starting HAART before your CD4+ cell count gets too low. Discuss these with your doctor so you understand your choices. To monitor the HIV infection and its effect on your immune system, a doctor will do two tests: Viral load, which shows the amount of virus in your blood. CD4+ cell count, which shows how well your immune system is working.

If you have no symptoms and your CD4+ cell count is at a healthy level, you may not need treatment yet. Your doctor will repeat the tests on a regular basis to see how you are doing. If you have symptoms or some other health problems, you should start treatment, whatever your CD4+ count is. After you start treatment, it is important to take your medicines exactly as directed by your doctor. When treatment doesn't work, it is often because HIV has become resistant to the medicine. This can happen if you don't take your medicines correctly. Ask your doctor if you have questions about your treatment.


Treatment has become much easier to follow over the past few years. New combination medicines include two or three different medicines in one pill. Many people with HIV get the treatment they need by taking just one or two pills a day. To stay as healthy as possible during treatment:

Don't smoke. People with HIV are more likely to have a heart attack or get lung cancer. Smoking can increase these risks even more. Eat a healthy, balanced diet to keep your immune system strong. Get regular exercise to reduce stress and improve the quality of your life. Don't use illegal drugs, and limit your use of alcohol. Learn all you can about HIV so you can take an active role in your treatment. Your doctor can help you understand HIV and how best to treat it. Also, consider joining an HIV support group. Support groups can be a great place to share information and emotions about HIV infection. PREVENTION HIV can be spread by people whether they know they are infected or not. To protect yourself and others: 1. Practice safe sex. Use a condom every time you have sex (including oral sex) until you are sure you and your partner are not infected with HIV or other sexually transmitted infection (STI). 2. Don't have more than one sex partner at a time. The safest sex is with one partner who has sex only with you. 3. Talk to your partner before you have sex the first time. Find out if he or she is at risk for HIV. Get tested together and retested 6 months later. Use condoms in the meantime. 4. Don't drink a lot of alcohol or use illegal drugs before sex. You might let down your guard and not practice safe sex. 5. Don't share personal items, such as toothbrushes or razors. 6. Never share needles or syringes with anyone.

(Pubic Lice) "Crabs" is the common term for lice found in the pubic hair of humans. Crabs is a parasite infection medically known as Pediculosis pubis or pubic lice. Barely the size of a pinhead, lice are organisms that live only with the help of another organism, called a host. There are thousands of types of lice, some of which have developed an attraction to humans. The official name for the organism responsible for pubic lice is Pthirus pubis. Other lice that often infect humans are Pediculus humanus capitis (head lice) and Pediculus humanus corporis (body lice). The term "crabs" seems to come from the microscopic appearance of the pubic louse. The pubic lice organisms are visible to the naked eye 190

in affected areas. The lice are typically seen attached to hair in pubic areas, but may sometimes appear in other areas of the body where coarse hair is present (such as beard, chest, armpits, etc.). The pubic louse is distinct morphologically (somewhat rounded with three pairs of legs on either side of the body from which it takes its descriptive name) from the head and body louse. The female lifespan is slightly shorter (three weeks), and she produces fewer eggs per day (three) than her counterparts. The eggs attach to the base of the pubic hair shaft for approximately six to eight days before hatching. Picture of pubic louse (crab)

CAUSES 1. The source of infection for pubic lice is intimate contact with an infected person. Therefore, pubic lice are often transmitted during sex. 2. Since transmission occurs during intimate contact, actual sexual intercourse is not necessary for the spread of pubic lice. 3. Pubic lice can also be transmitted by contact with contaminated belongings such as towels, bed sheets, or clothing. 4. Crabs are transmitted through any intimate contact. Lice do not jump or fly, so actual contact is necessary for transmission. An individual may acquire an infection by sharing bedding or towels. 5. Cats, dogs, and other pets are not involved in the spread of human lice. Your pet cannot become infested with human lice and transmit the lice to another person. SYMPTOMS The main symptoms of infection with the pubic lice of crabs are itching and burning of the pubic area.


The itching may spread as the pubic lice move to other moist areas of the body such as the armpit. For many people who have crabs the itching is worse at night. Intense or prolonged scratching may lead to skin injuries that may become infected by bacteria. TREATMENT Generally, pubic lice can be cured with an application of certain medications, but in some circumstances it may be necessary to seek a doctor's care. 1. One of the main concerns with pubic lice is that people often scratch incessantly, and this scratching can lead to a secondary bacterial infection. 2. When scratching is intense for long periods, the skin can be worn and broken. 3. If you notice a large area of redness or pus in the area, you may have a skin infection. 4. Other signs of a pubic infection include a fever, burning when you urinate, or a genital discharge. 5. Permethrin (Elimite) is a lice-killing product that is available over-the-counter without a prescription. When using this product it is important to exactly follow the instructions on the package. 6. Avoid mucous membranes, which are found at the tip of the penis and the opening of the vagina. 7. Repeat anti-lice treatment in seven to 10 days to kill nits that may have hatched.

8. Lindane (Kwell): An alternative treatment when permethrin (Elimite) is not available. Lindane requires a doctor's prescription. 9. Apply for 10 minutes then rinse with warm water. 10. Lindane should not be used on children. Lindane can be toxic to the brain and nervous system and should only be used when other treatments have failed. 11. Malathion lotion (Ovide) and ivermectin (Stromectol) are other prescription medications that have been shown to be effective against pubic lice or crabs. 12. Use over-the-counter antihistamines such as diphenhydramine(Benadryl) for itching. PREVENTION Crabs are usually spread by direct skin-to-skin intimate contact. Avoid contact with known infected people and textiles or clothing that may have been contaminated by someone who is infected with pubic lice. After treatment has been completed, ensure that all clothing and linens have been disinfected to avoid re-infection or spread of the infection to someone else in the home.