Illustrated Manual of Infectious Diseases of Livestock in Afghanistan

ILLUSTRATED MANUAL OF INFECTIOUS DISEASES OF LIVESTOCK IN AFGHANISTAN
Fort Valley State University
Department of Veterinary Science 1005 State University Drive Fort Valley, GA, US, 31030 Phone: 478-825-6427 Fax: 478-825-6376 Internet: www.FVSU.edu email: mobinis@fvsu.edu
Copyright 2008 Fort Valley State University

ALL RIGHTS RESERVED by
Library of Congress Catalogue Card Number: 2008935063 ISBN: 978-0-9659583-3-2
Published by: Boca Publications Group, Inc. 2650 N. Military Trail, 240-SZG Boca Raton, Florida, US 33431 email: bocagroup@aol.com Printed in Canada
ILLUSTRATED MANUAL OF INFECTIOUS DISEASES OF LIVESTOCK IN AFGHANISTAN
AUTHORS
Dr. Seyedmehdi Mobini (Fort Valley State University, USA) Dr. Corrie Brown (University of Georgia, USA) Dr. Daad Mohammad Amir (Dutch Committee for Afghanistan) Dr. Ezatullah Jaheed (Kabul University) Dr. Afzal Masoodi (Afghanistan Ministry of Agriculture, Irrigation, and Livestock) Dr. Abdulhabib Nawroz (UN Food and Agriculture Organization) Dr. Azizullah Osmani (Afghanistan Ministry of Agriculture, Irrigation, and Livestock) Dr. Fridoon Oria (Afghanistan Ministry of Agriculture, Irrigation, and Livestock) Dr. Lutfullah Rlung (UN Food and Agriculture Organization) Dr. Said Gul Safi (Afghanistan Veterinary Association) Dr. Fatima Safi (Afghanistan) Dr. Abdul Qader Samsor (Accelerating Sustainable Agriculture Program, US Agency for International Development) Dr. Robert M. Smith (Coordinator for Animal Health, US Agency for International Development, US Department of Agriculture; Kabul, Afghanistan) Dr. Ghulam Mohammad Ziay (Afghanistan Ministry of Agriculture, Irrigation, and Livestock)
Infectious Diseases of Livestock in Afghanistan
PREFACE
In Afghanistan, agriculture is the major form of livelihood for the majority of the population, and livestock serves as a key source of protein and income through edible and inedible products. The need to develop a capacity to correctly recognize and identify relevant livestock diseases was established between 2002 and 2007 by U.S. and international agencies working in reconstruction and capacity-building activities in this war-torn country. Early and accurate field recognition of these livestock diseases by animal health workers and individuals who provide humanitarian assistance and development is vital. It will enhance rapid reporting with subsequent field investigation and response by public and private sectors in veterinary medicine and public health. A team of U.S. and Afghan veterinarians worked together to produce this Illustrated Manual of Infectious Diseases of Livestock in Afghanistan. As a group, essential topics and diseases were selected, and the writing was shared by all team members. Our hope is that this manual will serve as a basic introduction to some of the major disease problems in the region, and that it will be used by veterinarians, assistant veterinarians, para-veterinarians, veterinary students, producers, and other animal health workers. All the chapters were initially written in English. Translation to Dari was by the Faculty of Veterinary Science of Kabul University (Dr. Noor Mohammad Ayubi, Coordinator), and translation to Pashto was by the Afghanistan Veterinary Association (Dr. Said Gul Safi, Coordinator). We are grateful to our colleagues and families for their support and contributions during the writing and production of this book.
We wish to acknowledge the United States Department of Agriculture, Foreign Agricultural Service, for funding provided to Fort Valley State University to develop and publish this book. We also wish to acknowledge additional funding from the United States Agency for International Development for support of travel for Drs. Brown and Mobini to Afghanistan to meet with all the authors. And, in particular, many thanks to Dr. Otto Gonzalez of the USDA Foreign Agricultural Service who manages USDA technical assistance to Afghanistan. << >>
PHOTO CREDITS
Photos in this Illustrated Manual courtesy of the authors, Drew Adams, and, LTC Richard Probst.
the Plum Island Animal Disease Center Audiovisual Services,
CONTENTS
CH. 1/ GENERAL TOPICS 1 Basic Necropsy 2 Sample Collection and Submission 3 Laboratory Testing 4 Carcass Disposal 5 Cleaning and Disinfection 6 Euthanasia CH. 2/ DISEASES OF MULTIPLE SPECIES 1 Anthrax 2 Clostridial Diseases 3 Crimean Congo Hemorrhagic Fever 4 Echinococcosis 5 Foot-and-Mouth Disease 6 Johnes Disease 7 Rabies CH. 3/ DISEASES OF CATTLE 1 Actinobacillosis 2 Actinomycosis 3 Anaplasmosis 4 Babesiosis (Red Water, Piroplasmosis, Tick Fever) 5 Bovine Spongiform Encephalopathy 6 Bovine Tuberculosis 7 Contagious Bovine Pleuropneumonia 8 Hemorrhagic Septicemia 9 Leptospirosis 10 Malignant Catarrhal Fever
1 12 18 22 25 28 35 39 46 49 52 56 60 65 67 69 72 75 78 81 84 87 90
11 External Parasites of Cattle 12 Internal Parasites of Cattle 13. Abortion Diseases of Cattle 14 Rinderpest 15 Theileriosis CH. 4/ DISEASES OF HORSES 1 Epizootic Lymphangitis 2 Equine Infectious Anemia 3 Equine Influenza 4 Equine Piroplasmosis 5 Equine Rhinopneumonitis 6 Equine Viral Arteritis 7 External Parasites of Horses 8 Glanders 9 Internal Parasites of Horses 10 Strangles 11 Surra CH. 5/ DISEASES OF POULTRY 1 Avian Influenza, Highly Pathogenic 2 Brooder Pneumonia (Aspergillosis) 3 Chlamydiosis, Avian 4 Chronic Respiratory Disease 5 Coccidiosis, Avian 6 Colibacillosis, Avian 7 Fowl Cholera 8 Hydropericardium Syndrome 9 Infectious Bronchitis 10 Infectious Bursal Disease 11 Infectious Laryngotracheitis 12 Mareks Disease 13 Newcastle Disease
93 97 101 106 109 115 118 120 123 126 128 130 133 136 140 143 147 151 154 157 160 162 165 168 171 174 176 179 181
14 Pullorum Disease 15 Tuberculosis, Avian CH. 6/ DISEASES OF SHEEP AND GOATS 1 Bluetongue 2 Caprine Arthritis Encephalitis 3 Contagious Agalactia 4 Contagious Caprine Pleuropneumonia 5 Contagious Ecthyma 6 External Parasites of Sheep and Goats 7 Internal Parasites of Sheep and Goats 8 Peste Des Petits Ruminants 9 Abortion Diseases 10 Scrapie 11 Sheep Pox and Goat Pox
184 187 191 194 198 200 203 206 209 215 219 228 230
CHAPTER
GENERAL TOPICS
Infectious Diseases of Livestock in Afghanistan / General Topics
1 BASIC NECROPSY
Necropsy is examination and dissection of a dead body to determine or confirm causes of death. It is also referred to as postmortem examination.
Recognizing and recording abnormalities are enhanced by developing a consistent routine in the dissection and collection of tissues. There is often a tendency to move quickly to the suspected lesion or body system, which risks missing important information. A good necropsy involves paying attention to ALL the clues that can be provided, so the routine has to be followed, with attention to detail at every step. The consistent routine entails 6 steps: 1. Obtain history. 2. Examine the animal externally. 3. Open the body. 4. Remove the organs and set aside for detailed examination and sampling. 5. Examine and sample the organs. 6. Write the report. Please note that the following is written for mammalian necropsy, but necropsy of birds follows the same general steps. Some specific differences for bird necropsies are noted at the end of the chapter.
1. Obtain the history A complete individual animal and herd history should be obtained. This history should include: age, breed, and sex of affected animals, husbandry conditions (including housing, feed), clinical signs, and any treatments administered and whether the animal died or was euthanized. 2. External examination Many people believe a necropsy begins when you start using the knife. But if you neglect to look at many external aspects of the carcass, some key findings can be missed.
Examine the site where the animal was found for clues; predators (dogs), lightning, poisons and poisonous plants, signs of trauma. Evaluate the general body nutritional and hydration status. Look at the external orifices for any discharges and for color of mucous membranes. Look at teeth for age and abnormal wear. Are there any skin lesions or external parasites?
3. Open the body. The next step in the necropsy is to expose the internal organs. Place the animal on its left side, and reflect right fore and hind limbs. Peel back the skin, remove the ribs on the right, and make a big window into the peritoneal cavity. 2
Limbs reflected and skin peeled back
Internal organs exposed
Note the color, position, and size of all organs and look for any adhesions or accumulations of fluid within cavities 4. Remove the organs Examination of the organs within the body is not very efficient. The following organs are removed and placed next to the carcass:
Lungs, heart, trachea, esophagus - removed in total after opening the skin along the ventral aspect of the head and neck.
Abdominal viscera Pull ventrally and cut the dorsal mesenteric attachments. Remove the spleen and liver from the rumen and intestines and set those organs aside.
Kidneys, adrenal glands, bladder - remove and set aside. Remove the reproductive tract.
Brain - Open the cranium and gently tease the brain out.
You should now have a collection of organs that might look like this.
5. Examine and sample the organs It is a good idea to go from the cleanest organs to the dirtiest. Usually this order is: spleen, lungs, heart, kidneys, reproductive tract, brain, liver, intestinal tract. Note any abnormalities for each (color, size, shape, consistency, exudates). Be sure to examine both capsular and cut surface. Make several cuts in each organ. Collect specimens for further diagnostic work.
Spleen - Normal appearance
Lungs - Should be pink and well aerated. Cut down the trachea and bronchi to look at mucosal airway surfaces.
Heart - Open all the chambers and look at the valves
Kidneys - Cut open and look for streaks, or pallor
Female reproductive tract
Opened testes
Liver examine the texture and color of the liver and make some slices for looking changes in the deeper structures of it.
Brain
Intestinal tract - Be sure to look at both serosal and mucosal surfaces.
Before finishing with organ examination, go back to the carcass and look at the superficial lymph nodes and muscles. Open some joints. Sample as necessary. For specific problems, you may want to take additional samples from key organs. For instance, if it is a skin disease, take more samples of skin and draining lymph nodes. If the animal has pneumonia, take additional lung samples and tracheobronchial lymph nodes. 6. Write the report. No necropsy is complete until all findings have been recorded in written form. The report should include at least the following information: Species, breed Age, sex History Died or euthanized? Nutritional, hydration status Findings from external examination: Findings by organ system: Lymphoreticular (spleen, lymph nodes) Respiratory Digestive Urogenital Musculoskeletal Nervous
Biosafety and Biosecurity

Many animal diseases are zoonotic. And many animal diseases if not properly contained can spread to other animals. Protection of the person doing the necropsy and protection of other animals in the vicinity are important. The following biosafety/biosecurity precautions should be taken during necropsy: Perform the necropsy in a dry area, away from other animals Wear personal protective equipment - gloves, apron, boots Dispose of carcasses appropriately, away from other animals
How is a bird necropsy different? The same six steps will be followed The only difference is in how the body is opened and sampling of the organs. Briefly, similarities and differences are as follows: The consistent routine entails 6 steps: 1. Obtain history - same as for mammals. 2. Examine the animal externally - same as for mammals. Pay special attention to the prominence of the keel bone, which is an indication of nutritional status.
3. Open the body - Before opening the body, wet the feathers. This is most easily done by immersing the bird in a bucket of soapy water. Put the bird on its back, abduct the legs, and cut through the skin below the keel. Then pull the skin forward over the keel to expose the breast muscles. Cut through the keel on both sides
Removing keel bone to expose viscera and remove the keel.
Checking air sacs
4. Remove the organs and set aside for detailed examination and sampling.
Digestive system removed, in entirety
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Lungs removed - these need to be dissected away from the thoracic body wall as they are closely adherent.
Kidneys, also apposed closely to the body wall, but in the abdomen.
5. Examine and sample the organs - Similar to the procedure for mammals. 6. Write the report - Same as for mammals.
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2 SAMPLE COLLECTION AND SUBMISSION Diagnosing infectious disease is a team effort. It is a chain event, starting with the animal in the field, and coming back to the animal in the field, but with many essential links in between, including veterinarians, paraveterinarians, veterinary assistants, and laboratory workers. See the diagram below. Two of the very critical links in this chain involve collection of appropriate samples and getting those samples to the laboratory. This chapter will focus on the two important processes of sample collection and sample submission. Collection of samples: From a dead animal One of the most frequently asked questions is, What samples should I collect in order for the laboratory to be able to diagnose a specific disease? Although many diseases are diagnosed based on specific tissues, what happens when it turns out that the animal doesnt have that specific disease, but may have some other malady? In fact, it is probably a better idea to collect a routine set of samples for all diseases. That way, if the first suspected disease is ruled out, then the laboratory still has many samples to choose from to see if another agent might be operating. In addition, depending upon the lesions seen at necropsy, there may be additional tissues collected. For instance, if there is pneumonia visible, also collect the tracheobronchial lymph nodes, if there is enteritis, collect also the mesenteric lymph nodes, etc. Any lesions with exudates (such as abscesses) can be swabbed and also tissues collected. If there is 12
enteritis, submit a fecal sample also. If internal or external parasites are noted, collect those as well into separate vials.
Treatment
Sick animal
Report back to veterinarian
Visit by animal health professional
Samples Taken Laboratory testing Samples submitted to lab
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The following tissues are considered essential for general disease diagnostic purposes: Spleen Liver Kidney Lung Prescapular or prefemoral lymph node Tied off piece of small intestine and large intestine, 3cm each (tied off at both ends) Brain (cut in half down the midline - with half for fresh and half for formalin) - ONLY IN CASES INVOLVING NEUROLOGIC SIGNS These tissues should be collected fresh and placed on a tray or into whirlpak bags, and replicate tissues should be placed in a jar of 10% formalin, with a 1:10 ratio of tissue to formalin.
Tissue collection tray which is useful during a necropsy procedure
From a live animal Of course, if the animal is not dead, there are many fewer options for sample collection. In that case, the following specimens can be collected: Whole blood, non-clotted - for blood parasite examination Serum (from clotted whole blood) - for serology - VIRUSES 14
Any external lesions with fluid or pus can be swabbed or placed in container - for BACTERIAL DISEASES Feces - for INTERNAL PARASITES External parasites Feed - for NUTRITIONAL DISEASES Submission of samples: The importance of how samples are submitted to the laboratory cannot be underestimated. Preservation of samples is critical. As soon as the animal dies, the process of autolysis begins. Cells throughout the body degrade and as they do so, they release many enzymes which can destroy the infectious agent under consideration. In addition, when the animal dies, one of the first things to happen is that bacteria in the intestine are able to move up into the bile duct, on into the liver, and from there through the body. These postmortem bacteria proliferate rapidly and can make it impossible to find the agent that caused the disease. So the two big problems are autolysis and bacterial overgrowth. Both contribute to the rotten state of the carcass and can complicate infectious disease diagnosis in the laboratory. A frequently asked question is, How will I know if the animal tissues are too rotten to be useful? The answer to that is, It depends. It depends on the size of the animal and the weather conditions. Both autolysis and bacterial overgrowth are temperature-dependent. Two big factors affect the body temperature after death - size of the animal and outside temperature. A large animal such as a cow will cool down slowly after death so that even though the skin may feel cool quite soon after death, the core temperature takes much longer to drop. On the other hand, for a smaller animal like a bird or a neonatal sheep, the temperature of the whole body drops rapidly after death. In either case, over time, the carcass temperature becomes the same as the 15
environmental temperature. So, if the carcass is left outside in the summer for two or three days, autolysis and putrefaction progress readily, whereas in the winter, the tissues might be preserved for quite a while. A quick test to tell if the tissues will be of any use to the lab: If the visceral organs, such as liver or kidney, are the consistency of paste. If the carcass is very malodorous If either of the above is true, probably best not to waste your time submitting tissue samples. Transport to the laboratory is also a critical issue. The tissues will continue to autolyze and bacteria will continue to proliferate in those tissues even after they are removed from the body. So keeping the samples cool and moist while awaiting shipment and during shipment will help. Finding the most rapid means to get the material to the laboratory will facilitate diagnosis. Of course, it is important to pack the samples to avoid leakage along the way also. Samples should be submitted with enough information that the laboratory workers have a good appreciation of what was happening at the field level. All laboratories are dependent on receiving complete information associated with the case. A complete history and detailed necropsy report will enhance the chances that an accurate diagnosis can be made in the laboratory.
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At the minimum, the following information should be included with the samples: 1. Description of the animals (species), location of outbreak 2. Number of animals in the affected group and number showing symptoms 3. Sex and age group affected 4. Number of deaths 5. Complete history and clinical signs observed by owner 6. Clinical signs observed by veterinarian 7. Clinical diagnosis and record of treatment or vaccination 8. Complete record of gross findings 9. Any other information pertinent to the diagnostic problem Note: In the case of a necropsy, many of these will be included in the necropsy report which is submitted with the samples.
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3 LABORATORY TESTING Veterinary diagnostic laboratories offer a unique set of diagnostic tests that is subject to changes as better tests become available. The protocols for sample collection and submission have been explained in a previous section. The practitioner and diagnostic laboratory staff should maintain good communication in order to complete their diagnostic efforts efficiently and provide optimal service to the animal owner. The aim of this chapter is to simplify the concepts of laboratory testing so that field personnel can have a better appreciation of what happens to the submitted samples. There are two big categories of testing for infectious diseases: Tests that are designed to detect the infectious agent (antigen). Tests that are designed to detect antibody production (acts against the infectious agent).
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Tests for detection of the agent (antigen) come in many forms. Visualization of the organism
Anthrax bacilli from a lymph node impression smear
Gram negative coccobacilli from an abscess
Whipworm egg in a stool sample
Trypanosomes in a blood smear
Growing the organism - bacterial culture
Samples are streaked onto agar and bacterial colonies grow
Specialized media can detect Salmonella
Antibiotic sensitivity of bacteria is determined
Biochemical reactions in panel form identify bacteria
19
Detecting the organism immunologically
Fluorescent antibody testing - labeled antibody highlights antigen in tissue or smear
Agar gel immunodiffusion (AGID) - antigen and antibody diffuse toward each other and if they meet, there is a line of precipitation in the agar.
ELISA - antibody is bound to the well, antigen binds, then a secondary antibody with a label highlights the presence of antigen.
Detecting nucleic acid of the organism Polymerase chain reaction (PCR)
Extremely low amounts of DNA or RNA specific for the agent can be multiplied to result in a product that is detectable.
20
Tests for detection of the response (antibody production) to the agent are all serologic tests. There are many of these and some have the same principles as those that are designed for detection of antigen, but in these cases, known antigen is put into the test and the unknown is the test serum: Indirect Fluorescent Antibody (IFA) testing - similar to the test for antigen but in this case the antigen is known, the serum is the primary antibody, and then there is a secondary antibody that is labeled. If the serum is positive, fluorescence results. AGID - similar to the test for the agent, but in this form, the known antigen is added, and the antibody is the unknown. A line of precipitation indicates the antibody is positive. ELISA - Antigen is bound to the bottom of a plate, serum is added, then a secondary antibody with a label. If the secondary antibody binds, there is a color reaction, indicating the presence of antibodies. For each disease in this book, one or more of the tests described above is used. In general, tests for detection of the agent can only be used while the disease is occurring, during the period of clinical illness. When the clinical illness is improving or after it has finished, there is no longer enough agent around to be able to detect. But it is also at this time that antibodies begin to develop and the serologic tests will begin to be useful. Antibodies can persist for months to years, so serology is helpful in looking at diseases over a longer period, such as surveillance efforts.
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4 CARCASS DISPOSAL In a disease outbreak situation, it is often necessary to dispose of animal carcasses. This is an often-overlooked aspect of infectious disease control. There are many factors that play a role in how carcasses are disposed and each situation requires individual attention and decisions in which several parties may play a role. Some of the factors to consider include: Species or animal for disposal Number of animals Amount of associated material - litter, eggs, milk, etc. Disease under consideration Zoonotic potential Environmental concerns General categories of carcass disposal used globally: Burial may be the easiest and safest method for all species. Over time, there is inactivation of almost all pathogens. Disadvantages occur if the water table is high or if there are many large carcasses for disposal, and this can potentially contaminate the public water supply. Burning / incineration is an excellent method that ensures destruction of pathogens. The main disadvantage is that it requires considerable fuel to burn the carcasses thoroughly, which is especially difficult with cattle. This method can also contribute to air pollution.
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Slaughtering is humane killing with subsequent consumption of the meat is suitable for diseases that are not transmissible to humans. Rendering involves the processing of animal tissues to high temperatures, resulting in disassociated proteins and fats that are then used for animal feeds. A major disadvantage is that rendering requires dedicated and often technically sophisticated facilities. Composting is a process in which animal tissue undergoes heatenhanced biological decomposition, resulting in total inactivation of pathogens. A disadvantage is that this is a slow process (days to weeks), and it is necessary to keep predators away during this time. Alkaline hydrolysis, also tissue digestion, is a method that combines heat, pressure and a high alkaline environment to completely break down animal tissue into a liquid that can be discharged into a sanitary sewer. Alkaline hydrolysis is the only disposal method that will inactivate prions (the cause of BSE). The major disadvantage of alkaline hydrolysis is that the equipment is very expensive. Commonly used methods for carcass disposal in Afghanistan: For all species, the most common method is slaughtering, with subsequent consumption. In the case of avian influenza, where there is danger of disease transmission to humans, burial is used. Chickens are buried 3 23
meters deep (without plastic) and covered with lime, and then with soil. Burial is also used for mammalian species with zoonotic disease in this case, burial is at least 2 meters deep, and covering with lime. The distance of the burial site should be 30 meters from a water well.
Example of burial with lime - chicken carcass at the bottom of a 3m hole (well).
Slaughter - an acceptable method when there is no danger of human disease
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5 CLEANING AND DISINFECTION After a disease has been diagnosed, it is often necessary to clean and disinfect the areas where the animals have been kept, to avoid replacement animals from becoming infected through exposure to the pathogen which is residual in the environment. The procedure for making a premise habitable for animals again in a safe manner is referred to as cleaning and disinfection. What is cleaning? Cleaning is the physical removal of organic matter, and it is what happens before disinfection. It is almost impossible to disinfect dirt, so dirt has to be removed first. Cleaning is usually a two-step procedure dry cleaning, following by wet cleaning. Dry cleaning means the carting away and disposal of litter, manure, bedding, carcasses, and feed. Because most disinfectants are rapidly inactivated with exposure to organic material, it is important to get rid of as much organic material as possible during the cleaning phase. Wet cleaning follows dry cleaning and involves actually washing surfaces. Soaps and detergents help a lot they break up stubborn materials and are mildly germicidal. Some compounds like Lysol or Dettol are detergents but also will kill some microorganisms as well. What is disinfection? Disinfection is the inactivation of the infectious agent. Dirt might not be visible, but the etiologic agent is still there and can infect new animals that are brought in to the area. 25
Most disinfectants are chemical agents that kill pathogens on contact. Many are readily available in the local marketplace. Each has advantages and disadvantages. See the table below:
Class of disinfectant Oxidizing agents Examples 5% Bleach, iodine, Virkon, hydrogen peroxide Caustic soda, lime Advantages Kills most viruses and bacteria Disadvantages Poor activity in the presence of organic material Irritating to respiratory membranes and skin Main use Decontaminate surfaces that may have virus or bacteria To cover carcasses or pathways
Alkalis
Acids
2% Vinegar, citric acid
Kill most viruses and bacteria Work even in the presence of organic matter Excellent for foot-andmouth disease
Do not work well for many agents
Decontaminate instruments after FMD
In addition, sunlight can be a powerful disinfectant, as ultraviolet rays within sunlight will kill many microorganisms. But unfortunately, ultraviolet rays do not penetrate very well and only the surface organisms will be inactivated. Both moist heat and dry heat are used to inactivate infectious agents. Moist heat and pressure are used together in autoclaves to sterilize 26
instruments. Dry heat can be supplied through flames and will kill almost all organisms. Many of the chemical disinfectants are available in Afghanistan at the local marketplace:
Common household bleach is an oxidizing agent that can effectively inactivate most infectious agents, but does not work well in the presence of organic matter, so cleaning should take place first. A 5% solution of bleach will inactivate many infectious agents.
Dettol is a phenolic compound good for general cleaning. This will NOT inactivate some viruses, such as FMD. Common household iodine solution and hydrogen peroxide are disinfectants that can be purchased at local stores.
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6 EUTHANASIA Euthanasia is defined as pain- and stress-free death of animals. For infectious disease diagnosis or control, it may be necessary to euthanize animals under the following circumstances: to obtain fresh specimens for laboratory diagnosis, to prevent spread of infection to other animals, to prevent human illness, in the case of zoonotic disease. There are many ways to euthanize animals and which method is chosen often depends on cultural environment, the species, the environment, the biological risk, and the importance of preserving adequate samples. But no matter what method is chosen, all need to fulfill the following criteria. -- Must be humane The method should induce loss of consciousness and death without causing pain, distress, anxiety, or apprehension for the animal. -- Must be socially and culturally acceptable If the method does not meet with community acceptance, there will be obstacles to continuing the practice and this will hamper further disease control efforts. -- Must be biosecure One of the reasons for euthanasia is to contain an infectious disease. If there is extensive exposure of bodily fluids, it could negate efforts to contain the disease. When possible, animals 28
should be killed on site, to minimize transport of infectious materials and spread of disease. -- Must be safe for people Many euthanasia methods entail considerable risk to human health. All operators should be well trained and fully cognizant of potential hazards to them or to others. Personal protective equipment (gloves, apron, boots, + respiratory protection) is usually required. The globally accepted methods for euthanasia, the species for which they are most applicable, and advantages and disadvantages of each, are all detailed in the table below: Method
Exsanguination (Halal slaughter in Moslem countries)
Species
All livestock and poultry
Advantages
Meat can be consumed, but only if animal was not physically ill No necessity for disposal of carcasses if meat is consumed Good for animals that are difficult to restrain, or are agitated, or in open fields
Disadvantages
May not work for diseases with zoonotic potential Often requires transport to slaughtering facility Blood exposure can spread disease
Free bullet
All livestock
Dangerous for people in the area Can spread bodily fluids Requires considerable operator skill to kill humanely Brain not available for examination
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Infectious Diseases of Livestock in Afghanistan / General Topics Captive bolt All livestock No need to move large animals off of premises Requires considerable operator skill to kill humanely as captive bolt delivery location varies from species to species No good if you want to examine brain Need to bleed out immediately to ensure death, therefore body fluids are disseminated Safety hazard for humans Requires electrical source Compressed gases can be difficult to obtain Good ventilation required after gassing to minimize human hazards
Electro-cution
Gases (CO2, CO)
Calves, sheep, goats, poultry Poultry, neonatal sheep and goats
No tissue or body fluid exposure All can be contained within a chamber, or room, can be sealed and gassed No tissue or blood exposure Time-tested method, may be most humane With some chemicals, must be followed by bleeding out to ensure death Least expensive Simple, minimal operator training
Injectable chemicals, such as barbiturates, magnesium sulfate, chloral hydrate, strychnine Cervical dislocation manual or with burdizzos
All livestock
Animals must be restrained appropriately Chemicals used are often controlled substances and difficult to obtain Chemicals can be expensive Reflex movements when first unconscious can be disconcerting Can be fatiguing when euthanizing large numbers
Poultry
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Practices in Afghanistan:
The most common method is exsanguination, to allow for cooking and consumption of meat. In the case of avian influenza, when the meat is not to be consumed, and carcasses are disposed, CO2 is the most accepted method.
For zoonotic diseases such as rabies, where close contact is dangerous, animals can be shot. Injectables are rarely used. Captive bolt is not practiced.
Drs. Farhad and Nawroz with CO2 and canister to contain the birds
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CHAPTER
DISEASES OF MULTIPLE SPECIES
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Infectious Diseases of Livestock in Afghanistan / Multi-Species
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1 ANTHRAX
This disease is known to occur in Afghanistan.
1. Definition Anthrax is a zoonotic disease of livestock that can cause sudden death in grazing animals and serious economic loss to the farmers. 2. Etiology The disease is caused by the spore forming bacterium, Bacillus anthracis. Anthrax can be found all over Afghanistan when grazing animals eat the bacteria present in soil or on the vegetation. The incidence of the disease may be high during drought or following flooding of pasture. 3. Transmission B. anthracis spores can remain infective in soil for many years. During this time, they are a potential source of infection for grazing livestock, but generally do not represent a direct infection risk for humans. Grazing animals may become infected when they ingest sufficient quantities of anthrax spores from the soil. The source of pasture contamination is animals that have died of anthrax and release the bacteria into the soil when they are decomposed. 4. Species affected Anthrax is most common in wild and domestic herbivores such as cattle, sheep, goats, and camels. The disease can also be seen in humans exposed to tissue from infected animals, contaminated animal products 35
or directly to B. anthracis spores under certain conditions. Humans should never consume the meat of animals that are suspected of dying from anthrax. Anthrax is a serious zoonosis! 5. Clinical signs Incubation period is 3-7 days (range 114 days). The clinical course ranges from peracute to chronic. The peracute form that is common in cattle, sheep, and goats is characterized by sudden onset and a rapidly fatal course. In acute cases, there is an abrupt fever and a period of excitement followed by depression, stupor, respiratory or cardiac distress, staggering, convulsions, and death. Often, the course of disease is so rapid that illness is not observed and animals are found dead. The body temperature may reach 41.5C, rumination ceases, milk production is materially reduced, and pregnant animals may abort. There may be bloody discharges from the natural body openings such as mouth , nostrils, ears, and anus. 6. Pathologic findings The body of an animal that has died of anthrax should never be opened or butchered because the bacteria exposed to air surrounds itself with a hard shell (spores) which makes the bacteria very resistant to destruction and the bacteria survives in the pasture for many years. Rigor mortis is frequently absent or incomplete. Dark blood may ooze from the mouth, nostrils, and anus with marked bloating and rapid body decomposition. The blood is dark and thickened and fails to clot readily. Hemorrhages of various sizes are common on the serosal surfaces of the abdomen and thorax as well as on the epicardium and endocardium. An enlarged, dark red or black, soft, semifluid spleen is common. The liver, 36
kidneys, and lymph nodes usually are congested and enlarged. Meningitis may be found if the skull is opened. 7. Diagnosis A diagnosis based on clinical signs alone is difficult. Confirmatory laboratory examination should be attempted if anthrax is suspected. The optimal sample is a cotton swab dipped in the blood and allowed to dry. Specific diagnostic tests include bacterial culture, PCR tests, and fluorescent antibody stains to demonstrate the agent in blood films or tissues. Anthrax should be differentiated from other conditions that cause sudden death such as clostridial infections, bloat, and lightning strike. Also, acute leptospirosis, bacillary hemoglobinuria, anaplasmosis, and acute poisonings by bracken fern, sweet clover, and lead must be considered in cattle. 8. Treatment Early treatment and vigorous implementation of a preventive program are essential to reducing losses among livestock. Livestock at risk should be immediately treated with a long-acting antibiotic such as oxytetrayclines, to stop all potential incubating infections. This is followed by vaccination 7-10 days after antibiotic treatment. Any animals becoming sick after initial treatment and/or vaccination should be retreated immediately and revaccinated a month later. 9. Prevention and control Anthrax is controlled through vaccination programs, rapid detection and reporting, quarantine, treatment of asymptomatic animals (postexposure prophylaxis), and burning or burial of suspect and confirmed cases. Livestock should be vaccinated 2-4 weeks before grazing season. The vaccination protection lasts for about one year, and should be repeated annually. (photo, next page) 37
Taking blood from animal suspected of dying of anthrax, to check for the bacteria in a smear.
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2 CLOSTRIDIAL DISEASES
1. Definition Clostridial diseases are caused by bacteria affecting cattle, sheep, goats and horses. The diseases go by many names depending on the specific bacteria causing the disease, or the clinical signs associated with it: blackleg (black quarter); bacillary hemoglobinuria (red water); enterotoxemia (overeating disease, pulpy kidney disease); infectious necrotic hepatitis (black disease); malignant edema, big head (swelled head); tetanus (lock jaw). 2. Etiology Clostridia are relatively large, anaerobic, spore forming, rod-shaped organisms. Associations with disease are as follows: Cl. chauvoei blackleg; Cl. haemolyticum - bacillary hemoglobinuria; Cl. perfringens types B, C and D enterotoxemia; Cl. novyi - infectious necrotic hepatitis; Cl. septicum - malignant edema; Cl. sordellii - big head; and Cl. tetani tetanus. 3. Transmission Clostridial bacteria are common in soil and the intestinal tract of animals, and are usually harmless. Under the right conditions, however, the bacteria grow rapidly and release toxins, quickly destroying tissue and often causing death. Flooding of low lying pasture may also bring the bacteria to the surface and increase the risk of exposure. These diseases are not contagious, meaning they do not spread from animal to animal. 39
4. Species affected blackleg: cattle and sheep bacillary hemoglobinuria: cattle and sheep enterotoxemia: sheep, cattle and goats infectious necrotic hepatitis: Sheep mainly, and sometimes cattle malignant edema: sheep mainly, cattle and goats big head: rams tetanus: horses are most susceptible, goats, sheep and cattle 5. Clinical signs Blackleg: Incidence of this disease is high in Afghanistan in summer and fall, and often strikes the biggest and healthiest cattle and sheep in the flock. The onset of the disease is sudden, and a few animals may be found dead without signs. Acute lameness and marked depression are common. Initially, there is a fever but, by the time clinical signs are obvious, body temperature may be normal or subnormal. Characteristic edematous and crepitant swellings develop in the hip, shoulder, chest, back, neck, or elsewhere. At first, the swelling is small, hot, and painful. As the disease rapidly progresses, the swelling enlarges, there is crepitation on palpation, and the skin becomes cold and insensitive as the blood supply to the area diminishes. Death occurs in 12-48 hours. Most cases of blackleg in cattle occur from 6 months to 2 years of age, and in sheep the disease more often occurs following some form of injury or wounds. Bacillary hemoglobinuria: Cattle may be found dead without any signs. Usually, there is a sudden onset of severe depression, fever, abdominal pain, dyspnea, dysentery, and hemoglobinuria. Anemia and jaundice are present in varying degrees. 40
Enterotoxemia: Infection with Cl. perfringens types B and C causes severe enteritis, dysentery, toxemia, and high mortality in young lambs, kids, and calves. Sudden death is often the first or only sign in lambs and kids. Some young animals may show additional signs before death, such as crying out and teeth grinding, muscular tremors, frothing at the mouth, yellowish or bloody diarrhea, and convulsions. High levels of starchy food in the diet and slowing of gut movement are predisposing factors. In calves, there is acute diarrhea, dysentery, abdominal pain, convulsions, and opisthotonos. Death may occur in a few hours, but less severe cases survive for a few days, and recovery over a period of several days is possible. Cl. perfringens type D causes pulpy kidney disease, a classic enterotoxemia of lambs that are either <2 wk old or weaned in feedlots and on a high-carbohydrate diet or, less often, on lush green pastures, seen less frequently in goats and rarely in cattle. Usually, sudden deaths in the best-conditioned lambs are the first sign. In some cases, excitement, incoordination, and convulsions occur before death. Opisthotonos, circling, and pushing the head against fixed objects are common signs of CNS involvement; frequently, hyperglycemia or glucosuria is seen. Diarrhea may or may not develop. Infectious necrotic hepatitis: There is sudden death in sheep with no well-defined signs. Affected animals tend to lag behind the flock, assume sternal recumbency, and die within a few hours. Most cases occur in the summer and early fall when liver fluke infection is at its peak. The disease is most prevalent in 1 to 4 year old sheep and is limited to animals infected with liver flukes. Malignant edema: General signs, such as anorexia, intoxication, and high fever, as well as local lesions, develop within a few hours to a few days after predisposing injury. The local lesions are soft swellings that pit on pressure and extend rapidly because of the formation of large 41
quantities of exudates that infiltrate the subcutaneous and intramuscular connective tissue of the affected areas. The muscle in such areas is dark brown to black. Accumulations of gas are uncommon. Severe edema of the head of rams develops after infection of wounds inflicted by fighting. Malignant edema associated with lacerations of the vulva at parturition is characterized by marked edema of the vulva, severe toxemia, and death in 24-48 hours. Big head: The disease is characterized by a nongaseous, nonhemorrhagic, edematous swelling of the head, face, and neck of young rams. This infection is initiated in young rams by their continual butting of one another. The bruised and battered subcutaneous tissues provide conditions suitable for growth of pathogenic clostridia, and the breaks in the skin offer an opportunity for their entrance. Tetanus: The incubation period varies from one to several weeks but usually averages 10-14 days. Localized stiffness, often involving the masseter muscles and muscles of the neck, the hind limbs, and the region of the infected wound, is seen first; general stiffness becomes proounced ~1 day later, and tonic spasms and hyperesthesia become evident. The animal is easily excited into more violent, general spasms by sudden movement or noise. Spasms of head muscles cause difficulty in prehension and mastication of food, hence the common name, lockjaw. In horses, the ears are erect, the tail stiff and extended, the nares dilated, and the third eyelid prolapsed. Walking, turning, and backing are difficult. Spasms of the neck and back muscles cause extension of the head and neck, while stiffness of the leg muscles causes the animal to assume a sawhorse stance. Sweating is common. General spasms disturb circulation and respiration, which results in increased heart rate, rapid breathing, and congestion of mucous membranes. Sheep and goats often fall to the ground and exhibit opisthotonos when startled. Consciousness is not affected. 42
6. Pathologic findings Blackleg: Edematous and crepitant swellings develop in the hip, shoulder, chest, back, and neck muscles. The affected muscle is dark red to black and dry and spongy; it has a sweetish odor and is infiltrated with small bubbles but with little edema. In sheep, because the lesions of the spontaneously occurring type are often small and deep, they may be overlooked. Bacillary hemoglobinuria: Dehydration, anemia, and sometimes subcutaneous edema are present. There is bloody fluid in the abdominal and thoracic cavities. The lungs are not grossly affected, and the trachea contains bloody froth with hemorrhages in the mucosa. The small intestine and occasionally the large intestine are hemorrhagic; their contents often contain free or clotted blood. An anemic infarct in the liver is virtually pathognomonic; it is slightly elevated, lighter in color than the surrounding tissue, and outlined by a bluish red zone of congestion. The kidneys are dark, friable, and usually studded with petechiae. The bladder contains dark urine. Enterotoxemia: Hemorrhagic enteritis with ulceration of the mucosa is the major lesion in all species. Grossly, the affected portion of the intestine is deep blue-purple and appears at first glance to be an infarction associated with mesenteric torsion. In young lambs, necropsy may reveal only a few hyperemic areas on the intestine and a fluid-filled pericardial sac. In older animals, hemorrhagic areas on the myocardium may be found as well as petechiae and ecchymoses of the abdominal muscles and serosa of the intestine. Rapid postmortem autolysis of the kidneys has led to the popular name, pulpy kidney disease; however, pulpy kidneys are by no means always found in affected young lambs and are seldom found in affected goats or cattle. Hemorrhagic or necrotic enterocolitis may be seen in goats. 43
Infectious necrotic hepatitis: The most characteristic lesions are the grayish yellow, necrotic foci in the liver that often follow the migratory tracks of the young flukes. Other common findings are an enlarged pericardial sac filled with straw-colored fluid, and excess fluid in the peritoneal and thoracic cavities. Usually, there is extensive rupture of the capillaries in the subcutaneous tissue, which causes the adjacent skin to turn black (hence the common name, black disease). Malignant edema: The local lesions consist of large quantities of serous exudates that infiltrate the subcutaneous and intramuscular connective tissue of the affected areas. The muscle in such areas is dark brown to black. Accumulations of gas are uncommon. Big head: There are areas of bruised and battered subcutaneous tissues of the head. Tetanus: The point of entry of organism cannot be found because the wound itself may be minor or healed. There are no remarkable lesions. 7. Diagnosis The most important thing to do when sudden deaths of stock occur is to get an accurate diagnosis. Anthrax should be considered as differential diagnosis since many of the clostridial diseases can look like anthrax. Animals suspected of dying from anthrax should not be moved or cut up in any way. Clostridial diseases are usually fatal. Death occurs rapidly with pulpy kidney, black disease and blackleg, but takes several days to weeks with tetanus. Laboratory testing should be considered to identify the bacteria or the toxin. Sample must be collected as soon as possible after death. 8. Treatment Clostridial diseases are difficult to treat because they progress so rapidly. Prevention, through proper management and vaccination, is far more 44
effective. Antitoxins should be used when available in conjunction with antibiotic therapy, such as penicillin. 9. Prevention and control The major factor in controlling these diseases is to develop satisfactory immunity within the animal at risk through vaccination. Passive immunity is transferred from the mother to the offspring in the first milk (colostrum). If the mother is boostered with a multi-valent colostridial vaccine about one month before the offspring is due to be born the level of protection and period of time for which the young animal is protected is increased. Active immunity requires a primary course of two doses of vaccine 4 to 6 weeks apart to give a reasonable period of protection. The first dose is usually given at 8 weeks of age or weaning time, when the protection from the mother's milk is starting to decline. Annual boosters are required to maintain the protection, as well as providing antibodies in the colostrum to protect the young until they are old enough to be vaccinated. Boosters should be given strategically before high-risk periods.
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3 CRIMEAN CONGO HEMORRHAGIC FEVER

This disease has not been diagnosed in Afghanistan.
1. Definition Crimean Congo Hemorrhagic Fever (CCHF) is a tick-borne viral disease that causes fever and mild illness in ruminants but that can be spread to humans causing a serious hemorrhagic disease. The disease was first characterized in Crimea in 1944 and given the name Crimean Hemorrhagic Fever. It was then later identified in 1969 as the cause of illness in the Congo, thus resulting in the current name of the disease. It currently has a wide geographic distribution, including Africa, eastern Europe, the Middle East and central Asia. 2. Etiology The causative agent, CCHF virus (CCHFV) is a member of the genus Nairovirus, Family Bunyaviridae. 3. Transmission Ixodid ticks, especially those of the genus Hyalomma, act as a reservoir and vector for the CCHF virus. In humans, however, the disease can also be acquired through exposure to contact with blood or bodily secretions from infected animals or humans. Slaughterhouse workers, veterinarians, paraveterinarians, and hospital employees are at greatest risk. Hospital outbreaks have been reported, due to exposure to virus-infected materials. 46
4. Species affected Numerous wild and domestic animals such as cattle, goats, sheep, horses, rabbits, and ostriches can all be infected and act as amplifying hosts for this virus, allowing for subsequent infection of more vector ticks. Disease in animals is usually subclinical or mild, with fever, depression, and recovery. Usually the disease is not recognized in animals. Infection in humans is, however, often severe. CCHF is a serious zoonosis! 5. Clinical disease Incubation period is 1-3 days following a tick bite, or 5-6 days after exposure to infected blood. Disease in animals is usually mild and selflimiting, and rarely diagnosed in the field. Disease in humans, however, is severe. There is high fever, dullness, abdominal pain, conjunctivitis, a skin rash, and often extensive hemorrhaging. Human fatality rate is 30%. 6. Pathologic findings Animals do not usually die from CCHF, so pathologic findings are not reported. In humans, there are extensive lesions associated with compromise of the vascular system and associated thrombosis and hemorrhaging. 7. Diagnosis Diagnosis of CCHF requires laboratory testing. Because the disease in animals is mild, it can be confused with many other disease entities. Diagnosis in animals is usually only made after it has been recognized in humans. 47
8. Treatment There is no known treatment for CCHF. 9. Prevention and Control CCHF is of minor importance as a livestock disease. However, it is a very serious zoonotic disease. Decreasing the prevalence among livestock requires control of the tick vector, and this can be achieved through acaricide treatments. Minimizing human exposure requires awareness and adequate protection among slaughterhouse workers, veterinarians, and paraveterinarians, and use of insect repellents such as DEET when working in tick-infested environments.
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4 ECHINOCOCCOSIS
1. Definition Echinococcosis (hydatid disease) is a parasitic infection caused by the intermediate stage of the Echinococcus tapeworm. 2. Etiology Echinococcosis is caused by Echinococcus granulosus, a tiny cestode parasite in the family Taeniidae. The parasite has an indirect life cycle, and must develop in both an intermediate host (sheep, goats, cattle) and a definitive host (dogs). 3. Transmission The definite host for E. granulosus, mainly canids, becomes infected when they ingest cysts in the tissue of the intermediate host (sheep, goats, cattle). The cysts develop into tapeworms, which mature in the canid small intestine. Eggs are shed in the canid feces and remain viable for several months in the pasture or gardens. When an intermediate host such as a sheep, goat, or cow, ingests them, the eggs develop into larvae and these larvae are carried out to different organs and develop cysts most frequently in liver and less frequently in the lungs. 4. Species affected The main animals affected by disease are sheep, goats, cattle, buffalo, and camels. Humans can also develop cysts in the organs such as liver, kidney, and brain when they ingest tapeworm eggs from the definitive 49
hosts. The eggs may be found on foods such as vegetables, fruits or herbs, or contaminated water. The dog-sheep cycle is most likely to result in human infections. Echinococcosis is a serious zoonosis! 5. Clinical signs Incubation period is prolonged. Clinical signs are only seen in the intermediate host and often the infestation is subclinical, with asymptomatic cysts found incidentally at slaughter. Most cysts are found in the liver and lungs, but they may also be found in other organs. When the cysts are large enough, they produce symptoms such as hepatic disorder, ascites and jaundice, as well as bronchopneumonia, heart failure, decreased growth, and weakness. 6. Pathologic findings In the intermediate hosts, cysts are usually individual, fluid-filled, and surrounded by a fibrous wall. Most are 1-7 cm in diameter, but some cysts may reach 20 cm. Some cysts become calcified, necrotic, or infected. Most of the cysts are found in the liver, and some in lungs. 7. Diagnosis Routine fecal examinations of the definitive hosts are not reliable because of similarity to other tapeworm eggs. In an intermediate host, echinococcosis is mainly diagnosed at necropsy or slaughter houses during meat inspection. Serological tests are not generally used in domestic animals. 8. Treatment In the definitive hosts, Echinococcus can be treated with a number of anthelminthic drugs including praziquantel (Droncit). There is no treat50
ment in the intermediate host, except surgical removal of the cysts which is not feasible in livestock. 9. Prevention and control Infections can be prevented in dogs and cats by not allowing them to eat carcasses, particularly the internal organs of infected intermediate hosts. Dogs should not be fed raw offal from sheep, goats, and cattle. Regular examination and treatment of dogs, particularly sheep dogs, can reduce echinococcosis in domestic livestock. For human protection, dogs should be kept out of vegetable plots to prevent contamination of the vegetables by eggs from dogs feces. Hygienic measures such as hand washing should also be observed before eating or after petting dogs. Most cysts in sheep and goats are fully infectious so slaughter workers should be especially careful. Most cysts in cattle are sterile, and therefore of minimal risk to humans.
Echinococcosis cysts in liver and lung, sheep
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5 FOOT-AND-MOUTH DISEASE
1. Definition Foot-and-mouth disease (FMD) is a highly contagious viral disease of all cloven-hoofed animals characterized by fever and vesicle formation in the mouth and on the feet. 2. Etiology The causative agent is foot-and-mouth disease virus (FMDV), a member of the Genus Aphthovirus in the Family Picornaviridae. Seven serotypes of FMDV have been identified (A, O, C, SAT1, SAT2, SAT3 and Asia1) and are distributed in different geographic regions of the world. 3. Transmission Foot-and-mouth disease virus is the most contagious disease known to exist. Infected animals exhale large quantities of virus which can then be carried as effective aerosols to neighboring animals and premises. Given the right climatic conditions, it is estimated that FMDV can travel several miles on the wind to infect animals in new areas. The virus can also survive within organic material such as bedding or manure, and animals can acquire the virus through oronasal exposure to this material. 4. Species affected All cloven-hoofed animals are susceptible to FMD. Cattle often show a more severe form of the disease than do sheep and goats. 52
5. Clinical disease Incubation period is 1-3 days. The disease is so contagious that morbidity is usually close to 100%. Animals become febrile (often remarkably so), with marked decreases in activity and feed consumption. Small blisters (vesicles) form on the tongue, dental pad, and on the feet, around the coronary band and in the interdigital cleft. These vesicles coalesce to become large, with subsequent rupture and exposure of painful ulcers. Secondary infection of these exposed regions is common. Animals usually recover completely but lose a great deal of condition during the short period of illness. Mortality is significant only in very young animals, in which the heart muscle is susceptible to infection, leading to myocardial failure and sudden death. 6. Pathologic findings Animals do not usually die from FMD, so pathologic findings are restricted to what is seen clinically - vesicles followed by ulceration on the feet and in the mouth. 7. Diagnosis Presumptive diagnosis of FMD can be made based on high morbidity and presence of vesicles in characteristic locations. Confirmation requires laboratory testing. A variety of tests exist: complement fixation, ELISA, virus neutralization. Differential diagnoses include: bluetongue, infectious bovine rhinotracheitis, bovine papular stomatitis, abrasive feed, and others. 8. Treatment There is no specific treatment for FMD. Ensuring that the animals are kept in a dry environment and have access to soft food can decrease problems due to bacterial secondary infections.
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9. Prevention and Control Prevention and control of FMD consumes considerable amounts of time for regulatory officials. The only truly effective prevention is to keep infected animals or animal products from entering an area. Once established, control is effected through the use of vaccination, which is often done in Afghanistan. Vaccines are serotype specific so it is important to know which serotype is circulating in an area. FMD can persist within organic material (e.g., bedding, manure) for days to weeks so decontamination of infected premises must be undertaken. Disinfectants include 2% acetic acid (halfstrength kitchen vinegar) or sodium hypochlorite (three parts laundry bleach, two parts water).
(photos, next page)
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Vesicle forming in interdigital cleft, bovine
Ruptured vesicle on tongue, bovine
Vesicle forming along coronary band, sheep
Ruptured vesicle, dental pad, sheep
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6 JOHNES DISEASE
1. Definition Johnes disease is a chronic debilitating infection of ruminants, seen in most parts of the world, causing significant morbidity and major economic losses through lowered production. 2. Etiology The causative agent is Mycobacterium avium subsp. paratuberculosis (Map), a hardy, slow-growing acid-fast bacterium. 3. Transmission Young animals acquire the infection from the environment, through the fecal-oral route or consumption of milk, within the first six months of life. Map survives well in the environment, and animals who are suffering from the clinical disease shed plenty of organisms in their feces, so local environmental contamination can be considerable. Although young animals pick up the infection, they do not show evidence of the disease until years later. Introduction of the disease into a noninfected herd is usually through replacement purchases. 4. Species affected Natural hosts include both domestic and exotic ruminants, and camelids, although disease may be noted rarely in other species. Most scientists do not believe that Johnes disease is zoonotic. There is however, some scientific evidence to suggest that people who drink milk from cows 56
infected with Map, might also become infected, and that Crohns disease, a chronic granulomatous inflammation of the ileum, is actually caused by Map. There is incomplete evidence that the agent of Johnes disease might also cause Crohns disease in humans. 5. Clinical disease The incubation period is long, 2-10 years. Morbidity is variable and dependent on the percentage of the herd that was exposed as young animals. Clinical signs rarely develop in cattle less than 2 years of age, and consist of chronic projectile diarrhea, weight loss, and low milk yield. The feces do not contain blood, mucus, or epithelial debris and are passed without straining. In sheep and goats, diarrhea is not a common feature and in advanced cases in sheep, wool may be shed. Animals remain bright and alert. The disease is progressive and ultimately terminates in emaciation and death. 6. Pathologic findings Grossly, the intestine has a thickened appearance, with numerous exaggerated transverse folds, creating a corrugated appearance. Mucosal thickening is most obvious in the ileum. Unlike the corrugations that may be seen in normal ruminant intestines at postmortem, those that are present due to Johnes disease do not disappear when the intestinal mucosa is physically stretched. Lesions may be multifocal to diffuse, with greatest concentration in ileum, but also occurring in jejunum and cecum. Focal granulomas may be present in the mesenteric lymph nodes, and in the intestinal wall in sheep and goats.
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7. Diagnosis Clinical signs and the gross appearance of the intestine is highly characteristic of Johnes disease. Laboratory confirmation can be obtained through seeing the acid-fast organisms within histologic sections of intestine in dead animals or in rectal scraping from live animals. Culturing the organism is difficult. There are no other diseases that will cause this clinicopathologic picture. Differential diagnoses include: internal parasites, salmonellosis, and clostridial enteritis. 8. Treatment There is no effective treatment for Johnes disease. 9. Prevention and Control The only way to control Johnes disease is to ensure that young animals do not have a chance to ingest the organism, which is shed in large numbers from diseased adults. Keeping actively infected (clinically diseased) animals away from young stock is essential. Good sanitation and management practices such as birthing in areas free of manure, feeding pasteurized colostrums in dairy calves and separate rearing area, elevating food and water troughs are all helpful in prevention.
(photos, next page)
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Johnes disease enlarged mesenteric lymph node.
Johnes disease mucosa of ileum is thickened and corrugated; also cecocolic lymph node is markedly enlarged.
Fluid feces, from a cow with Johnes disease
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7
RABIES
1. Definition Rabies is an acute viral encephalomyelitis that can affect any mammal. It is characterized by nervous signs that may include stupor, excitability, aggression, and terminates in paralysis and death. 2. Etiology The causative agent is rabies virus, a member of the Genus Lyssavirus in the Family Rhabdoviridae. There are many strains of rabies, with each strain having a particular reservoir, therefore there is canine rabies, fox rabies, bat rabies, etc., although all strains will cause disease in many species.
Transmission is almost always by introduction of virus-laden saliva into the tissues, usually by the bite of a rabid animal. Other means include licking of open wounds by a rabid animal, splashing of body fluids onto mucous membranes, such as might occur during the necropsy or slaughter of an infected animal, or inhalation of virus in a cave in which many rabies-infected bats are residing. Animals are shedding virus in saliva at the time of clinical illness and also for several days prior to the onset of clinical illness.
3. Transmission
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4. Species affected All mammals are susceptible to the development of rabies. Rodents and rabbits are somewhat refractory. The disease is seen in all of the domestic species. Humans are very susceptible to rabies and it causes a fatal encephalomyelitis.
Rabies is a fatal zoonosis!
5. Clinical disease Incubation period is prolonged. The virus is introduced into a skin wound and travels up the peripheral nerves to the brain. Depending on the location of entry, it can take weeks to months for the virus to reach the brain, at which time disease becomes apparent. Clinical signs of rabies are rarely definitive. Rabid animals of all species usually exhibit typical signs of CNS disturbance, with minor variations among species. The most reliable signs, regardless of species, are acute behavioral changes and unexplained progressive paralysis.
The clinical course may be divided in to 3 phases - prodromal, excitative, and paralytic/end stage. During the prodromal period, which lasts 1-3 days, animals show only vague CNS signs, which intensify rapidly. Then more marked behavioral changes appear. The term furious rabies refers to animals in which aggression (the excitative phase) is pronounced. This is the form seen most commonly in dogs and cats, where mild stimuli may provoke severe irritability and they will attack without provocation. During this phase, animals may salivate extensively. "Dumb or paralytic rabies" refers to animals in which the behavioral changes are minimal, and the disease is manifest principally by paralysis. This form is most common in cattle and horses. All cases, if allowed to progress, end in paralysis and death. 61
6. Pathologic findings At postmortem, the brain may have congested meningeal vessels, giving it an overall reddened appearance, but this is not diagnostic. 7. Diagnosis Unfortunately, although the clinical picture of rabies disease is somewhat typical, it is not diagnostic. Because of the grave danger to humans who have been in contact with the animal, definitive diagnosis is necessary. Laboratory confirmation is done by fluorescent antibody testing on brain smears.
There is no effective treatment for rabies once clinical signs are apparent. For exposed humans, there is postexposure treatment, which involves inoculation of hyperimmune serum, to inactivate the virus before it reaches the brain.
8. Treatment
9. Prevention and Control Most cases of rabies in Afghanistan are due to infected dogs and cats. Excellent commercial vaccines are available and all pets should receive vaccinations. Control of stray and ownerless dogs is important. Public education regarding the importance of rabies and what to do if bitten by an animal will decrease the incidence of human rabies. Any animal that bites without provocation and has no history of vaccination, should be killed and the brain tested for rabies antigen.
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CHAPTER
DISEASES OF CATTLE
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Infectious Diseases of Livestock in Afghanistan / Cattle
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1 ACTINOBACILLOSIS
1. Definition Actinobacillosis (wooden tongue) is a chronic disease of cattle, and rarely sheep, primarily causing tumor-like masses in the tongue, and leading to lack of productivity because of inability to eat. 2. Etiology Actinobacillus lignieresii, a gram-negative coccobacillus, is the causative agent of the disease. 3. Transmission The organism is part of the normal mucosal flora of the upper gastrointestinal tract and causes disease when it gains access to adjacent soft tissues of the mouth through epithelial damage associated with rough fodder containing sharp stems or thorns, where it multiplies locally. It causes localized infection and can spread through lymphatics to other tissues. 4. Species affected The disease is primarily seen in cattle and sometimes in sheep. It usually occurs sporadically on pasture with abrasive weeds. 5. Clinical signs Incubation period is long. Morbidity is very low. Swelling of the tongue due to expanding and firm abscesses, and tongue chewing are the main 65
clinical signs. The animal is unable to eat or drink for several days due to painful and swollen tongue. Animals may occasionally die from starvation and thirst in the early stages of the disease. As the infection becomes more chronic, fibrous tissue is deposited and the tongue becomes shrunken and immobile and eating is very difficult. The organism may also cause polygranulomatous lesion in the soft tissue of the head, neck, limbs, and occasionally lungs, pleura, udder and subcutaneous tissue. 6. Pathologic findings There are pyogranulomatous lesions of the tongue, neck, limbs, and occasionally lungs, pleura, udder and subcutaneous tissues. Pus from abscesses contains small, hard yellow to white granule containing microcolonies, giving the appearance of sulfur granules and has a sandy consistency. 7. Diagnosis The lesion in the tongue is highly characteristic and allows for a tentative diagnosis. The pus from the lesion is also distinctive, with yellowish grain-like 1mm diameter granules (sulfur granules). Under the microscope, the pus has typical microcolonies surrounded by cuplike spicules of calcium.Differential diagnoses: tumor,infection by Actinomyces bovis. 8. Treatment Systemic antibacterial therapy with oxytetracycline or erythromycin may be effective. Surgical debridement may be of some value in the treatment of advanced cases. Systemic treatment with potassium iodide has been used successfully in the past but is no longer recommended due to food safety issues. 9. Prevention and control Removal of external objects such as wires and sticks reduces the chances of disease development. 66
2 ACTINOMYCOSIS
1. Definition Actinomycosis (lumpy jaw) is primarily a disease of cattle causing chronic, progressive, pyogranulomatous inflammation of both soft and bony tissues of the head. 2. Etiology The causative agent is Actinomyces bovis, a Gram-positive filamentous bacteria. 3. Transmission Actinomyces bovis is part of the normal flora of the oral and nasopharyngeal mucous membranes of cattle. Disease occurs when the organism is introduced to underlying soft tissue, via penetrating wounds of the oral mucosa from wire, sticks, or coarse feed. 4. Species affected Cattle are the primary species affected. Infrequently sheep are affected. 5. Clinical signs Incubation period is long. Morbidity is low. The clinical presentation of lumpy jaw is a hard non-movable swelling that most frequently involves the mandible, the maxilla, or other bony tissues in the head. The lesion may open and drain with a suppurative exudate that has yellow, sand-like granules. Involvement of bone frequently results in facial distortion and 67
loose teeth which make chewing difficult. Extension into the nasal cavity causes dyspnea. 6. Pathologic findings Animals do not usually die from lumpy jaw. Pathological findings are limited to the lesions at mandible and maxillae or other bony tissues in the head. The lumps consist of honeycombed masses of thin bone filled with pus. 7. Diagnosis Diagnosis can be based on clinical signs alone, but confirmed by demonstration of Gram-positive rods in yellowish sulfur granules from the purulent material, as well as bacteriological culture and histopathology. The organism appears as long filaments, rods, and cocci in exudates from active lesions. The main differential diagnoses are wooden tongue (actinomycosis) and tumors. 8. Treatment Treatment is not successful in chronic cases in which bone is extensively involved, due to poor penetration of antibacterial agents into the infection site. In less advanced cases, penicillin or oxytetracycline may be effective. Systemic treatment with potassium iodide has been used successfully in the past but is no longer recommended due to food safety issues. 9. Prevention and control Removal of external objects such as wires and sticks in the feed reduces the chances of disease development.
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3 ANAPLASMOSIS
1. Definition Anaplasmosis is a rickettsial disease of ruminants characterized by anemia, high fever, and jaundice. 2. Etiology Anaplasmosis is most commonly caused by Anaplasma marginale. Cattle could also get infected with A. centrale, which generally results in mild disease. A. ovis may cause mild to severe disease in sheep, deer, and goats. 3. Transmission Anaplasmosis is transmitted through ticks. Numerous species of tick vectors can transmit Anaplasma spp. Boophilus spp. and Dermacentor spp. have been incriminated as the main vectors. Mechanical transmission via horse flies and stable flies occurs in some regions. Transplacental transmission has been reported and is usually associated with acute infection of the dam in the second or third trimester of gestation. Anaplasmosis may also be spread through the use of contaminated needles, tattooing, dehorning or other surgical instruments. 4. Species affected All cattle are susceptible. There is a strong correlation between age of cattle and severity of disease. Calves are much more resistant to disease than older cattle. In endemic areas where cattle first become infected 69
with A. marginale early in life, losses are minimal. Serious losses occur when cattle more than two years of age with no previous exposure are moved into endemic areas. After recovery from the acute phase of infection, cattle remain chronically infected carriers but are generally immune to further clinical disease. Carriers serve as a reservoir for further transmission. Sheep, goats and wild ruminants can get inapparent infections and become a reservoir for the disease. 5. Clinical signs Incubation period is directly related to the infective dose and typically ranges from 15-36 days. After the prepatent period, peracute, acute, or chronic anaplasmosis may follow. Acute disease is most common and usually occurs in summer and fall during peak vector season. Clinical signs include fever (41C), anorexia, rapid loss of body condition, severe decrease in milk production, pale and icteric mucous membranes, increased heart and respiratory rates, and muscle weakness. 6. Pathologic findings The carcasses of cattle that die are generally markedly anemic and jaundiced. Blood is thin and watery. The spleen is characteristically enlarged and soft, with prominent follicles. The liver may be mottled and yellow-orange. The gallbladder is often distended and contains thick brown or green bile. 7. Diagnosis In endemic area anemia without hemoglobinuria and jaundice may be indicative of anaplasmosis. Microscopic examination of Giemsa-stained blood smear and identification of the organism would confirm the diagnosis. There are serologic tests as well. Differential diagnoses include babesiosis, leptospirosis, and theileriosis. 70
8. Treatment Tetracycline antibiotics and imidocarb are used for treatment, and need to be given in the early phase of disease. The carrier state may be eliminated by administration of a long-acting oxytetracycline preparation. 9. Prevention and control In some areas, sustained stringent control or elimination of the arthropod vectors and flies, together with good biosecurity would be a viable control strategy. Vaccination if available is recommended. Proper disinfection of needles, tattooing, dehorning or other surgical instruments in between animal use, is another important preventive measure.
Anaplasma marginale in bovine blood. The organisms appear as basophilic, spherical inclusions located near the margin of red blood cell.
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4 (Red Water, Piroplasmosis, Tick Fever)

BABESIOSIS
1. Definition Babesiosis is a tickborne intraerythrocytic protozoan parasitic disease of ruminants characterized by anemia, hemoglobinuria, high fever, and jaundice. 2. Etiology Two important species of Babesia in cattle, B. bigemina and B. bovis are the causative agents of the disease which is widespread in tropical and subtropical areas. 3. Transmission The main vectors of B. bigemina and B. bovis are 1-host Boophilus spp. ticks, in which transmission occur transovarially. The disease is more common in Afghanistan provinces with hot climate, and has been diagnosed in Nangarhar, Balkh, Heart, Khost, Takhar, Kunduz, and Kandahar provinces. In endemic areas, calves have a degree of immunity that persists for ~ 6 mos, and animals that recover from Babesia infections are generally immune for life. 72
4. Species affected These two species of Babesia affect only cattle. However, there are other species of babesias which may infect other domestic animals, including horses, sheep and goats. 5. Clinical signs Incubation period is 7-35 days. The acute disease generally runs a course of ~1 week. The first sign is fever (41-42C), and is accompanied later by inappetence, increased respiratory rate, muscle tremors, anemia, jaundice, and weight loss; hemoglobinemia and hemoglobinuria occur in the final stages. CNS involvement could occur with B. bovis infections. Either constipation or diarrhea may be present. Late-term pregnant cows may abort, and bulls may undergo temporary infertility due to transient fever. 6. Pathologic finding Lesions include an enlarged and friable spleen; a swollen liver with an enlarged gallbladder containing thick granular bile; congested, darkcolored kidneys; and generalized anemia and jaundice. The urine is often, but not invariably, dark red. Other organs, including the brain and heart, may show congestion or petechiae. 7. Diagnosis Clinically, babesiosis can be confused with other conditions that cause fever, anemia, hemolysis, jaundice, or red urine. Confirmation of a diagnosis by microscopic examination of Giemsa-stained blood or organ smears is essential. From the live animal, thick and thin blood smears should be prepared, preferably from capillaries in the ear or tail tip. Smears of heart muscle, kidney, liver, lung, brain, and from a blood vessel in lower leg should be taken at necropsy. A number of serologic tests such as indirect fluorescent antibody test and ELISA are available for the detection of carrier animals. 73
Differential diagnoses include anaplasmosis, and other conditions that result in anemia and jaundice, such as leptospirosis and theileriosis. 8. Treatment Diminazene aceturate (Brenil) and imidocarb dipropionate (Imzol) are the two common drugs in use. These drugs may not be available in all endemic countries. Supportive treatment is advisable, particularly in valuable animals. Blood transfusions may be life-saving in very anemic animals. 9. Prevention and control Vaccination using live, attenuated strains of the parasite has been used successfully in countries that vaccine is available. Controlling the tick vector can break the transmission cycle.
Babesia bigemina parasites in bovine blood, Wright-Giemsa stain
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5 BOVINE SPONGIFORM ENCEPHALOPATHY

1. Definition Bovine spongiform encephalopathy (BSE), also known by the name mad cow disease, is a chronic, nonfebrile, noncontagious disease of the central nervous system characterized by progressive loss of awareness and progressive ataxia. 2. Etiology BSE is not caused by an infectious agent. It is caused by a malformed neuronal protein that is similar to a normal neuronal protein, both of which are known as prion proteins. When the abnormal prion is ingested, it eventually finds its way to the central nervous system, where it causes the normal prions to change configuration and become abnormal also. The abnormal proteins are not capable of being degraded during normal cellular metabolism, and so they build up in large quantities within the neurons, hindering function of the cell. When viewed under the microscope, these abnormal prion protein accumulations appear as big clear areas that distend the cell and the brain takes on a spongey appearance, hence the name of the disease. 3. Transmission BSE can only be transmitted if a susceptible cow consumes nervous system tissue from an affected cow. This has happened in many areas of the world because of the practice of rendering - gathering the nonconsumption material at slaughter and processing it to high protein feedstuff to feed back to animals as a protein supplement. 75
4. Species affected BSE is a disease of cattle. However, some humans have become affected by BSE, and contract a disease known as variant Creutzfeld-Jacob disease (vCJD). To date, less than 200 people have been diagnosed with vCJD. Consumption of meat containing the BSE protein has been incriminated. The disease in humans is fatal. BSE causes vCJD in humans, which is a fatal zoonosis. 5. Clinical signs The incubation period for BSE is 2-8 years. Morbidity is sporadic; only one animal in a herd might show clinical signs. There is no fever. All signs are referrable to the nervous system and include behavioral changes, nervousness, hyper-reactivity, agitation, and ataxia. The disease is progressive and animals do not recover from BSE. 6. Pathologic findings There are no gross changes noted in the carcass. Histologic changes are characteristic and consist of a very spongey appearance to the brain, because of vacuolation of neurons, especially those neurons within the midbrain at the area of the obex. 7. Diagnosis There is no way to determine if BSE is present based only on clinical signs. The diagnosis is made in the laboratory, through examining brain material microscopically, or through utilizing brain material in a Western blot or ELISA test. Differential diagnoses for the clinical syndrome include: milk fever, hypomagnasemia, plant toxicities, rabies, or any other encephalitic disease. 76
8. Prevention and control BSE can be completely prevented by not feeding ruminant-based feed supplements to cattle. Once BSE is detected in an animal within a herd, the entire herd is depopulated because other animals in the herd may be harboring the abnormal prion protein which could get transmitted to humans through meat.
BSE: Midbrain and hindbrain - black line shows section to sample for diagnosis (this is the obex).
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6 BOVINE TUBERCULOSIS
1. Definition Bovine tuberculosis (TB) is a chronic infectious and debilitating granulomatous disease. 2. Etiology Bovine TB is caused by Mycobacterium bovis, a hardy bacillus that can persist in the environment. M. bovis can cause progressive disease in most warm-blooded vertebrates, including humans. 3. Transmission Inhalation of infected droplets expelled from the lungs is the usual route of infection, although ingestion, particularly via contaminated milk, also occurs. 4. Species affected Bovine TB infects predominantly cattle but may on rare occasions affect some other mammals. Humans are quite susceptible to bovine TB. Infections in humans occurs through consumption of infected raw milk, raw milk products, and through inhalation. Bovine TB can cause a disease in humans that is very similar to human TB.
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5. Clinical signs The clinical signs reflect the extent and location of lesions plus the underlying toxemia. Generalized signs include progressive emaciation, lethargy, weakness, anorexia, and a low-grade, fluctuating fever. The bronchopneumonia of the respiratory form of the disease causes a chronic, intermittent, moist cough with later signs of dyspnea and tachypnea. The destructive lesions of the granulomatous bronchopneumonia may be detected on auscultation and percussion of the lungs. Superficial lymph node enlargement may be a useful diagnostic sign when present. Affected deeper lymph nodes cannot always be palpated, but they may cause obstruction of the airways, pharynx, and gut, leading to dyspnea and ruminal tympany. 6. Pathologic findings TB granulomas may be found in any of the lymph nodes, particularly in bronchial, retropharyngeal, and mediastinal nodes. In the lungs, miliary abscesses may extend to cause a suppurative bronchopneumonia. The pus has a characteristic cream to orange color and varies in consistency from thick cream to crumbly cheese. TB nodules may appear on the pleura and peritoneum. 7. Diagnosis The single most important diagnostic test for TB is the intradermal tuberculin test. Diagnosis on clinical signs alone is very difficult, even in advanced cases. Microscopic examination of sputum and other discharges is sometimes used. Necropsy findings of the classic tuberculous granulomas are often very suggestive of the disease. Confirmation of diagnosis is by isolation and identification of the organism, with culture usually taking 4-8 weeks, or by PCR, which requires only a few days.
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8. Treatment Treatment is illegal in some countries and destruction of TB positive animal should be attempted due to zoonotic nature of the disease. 9. Prevention and control The main reservoir of infection for bovine TB is cattle. A test and slaughter policy is used in many countries to eradicate the disease. In an affected herd, testing every 3 mo is recommended to rid the herd of individuals that can disseminate infection. Pasteurization of the milk is a major step in the fight against human TB and continues to be an important control procedure in many countries.
Granulomatous lesions in the lung of a cow infected with Mycobacterium bovis. Courtesy of the Department of Pathobiology, University of Guelph
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7 CONTAGIOUS BOVINE PLEUROPNEUMONIA

This disease is known to occur in Afghanistan but is RARE.
1. Definition Contagious bovine pleuropneumonia (CBPP) is an infectious mycoplasma disease, of cattle, causing primary damage in the lung. 2. Etiology CBPP is caused by Mycoplasma mycoides subspecies mycoides smallcolony or bovine type (MmmSC). MmmSC does not survive well in the environment or in meat or meat products. 3. Transmission CBPP is spread by inhalation of droplets from an infected, coughing animal. Outbreaks usually begin as the result of movement of an infected animal into a naive herd. 4. Species affected All breeds of cattle and buffalo are susceptible. 5. Clinical disease Incubation period is long, weeks to months. Morbidity depends on degree of contact, varying from 20-80%. The mortality rate with CBPP ranges from 1070%. Usually the first abnormality noticed is a depressed, inappetent animal with fever. Coughing may be the next sign, followed by evidence of thoracic pain and an increased respiratory rate. When pulmonary involvement is extensive and severe, there will be 81
labored respiration and, sometimes, open-mouthed breathing. As pneumonia progresses and animals become increasingly dyspneic, animals are inclined to stand with elbows abducted in an attempt to decrease thoracic pain and increase chest capacity. Contagious bovine pleuropneumonia often evolves into a chronic disease. This form, characterized by ill thrift and recurrent low-grade fever, may be difficult to recognize as pneumonia. In calves, the mycoplasmemia results in a polyarthritis which may be the primary presenting complaint, often without an accompanying pneumonia. Animals affected in this manner may stand stiffly with a distinctly arched back and be very reluctant to move. 6. Pathologic findings In the lung, gross pathologic features of CBPP are characteristic. There is usually extensive, and often unilateral, inflammation of the lung and associated pleurae. The predominant gross change is consolidation, or thickening, of individual lobules that become encased in markedly widened interlobular septa, resulting in the characteristic marbled appearance. The overlying pleura may be thickened by an irregular layering of yellow fibrin which, with time, becomes fibrosed. Sequestrum, or vascular dead spots can form within the lung, and here the organism can survive for months to years, and these animals serve as carriers. In calves, joints may be filled with abundant turbid fluid that clots on exposure to air because of the excessive amounts of fibrin. 7. Diagnosis Diagnosis is based on clinical signs and necropsy lesions. Confirmation can be done through complement fixation test or isolation of the organism. The most common differential diagnosis is pneumonia due to Mannheimia or Pasteurella, but unlike CBPP, this pneumonia is almost always bilateral. 82
8. Treatment The organism is susceptible to tetracycline and tylosin. If not given early enough in the course of the disease, antimicrobial therapy may only serve to slow the progression of the disease or may even in some cases favor the formation of sequestra. 9. Prevention and Control Successful control of the spread of CBPP rests on removing susceptible animals from any possible contact with CBPP-infected animals, whether they are clinically affected or only subclinical carriers. An attenuated strain of MmmSC (T1) is used as a vaccine in enzootic areas. It is delivered subcutaneously. The vaccine may generate local necrosis, so it is usually given in the tail tip.
CBPP - pleural surface is covered with fibrin deposits
CBPP Cut section of lung showing extensive marbling due to fibrin and edema in interlobular septa.
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8 HEMORRHAGIC SEPTICEMIA
1. Definition Hemorrhagic septicemia is a peracute or acute systemic bacterial disease of cattle. 2. Etiology Hemorrhagic septicemia is caused by 2 serotypes of Pasteurella multocida, 6:B and 6:E (formerly known as B:2 and E:2). The 6:B organism is found predominantly in Asia. 3. Transmission Transmission occurs through exposure to infected animals, carrier animals, or fomites. Stress can precipitate disease in an animal harboring the organism subclinically. The bacteria do not survive well in soil. The route of entry is presumed to be oronasal. Shortly after an outbreak, as many as 20% of the surviving animals may be carriers; after 6 months, survivor carrier rate is probably less than 5%. Close contact of animals in situations that induce crowding facilitates spread. 4. Species affected Cattle 6 to 18 months of age are the principal hosts of hemorrhagic septicemia. Although outbreaks of hemorrhagic septicemia have been reported in sheep, it is not a frequent or significant disease. 84
5. Clinical disease Incubation period is short. Morbidity can be high. Mortality is high. Clinical disease usually lasts less than 72 hours. First signs may be dullness and reluctance to move. There may be respiratory distress, with frothing at the mouth, and recumbency. Edematous swellings can be seen in the throat region, neck, and brisket. 6. Pathologic findings Lesions seen are those of severe sepsis, with extensive damage to the capillary bed. There are widely distributed hemorrhages and edema, especially of the head, neck, and brisket region. Incision of the edematous swellings reveals a coagulated, serofibrinous mass with straw-colored or blood-stained fluid. Petechiation is present in multiple organs and serosal surfaces. There may be serosanguinous effusions in body cavities. There is an interstitial reaction in the lung, typical of a toxic state, and represented by a diffuse congestion and a rubbery feel to the lungs grossly. 7. Diagnosis Some epidemiological and clinical features aid in recognition of the disease. Characteristic necropsy lesions support the clinical diagnosis. In endemic regions, acute salmonellosis, anthrax, pneumonic pasteurellosis, and rinderpest should be considered for differential diagnosis. 8. Treatment Usually, by the time the disease is diagnosed, it is too late to institute treatment, although it may be possible to prophylactically administer antibiotics to animals in the herd that are not yet clinically ill. Various antibiotics, such as sulphonamides, tetracyclines, and penicillin are effective if administered early.
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9. Prevention and control Vaccination is routinely practiced in endemic areas, with bacterins or a modified live product. Avoiding crowding, especially during wet conditions, will also reduce the incidence of disease. Animals that are to be shipped should be vaccinated.
Extensive edematous swelling of the head and neck, hemorrhagic septicemia.
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9 LEPTOSPIROSIS
1. Definition Leptospirosis is a common and contagious disease of cattle affecting both beef and dairy animals, and causes lost production and reduced milk yield. Morbidity and mortality are higher in calves than in adult cattle. 2. Etiology The disease is caused by a thin, spiral-shaped bacterium called Leptospira. Leptospira serovars hardjo, pomona, and grippotyphosa are most common. However, serovars canicola, bratislava, autumnalis, and icterohaemorrhagiae, also have been isolated. 3. Transmission Cattle, which recover from the disease, may become carriers and shed the organism in their urine, sometimes for over 12 months. If the urine is passed into a moist environment, the bacteria can survive for a number of weeks. Muddy areas around water troughs and water holes are sites of infection. 4. Species affected Cattle are the principal species affected. Prevalence of leptospirosis in sheep is lower than in cattle, possibly due to less intensive husbandry methods and the tendency of sheep to avoid contact with surface water. Leptospirosis may be transmitted from cattle to humans. Symptoms can vary from fatal infection to a mild, influenza-like condition. Humans can 87
become infected either by direct contact with infected urine when handling cattle at milking, or indirectly through contact with contaminated water. Leptospirosis is a zoonosis. 5. Clinical signs Acute leptospirosis is seen mainly in calves. Calves may have fever, anorexia, dyspnea, icterus, hemoglobinuria, and hemolytic anemia. Body temperature may rise suddenly to 40.5-41C. Hemoglobinuria may last 48-72 hr. In older cattle, signs vary greatly and diagnosis is more difficult. Enzootic infections of naive cattle with serovar hardjo are more obvious in dairy than in beef cattle. Signs usually are restricted to a sudden drop in milk production; a hemolytic crisis does not occur. The milk is thick, yellow, and blood-tinged, with thick clots and a high somatic cell count; milk production can drop 10-75%, depending on the infecting strain. The udder is typically soft and flabby. The chronic forms of leptospirosis manifest as abortion and stillbirth. Abortion generally occurs 6-12 wk after initial infection and is more common during the third trimester. Stillbirths and birth of premature or weak infected calves also occur. 6. Pathologic findings In the acute form anemia, icterus, hemoglobinuria, and submucosal hemorrhage are prominent. The kidneys are swollen and dark, with multifocal petechial and ecchymotic hemorrhage. The liver may be swollen, pale, and friable, with minute areas of focal necrosis. 88
7. Diagnosis Serology with paired serum samples, direct culture in special media, or fluorescent antibody techniques on tissues are used to confirm clinical and postmortem findings. Differential diagnoses for the acute form include babesiosis and plant toxicities. Differential diagnoses for the abortion form include brucellosis, campylobacteriosis, and trichomoniasis. 8. Treatment In acute cases, treatment with anitibiotics such as tetracycline, oxytetracycline, erythromycin, and enrofloxacin have been reported to be successful if given early. Treatment has limited effect on the course of disease once uremia has developed. Blood transfusions may be indicated in severely anemic animals. 9. Prevention and control Yearly vaccinations, confinement rearing, and chemoprophylaxis are used for control of the disease. Annual vaccination should be used in closed herds, whereas semi-annual vaccination is recommended for open herds. Fencing cattle from potentially contaminated streams and ponds is recommended.
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10 MALIGNANT CATARRHAL FEVER

1. Definition Malignant Catarrhal Fever (MCF) is a chronic and severe viral disease of cattle, characterized by rhinitis, keratoconjunctivitis, lymphadenopathy, and generalized wasting. 2. Etiology The etiologic agent of bovine MCF is ovine herpesvirus-2 (OHV-2). This virus is carried subclinically by most sheep, and is spread at the time of lambing. OHV-2, to date, has resisted attempts to isolate it.There are other MCF viruses (alcelaphine herpesvirus-1, caprine herpesvirus-2, MCFV-WTD), which may cause disease, but they are of minimal relevance to Afghanistan, either because the reservoir host is not present, or because the target species is not present. 3. Transmission Sheep carrying OHV-2 virus are the primary source of infection for cattle. In sheep infection occurs early in life with most lambs being infected early in life. In the earliest stages of infection, lambs will shed the virus in nasal and oral secretions, and cattle become infected through exposure to these shedding lambs. Older lambs and adult sheep do not shed the virus and so are not infectious for cattle. Similarly, infected cattle are not contagious for other cattle. 4. Species affected Cattle are the principal victims of OHV-2. 90
5. Clinical disease Incubation period is long, on the order of weeks to months. Morbidity is low - usually only one or very few animals in a herd are affected. General clinical signs of MCF are depression, separation from the herd, persistent fever, and anorexia. Severe erosions, with deposition of abundant mucus and necrotic debris causing partial occlusion occur in the anterior nasal cavity, with resulting loud and labored breathing. Corneas become opaque. Lymph nodes throughout the body enlarge remarkably. Erosions can be present anywhere in the oral cavity, but especially on the buccal papillae. Affected animals may have diarrhea (occasionally with blood), or hematuria. Mortality in affected animals is 100%. 6. Pathologic findings Post mortem lesions include all the erosions and ulcers that were described under clinical signs, as well as generalized lymphoid enlargements throughout the body. There may be infarcts in visceral organs (especially kidney). All lesions relate to the pathogenesis of the virus, which is to infect the host and cause a pseudoneoplastic proliferation of killer lymphocytes, which then go on to attack the host tissues, especially blood vessels and stratified squamous epithelium, particularly nasal and oral epithelium, resulting in severe erosions and ulcerations. Infection of blood vessels causes vasculitis and infarctions. The generalized lymphoid enlargements are due to the virally-induced generalized lymphoid proliferations. 7. Diagnosis The clinical signs and pathologic features are diagnostic for MCF. The only laboratory test that might be helpful for confirmation is histopathology. Differential diagnoses are minimal but may include: lymphosarcoma, infectious bovine rhinotracheitis, and foot-and-mouth disease. 91
8. Treatment There is no effective treatment for MCF. Supportive care may prolong the clinical course, but case fatality rate is generally 100% regardless of therapy. 9. Prevention and control There is no vaccine to protect against MCF. Prevention is aimed at minimizing risk factors associated with the occurrence of MCF. It is good practice to avoid any contact with sheep, especially around the time of lambing.
MCF - conjunctivitis, nasal discharge, drooling.
MCF - enlarged lymph node, as palpated through the skin
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11 EXTERNAL PARASITES OF CATTLE

These parasites are known to occur in Afghanistan.
1. Definition External parasites (ectoparasites), for the most part, are a nuisance and can cause reduced weight gain and weight loss simply because the animal spends more time and energy combating them than feeding. Physical injury occurs when irritation and scratching result in open wounds that then can become infected or subject to infestation with fly larvae. Many ectoparasite species act as vectors of disease for both animals and humans. 2. Etiology There are a number of fly species which are primarily a nuisance. Blood loss due to large numbers of feeding mosquitoes may lead to anemia, unthriftiness, and weight loss/reduced gains. Lice and mites (mange) are relatively permanent residents on the animal. Infestation (commonly called mange when mites are involved) may be seen as intense irritation with the animal scratching and chewing creating skin lesions that can become ugly. Ticks thrive on blood obtained from the host. They are subdivided into hard and soft ticks according to structural characteristics. The cattle grub (Hypoderma bovis), which is a fly larva, can cause serious damage to hides and carcasses. 93
3. Transmission Lice and mites thrive and reproduce during the cooler months of the year. Transmission from animal to animal is by contact, so crowding should be avoided. Cattle grub flies attach their eggs on the hair of cattle in late spring or early summer, particularly on the legs and lower body regions. The eggs hatch in 3-7 days, and first-stage larvae travel to the base of the hair shaft and penetrate the skin. They then move to subdermal tissue along the back after 2-3 months emerge from the breathing hole, fall to the ground, pupate and emerge as adult flies 3-5 weeks later. 4. Species affected Both dairy and beef cattle are affected. 5. Clinical signs Affected animals may be distracted by external parasites and rub or scratch. Some external parasites produce crust, hair loss, dullness, lethargy, weakness, and signs of anemia. Warbles which are the larval form of the cattle grub fly (Hypoderma bovis) may occur in the back from tailhead to shoulders, and from topline to about one-third the distance down the sides. Cysts may occasionally develop into large, suppurating abscesses. The emergence of the grub, its forced expulsion, or its death within the cyst usually results in healing of the lesion without complications. Death of first-stage larvae of H. bovis in the spinal canal of cattle after systemic insecticide treatment has resulted in stiffness, ataxia, muscular weakness, and paralysis of hindlimbs.
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6. Pathologic findings There are no specific gross findings except lesions associated with anemia. Cattle grub cysts are firm and are raised considerably above the normal contour of the skin. In each cyst, there is a breathing hole, ranging in size from a small slit to a round hole (3-4 mm in diameter) for more mature larvae. Carcasses and hides of cattle infested with cattle grubs show marked evidence of the infestation and are reduced in value. 7. Diagnosis In general, most external parasites can be collected with various equipments for diagnosis such as nets, jars, traps, combs and forceps. For mites, skin scrapings are used. Most external parasites can be seen readily and identified using published descriptions and keys. However, the use of a microscope is usually necessary. 8. Treatment Treatment with various drugs to reduce or eliminate ectoparasites is often required to maintain health and to prevent economic loss. The choice and use of ectoparasiticides depends to a large extent on husbandry and management practices, as well as on the type of ectoparasite causing the infestation. Accurate identification of the parasite is necessary for selection of the appropriate drug. The selected agent can be administered or applied directly to the animal in the form of dipping, high pressure sprays, back rubs, insecticide impregnated ear tags, and pour-ons, or introduced into the environment to reduce the arthropod population to a level that is no longer of economic or health consequence. 9. Prevention and control Many ectoparasite infestations are seasonal and predictable and can be countered by prophylactic use of ectoparasiticides. For example, flies are seen predominantly from late spring to early autumn, tick populations increase in the spring and autumn, and lice and mites during the autumn 95
and winter months. Prevention and control could therefore be targeted at anticipated times of peak activity as a means of limiting disease and parasite populations.
Cow with mange infestation
Steer with tick infestation
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12 INTERNAL PARASITES OF CATTLE

1. Definition Parasitism and gastrointestinal nematode parasitism in particular, is arguably the most serious constraint affecting cattle production in Afghanistan. Economic losses are caused by decreased production, cost of prevention, cost of treatment, and death of infected animals. 2. Etiology Although there are many species of worm parasites harbored in the gastrointestinal and respiratory tracts of cattle, only a few target species are clinically and economically important. These include Haemonchus placei (barber pole worm, large stomach worm, wire worm), Ostertagia ostertagi (medium or brown stomach worm), Trichostrongylus axei (small stomach worm), Eimeria bovis (coccidian), Fasciola hepatica (liver fluke), and Dictyocaulus (lungworm). 3. Transmission Adult parasites lay microscopic eggs, which are passed in the feces and hatch in dung pats. Microscopic larvae are then dispersed, with some trickling deep into the soil and others carried onto surrounding grass. The free-living larvae feed on fungi and other soil and grass microorganisms and represent pasture contamination. When these larvae have developed to an infective stage, they may be found on blades of grass in dew drops early in the morning and seasonally in late spring and late summer/early fall. Cattle become infected while grazing. 97
4. Species affected Worm problems are seen most frequently in young beef cattle from time of weaning, and in segregated groups of dairy calves during the first season at grass. Young animals are more often affected, but adults not previously exposed to infection frequently show signs and succumb. 5. Clinical signs Clinically, the parasites of the stomach and intestine cause anemia, scouring, depression, progressive weight loss, weakness, rough coat, anorexia, and even death, but clinical parasitism occurs infrequently. The effects of parasitism usually are insidious and subclinical, such as indigestion and poor feed conversion, inadequate weight gain and decreased milk production. Lungworms cause verminous pneumonia and provide an environment conducive for viral and bacterial pneumonia. O. ostertagi, T axei, and Haemonchus can all cause hypoproteinemia and edema, particularly under the lower jaw (bottle jaw) and sometimes along the ventral abdomen. In addition, Haemonchus infection can cause severe anemia. Fasciolosis is usually asymptomatic in cattle. Coccidiosis is commonly a disease of young cattle (1-2 months to 1 yr) and occurs sporadically during the wet seasons of the year in cattle on pasture. Cattle confined to feedlots are susceptible to coccidiosis throughout the year. Outbreaks usually occur within the first month of confinement. The incubation period is 17-21 days. Calves may appear unthrifty and have fecal-stained perineal areas. The most characteristic sign of clinical coccidiosis is watery feces, with little or no blood, and the animal shows only slight discomfort for a few days. Severe infections are rare. Severely affected cattle develop thin, bloody diarrhea that may continue for >1 wk, or thin feces with streaks or clots of blood, shreds of epithelium, and mucus. They may develop a fever; become anorectic, depressed, and dehydrated; and lose weight. Tenesmus is common. 98
6. Pathologic findings Some parasites can readily be seen and identified in the abomasum, and small petechiae may be seen where the worms have been feeding. The most characteristic lesions of Ostertagia infection are small, umbilicated nodules 1-2 mm in diameter throughout the abomasum. These may be discrete, but in heavy infections they tend to coalesce and give rise to a cobblestone appearance. In T.axei infections, the mucosa of the abomasum may show congestion and superficial erosions, which are sometimes covered with a fibrinonecrotic exudate. In coccidiosis, the large intestinal mucosa may be hemorrhagic and ulcerated. 7. Diagnosis The clinical signs associated with gastrointestinal parasitism are common to many diseases and conditions; however, presumptive diagnosis based on signs, grazing history, and season is often justified. Infection usually can be confirmed by demonstrating parasite eggs. The advent of safe and effective broad-spectrum anthelmintics has largely reduced the need for differentiating the genera and species of these parasites. 8. Treatment In many management situations, high levels of infection can be expected, particularly after favorable temperatures and rainfall conditions in certain seasons. Anthelmintics are recommended when eggs are few or absent, yet history and signs suggest infections. A clinical response to a broadspectrum anthelmintic permits a retrospective diagnosis, but the animals should be placed on clean pastures after treatment to avoid reinfection. Coccidiosis is a self-limiting disease, and spontaneous recovery without specific treatment is common when the multiplication stage of the coccidia has passed.
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9. Prevention and control Effective worm control cannot always be achieved by drugs alone; however, anthelmintics play an important role. They may be used to reduce pasture contamination, particularly at times when seeding of the pasture with parasite eggs is a prerequisite for the development of an infective challenge necessary to cause clinical parasitism. Coordination with other methods of control, such as alternate grazing of different host species, integrated rotational grazing of different age groups within a single host species (including creep grazing), and alternation of grazing and cropping, are other management techniques that can provide safe pasture and give economic advantage when combined with anthelmintic treatment. Coccidiostats are used for the control of naturally occurring coccidiosis. The ideal coccidiostat suppresses the full development of the life cycle of the coccidia, allows immunity to develop, and does not interfere with production performance.
Calf showing diarrhea and rough hair coat
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13 ABORTION DISEASES OF CATTLE

These diseases are known to occur in Afghanistan.
1. Definition Abortion in cattle is commonly defined as a loss of the fetus between the age of 42 days and approximately 260 days of gestation. Infectious agents such as Brucella abortus (Bangs disease), Leptospira, Campylobacter, and Trichomonas are perhaps the most frequent causes of bovine abortion. 2. Etiology Brucellosis is a bacterial disease caused by Brucella abortus. Leptospirosis is a bacterial infection of which five common serovars have been identified as causing abortion in cattle: Leptospira canicola, L. icterohaemorrhagiae, L. grippotyphosa, L. hardjo and L. pomona. Campylobacteriosis is caused by the bacterium Campylobacter fetus, which lives in the crevices of a bulls prepuce (foreskin), but usually does not become established in the bull until it is about 4 years old or older. Trichomoniasis is caused by the protozoan Tritrichomonas fetus. 3. Transmission Brucellosis: The bacteria are spread among cattle by contact with aborted tissues and fluids. The discharges then contaminate the pasture 101
and other feeds, such as hay, threatening other cattle. Although infection usually occurs via ingestion, a susceptible animal may also pick up bacteria through the skin or eye. Leptospirosis: The Leptospira bacteria are spread by infected urine or contaminated water (oral ingestion). Droplets of urine from infected cows can infect normal cows after contact with the eye or mucous membranes of the nose or mouth. Campylobacteriosis: The disease is spread from an infected bull to a cow during breeding. Bulls also may be infected by breeding infected cows. This disease can be transmitted through artificial insemination. Untreated, infected bulls can remain carriers for a long time. Trichomoniasis: This organism is spread at breeding (venereal) only. The majority of cows clear themselves of the infection after several estrus cycles. Bulls tend to remain infected and carry the organism from one breeding season to the next. 4. Species affected Brucellosis and leptospirosis are zoonotic. Owners should be advised to wear gloves when handling aborted fetuses and to burn or bury any placentas and fetuses not needed for diagnostic efforts. In addition pasteurization of milk for human consumption should be stressed. Both Brucella abortus and Leptospira spp. can cause serious zoonotic diseases! 5. Clinical signs Brucellosis: Brucellosis causes abortions in the second half of gestation (usually ~7 months), produces weak calves, retained placenta or causes cows have trouble breeding back. Abortion or stillbirth occurs 2 weeks to 102
5 months after initial infection. Orchitis and inflammation of the accessory sex glands can occur in males. Leptospirosis: The disease causes repeat breeders, low-grade uterine infections, abortions, mastitis and occasionally systemic infection. Cattle abortion may occur at any stage of gestation but is more common during the last trimester. Some calves may be born alive but weak or they may die in-utero and be retained for up to 72 hours. The aborting dam is usually not ill. Campylobacteriosis: The disease usually results in infertility but occasionally causes abortion between 5 and 8 months of gestation. Trichomoniasis: The disease usually results in infertility and repeat breeders, but occasionally causes abortion in the first half of gestation. 6. Pathologic findings Brucellosis: Affected cotyledons may be normal to necrotic, and red or yellow. The intercotyledonary area is focally thickened with a wet, leathery appearance. The fetus may be normal or autolytic with bronchopneumonia. Leptospirosis: The leptospires cause a diffuse placentitis with avascular, light tan cotyledons and edematous, yellowish intercotyledonary areas. The fetus usually dies 1-2 days before expulsion and therefore is autolyzed. Campylobacteriosis: The fetus can be fresh with partially expanded lungs or severely autolyzed. Mild fibrinous pleuritis and peritonitis may be noted, as well as bronchopneumonia. Placentitis is mild with hemorrhagic cotyledons and an edematous intercotyledonary area. 103
Trichomoniasis: Placentitis is relatively mild with hemorrhagic cotyledons and thickened intercotyledonary areas covered with flocculent exudate. The placenta is often retained, and there may be pyometra. The fetus has no specific lesions. 7. Diagnosis Given the low diagnostic success rate, the high cost of laboratory work, and the low profit margin in both the beef and dairy industries, investigators should not attempt to make an etiologic diagnosis in every abortion. Instead, they should become concerned if fetal loss is >3-5% per year or per month. Brucellosis: Diagnosis can be made by maternal serology combined with fluorescent antibody staining of placenta and fetus or isolation of B. abortus from placenta, fetus, or uterine discharge. Leptospirosis: Placenta and fetus should be submitted to the laboratory for fluorescent antibody staining or PCR testing for Leptospira. Urine from the dam can be used to culture the organism for up to two weeks after aborting. Campylobacteriosis: The preferred samples for diagnostic work are the fetus and placenta, cervical mucus from the dam, or sample swabs from the genitalia of the bull. Campylobacter spp. can be identified by darkfield examination of abomasal contents or culture of placenta or abomasal contents. Trichomoniasis: Diagnostic samples can include the fetus, placental fluids and cervical mucus from the dam. Preputial scrapings from the bulls can also be used to grow and identify Tritrichomonas. 8. Treatment Brucellosis: Treatment is unsuccessful. 104
Leptospirosis: In an outbreak, antibiotics such as tetracycline, or erythromycin could be used to reduce shedding. Campylobacteriosis: Treatment with a topical antibiotic ointment containing neomycin and erythromycin is an option for valuable bulls. Trichomoniasis: Treat the uterine infection in the female and provide sexual rest. Usually a 90-day period of sexual rest eliminates the organisms from the uterus. 9. Prevention and control Safe and efficacious vaccines are available for many of the infectious diseases that can cause abortions in cattle. It is generally accepted that a vaccination program targeted at reproductive diseases should include, at a minimum, Leptospirosis (usually 5 serovars are included). Long-term regulatory programs involving calfhood vaccination and testing and slaughter of carrier cows are required for brucellosis eradication. Special attention should be focused on the health status of bulls in herds that utilize bulls in their lactating cow or heifer herds. Purchased bulls can not only introduce disease into the herd, but may also spread venereal diseases within a herd. In situations where bulls are introduced to the herd from outside sources, a minimum 10-14 day quarantine period should be routinely imposed in order to evaluate the health status of the imported animals. Bulls should be purchased only from herds that have a good herd health program in place and whose health status is known.
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14 RINDERPEST
This disease has been eradicated from Afghanistan.
1. Definition Rinderpest is an acute viral disease of large cloven hoofed animals characterized by fever, necrotic stomatitis, gastroenteritis, lymphoid necrosis and high mortality. 2. Etiology The infectious agent, rinderpest virus (RPV), is a morbillivirus, closely related to the viruses causing peste des petits ruminants, canine distemper and measles. Strains of rinderpest virus vary markedly in host range and virulence. 3. Transmission Transmission requires direct or close indirect contact; infection is via droplets - from the oronasal, ocular, or fecal secretions/excretions of infected animals. There is no carrier state; the virus maintains itself by continual transmission among susceptible animals. 4. Species affected All cloven-hoofed species are susceptible to rinderpest, with cattle suffering the worst disease clinically. Rinderpest can infect wild ruminants and circulate there. 5. Clinical disease An incubation period of 3-15 days is followed by fever, anorexia, and depression; oculonasal discharge develops1-2 days later. Within 2-3 106
days pinpoint necrotic lesions, which rapidly enlarge to form cheesy plaques appear on the gums, buccal mucosa, and tongue. The hard and soft palates are often affected. The oculonasal discharge becomes mucopurulent, and the muzzle appears dry and cracked. Diarrhea occurs during the final stages of the disease and may be watery, or contain blood, mucus, and epithelial fragments. In endemic areas, morbidity is low and clinical signs are often mild; in epidemic areas, morbidity is often100% and mortality is up to 90% 6. Pathologic findings Gross pathologic changes are evident throughout the gastrotinestinal tract, as areas of necrosis, erosion, ulceration, and hemorrhage. Lesions are particularly severe over the Peyers patches. Lymph nodes may be edematous. Zebra striping, that is, longitudinal congestion and hemorrhage in mucosal folds of the rectum, is common. 7. Treatment Treatment usually is not attempted, but nursing care with supportive fluid and antibiotic therapy such as penicillin or oxytetracycline (for secondary bacterial infection) may aid recovery of valuable animals. 8. Prevention and control Control in endemic areas is by immunization of all cattle and domestic buffalo >1yr old with attenuated cell culture vaccine. In these areas, outbreaks are controlled by quarantine and 'ring vaccination' and someimes by slaughtering. In epidemic areas, the disease is best eliminated by imposing quarantine and slaughtering affected and exposed animals. Control of animal movement is paramount because most outbreaks are due to introduction of infected cattle. Countries that are free of the disease and that border endemic areas must be extremely vigilant or vaccinate as a precaution. 107
Over the past few years, the FAO global control program for rinderpest has resulted in greatly decreased prevalence of the disease. Adherence to the Global Rinderpest Eradication Program (GREP) guidelines has enabled many countries to declare freedom from disease. Should it recur in clinical form, control will be through quarantine and ring vaccination. The vaccine for rinderpest, a modified live virus, provides excellent and long-term immunity to all strains of the virus.
Shooting diarrhea characteristic of rinderpest
Rinderpest - Feces, showing mucus, blood
Rinderpest - ulceration of Peyers patch, small intestine
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15 THEILERIOSIS
1. Definition Tropical theileriosis is a tickborne disease of cattle and camels, caused by Theileria annulata, and characterized by anemia, jaundice, ill thrift, dyspnea, and hemorrhagic diarrhea. 2. Etiology The causative agent is a protozoan parasite, Theileria annulata. Sporozoites in the saliva of the Hyalomma tick vector are inoculated during feeding and these sporozoites invade macrophages, and B lymphocytes to a lesser extent. In these cells they mature to become macroschizonts, which eventually differentiate into microschizonts, leading to merozoites that invade erythrocytes. Within the erythrocytes, the organisms are usually referred to as piroplasms. Ticks feeding on infected animals will ingest the infected erthyrocyte and there is further development to a sporozoite within the salivary gland of the tick. 3. Transmission The disease is transmitted by ticks of the Hyalomma spp. 4. Species affected Cattle are the principal victims of theileriosis. The parasite will also infect buffalo and camels. 109
5. Clinical signs The incubation period is 10-25 days. The number of animals sick is influenced by a variety of factors, including tick infectivity, tick challenge, and pre-existing immunity in the host herd. In the acute disease, death occurs 15-25 days after infection. Clinical signs might include pale mucous membranes (anemia) or jaundice, as the piroplasms will precipitate destruction of red blood cells. During the stage when there is great production of macroschizonts within macrophages, there could be enlarged lymph nodes, lacrimation, and a generalized loss of condition and muscle wasting due to massive release of cytokines from infected cells. Early there is constipation, but there may be hemorrhagic diarrhea in the terminal stages. In susceptible cattle introduced into endemic areas, mortality is high, between 40-90%. Mortality among local breeds is much lower. 6. Pathologic findings There are no specific lesions associated with tropical theileriosis. Shortly after infection, the lymph node draining the site of the tick bite will be enlarged. At the time of severe clinical disease or death, anemia, jaundice, enlarged lymph nodes, muscle wasting, pulmonary edema, and hemorrhage in the reticulum, and hemorrhagic enterocolitis may all be present. 7. Diagnosis Diagnosis of disease rests on finding the infectious organisms in blood smears or impression smears of lymph nodes. Differential diagnoses include: babesiosis, anaplasmosis, hemorrhagic septicemia, plant toxicities, and nutritional disorders. 8. Treatment Anti-protozoal drugs (buparvaquone) can all be used in the face of clinical infection and will diminish clinical signs, but do not sterilize the infection. 110
9. Prevention and Control Endemic stability between tick challenge and host immunity is operative in many areas but this can be easily disturbed through a number of factors, including sudden increase or decrease in tick burdens, failure to vaccinate, or introduction of nave stock. The greatest problems occur when nonnative cattle are introduced into an area of endemicity. Protecting these animals through vaccination is practicable. Two methods of vaccination exist - intentional low dosing of sporozoites, or using an attenuated product of schizont-containing cells. Use of ivermectin will decrease tick burdens.
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CHAPTER
DISEASES OF HORSES
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Infectious Diseases of Livestock in Afghanistan / Horses
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1 EPIZOOTIC LYMPHANGITIS
1. Definition Epizootic lymphangitis is a chronic fungal disease of the skin of horses, characterized by exudative and ulcerative inflammation along lymphatic tracts and on the conjunctiva. 2. Etiology The causative organism is a dimorphic fungus, Histoplasma capsulatum var. farciminosum. In tissues, the fungus occurs as a yeast form, whereas in the environment, it exists in the hyphal form, hence the designation dimorphic. 3. Transmission The organisms are present in the exudates of active lesions and can survive in the environment for a long period. Most cases are due to flies carrying the organism from the exudates on one animals skin to an open wound on a susceptible animals skin. Additionally, grooming equipment or harnesses can act as fomites, transferring the disease to the next animal in contact. The fungus can remain in bedding for months. 4. Species affected Donkeys, horses, and mules are the only species affected.
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5. Clinical signs Incubation period is long, probably on the order of weeks. Morbidity is variable and depends on the proximity of animals and the overall fly burden. Animals do not appear to be clinically ill and remain bright and alert. A nodule appears in the subcutis, will ulcerate, heal, ulcerate again, and may progress along lymphatics to do the same process at nearby locations. The repeated bouts of inflammation can cause nodules to become firm with abundant scar tissues. Lesions are most common on the limbs but also on the face. Lymphatics can become cord-like. Conjunctiva are frequently affected. Epizootic lymphangitis is not a fatal disease except that infected animals may be euthanized to prevent spread. 6. Pathologic findings Animals rarely die of epizootic lymphangitis. The pathologic findings are basically the same as those described under clinical disease. There are ulcerative pyogranulomas that undergo recurring cycles of activity and healing. 7. Diagnosis The clinical picture is characteristic but not diagnostic, because the skin form of glanders is almost identical. Making an impression smear and staining with Giemsa or DiffQuik can highlight the Histoplasma yeast. This is the most useful laboratory test. The organism is very difficult to culture. Differential diagnoses include: skin form of glanders (farcy), habronemiasis. 8. Treatment Treatment with anti-fungal drugs such as sodium iodide, potassium iodide, or amphotericin B is possible but recurrence is common.
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9. Prevention and control Infected animals with productive lesions need to be separated from susceptible animals. Cleaning of lesions and the surrounding environment will decrease transmission. Environmental contamination, once it occurs, can remain for months to years. There is no commercially available vaccine.
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2 EQUINE INFECTIOUS ANEMIA

1. Definition Equine Infectious Anemia (EIA), also known as swamp fever, is an acute to chronic viral disease affecting all equidae species (horses, mules and donkeys), and characterized by progressive anemia, weakness, and poor growth. 2. Etiology The causative agent is equine infectious anemia virus (EIAV), a lentivirus in the Family Retroviridae. Once infected with EIAV, an animal is considered infected for life. 3. Transmission Equine Infectious Anemia is spread mechanically through transfer of blood from one horse to another. This can happen through biting flies (tabanids and stable flies) that are irritating as they feed on the horse, so the feeding is interrupted and the fly immediately moves to another horse to finish the feeding, taking blood with it. The other common means of transmission is through the use of syringes, needles, or surgical tools. 4. Species affected All equidae can be infected with EIA. 5. Clinical Disease Most infections with EIAV are inapparent. However, animals are infected for life and if stressed or immunocompromised, disease can be 118
precipitated. In animals that become clinically ill, the disease can appear as acute or chronic, with chronic being far more common. In the acute form, there is fever and hemorrhaging, often with death occurring within two weeks. The most classical cases of EIA are seen in chronically infected horses. These animals experience episodes of fever, weight loss, depression, progressive weakness, anemia, jaundice, and dependent edema. These signs occur every two weeks in recurring cycles. Pregnant mares may abort. 6. Pathologic findings Gross pathological findings in acute cases include edema and hemorrhage in multiple organs, especially lung. In the chronic cases, in addition to the pallor and edema that was noticeable clinically, internal findings may include a large pulpy spleen, enlarged soft liver, and hemorrhage over many serosal surfaces. 7. Diagnosis A clinical presumption of EIA requires laboratory diagnosis via the agar gel immunodiffusion test. Differential diagnoses include: purpura hemorrhagica, babesiosis, leptospirosis, phenothiazine toxicity, and autoimmune hemolytic anemia. 8. Treatment There is no known treatment that can eliminate the virus from the body. 9. Prevention and Control There is no vaccine to prevent infection. Once infected, animals remain so for life, consequently the only effective strategy is to prevent infection. An agar gel immunodiffusion test (Coggins test) exists for detection of infection, so isolation of infected horses to prevent infection of others nearby is important. Sterilization of needles and instruments will prevent iatrogenic transmission. 119
3 EQUINE INFLUENZA
1. Definition Equine influenza is highly contagious, rapidly spreading viral disease of horses causing flu-like signs. 2. Etiology The causative agent is equine influenza virus, a type A influenza virus in the Orthomyxovirus family. 3. Transmission The virus can be spread easily from horse to horse as a result of aerosols, droplets and also from nasal discharge and from things like infected brushes and rugs. The disease is fairly contagious and there is almost 100% infection rate in a population that has been previously unexposed to the virus. 4. Species affected Equine influenza virus can infect horses, donkeys, and zebras. The disease is most common in young horses, especially those grouped together and also during transport. 5. Clinical signs The incubation period of influenza is 1-3 days. Poor performance may be the first indication of illness. Clinical signs begin abruptly and include a dry, nonproductive cough, depression, anorexia, fever (up to 41.1C), 120
serous nasal discharge, and enlarged and tender submandibular and retropharyngeal lymph nodes. Secondary bacterial infections may occur and can cause a mucopurulent nasal discharge, guttural pouch empyema and sinusitis. Mildly affected horses recover uneventfully in 2-3 weeks; severely affected horses may convalesce for up to 6 months. Recovery may be hastened by complete restriction of strenuous physical activity. 6. Pathologic findings Necropsy material is rarely available since the disease is not usually fatal. Foals dying of acute respiratory distress associated with influenza infection have severe diffuse interstitial pneumonia. 7. Diagnosis The presence of a rapidly spread respiratory infection in a group of horses characterized by rapid onset, high fever, depression, and cough is presumptive evidence of equine influenza. Definitive diagnosis can be determined by virus isolation, influenza A antigen detection, or paired serology (hemagglutination inhibition). Nasopharyngeal swabs are obtained for virus isolation and antigen detection. These samples should be obtained as soon as possible after the onset of illness. 8. Treatment Horses that do not develop complications require rest and supportive care. Horses should be rested with a minimum of 3 weeks rest. Antiinflammatory drugs are recommended for horses with a fever of 40C. Antibiotics are indicated when fever persists beyond 3-4 days or when purulent nasal discharge or pneumonia are present. A booster vaccination during an outbreak may help. Severe cases may take 3-4 months to resolve. Quarantine any affected barn for at least 4 weeks. Clean and disinfect stalls, equipment, transport vehicles after recovery.
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9. Prevention and control Prevention of influenza requires hygienic management practices and vaccination. Exposure can be reduced by isolation of newly introduced horses for 2 weeks. Numerous vaccines are commercially available for the prevention of equine influenza.
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4 EQUINE PIROPLASMOSIS
1. Definition Equine piroplasmosis is a tickborne protozoal infection of horses characterized by acute fever, inappetence, anemia, jaundice, sudden death, or chronic weight loss and poor exercise tolerance. 2. Etiology Equine piroplasmosis results from infection by the protozoa Babesia (Theileria) caballi or Babesia equi. The two organisms may infect an animal concurrently. 3. Transmission Babesia caballi and B. equi are transmitted by ticks in the genera Dermacentor, Hyalomma, and Rhipicephalus. Equine piroplasmosis can also be spread by contaminated needles. Intrauterine infection of the foal is fairly common, particularly with B. equi. After recovery, horses may become carriers for long periods of time. The disease is more common in Afghanistan in hot seasons of the year. 4. Species affected Equine piroplasmosis affects all members of the equidae family (horses, mules, donkeys). Mules and donkeys are less susceptible than horses.
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5. Clinical signs Incubation period is 7-22 days. Disease can be mild to severe, depending on the virulence of the parasite. In rare peracute cases, animals may be found dead or dying. More often, piroplasmosis presents with fever, inappetence, malaise, labored breathing, congestion of the mucous membranes, and small, dry feces. Anemia, jaundice, hemoglobinuria, sweating, petechial hemorrhages on the conjunctiva, a swollen abdomen, and posterior weakness or swaying may be also seen. Less severe cases may have a fever (40C), inappetence, malaise, weight loss, signs of mild colic, and mild edema of the distal limbs. The mucous membranes can be pink, pale pink, or yellow, and may have petechiae or ecchymoses. In chronic cases, common symptoms include mild inappetence, poor exercise tolerance, weight loss, and transient fever. 6. Pathologic findings In severe cases, the animal is usually emaciated, jaundiced, and anemic. The liver is typically enlarged and dark orangebrown. The spleen is enlarged, and the kidneys are pale and flabby. Petechial hemorrhages may be seen in the kidneys and subepicardial and subendocardial hemorrhages in the heart. There may also be edema in the lungs perhaps along with pneumonia. 7. Diagnosis Equine piroplasmosis should be suspected in horses with anemia, jaundice, and fever; however, the clinical signs are often variable and nonspecific. The disease can be diagnosed by identification of the organisms in Giemsa stained blood or organ smears. The organisms can be difficult to detect in carriers and serology is often the diagnostic method of choice. Serologic tests include complement fixation, indirect fluorescent antibody (IFA), and enzymelinked immunosorbent (ELISA) assays. The IFA test can distinguish between B. equi and B. caballi, and a PCR assay can detect the organisms from the blood of horses recovered 124
from acute babesiosis. Differential diagnoses include surra, equine infectious anemia, dourine, African horse sickness, and purpura hemorrhagica. 8. Treatment Diminazene aceturate (Berenil) and imidocarb dipropionate (Imzol) are the two common drugs in use. These drugs may not be available in all endemic countries. There are no vaccines for horses. 9. Prevention and control Disinfectants and sanitation are not generally effective against the spread of tickborne infections. However, preventing the transfer of blood from one animal to another is vital.
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5 EQUINE RHINOPNEUMONITIS
1. Definition Equine rhinopneumonitis is an acute and contagious viral disease of horses and donkeys that results in respiratory problems, especially in young animals, and abortion in pregnant mares. 2. Etiology The causative agent is equine herpesvirus-1 (EHV-1). 3. Transmission The disease travels readily through a herd, spread primarily by aerosol from respiratory secretions of infected animals. It can also spread via fomites. This is the main means of transport between herds. 4. Species affected Both horses and donkeys are susceptible to equine rhinopneumonitis. 5. Clinical signs Incubation period is 2 to 10 days. Morbidity is usually high. There is an initial fever, followed by respiratory signs with dyspnea and nasal discharge. Respiratory disease is more severe in foals. Mares can abort following a bout of respiratory disease, as the virus moves systemically, passes through the placenta, and kills the fetus. Occasionally, EHV-1 will also attack the nervous system, resulting in ataxia and paresis. 126
6. Pathologic findings Animals rarely die of equine rhinopneumonitis. In aborted fetuses, there may be multiple pinpoint white foci in the liver, lung, and kidney (representing multifocal necrosis). 7. Diagnosis Clinical diagnosis is not possible, as equine rhinopneumonitis can mimic many other equine respiratory diseases. Laboratory confirmation is essential and the tests include virus isolation, indirect fluorescent antibody testing, and serology. Differential diagnoses for the respiratory illness include glanders, equine influenza, lymphangitis, and for abortion include equine viral arteritis, leptospirosis, and bacterial placentitis. 8. Treatment There is no specific treatment for equine rhinopneumonitis. Supportive therapy, good nutrition, and antipyretics will help speed animals recoveries and antibiotics will decrease possibility of secondary bacterial infection. 9. Prevention and Control There are excellent vaccines available. Modified live vaccine provides longterm immunity; killed vaccines can be used in pregnant mares. Preventing the disease from entering a herd can be facilitated through isolating new arrivals for 3-4 weeks prior to mixing with the rest of the herd. As sometimes the disease is transmitted herd to herd through fomites, veterinarians and farriers should ensure that their equipment and clothing is adequately cleaned after working on an infected premise.
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6 EQUINE VIRAL ARTERITIS

1. Definition Equine viral arteritis is a contagious viral disease of horses and donkeys, causing fever,depression, conjunctivitis, edema,pneumonia and abortion. 2. Etiology The causative agent is equine arterivitis virus (EAV), a member of the Genus Arterivirus, Family Arteriviridae. 3. Transmission The most common means of transmission are respiratory and venereal. Acutely infected horses exhale virus as they breathe and animals nearby are infected by droplets. Fomite transmission from these respiratory droplets can occur but is not of major importance for the disease. Stallions can become persistently infected; these animals are not clinically ill but they transmit the virus to susceptible animals in their semen, either through natural breeding or artificial insemination. Additionally, an acutely infected mare will pass the infection to her fetus, resulting in abortion. 4. Species affected Both horses and donkeys are susceptible to equine viral arteritis. 5. Clinical signs The incubation period is 3-7 days. Many animals in a herd may be infected but most animals infected with EVA do not experience clinical 128
disease. Those that become ill have fever, inappetence, and depression. There may be a skin rash, muscle soreness, or edema of dependent regions and also around the face and genital area. A serous conjunctivitis is frequently seen. Respiratory signs consist of nasal to mucoid discharge, coughing, and dyspnea. In pregnant animals that become infected, the abortion rate is 10-70%. 6. Pathologic findings Adult animals usually recover. In the few that die, there is edema in numerous locations, especially lung. In aborted foals, there is fluid in the body cavities and interlobular edema in the lung. 7. Diagnosis The clinical signs are similar to many other respiratory diseases of horses, so laboratory diagnosis is essential. Tests done in the laboratory include virus isolation, and serology. Differential diagnoses include: equine rhinopneumonitis, equine influenza, African horse sickness, and equine infectious anemia. 8. Treatment There is no specific treatment for horses with EVA. Rest, adequate nutrition, and antibiotics will all help with recovery and decrease the possibility of pneumonia due to secondary bacterial infection. 9. Prevention and Control An effective attenuated vaccine is commercially available and will protect animals from respiratory infection. This vaccine should not be used in pregnant mares as it may result in abortion. Infected stallions carry the virus in their accessory glands and will continue to shed the virus for years, so they need to be culled, castrated, or only bred to mares that have been well vaccinated. 7 129
EXTERNAL PARASITES OF HORSES

1. Definition The primary ectoparasites of horses are houseflies, stable flies, mosquitoes, and, to a lesser extent, horse and deer flies. 2. Etiology The common housefly (Musca domestica) is by far the most common pest for horses. The stable fly (Stomoxys calcitrans) is the most common blood-feeding fly pest for horses. The stable fly resembles the housefly but has a slender tubular beak that it uses to pierce the skin and suck blood. Mosquitoes are serious disease vectors, in addition to their annoying bites. Mosquitoes can carry West Nile virus and encephalitis. Both the horse fly and deer fly are biting flies that are annoying to horse. Horse flies are about the size of your thumb and make a loud buzzing noise when flying. 3. Transmission Houseflies are a nuisance as well as carriers of disease to humans and horses. Horse manure is a favorite larval food of houseflies. Mucous secretions and wounds on horses are a protein source for the adult housefly. Old bedding, wet hay, manure and other moist organic debris are also stable fly breeding areas. Adult stable flies can travel 130
considerable distances, resulting in large numbers of flies appearing at horse facilities that have minimal stable fly breeding areas. All mosquitoes must have water in which to complete their life cycle. 4. Species affected All horses are affected. 5. Clinical signs Houseflies feed around the eyes, nose, genital openings, and wounds on a horse. In high fly-populated areas, this feeding can be very annoying and potentially dangerous for the horse. Stable flies usually feed on the horse's lower front legs. Horses will stomp their feet in reaction to the fly's painful bite. Foundered or lame horses that can't stomp are especially prone to attack. Horse flies have a bite that is relatively painful, and most horses will attempt to get away from a horse fly if it lands on them. 6. Pathologic findings There are no specific gross findings except lesions associated with fly bites. 7. Diagnosis Most external parasites can be seen readily and identified using published descriptions and keys. 8. Treatment On-site treatments can be applied by spraying potential fly nesting sites with a residual insecticide and sticky traps. Fly repellent sprays are available for individual horse application.
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9. Prevention and control Environmental control through good sanitation is essential to minimize housefly populations. Manure and wet bedding should be removed from stalls at least once a week. Leaky waterers should be fixed, and muck holes in stalls should be filled in and kept dry. Edges of feed bunks and under fence lines and other protected places that may provide a fertile larval breeding ground should be cleaned regularly. Controlling stable flies involves weekly disposal of manure and other breeding sources, such as urine-soaked straw, moist decaying vegetation, and compost piles.
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8 GLANDERS
1. Definition Glanders is a contagious disease of horses characterized by granulomatous lesions in the lungs, nasal cavity and lymphatic system. 2. Etiology The causative agent is the Gram-negative bacteria Burkholderia mallei. 3. Transmission The bacteria are present in exudates and secretions from infected animals. Ingestion or inhalation of bacteria is the most common route of infection. Contamination of feed bunks and watering troughs is probably important in disseminating the disease through a herd. 4. Species affected Glanders can infect and cause disease in many species. Horses are the principal victims, donkeys and mules less so. Cats, both wild and domestic, that feed on meat from infected horses can contract the disease. Humans are also susceptible to infection and glanders is considered an occupational hazard for veterinarians and paraveterinarians. Glanders is a serious zoonosis! 133
5. Clinical signs Incubation period is 2-10 days, but the disease is usually chronic and often not noticed until some weeks after infection. Morbidity depends on husbandry conditions and confinement. Herds kept in close quarters will have higher morbidity rates. The disease affects lymphatic and respiratory systems. In both forms, animals show intermittent high fever and lose considerable condition. The lymphatic, or skin form, also referred to as farcy, is associated with nodular thickening of cutaneous lymphatics, often with breakout granulomatous lesions along the affected tract. Draining lymph nodes are markedly enlarged and firm. In the respiratory form, either nasal cavity or lungs or both may be affected, with dyspnea, and mucopurulent nasal discharge. Mortality is high, but may be falsely elevated because infected animals are often euthanized due to regulatory or public health concerns. Infection in humans is characterized by severe illness, with nodular lesions on the skin, and respiratory distress. 6. Pathologic findings Skin lesions consist of frequent to continuous pyogranulomatous inflammation of the lymphatics and large reactive draining lymph nodes that have multiple areas of necrosis or caseation. In the nasal mucosa, glanders ulcers are characterized by extensive mucopurulent and necrotic exudates and are often stellate in shape. Pulmonary lesions consist of multiple variably-sized soft, caseating or pyogranulomatous nodules, randomly scattered throughout the parenchyma. 7. Diagnosis The typical nodules, ulcers, scar formation, and debilitated condition may provide sufficient evidence of clinical diagnosis. The bacteria can be grown in the laboratory and identified through biochemical tests. Differential diagnoses include: pneumonia of any cause, epizootic lymphangitis. 134
8. Treatment Broad-spectrum antibiotic therapy such as doxycycline, gentamicin, or trimethroprim sulfate is recommended for infected animals. However, because of the public health concerns, isolation or euthanasia is often considered as well. 9. Prevention and Control There is no vaccine to protect against glanders. Detection of subclinically infected carrier animals can be done through the mallein test, which is similar to tuberculin testing. A small amount of bacterial lysate is inoculated into the eyelid and if swelling occurs in one to three days, it is presumed that the animal has been infected at some time previously and may still be infected. Isolation or destruction of these animals is recommended to prevent local spread. Thorough cleaning of the environment around infected animals is essential.
Glanders - affected lung with multiple caseating nodules
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9 INTERNAL PARASITES OF HORSES

1. Definition Internal parasites are the greatest single cause of colic in horses and are often a causative or contributing factor in many respiratory, digestive, and performance problems. 2. Etiology The four most common internal parasites found in horses are strongyles, ascarids, bots, and pinworms. Large and small strongyles, ascarids and tapeworms present the greatest health risks. Strongylus vulgaris (bloodworm) is the most significant and the most common of all the internal parasites of horses. Strongyles are commonly divided into two groups: the large strongyles and small strongyles. The ascarid (Parascaris equorum) is a large roundworm that primarily affects foals and young growing horses. Horse bots, which are found in the stomach, are the larvae of botflies, Gasterophilus spp., which can cause a mild gastritis. Adult pinworms (Oxyuris equi) are found primarily in the colon and rectum of horses and lay their eggs around the anus. 136
Tapeworms (Anoplocephala) occur in horses of all ages and may lead to varying degrees of colic. 3. Transmission Strongyles are very dangerous because the immature worms migrate through blood vessels of the intestine, and produce intestinal inflammation which may result in "fatal" colic. Horses acquire the parasite by consuming contaminated water, grain, hay or grass. Strongyle larvae are extremely resistant to adverse weather conditions because they are enclosed in a sheath. The life cycle of the ascarid starts as the horse swallows eggs with feed, pasture or water. These eggs hatch, and the resulting larvae migrate into the wall of the small intestine where they migrate into the veins. Adult botflies lay their eggs during the warm months of late summer and early fall, on the hair of various parts of the horse, especially the chest, forelegs, throat, and nose. Stimulated by the horse's licking, the larvae hatch and enter the horse's mouth, where they settle in the tissues of the gums, cheek and tongue. After about a month, the larvae migrates to the stomach, where they attach to the stomach lining. The damage produced by pinworms is minor. They do produce a severe irritation around the tail area which causes the horse to rub its tail. Transmission of tapeworms requires an intermediate host, the oribatid mite which exists as a free living form on pastures. The horse ingests the mite from pastures, and it takes about two to four months for the tapeworm to mature in the horse. 4. Species affected Horses of all ages are infected with strongles, except the neonatal foals. Ascarids affect young horses more than mature ones. 137
5. Clinical signs Horses with strongyles may lose condition, weaken, and have diarrhea. They may become anemic due to the parasites' blood sucking. Horses in good physical condition may have a large number of strongyle larvae that can create arterial aneurysms (a balloon-like defect) which can cause sudden death if the artery ruptures at the aneurysm. Signs of ascarid infection in foals include unthriftiness, pot belly, rough hair coat, slow growth and depression. Some foals will develop a cough and nasal discharge that does not respond to antibiotic treatment. It is not unusual for several hundred bots to attach to the stomach, causing irritation, interfering with digestion, and obstruction to the opening of the small intestine. Pinworms are less dangerous than other internal parasites, and are annoying to the horse because they cause severe anal itching. Large numbers of tapeworms can cause ulceration in the large intestine and cecum, colic, and a severe form of intestinal blockage. 6. Pathologic findings Dead animals should be opened and inspected for worms. Some worms could be seen with naked eye. The larvae of S. vulgaris migrate extensively in the cranial mesenteric artery and its branches, where they may cause parasitic thrombosis and arteritis. Therfore, these areas should be examined in horses dying of colic. 7. Diagnosis Diagnosis of mixed parasite infection is based on demonstration of eggs in the feces. Specific diagnosis can be made by identifying the infective larvae after fecal culture. When colic due to verminous arteritis is 138
suspected, a painful enlargement at the root of the mesentery may be palpable per rectum. 8. Treatment Many different commercial products are available to remove internal parasites from horses. These drugs are available in several different physical forms and are sold under various trade names. A drug control program to reduce or eliminate internal parasites should be used in combination with a good management control program. Pinworms can be treated successfully with the same drugs that are effective against strongyles and ascarids. It is important to include treatment for tapeworms in your deworming plan. Because many deworming agents do not kill tapeworms, a specific product may need to be added to your deworming program. 9. Prevention and control A universal protocol to eliminate internal parasite infection in the horse does not exist. Each situation is different and is affected by many factors, including climate, season of the year, humidity, rainfall, age of the horse and concentration of horses on the land. Management and medication are the primary methods used to control parasite concentration and influence productivity in the horse. Breaking the life cycle of parasites is as important as administering dewormers. Manure should be removed daily in stalls and weekly in pastures. Pastures and paddocks should be well drained and not overpopulated. Fly control programs help with bot prevention and general well-being.
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10
STRANGLES
1. Definition Strangles is an acute to subacute contagious bacterial disease of equids affecting the upper respiratory tract and associated lymph nodes. 2. Etiology The causative agent is Streptococcus equi subsp. equi, a Gram positive coccus. 3. Transmission The bacteria move from animal to animal mostly by direct contact, but also indirect contact through contaminated items. The pus discharges contain abundant bacteria which then, if aerosolized and inhaled, can penetrate the nasopharyngeal epithelium and move to the local lymph nodes where they incite the formation of abscesses. 4. Species affected Both horses and donkeys are susceptible to the development of strangles. 5. Clinical signs Incubation period is 4 to 14 days. The disease usually occurs in outbreak form in groups of young horses under crowded conditions. Animals have fever (39.4-41.1C), and then develop enlarged parotid or retropharyngeal lymph nodes. Mucopurulent nasal discharge is common. Some are reluctant to eat or swallow because of the pain associated with the expanding abscesses. Some abscesses may rupture and discharge to the out140
side. About 20% of infected horses experience some complication, and these can include guttural pouch infection, abscesses that might form in other parts of the body (lung, brain, mesentery), or an autoimmune reaction to the bacteria which presents as diffuse and petechial hemorrhages, otherwise known as purpura hemorrhagica. Mortality is low. 6. Pathologic findings Animals do not usually die from strangles. 7. Diagnosis Diagnosis of strangles is usually made on the basis of clinical signs, when enlarged, painful, pus-filled lymph nodes are present in the head or neck. There are no other differential diagnoses for this common form of the disease. Confirmation of strangles is by laboratory culture and the organism is easily identified through standard biochemical tests. When abscesses are present in other parts of the body, diagnosis is problematic as clinical signs could mimic so many other diseases. 8. Treatment Penicillin is the drug of choice for strangles. However, if abscesses are already well-formed, treatment is contraindicated as it prolongs the course of the disease. Once abscesses are readily visible, it is better to let the disease run its full course, allow the abscesses to rupture and heal, rather than treating with antibiotics that might inhibit the rupture of the abscesses or prolong the period of shedding. Supportive therapy, including adequate rest, and ready access to soft food and plenty of water is recommended. 9. Prevention and Control The organism does not persist for long in the environment. Most infectious material comes from acutely infected animals that are shedding the bacteria in the purulent nasal secretions, so keeping these 141
animals separated from other susceptible animals is essential. Approximately 10% of animals might be chronic subclinical carriers after they recover.
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11 SURRA
1. Definition Surra is an endemic chronic protozoal disease of mainly horses and camels characterized by intermittent fever, anemia, and weight loss. 2. Etiology Surra is caused by Trypanosoma evansi, a protozoan parasite. 3. Transmission Any biting or blood sucking insect or tick may serve as a vector. Horse flies (Tabanus) and stable flies (Stomoxys) are commonly implicated. T. evansi does not require a period of maturation in an insect vector. Mechanical transmission by contaminated needles is also possible. 4. Species affected The disease mainly affects camels and horses, but buffaloes and cattle can also be affected. Surra is one of the most important diseases of camels. 5. Clinical signs The incubation period is 5-60 days. Severity of disease varies from mild to acute. Acute surra is characterized by depression, weakness and edema of the legs, brisket and abdomen, and secondary pneumonia. Females may abort and milk of lactating animals may become caseous. 143
Death may occur in 2 weeks to 4 months. Chronic surra is characterized by intermittent fever, anemia, subcutaneous edema, and emaciation. 6. Pathologic findings The lesions are not very specific. The carcass is pale, emaciated, and icteric, with ascites and hydrothorax present. 7. Diagnosis Identification of the parasite can be attempted from Giemsa stained blood smears. Sampling from deep vessels will increase the chances of having a positive result. The most sensitive rapid method is parasite detection by examination of buffy coat area of a PCV tube after centrifugation. Serological tests are available, including complement fixation, indirect haemagglutination, indirect fluorescent antibody test, enzyme linked immunosorbent assay (ELISA) or card agglutination tests. Differential diagnosis includes other infections that cause anemia and weight loss, such as babesiosis, anaplasmosis, theileriosis, chronic parasitism, and malnutrition. 8. Treatment Quinapyramine sulfate (Quintrycide) is used for treatment in camels, and diminazene aceturate (Berenil) in horses and camels. 9. Prevention and control Control of surra can be difficult as there are many possible vectors and a wide range of hosts. Control methods include detection and treatment of infected animals, prophylactic treatment of susceptible animals, and their protection from biting flies when possible. There is no vaccine.
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CHAPTER
DISEASES OF POULTRY
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Infectious Diseases of Livestock in Afghanistan / Poultry
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1 AVIAN INFLUENZA, HIGHLY PATHOGENIC

This disease has been diagnosed in Afghanistan.
1. Definition Highly pathogenic avian influenza is a severe, contagious viral disease of poultry causing significant morbidity and mortality and serious economic loss. 2. Etiology Influenza viruses are all members of the Influenza A group of viruses within the Genus Influenza, Family Orthomyxoviridae. Influenza A strains are classified based on two surface molecules - hemagglutinin (H), of which there are 16 varieties, and neuraminidase (N), of which there are 9 varieties. All H and N types occur in birds. Most strains of avian influenza do not cause disease. Those that cause severe disease are referred to as highly pathogenic avian influenza (HPAI). Highly pathogenic avian influenza viruses are all of the H5 or H7 designation. Bird flu refers only to the H5N1 strain. There are many other strains of HPAI in addition to H5N1 but none of these are referred to as bird flu. 3. Transmission Transmission is by contact with secretions and excretions from infected birds. Aerosol transmission can occur over one meter distance. Fomite transmission occurs through transfer of contaminated cages or other equipment. 147
4. Species affected Many bird species can be infected with highly pathogenic avian influenza. Clinical disease is usually seen only in poultry. Some strains can infect humans. The H5N1 strain has infected hundreds of people with an approximately 50% mortality rate. HPAI H5N1 is a serious zoonosis! 5. Clinical signs The incubation period is 1-7 days. Morbidity is very high and usually almost all contact birds will become ill. Clinical disease, if noticed, is short and consists of severe depression and perhaps watery diarrhea or neurologic signs just before death. Period of clinical disease is short, sometimes only 24 hours. Mortality is close to 100%. 6. Pathologic findings There can be edema and hemorrhage in many organs. Typically there is subcutaneous edema in the neck and head, especially comb and wattles, which may even appear cyanotic. Hemorrhage along the shanks and in the trachea is also frequent. There are petechial hemorrhages over serosal surfaces. Lungs can be edematous and hemorrhagic. But none of these lesions is so highly characteristic that HPAI can be diagnosed without laboratory confirmation. 7. Diagnosis Highly pathogenic avian influenza cannot be reliably diagnosed on clinical and pathologic findings only. There are many quick tests that can be used to determine if influenza A is present, but laboratory confirmation, using ELISA or PCR should be pursued to determine the type. Differential diagnoses include: Newcastle disease, infectious laryngotracheitis, and Gumboro disease. 148
8. Treatment There is no treatment for HPAI in birds. 9. Prevention and Control Control of HPAI requires keeping infected birds away from those that are susceptible. High biosecurity is recommended to minimize contact or fomite transmission and propagation of the outbreak. A number of vaccines have been developed and can be used to protect birds in the face of an outbreak.
(photos, next page)
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HPAI Cyanosis of the comb
HPAI Edema of the neck
HPAI Edema and hemorrhage, lungs
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2 BROODER PNEUMONIA (ASPERGILLOSIS)

1. Definition Brooder pneumonia is a subacute to chronic fungal respiratory disease of chickens and other birds. Other names for the disease include: aspergillosis, Pneumomycosis, Mycotic pneumonia, pneumonomycosis, air-sac disease, pseudo-tuberculosis. 2. Etiology The causative agent is Aspergillus fumigatus, a fungus that is found in many environments and the number of spores produced increases with warm, moist conditions. 3. Transmission Birds become infected through inhaling spores of the fungus. The greater the environmental contamination with fungus, the larger the number of animals that will be affected with the disease. Moldy food or litter can contain abundant organisms. A serious problem happens when hatcheries are infected, as the spores can penetrate the egg shell and result in disease in large numbers of hatched chicks. 4. Species affected Chickens, turkeys, geese, ducks, pheasants, and canaries are all susceptible to infection with Aspergillus and development of disease. It is also a very common disease of pigeons and zoological birds. 151
Care should be taken when working over open carcasses of birds with aspergillosis as the spores from the fungal masses can aerosolize and infect humans through inhalation. Disease in humans can be severe, especially in the immunocompromised. Aspergillus spores from the lesion can infect humans and cause a fungal respiratory disease. 5. Clinical signs Incubation period is 2-6 weeks. Morbidity is usually low but can be high in cases of massive hatchery infection. Birds are inappetent and become emaciated. There is nasal discharge, dyspnea, and gasping. Birds become debilitated and susceptible to many other infections. In some cases the fungus invades the brain or eye and then there is encephalitis or blindness. Mortality is usually high. 6. Pathologic findings Grossly, there can be caseous or necrotic masses in multiple locations, especially the respiratory tract, where the fungus can grow in large accumulations and form visible masses. These can appear as plaques in the nasopharynx. In the air sac, they appear as fuzzy buttons, often with the appearance of stemless mushrooms, attached to the wall, and the surface consisting of a mycelia mat that can discharge spores. In the lungs, the lesions are more nodular and distributed throughout the parenchyma. 7. Diagnosis The appearance of the lesions is highly characteristic. Field or laboratory confirmation can be done by an impression smear. For this, a small piece of nodule or scraping is crushed in 10% potassium hydroxide or sodium hydroxide, put on a slide with a cover slip, and mycelia structures with fruiting bodies are evident. Additional confirmation can be done through 152
culturing of the fungus. Differential diagnoses for clinical disease includes: Newcastle disease, infectious bronchitis, chronic respiratory disease, pullorum disease. 8. Treatment There is no effective treatment for birds with aspergillosis. 9. Prevention and Control Affected chicks should be removed and destroyed. Fumigation of litter will kill the spores. Hatchery should not be located near feed mills or other installations which exhaust organic dust that could have spores. Overcrowding and moist litter should be avoided.
Aspergillus miliary nodules, lung
Aspergillus plaque on the palate of a starling
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3 CHLAMYDIOSIS, AVIAN
1. Definition Avian chlamydiosis, also known as ornithosis (and known as psittacosis in pet birds), is a contagious, subacute to chronic bacterial disease of poultry, especially turkeys, characterized by systemic illness and respiratory illness. 2. Etiology The causative agent is an obligate intracellular bacteria, Chlamydophila psittaci. 3. Transmission Transmission is most commonly by inhalation of infective aerosols or ingestion of contaminated material. Birds that are clinically ill shed large amounts of the bacteria in respiratory secretions and feces. Some birds do not appear clinically ill but may be long-term shedders. 4. Species affected Many bird species can be infected with Chlamydophila psittaci. It is well recognized in pet birds, but also causes significant problems in turkeys and pigeons. It is not much of a problem in chickens. Humans become infected through inhalation of infectious aerosols, which happens most frequently with farm workers and poultry inspectors at 154
processing plants. Humans that are infected often have pneumonia, headaches and muscle pain. Avian chlamydiosis can be transmitted to humans. 5. Clinical signs The disease is most severe in turkeys, where it may occur in outbreak form, with high morbidity. Incubation period is 5-10 days. Birds are depressed, off feed, and have conjunctivitis and respiratory distress. Feces become gelatinous and yellow-green. Egg production decreases markedly. Mortality ranges from 1-30% depending on the virulence of the strain. In pigeons, the disease tends to be endemic and may show up in only a few birds or may appear in more outbreak-like form if all the birds in a flock are nave. 6. Pathologic findings Conjunctiva are thickened and crusty and fibrinonecrotic exudates are present at the nares. Lungs are congested and there may be fibrinohemorrhagic pleural exudates. Pericardium, air sacs, and various mesenteric surfaces can all be covered with fibrin. 7. Diagnosis The clinical disease can resemble several other systemic illnesses of birds. The Chlamydophila organisms have a characteristic microscopic appearance and so stained smears or histologic sections can help to render a diagnosis. Isolation of the organism is also possible but difficult. Serology is helpful for determining flock status. Differential diagnoses include: pasteurellosis, mycoplasmosis, colibacillosis. 155
8. Treatment Chlortetracycline added to the feed will help to decrease the number of affected birds in a flock. 9. Prevention and Control Preventing contact with infected birds is difficult but could be practicable in an intensive rearing situation. Sanitation will help decrease pathogen burden in the environment. There are no vaccines for chlamydiosis.
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4 CHRONIC RESPIRATORY DISEASE

1. Definition Chronic respiratory disease (CRD), caused by a mycoplasma bacteria, is a problem of chickens and turkeys, characterized as an insidious illness, with major signs in the respiratory tract, and resulting in lowered production and major economic losses. 2. Etiology CRD is caused by Mycoplasma gallisepticum (MG), a bacteria. This same organism, in addition to causing CRD in turkeys, will also cause infectious sinusitis in turkeys, with filling of the infraorbital sinus with caseous and purulent exudate. In chickens with CRD, Mycoplasma gallisepticum may move further into the respiratory tract to cause, in concert with E. coli, airsacculitis. 3. Transmission Mycoplasma gallisepticum is transmitted from bird to bird by direct contact. Some birds may be carriers and introduce the organism into a flock. A major means of MG transmission is through eggs. Infected hens lay eggs that contain the organism and the chick is infected at hatching. 4. Species affected Both chickens and turkeys are susceptible to infection with MG.
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5. Clinical signs CRD can be triggered by Newcastle disease or infectious bronchitis. These maladies allow the MG to gain hold within the body and create longer term inflammation. Respiratory signs are often mild and referable to the upper respiratory tract, with nasal discharge, snicking, coughing and sneezing. Growth rate is poor. If the organism progresses into the air sac and teams up with E. coli to create airsacculitis, clinical disease can be more severe with dyspnea, depression, marked drop in feed consumption, and rapid weight loss. 6. Pathologic findings With CRD, the nasal sinuses are filled with catarrhal exudates. If CRD has progressed to airsacculitis, the air sacs can be filled with fibrinocatarrhal exudates. 7. Diagnosis Tentative diagnosis of CRD is based on flock history, clinical signs and pathologic lesions. Definitive diagnosis is usually via serology - testing for antibodies to MG in the chickens. As with many mycoplasmas, MG is very difficult to grow in the laboratory. 8. Treatment MG is sensitive to some antibiotics (tylosin, aureomycin, gallimycin, terramycin) and these can be given by injections or through the drinking water or feed. Treatment should be at a high enough level to kill all the organisms. If not, disease may be cleared, but the bacteria will persist to cause problems again. 9. Prevention and Control Preventing the disease requires attention to new introductions and purchasing hatching stock from known MG-free sources. Once diagnosed, treatment with high levels of antibiotics will help to eradicate 158
the disease from the flock. MG does not survive well in the environment and is very susceptible to most disinfectants.
Chronic respiratory disease - nasal sinuses contain abundant mucopurulent exudate.
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5 COCCIDIOSIS, AVIAN
1. Definition Avian coccidiosis is caused by a number of related protozoan parasites in the genus Eimeria that invade the intestinal epithelium and cause ulceration and hemorrhage of the intestinal tract. 2. Etiology There are seven species of Eimeria that cause disease in chickens - they may occur separately or together. The two that cause the most severe disease are Eimeria necatrix which affects the small intestine, and Eimeria tenella which targets the ceca. 3. Transmission The disease is contagious. Oocysts are passed in the feces of infected birds and after two days on the ground have sporulated and then are infectious when ingested by other birds. 4. Species affected The chicken is the only natural host. Younger birds tend to have more severe disease than older ones, and disease is often most severe in the 36 week age range. Birds develop immunity but there is no cross-species immunity, so infection with one Eimeria species does not confer protection against another. 160
5. Clinical signs Disease depends on the number of ingested oocysts and the pre-existing immunity in the flock. Ingestion of just a few oocysts will result in subclinical or mild disease and subsequent immunity. However, if many oocysts are present and there is no previous exposure in the flock, disease can be florid. Within 2 to 3 days of ingestion, there is bloody diarrhea and birds are markedly depressed and dehydrated. Morbidity is high. Mortality is variable. Birds surviving infection may be predisposed to other infections such as Salmonella or Clostridium. 6. Pathologic findings Gross changes are quite specific. Depending on the species of infecting Eimeria, certain segments of intestine are ulcerative and hemorrhagic. Mucosa may be markedly thickened, with necrotic cores in the lumen. Eimeria necratix affects the small intestine whereas Eimeria tenella damage is focused on the ceca. 7. Diagnosis Diagnosis is straightforward and often based on clinical signs and pathologic features. A smear of intestinal contents will reveal protozoan schizonts. 8. Treatment There are numerous anticoccidial drugs available, but many suffer from problems of resistance developing within the parasites. Because the anticoccidial drugs all work at different parts of the life cycle, alternating drugs is recommended to minimize development of resistance. 9. Prevention and Control Prevention of coccidiosis is difficult as the protozoa are found worldwide and in all types of poultry husbandry. The goal is to use anticoccidials and hygiene to minimize damage. 161
6 COLIBACILLOSIS, AVIAN
1. Definition Colibacillosis is a common bacterial disease of poultry, caused by E. coli, and characterized by systemic illness and poor production. 2. Etiology The causative agent is Escherichia coli. These bacteria are ubiquitous in the environment, and access to the body is predisposed by immunologic immaturity, immune suppression, respiratory disease, and poor hygiene. 3. Transmission The bird acquires the organism from the environment. Colibacillosis usually occurs after respiratory disease such as infectious bronchitis virus or Mycoplasma gallisepticum. Damage to the mucous membranes allows the E. coli access into the body. Also, subsequent to Gumboro disease, the chicken has enough immunosuppression that E. coli can gain entrance to the body. 4. Species affected All poultry species are susceptible to the development of colibacillosis. 5. Clinical signs Incubation period is 2-10 days. Morbidity is variable. There is a septicemia with seeding of serosal surfaces, as well as some solid organs - lungs, liver, and spleen. Signs of colibacillosis include coughing, 162
dyspnea, severe depression, inappetence, and poor growth rate. Mortality is 5-20%. 6. Pathologic findings At postmortem, there can be fibrinous inflammation on any serous surface. Consequently it is possible to see airsacculitis, pericarditis, peritonitis, perihepatitis, and synovitis. Any of these surfaces will be covered by a yellow-white thin membrane of fibrin. Additionally, the bacteria may have invaded into solid organs, especially liver and spleen, with swelling of these organs and formation of granulomas or develop-ment of caseous exudates. 7. Diagnosis Pathologic lesions are highly characteristic. Definitive diagnosis requires culturing the bacteria in the laboratory. Differential diagnoses include: chronic respiratory disease, fowl cholera, pullorum disease. 8. Treatment A variety of antibiotics, such as amoxicillin, tetracyclines, genamycin, ceftiofur, and fluoroquinolones, will kill the E. coli within the bird. However, E. coli is extensive in the environment and there are predisposing factors that allow E. coli to enter and cause disease. Attention to these predisposing factors will help the flock more than any antibiotic therapy. 9. Prevention and Control Commercial vaccines are available but are not in wide use. Because immunosuppressive and respiratory diseases (Gumboro disease, infectious bronchitis virus, Mycoplasma gallisepticum) can predispose to colibacillosis, control of these is important. 163
Good sanitation and adequate nutrition will prevent many cases of colibacillosis. Hygiene in the hatchery is especially important for preventing navel infections.
Colibacillosis - with fibrin covering the surface of the liver
Colibacillosis - fibrin and caseous exudates on the surface of the lungs, and fibrin covering the spleen
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7 FOWL CHOLERA
1. Definition Fowl cholera is a systemic bacterial disease affecting all poultry species, characterized by systemic illness, diarrhea, arthritis, and poor production. 2. Etiology The causative agent is Pasteurella multocida. This organism is abundantly present within feces of infected birds and in carcasses of animals that have died of the disease and it can persist in the environment for months. Feces from infected birds may contaminate water supplies. In addition, other animals such as dogs, cats, and rodents, may harbor Pasteurella multocida and spread it to new locations. Also, humans may take it to new locations by contaminated clothing or shoes. 3. Transmission The organism enters a susceptible bird through the oropharynx, i.e., the mouth or the respiratory tract. 4. Species affected Many species of birds can suffer from fowl cholera. Both wild and domestic birds are affected by the disease. 5. Clinical signs Incubation period is 2-10 days. Morbidity is often high. Disease is most common in adult birds. It may be peracute in which case the first sign of 165
the disease is death. In animals that survive longer, there is systemic illness, including inappetence, poor production, dyspnea, watery diarrhea, swollen joints. The comb and wattles may be swollen and cyanotic. Mortality is 5-30%. 6. Pathologic findings In animals that die in the very acute stage, there may be no lesions. Those that survive longer can have evidence of systemic inflammation. Spleen is large and reactive, with numerous white (lymphoid) nodules visible on cut surface. There may be petechial hemorrhages scattered over mucosal and serosal surfaces. Liver is pale throughout. The cranial portion of the intestine (duodenum and jejunum) is reddened with fibrinocatarrhal contents. Joints cavities can contain caseous exudates. Similar caseous material may be found in the sinuses of the head, including the inner ear. 7. Diagnosis The typical picture at the flock level - adult birds, systemic illness, pathologic lesions, can lead to a suspicion of fowl cholera. Confirmation of the diagnosis requires isolating the organism in the laboratory. Differential diagnoses include: fowl typhoid, highly pathogenic avian influenza, colibacillosis. 8. Treatment Pasteurella multocida is susceptible to a variety of antibiotics and these will cure the infection temporarily. Unfortunately treatment with antibiotics can promote a carrier state and leave additional birds at risk. Also, birds can break out with the disease again at the end of the antibiotic treatment period. So, although antibiotics will work, if other measures are available, such as vaccination, this is preferable to using antibiotics to control the disease. 166
9. Prevention and Control Bacterins are available but do not completely prevent infection. They should be used in combination with a strong program of sanitation that would include cleaning and disinfection after an outbreak, rodent control, provision of clean drinking water, and adequate disposal of dead birds.
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8 HYDROPERICARDIUM SYNDROME
1. Definition Hydropericardium syndrome is a recently emerged infectious disease of poultry characterized by fluid buildup around the heart, and often hepatic necrosis. It was first described in India and Pakistan and has since spread to other parts of the world. It has been popularly called litchi heart disease. 2. Etiology The causative agent is fowl adenovirus, serotype 4, a member of the Genus Adenovirus in the Family Adenoviridae. 3. Transmission The disease is contagious and the virus is transmitted horizontally by mechanical means and by contamination with infected feces. Humans may take the disease from one farm to another on contaminated clothing or equipment. 4. Species affected Broilers in the 3 to 6 week age range are especially susceptible. Layers and breeders can also be affected, but morbidity and mortality are lower. Other poultry can also be affected, notably pigeons. 5. Clinical signs Disease usually occurs suddenly. Incubation period is 5 to 17 days. Morbidity is high. Clinical signs are not specific. Birds are depressed 168
with ruffled feathers and may be partially recumbent with chest and beak resting on the ground. Mortality is up to 80% in broilers, but less than 10% in layers. 6. Pathologic findings More than 90% of birds dying of this disease have an accumulation of straw-colored, jelly-like fluid in the pericardium. It is this appearance of the heart floating in jelly-like fluid that gave the name leechy disease or litchi disease because of the similarity to lichee fruit. Livers are often swollen, discolored, and friable. Urates are seen in kidneys, characteristic of severe dehydration. There may be thymic and bursal atrophy. 7. Diagnosis Diagnosis on clinical signs is not possible. At necropsy, the presence of hydropericardium in multiple birds is highly suggestive. There are many serologic tests to confirm the diagnosis. Histopathology is also definitive, with prominent adenoviral intranuclear inclusions visible in multiple organs. Differential diagnoses are minimal; no other disease will cause this characteristic hydropericardium. 8. Treatment There is no effective treatment. 9. Prevention and Control Formalin-inactivated vaccines, made from infected liver homogenate or from cell cultures, have been shown to be effective, significantly reducing mortality. The vaccines will work in the face of a natural outbreak.
(photo, next page)
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Hydropericardium syndrome - Heart is suspended in straw-colored, jelly-like fluid and liver displays extensive mottling.
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9 INFECTIOUS BRONCHITIS
1. Definition Infectious Bronchitis (IB) is an acute contagious disease of birds, found worldwide, and causing primarily respiratory disease and lowered production. 2. Etiology A coronavirus, infectious bronchitis virus (IBV), is the causative agent. There are numerous strains, with varying virulence. Some strains specifically target the kidney, causing lesions there. 3. Transmission Transmission is mostly through contact and aerosol and droplet virus shed through respiratory secretions and feces. Contaminated feed and water, contact with animals or materials, importation of infected chicken or husbandry materials can be sources of infection. Transmission from farm to farm is by movement of contaminated workers, equipments and vehicles. Recovered birds may shed virus for weeks. There is no transmission through eggs. 4. Species affected Infectious Bronchitis is disease of chicken. All ages of chickens are susceptible to infection, but the severity of disease varies with age. 171
5. Clinical disease Incubation period is 36-48 hours. Morbidity approaches 100%. Affected chicks are depressed and tend to huddle near heat source; clinical signs include coughing, snicking, sneezing, rales, nasal discharge, and frothy exudates from the eyes. There is a 5-10% drop in egg production lasting for 10-14 days and eggs may have thin and irregular shells, and watery albumen. Mortality varies, but is often as high as 25%. Secondary infections with other organisms, such as M. gallisepticum, can worsen the clinical disease significantly, with more severe respiratory disease and a further drop in egg production. The kidney-targeting strains may cause higher mortality. 6. Pathologic findings Lesions seen in the respiratory tract include edema, hemorrhages, and perhaps some fibrin in nasal cavity, trachea, and bronchi. Sometimes air sacs are involved as well. Kidney damage may be significant after infection with nephrogenic strains, and they appear pale and swollen, with urate deposits in the kidney and ureters, which may even be occluded. Laying bird smay have yolk material in the body cavity and developing eggs in the ovary may be flaccid. Cystic oviduct may be seen in young birds. 7. Diagnosis Typical clinical signs are highly suggestive of IB. Laboratory diagnosis includes serology or virus isolation. Differential diagnoses include Newcastle disease, Infectious Laryngeotrachitis, and Infectious Coryza. 8. Treatment There is no known treatment for IB. 9. Prevention and Control Prevention of IB is best achieved through an effective biosecurity program. As a second line of defense, chickens in endemic areas should 172
be vaccinated with modified live vaccines to provide protection. There is a significant amount of cross protection to heterologous challenge, but choosing vaccines based on the knowledge of the strains present in the region is the most cost effective and efficacious.
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10 INFECTIOUS BURSAL DISEASE

1. Definition Infectious bursal disease (IBD), also known as Gumboro disease, is an acute viral disease of growing chickens causing extensive destruction of the Bursa of Fabricius, diarrhea, and subsequent immunosuppression. 2. Etiology The causative agent, IBD virus, is a member of the Birnavirus Family. It is highly resistant in the environment. There are several strains and they vary in virulence. 3. Transmission Environmental contamination is the major means of transmission. Virus is shed into the environment from actively infected birds and persists in the litter, on equipment, and fomites. Spread between flocks happens through fomites. 4. Species affected Only chickens are naturally infected. Egg laying breeds tend to be more susceptible. Susceptibility is greatest at the time of maximal development of the Bursa of Fabricius, 3-15 weeks of age. 5. Clinical signs The incubation period is 3-4 days. Morbidity is 10-80%. There is depresssion and anorexia, with watery diarrhea that may be whitish and mucoid. Bursa is palpably enlarged initially, but as disease progresses, 174
it becomes small. Animals are incoordinated and may be recumbent. Deaths begin to occur at about the third day of clinical illness. Mortality is usually around 10% but may be as high as 30%. One of the major clinical problems with IBD is that they remain immunosuppressed and so are less able to resist infection with other viruses, and also are less able to respond effectively to vaccination. 6. Pathologic findings The Bursa of Fabricius is the primary site of viral replication, and most characteristic changes are seen here. In acute cases, it is markedly edematous and swollen, to 2-3 times normal size. As the disease progressses, it may be hemorrhagic or atrophic, with a gelatinous, yellow exudates on the surface. Carcass is dehydrated, with dark appearing musculature. Spleen is usually enlarged. Liver may be swollen and friable. Urates are present in the kidney, as a result of the dehydration. 7. Diagnosis History, clinical signs, and postmortem lesions are often enough to make a diagnosis of IBD. Laboratory testing involves isolation of the virus, or agar gel immunodiffusion test for serology. Differential diagnoses include: infectious bronchitis, Mareks disease, Newcastle disease, highly pathogenic avian influenza. 8. Treatment There is no effective treatment for IBD. A change to low energy, low protein diet is recommended until the disease outbreak subsides. 9. Prevention and Control Both modified live and inactivated vaccines exist for IBD and have good efficacy. Critical period for exposure is during the time when maternal immunity wanes and so vaccination should be targeted then. Strict biosecurity will prevent entry of viruses. Disinfection after an outbreak is essential. 175
11 INFECTIOUS LARYNGOTRACHEITIS
1. Definition Infectious laryngotracheitis (ILT) is a viral disease of poultry causing acute and severe respiratory disease, usually in outbreak form. 2. Etiology The causative agent of ILT is a herpesvirus, ILT virus (ILTV). The virus has poor survival in the environment and is sensitive to most common disinfectants. However, it can survive for months if protected by organic material such as manure. 3. Transmission Birds contract the virus through droplet infection, with entrance through respiratory tract or conjunctiva. Transmission is most frequent through actively infected birds, but some birds act as carriers and can move the virus from flock to flock. Fomite transmission is also possible, with footwear or equipment contaminated with organic material taking the virus to new locations. As with many herpes viruses, ILT can be latent in re-covered birds, and then these birds may begin to shed the virus when stressed. There is no vertical transmission.
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4. Species affected ILT is a disease of chickens. However, some related birds, such as pheasants, peafowl, and turkeys, might contract the disease also. Wild birds may act as mechanical vectors of the virus. 5. Clinical signs Incubation period is 6-12 days. Morbidity is often 100%. The first sign is that birds have some degree of dyspnea, and coughing or gasping begins. There is discharge from the eyes and nostrils. Dyspnea becomes severe as the trachea fills with exudates and birds can expectorate quantities of blood and mucus that spatters on the wall. Sinuses may be distended and conjunctiva swollen. The course of the disease can be as long as six weeks. Egg production decreases markedly but there are no eggshell abnormalities. Mortality varies between 10-70%. 6. Pathologic findings The trachea can be filled with caseous or bloody casts. The mucosa has multifocal ulceration, with fibrinonecrotic debris covering. Sinuses may be filled with fibrinous or necrotic exudates. Conjunctivae are edematous and can have fibrinonecrotic exudates. 7. Diagnosis ILT is the only disease that will cause such severe ulcerative and hemorrhagic lesions in the trachea. Milder cases could be confused with Newcastle disease or infectious bronchitis virus. Confirmation of the diagnosis of ILT requires histopathology or culturing of the agent in the laboratory. 8. Treatment There is no effective treatment for ILT. 177
9. Prevention and Control The best prevention for ILT is biosecurity. Vaccines are available and can be used in the face of an outbreak, but have some drawbacks. The vaccines for ILT are all modified live virus, and can introduce a circulating strain into the flock, with danger of reversion to virulence. Also, the ILT vaccines protect against disease, but not against infection, so vaccinated birds could still replicate virulent ILT, and spread it to susceptible birds.
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12 MAREKS DISEASE
1. Definition Mareks disease (MD) is a virally-induced chronic lymphoproliferative disease of chickens, and occasionally turkeys, characterized by paralysis, formation of lymphoid tumors in multiple locations, and general loss of condition. 2. Etiology The causative agent of Mareks disease is a herpes virus, gallid herpesvirus-2. 3. Transmission Virus enters susceptible birds through the respiratory tract. Virus is very hardy in the environment and is shed in epithelial cells of the feather follicle, dander, feces and saliva, from infected birds. There is no egg transmission. 4. Species affected MD is a disease of chickens. 5. Clinical signs Incubation period is long, weeks to months. Morbidity is 10-50% in a flock. Disease is only seen in birds older than 6 weeks of age. Onset of clinical symptoms may begin at 6 weeks of age, but more commonly is seen 12-24 weeks of age. All signs are related to the neoplastic 179
proliferation, which occurs most commonly around nerves, but also in some visceral organs. Most common sign is progressive unilateral paralysis of legs or wings, and then the bird becomes recumbent. There may be torticollis as nerves supplying the head and neck are affected. Crop dilation and inability to swallow easily happens when the vagus nerve is involved. Infiltration of the iris with neoplastic cells can cause blindness. Proliferation of neoplastic cells around cutaneous nerves results in multifocal nodules in the skin. Due to the compromising nature of the peripheral nerve involvement, there are many nonspecific signs such as weight loss, anorexia, and diarrhea. Mortality is close to 100% 6. Pathologic findings Lesions consist of gray-white thickening around nerves. Rather than the normal striated glistening white appearance of the nerves, they are thickened, amorphous, and grayish. Nerves commonly affected include sciatic, brachial, and intercostals. In the visceral form of the disease, gray-white infiltrations or enlargements might be seen in ovaries, liver, spleen, kidney or heart. 7. Diagnosis MD lesions are characteristic but cannot be reliably differentiated from those of lymphoid leukosis. Confirmation of MD requires laboratory testing - virus isolation or agar gel immunodiffusion. 8. Treatment There is no treatment for MD. 9. Prevention and Control Several commercial vaccines are available for MD and provide good protection against the disease. Increasing hygiene standards will decrease the environmental infectious load. 180
13
NEWCASTLE DISEASE
1. Definition Newcastle disease (ND) is a highly contagious systemic viral disease of poultry causing significant morbidity and mortality and often occurring in outbreak form. 2. Etiology The causative agent is Newcastle disease virus (NDV), also known as avian paramyxovirus-1 (APMV-1), and is a member of the Genus Avulavirus in the Family Paramyxoviridae. Newcastle disease viruses are divided into two classification schemes, both are reflective of virulence. In the older classification, viruses were velogenic, mesogenic, and lentogenic, with the velogenic viruses being of most concern. In the newer system, NDVs are classified according to an intracerebral pathogenicity index (ICPI) and higher scores using this system are indications of virulence (>0.7 is considered virulent). 3. Transmission Secretions and excretions from sick birds contain abundant virus. Disease is transmitted through contact and fomites. Insufficient cleaning of cages is a common means of transmission. 4. Species affected More than 250 species of birds can be infected with NDV. The disease is recorded most commonly in domestic birds. NDV can infect humans 181
and will cause a self-limiting conjunctivitis, most commonly seen in poultry workers. NDV can cause a mild zoonotic illness! 5. Clinical signs The incubation period is 2-15 days. Morbidity is usually very high. With mild strains there may be a slight drop in production or mild respiratory disease. With the velogenic isolates, disease takes one of two forms viscerotropic or neurotropic. In the neurotropic form, birds become progressively depressed and disoriented, with torticollis and opisthotonus preceding paralysis and inability to right themselves. In the viscerotropic form, which is more rapid than the neurotropic form, birds are very depressed, may have conjunctivitis, and develop diarrhea. Mortality with the velogenic strains is close to 100%. 6. Pathologic findings Gross lesions are only seen with the viscerotropic velogenic strains. The most characteristic feature is an enlarged, friable and mottled spleen (necrosis), and hemorrhage in the cecal tonsils and other lymphoid patches in the intestines. Other possible lesions include pancreatic necrosis and pulmonary edema. With the neurotropic strains, even though neurologic signs may be dramatic, all tissues, including brain, may be grossly normal. 7. Diagnosis Velogenic Newcastle disease cannot be reliably distinguished from highly pathogenic avian influenza on clinical and gross findings along. Laboratory testing is required to confirm diagnosis, and involves hemagglutination and/or PCR. Differential diagnosis for velogenic Newcastle disease includes: avian influenza, fowl cholera, Gumboro 182
disease, lack of ventilation (heat stroke), or lack of water (severe dehydration). 8. Treatment There is no effective treatment for birds infected with NDV. 9. Prevention and Control The most reliable means is to prevent introduction of the disease into a flock. Vaccines are commercially available but protect against the milder strains primarily and will not completely protect against challenge with the velogenic isolates.
NDV - enlarged, mottled spleen
NDV - Hemorrhage seen through the wall of the intestine, cecal tonsils
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14 PULLORUM DISEASE
1. Definition Pullorum disease is a contagious, often fatal diarrheal bacterial disease of young poultry, characterized by moribund and dead birds at hatching time. It usually occurs in an acute systemic form in chicks and poults, but in adults can be more chronic. 2. Etiology The causative organism is Salmonella pullorum, a non-motile bacteria highly adapted to chickens and turkeys. 3. Transmission The route of infection is oral or via the navel/yolk. Transmission may be transovarial or horizontal mainly in young birds and may sometimes be associated with cannibalism. The organism can penetrate to eggshell and infect the embryo. Mechanical transmission via fomites (carried around on clothes, shoes or equipment) is also possible. Survivors become infected breeders (cycle begins again). 4. Species affected The organism is fairly well adapted to chickens and turkeys. People consuming raw eggs can get a mild three-day diarrhea.
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Salmonella pullorum can cause a mild diarrheal disease in humans. 5. Clinical signs Morbidity is 10-80%; mortality is increased in stressed or immunocompromised flocks and may be up to 100%. Chicks from infected eggs are weak and often die within several days. Affected birds tend to huddle under brooders and are depressed. They frequently give out a shrill cry when voiding droppings, which are white and pasty. Growth is retarded and feathers are poor. Gasping may also be observed as the lungs are often infected. Adult birds usually don't show clinical signs, however, there may be a reduction in egg production and fertility. 6. Pathologic findings Gross lesions may be seen in chronic disease, but are usually absent in peracute disease. When lesions occur, they consist of enlarged and congested liver, spleen and kidneys. Yolk sac can be retained with creamy or caseous yolks material. White caseous nodules may be present in the lung, heart, and intestinal tract, especially ceca. Joints are often swollen with yellow viscous fluid. 7. Diagnosis Tissue and fecal samples can be submitted for bacterial identification through culture or genetic techniques. Serologic testing alone is not considered adequate for a positive diagnosis. Differential diagnoses include fowl typhoid, fowl cholera, erysipelas, and others. 8. Treatment Pullorum disease can be slowed by antibiotics, but no drug is capable of eliminating pullorum from a flock. 185
9. Prevention and Control If introduced, control should focus on eradication of the disease through isolation and destruction of contaminated flocks, proper disposal of carcasses and disinfection of fomites. As with other salmonella, recovered birds are resistant to the effects of infection but may remain carriers. Vaccines are not normally used as they interfere with serological testing and elimination of carriers. S. pullorum may survive for years in a favorable environment, but is less resistant to heat, cold, and most disinfectants.
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15 TUBERCULOSIS, AVIAN
1. Definition Avian tuberculosis is a chronic debilitating infectious bacterial disease characterized by the formation of multiple caseating granulomas in internal organs. 2. Etiology The causative agent is Mycobacterium avium, an acid fast bacillus. 3. Transmission The organism is shed in abundance in fecal material and respiratory secretions from infected birds. It has long survivability in the environment, as long as 4 years in soil. Susceptible birds acquire the infection from contaminated environmental sources. 4. Species affected All species of birds can be infected with M. avium. Disease is reported in many species of poultry, and also in numerous wild birds. M. avium can also infect and cause disease in mammals, including humans, especially those who are immunocompromised. Mycobacterium avium can cause debilitating disease in immunocompromised humans.
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5. Clinical signs Incubation period is prolonged, and can be on the order of weeks to months. Usually only adult birds are affected. Morbidity is usually low and only one or a few animals in a flock might be affected. Clinical signs are not specific. Birds are unthrifty, dull, and have ruffled feathers. The disease can progress to atrophy of musculature and emaciation. Mortality is high. 6. Pathologic findings Lesions of avian tuberculosis are very characteristic. There are pinpoint to extensive gray-yellow masses in multiple visceral organs. These masses (granulomas) have a caseous and yellow center, and may be surrounded by fibrous tissue. The granulomas are most frequently found in liver, spleen and intestine, but bone marrow is often affected as well. 7. Diagnosis Diagnosis on clinical signs is not possible. On necropsy, the presence of multiple granulomatous masses is highly suggestive. Histopathology of the masses to reveal granulomas and multinucleate giant cells is diagostic. It is also possible to culture Mycobacterium avium, but this requires specialized media and prolonged incubation. Differential diagoses include colibacillosis and pullorum disease. 8. Treatment There is no effective treatment for avian tuberculosis. 9. Prevention and Control The best prevention is to maintain tuberculosis-free flocks. Tuberculintesting of birds prior to introduction is one safeguard. Ensuring no contact with wild birds is also helpful. Thorough cleaning of premises after diagnosis will help prevent recurrence. 188
CHAPTER
DISEASES OF SHEEP AND GOATS
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Infectious Diseases of Livestock in Afghanistan / Sheep and Goats
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1 BLUETONGUE
1. Definition Bluetongue (BTV) is an acute, insect-transmitted viral disease affecting primarily sheep, and characterized by lameness, oral erosions, and stiffness. 2. Etiology Bluetongue virus (BTV) is a member of the Orbivirus genus in the Family Reoviridae. There are 24 serotypes of BTV identified. 3. Transmission BTV is transmitted through the bite of an infected Culicoides fly. These flies are biological vectors. Virus can also be transmitted vertically from viremic dams to the developing fetus or from male to female through semen during the period of peak viremia. Cattle can be viremic for several weeks, and so they act as temporary reservoirs of the virus. 4. Species affected BTV infects many ruminant species but disease is usually manifest only in sheep. Cattle, goats, and camels can be infected, as well as many wild species of ruminants. 5. Clinical Disease Incubation period is 7-10 days. Morbidity is variable, but often high. Sheep become febrile, and soon after that there is excessive drooling 191
along with the development of oral erosions. Buccal and nasal mucosa, as well as tongue, may become swollen and hyperemic, and rarely cyanotic (but this rarely seen feature is the source of the name of the disease). Hyperemia of coronary bands occurs along with the onset of lameness. In severe cases sloughing of hooves is possible. In addition, animals will be weak, depressed, and unwilling to walk. Mortality with BTV infection is usually less than 10%. Recovered animals may have a dark line in the wall of the hooves, or may have a wool break. Virus can cross the placenta, causing abortion, stillbirth, or congenital abnormalities. 6. Pathological findings Pathological findings depend on the strain of the virus and host susceptibility. In the worst cases, the swelling of the oral mucous membranes creates facial edema. Erosions in the oral and nasal cavities may progress to ulcers and be covered with necrotic debris. Crusty exudates may be present at the nares. Hyperemia and occasional erosions are present in the reticulum and rumen. In some cases there is a terminal pulmonary edema and these animals will have abundant froth in the trachea. A significant lesion that is thought to occur only in BTV infection is hemorrhage within the pulmonary artery at the base, near the heart. Striated muscle, especially of the limbs, may have areas of pallor indicating acute necrosis. 7. Diagnosis Diagnosis is based on typical clinical signs and known presence of Culicoides in the area. Differential diagnoses include: white muscle disease, foot rot, and foot-and-mouth disease. 8. Treatment Supportive care may help an animal to survive infection with BTV. Supplying soft food, cleaning the nares and oral cavity of debris, and ensuring easy access to drinking water will all help. 192
9. Prevention and control Vaccination has been the primary means of controlling BT disease in sheep with live attenuated vaccines. Vaccine serotypes should be matched to those circulating in the area to prevent introduction of a novel serotype. Many viruses can cross the placenta to infect the fetus at a critical period of development resulting in abortion or malformation, especially of the nervous system. Control of the Culicoides vector will help to decrease spread, but is challenging.
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2 CAPRINE ARTHRITIS ENCEPHALITIS

1. Definition Caprine arthritis encephalitis (CAE) is a viral disease causing polyarthritis in adult goats and less commonly as progressive paresis in kids. Subclinical or clinical interstitial pneumonia, mastitis (hard udder), and chronic wasting have also been attributed to infection with this virus. 2. Etiology The CAE virus is an enveloped, single-stranded RNA lentivirus in the family Retroviridae. 3. Transmission The chief mode of spread of CAE is through ingestion of virus-infected goat colostrum or milk by kids. Horizontal transmission also contributes to disease spread within herds and may occur through direct contact, exposure to fomites at feed bunks and waterers, ingestion of contaminated milk in milking parlors, or serial use of needles or equipment contaminated with blood. 4. Species affected CAE virus infection is widespread among dairy goats in most industrialized countries but rare among indigenous goat breeds of developing countries unless they have been in contact with imported goats. 194
5. Clinical signs Most goats are infected at an early age, remain virus positive for life, and develop disease months to years later. Clinical signs in adult goats include joint capsule distention, especially carpal joints, and varying degrees of lameness. Affected goats lose condition and usually have poor hair coats. Encephalomyelitis is generally seen in kids 2-4 months old but has been described in older kids and adult goats. Affected kids initially exhibit lameness, ataxia, and hind limb placing deficits. Hypertonia and hyperreflexia are also common. Over time, signs progress to paraparesis or tetraparesis and paralysis. Depression, head tilt, circling, opisthotonos, torticollis, and paddling have also been described. The interstitial pneumonia component of CAE virus infection rarely produces clinical signs in kids. However, in adult goats with serologic evidence of CAE virus infection, chronic interstitial pneumonia that leads to progressive dyspnea has been documented. The hard udder syndrome attributed to CAE virus infection is characterized by a firm, swollen mammary gland and agalactia at the time of parturition. 6. Pathologic findings Lesions in joints are characterized by thickening of the joint capsule and marked proliferation of synovial villi. In chronic cases, soft-tissue calcification involving joint capsules, tendon sheaths, and bursae is common. Severe cartilaginous destruction, rupture of ligaments and tendons, and periarticular osteophyte formation has also been described in advanced cases. Lungs of affected goats are firm and gray-pink with multiple, small, white foci, and do not collapse. 7. Diagnosis A presumptive diagnosis of CAE can be based on clinical signs and history. Traumatic arthritis, and infectious arthritis caused by 195
Mycoplasma spp, are differential diagnoses for arthritis induced by CAE virus. Differential diagnoses for the progressive paresis and paralysis exhibited by young kids should include enzootic ataxia, spinal cord abscess, cerebrospinal nematodiasis, spinal cord trauma, and congenital anomalies of the spinal cord and vertebral column. If neurologic examination indicates brain involvement, polioencephalomalacia, listeriosis, and rabies should be considered as possible causes. The pulmonary form of caseous lymphadenitis may have a similar clinical presentation to the pulmonary form of CAE in adult goats. Serologic tests available for diagnosis are the agar gel immunodiffusion (AGID) and ELISA. A positive test result in an adult goat implies infection but does not confirm that the clinical signs are caused by CAE virus. 8. Treatment There are no specific treatments for any of the clinical syndromes associated with CAE virus infection. 9. Prevention and control In commercial dairy herds, the following is recommended for control of CAE: permanent isolation of kids beginning at birth; feeding of heattreated colostrum (56C for 60 min) and pasteurized milk; frequent serologic testing of the herd (semiannually), with identification and segregation of seronegative and seropositive goats; and eventual culling of seropositive goats. (photos, next page)
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Lame goat with carpal joints swelling Arthritis with thickening of the joint capsule
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3 CONTAGIOUS AGALACTIA
1. Definition Contagious agalactia (CA) is a mycoplasmal disease affecting sheep and goats, characterized by mastitis and agalactia in milking animals and polyarthritis, keratoconjunctivitis, and respiratory disease in nonlactating animals. 2. Etiology Typically, CA is caused by Mycoplasma agalactiae (Ma) but some other mycoplasmas may cause very similar syndromes. 3. Transmission The organism is present in milk, urine, feces, and oculonasal discharges and transmission occurs by ingestion. It can also be transmitted through the teat canal, as uninfected animals are milked subsequent to infected animals. 4. Species affected Both goats and sheep are susceptible. Goats may suffer a more severe form of the disease. 5. Clinical disease Incubation period is long, 1 to 8 weeks. Morbidity can be high, especially just after the time of parturition. Early disease is characterized 198
by fever, malaise, and inappetence. In lactating animals, as mastitis develops, milk can turn greenish-yellow or grayish-blue. In young and nonlactating animals, septicemia leads to polyarthritis, with swollen joints, ocular discharge and corneal opacity, and respiratory compromise due to the developing pneumonia. Animals may be reluctant to stand or walk. Tarsal and carpal joints are preferentially affected. Mortality is less than 20%, but damage to mammary gland or joints can be so severe that animals are rendered useless for production. 6. Pathologic Findings The mastitis is characterized by interstitial inflammation followed by chronic progressive fibrosis and atrophy. Polyarthritis affects carpal joints most severely, with hyperemic synovial membranes and turbid joint fluid that can be hemorrhagic. Conjunctivitis is mucopurulent and there is associated corneal inflammation sometimes with ulceration. 7. Diagnosis The simultaneous occurrence of mastitis, polyarthritis, and conjunctivitis within a herd or flock leads to a strong suspicion of CA. Laboratory testing involves growth of the organism. Differential diagnoses include: caprine arthritis-encephalitis, and mastitis of any etiology. 8. Treatment Treatment with antibiotics (tetracycline, florfenicol, fluoroquinolones) in the early stages of the disease is effective. 9. Prevention and control Good biosecurity, especially regarding milking practices, will help to prevent spread. Some animals that recover from the mastitis may still carry the organism and can be sources of bacterial shedding, and so need to be identified and removed from the herd or flock. Vaccines are available but efficacy is low. 199
4 CONTAGIOUS CAPRINE PLEUROPNEUMONIA

1. Definition Contagious caprine pleuropneumonia (CCPP) is a contagious mycoplasmal disease of goats characterized by severe respiratory lesions and high morbidity and mortality. 2. Etiology The causative agent of CCPP is Mycoplasma capricolum subsp. capripneumoniae (Mccp), originally known as the F38 biotype. There are other related mycoplasmal organisms, such as Mycoplasma mycoides capri and Mycoplasma mycoides mycoides Large Colony (LC) type, and these can also cause pleuropneumonia but the pulmonary lesions are usually part of a spectrum of systemic illness and they are not strictly specific for lung. 3. Transmission Transmission of CCPP is through droplet infection, respiratory secretions from a coughing animal must land in the respiratory tract of a susceptible host. Gathering or housing animals together facilitates spread of the disease. 4. Species affected Only goats are susceptible to infection with Mccp. The other two may also affect goats and sheep. 200
5. Clinical disease Morbidity can be 100% and mortality 60-100%. Incubation period is 1-4 weeks. Weakness, anorexia, cough, hyperpnoea, and nasal discharge accompanied by fever (41C) are often found. Exercise intolerance is common. 6. Pathologic findings Typically, the thorax contains an excess of straw-colored fluid, and there is acute fibrinous pneumonia, with extensive consolidation, and overlying fibrinous pleuritis. All lobes of the lung can be involved. Chronic cases may have severe pleural adhesions and multiple abscesses of variable size. 7. Diagnosis When an entire group of goats develops high fever, respiratory distress, and the postmortem lesions are typical, a tentative diagnosis of CCPP can be made. Laboratory confirmation entails isolation of the causative organism, which is challenging. 8. Treatment Whenever possible, treatment should be based on bacterial culture and sensitivity, especially in herd outbreaks, when valuable animals are involved, or in acute or chronic cases when initial therapeutic attempts have failed. Commonly recommended antibiotics are oxytetracycline (15mg/kg) and tylosin (10-20 mg/kg). Therapy should continue for at least 24-48 hr after body temperature has returned to normal. Duration of treatment usually is 4-5 days. 9. Prevention and control Inadequate ventilation, crowding, commingling of animals from various farms (feedlot or market situations), poor nutrition, failure of passive transfer of antibodies, transportation and other stresses have all been associated with pneumonia outbreaks, consequently control and 201
prevention lies with correction of the predisposing factors whenever practical. In Afghanistan many animals, both sheep and goats, are given an M. capri vaccine, and this is useful in preventing outbreaks of mycoplasmal pneumonia. Vaccine should be given before the start of the cold and rainy season.
CCPP - Severe consolidation and extensive fibrin deposition on the overlying pleura.
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5 CONTAGIOUS ECTHYMA
1. Definition Contagious ecthyma (Orf, Sore Mouth) is an infectious dermatitis of sheep and goats causing sores primarily on the lips of young animals. The disease is usually more severe in goats than sheep 2. Etiology The causative agent, contagious ecthyma virus, is in the Genus Parapoxvirus in the Family Poxviridae. 3. Transmission Infection occurs by contact with carriers, infected animals, or fomites. The virus is highly resistant to desiccation and survives in the crust for years. The virus has reportedly been recovered from dried crust after 12 years. Animals feeding on acidic garbage or on very rough materials are especially susceptible to inoculation because of mucosal erosions. 4. Species affected Sheep and goats are the primary affected species. This disease is found worldwide and may occur in young lambs and kids in early spring and occasionally in mature animals that do not acquire immunity from natural exposure. Humans are occasionally affected with blisters on their hand after handling lesions of affected animals. 203
Contagious ecthyma can infect humans! 5. Clinical signs The primary lesion develops on the skin of lips and frequently in the corner of the mouth and on the ears. Lesions are occasionally found in between the digits of the feet, and around the coronary band. Sheep and goats nursing young lambs or kids may develop lesions on the teats. The lesions develop as papules and progress to vesicular and pustular stage before forming proliferative crusts and scabs. After about 1 to 4 weeks, the scabs drop off and tissues heal without scarring. During active stages of infection, more severely infected animals fail to eat and lose weight, especially if secondary infections have taken place. Extensive lesions on the feet may lead to lameness. Animals with lesions on the teat may develop mastitis. 6. Pathologic findings Animals do not usually die from sore mouth, except for very young animals that are too sore to suckle. The skin lesions are as described under clinical signs. 7. Diagnosis The lesions of sore mouth are characteristic in their distribution and age susceptibility. Definitive diagnosis can be done in the laboratory through histopathology, electron microscopy, or viral isolation. 8. Treatment The disease is usually self-limiting and affected animals do not need any treatment. Severely affected lambs and kids should receive supportive therapy if they are not able to nurse or eat. Antibacterials such as 204
penicillin and oxytetracycline may be indicated in severe case to combat secondary bacterial infection. 9. Prevention and control Animals that have recovered from natural infection develop immunity and are highly resistant to re-infection. There is a live vaccine available in some countries that produces fair immunity. However, vaccines should be used cautiously to avoid contaminating uninfected premises. Vaccinated animals should be segregated until the scabs have fallen off. Vaccination for sore mouth is not indicated unless the disease exists in a herd. Vaccination is not practiced in Afghanistan. Persons handling affected animals with active lesion around the mouth should use reasonable protective precautions such as wearing gloves.
Sore Mouth papule on the finger of a person
Sore Mouth scabs on the lip
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6 EXTERNAL PARASITES OF SHEEP AND GOATS

1. Definition External parasites, for the most part, are a nuisance and can cause reduce weight gain and weight loss simply because the animal spends more time and energy combating them than feeding. Physical injury occurs when irritation and scratching result in open wounds that then can become infected or subject to infestation with fly larvae. 2. Etiology There are a number of fly species which are primarily a nuisance. Blood loss due to large numbers of feeding mosquitoes may lead to anemia, unthriftiness, and weight loss/reduced gains. Lice and mites (mange) are relatively permanent residents on the animal. Infestation (commonly called mange when mites are involved) may be seen as intense irritation with the animal scratching and chewing creating skin lesions that can become ugly. Ticks thrive on blood obtained from the host. They are subdivided into hard and soft ticks according to structural characteristics. The sheep nose botfly, Oestrus ovis, is a parasite that in its larval stages inhabits the nasal passages and sinuses of sheep and goats. 206
3. Transmission Lice and mites thrive and reproduce during the cooler months of the year. Transmission from animal to animal is by contact, so crowding should be avoided. The female nose botfly deposits larvae in and about the nostrils. These small, clear-white larvae migrate into the nasal cavity. As the larvae (bots) mature, they become cream-colored, and then darken. When mature, the larvae leave the nasal passages, drop to the ground, burrow down a few inches, and pupate. 4. Species affected Both sheep and goats can be affected. 5. Clinical signs Affected animals may be distracted by external parasites and rub or scratch. Some external parasites produce crusting, hair loss, dullness, lethargy, weakness, and signs of anemia. In nosebot infestation cases, a profuse discharge occurs, at first clear and mucoid, but later mucopurulent and frequently tinged with fine streaks of blood. Continuing activity of the larvae, particularly if they are numerous, causes a thickening of the nasal mucosa that, together with the mucopurulent discharge, impairs respiration. Larvae present in the sinuses are sometimes unable to escape; they die and may gradually become calcified or lead to a septic sinusitis. The purulent inflammation produced in the sinuses occasionally may spread to the brain with fatal results. 6. Pathologic findings There are no specific gross findings except lesions associated with anemia.
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7. Diagnosis In general, most external parasites can be collected with various equipments for diagnosis such as nets, jars, traps, combs and forceps. For mites, skin scrapings are used. Most external parasites can be seen readily and identified using published descriptions and keys. However, the use of a microscope is usually necessary. 8. Treatment Insecticides for ectoparasites will control flies, lice, mites and ticks. Dipping or high pressure sprays provide the best results. Sheep and goats may have to be treated every 3 weeks in endemic areas. Insecticide impregnated ear tags and pour-ons are also available in some areas. Ivermectin is highly effective against all stages of the nose botfly larvae for treatment. 9. Prevention and control There are many insecticides that can be used for control when necessary. Routine disposal of manure and organic materials will help control nuisance flies and mosquitoes.
Hair loss in sheep due to external parasites
Sheep with nosebot infestation
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7 INTERNAL PARASITES OF SHEEP AND GOATS

1. Definition Parasitism and gastrointestinal nematode parasitism in particular, is arguably the most serious constraint affecting sheep and goat production in Afghanistan. Economic losses are caused by decreased production, cost of prevention, cost of treatment, and the death of infected animals. 2. Etiology Although there are a number of worms found in sheep and goats, the predominant and usually the most pathogenic ones are gastrointestinal nematodes (worms). Amongst them, Haemonchus contortus (Barberpole Worm, Wire Worm) is a voracious blood feeding worm. These worms thrive under hot and moist environmental conditions. Telodorsagia (Ostertagia) circumcincta (Brown Stomach Worm) feed mostly on nutrients in mucous and do not feed on blood. This worm thrives in cooler wet environmental condition. Trichostrongylus colubriformis (Bankrupt worm) seems to thrive better under more cool and wet conditions feeding on nutrients in mucous and interferes with digestive function resulting in diarrhea. It is called the bankrupt worm because death is seldom the end result and animals just become poor doers leading to loss of production and income. Oesophagostomum spp. (Nodular worm) resides in the large intestine 209
feeding on blood and can contribute to the overall anemia being caused by H. contortus. Trichuris spp. (Whipworm) are usually found in small numbers and are also blood feeders contributing to the overall blood loss due to other worms. Moniezia (Tapeworm, white rice grain-like "worms") absorb nutrients from digested feed and cause very little damage. However, growth in kids (not adults) may be somewhat reduced and intestinal blockage may rarely occur. Fasciola hepatica (Liver fluke) can be a major problem in low lying perennial wet areas in Afghanistan. Liver flukes reside in and damage the liver resulting in unthriftiness, weight loss/reduced gains, and sometimes death. Dictyocaulus filaria, Muellerius, Protostrongylus (Lungworms) infection result in respiratory distress (chronic coughing), unthriftiness, and sometimes death. Eimeria spp. (Coccidia) is a disease associated with filth, moisture and times of depressed immunity such as kidding, weaning or during transportation. Infection results in destruction of the intestinal lining leading to scours, unthriftiness, weight loss/reduced weight gains, and sometimes death. 3. Transmission The worm life cycle consists of part of their life being spent inside the animal and part of their life on the pasture. Worms mate in the host and females lay eggs that pass out in the feces. The eggs hatch and develop to infective young worms (larvae) while remaining in the feces. The infective larvae then move out of the feces onto the surrounding forage 210
where they can be consumed during grazing thus completing the cycle. Spring is the most dangerous time for animals to become infected with worms. In the summer when it is hot, parasite eggs and larvae may not survive so well on pasture. However, there may be another high risk of the disease in autumn, when temperatures begin to fall and the young worms once again can survive on pastures until the cold temperature of winter arrive. Transmission of parasites can be reduced by implementing control measures to eliminate the worms from the animal (deworming) and/or reducing the chances that infective larvae have to re-infect the animal (management). Transmission of liver flukes ceases in late spring/early summer. 4. Species affected Young lambs and kids are very susceptible to the effect of worms, and often become sick and die. Adult sheep and goats are also susceptible. 5. Clinical signs Animals affected by parasites show many signs of infection depending on the parasites present. The general signs include rough hair coat, diarrhea, thriftiness, depression, weight loss (or reduced weight gain), bottle jaw and anorexia (off feed). H. contortus infected animals show symptoms associated with blood loss (anemia), which include pale mucous membranes (most visible by viewing inside the lower eyelid) and bottle jaw (an accumulation of fluid under the chin). The greater the infection level the more blood is lost and eventually the animal may die. When infections with Telodorsagia (Ostertagia) circumcincta and Trichostrongylus colubriformis reach levels that cause disease to be seen, the primary symptom is diarrhea.
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6. Pathologic findings Dead animals should be opened and inspected for worms in the intestines, stomach and liver. Some worms could be seen with naked eye attached to the lining or squeezed out of the organ. 7. Diagnosis Laboratory diagnostic findings may include anemia (low PCV), increased fecal egg count (FEC) and loss of plasma protein. Level of anemia can be roughly evaluated by observing the color of mucous membranes of the lower eye lids. The FAMACHA eye color chart system was developed in South Africa to help producers monitor and evaluate level of anemia without having to rely on laboratory testing. In this method, the lower eyelid mucous membranes are examined and compared to a laminated color chart bearing pictures of sheep eyes at 5 different levels of anemia.: 1 (red, non-anemic); 2 (red-pink, non-anemic); 3 (pink, mild-anemic); 4 (pinkwhite, anemic); 5 (white, severely anemic). Since anemia is the primary pathologic effect from infection with H. contortus, this system can be an effective tool for identifying those animals that require treatment (but only for H. contortus). 8. Treatment Dewormers (anthelmintics) are available in various formulation and variety of forms for administration by drenching, pill, injection or incorporation in feed and water. Treatment schedules vary between regions and with different species of parasites. The most important aspect of using dewormers is to conserve their effectiveness. This can be achieved by using them as little as possible and only when infection levels dictate that intervention is necessary. It would be prudent to establish which dewormers are effective against a worm population. This can be achieved by conducting FEC reduction testing and should be done by a qualified professional such as a veterinarian, veterinary school parasitology lab or a diagnostic lab that 212
offers such a service. Animals should be dewormed based on need using FAMACHA and Smart Drenching approach, or strategic deworming during favorable conditions for the parasite, especially in the spring and autumn and around the time of kidding and lambing. 9. Prevention and control The major problem encountered in controlling nematode parasitism in sheep and goats is the resistance that many worm populations (specifically H. contortus) have developed to essentially all of our dewormers. Resistance has developed primarily because dewormers have been used and rotated too frequently and many times under-dosing occurs. Effective worm control and treatment can not always be achieved by drugs alone. Anthelminthics should be combined with other methods such as rotational grazing and elimination of host species.
(photos, next page)
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Bottle jaw accumulation of fluid under the chin.
FAMACHA eye color chart being used to check level of anemia.
Adult lungworms in the bronchi of the lungs.
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8 PESTE DES PETITS RUMINANTS

1. Definition Peste des petits ruminants (PPR) is an acute or subacute viral disease of goats and sheep characterized by sudden onset of depression, fever, nasal and ocular secretions, foul-smelling diarrhea, and respiratory signs. 2. Etiology PPR virus (PPRV) is a member of the Genus Morbillivirus in the family Paramyxoviridae. It is closely related to the rinderpest, measles, and canine disemtper viruses. PPRV does not survive well in the environment. 3. Transmission Secretions and excretions of sick animals are the sources of infection and transmission increases with close contact, particularly when affected animals cough and sneeze. Animal markets greatly increase the chance for infection. As in rinderpest in PPR it is generally accepted that there is no carrier state. Although cattle and camels are susceptible to infection, they usually do not exhibit clinical signs or transmit the disease. 4. Species affected Sheep and goats are the main victims of PPR. Goats are more susceptible to the disease than sheep. Cattle and camels can be subclinically infected. 215
5. Clinical disease The incubation period is 4-5 days. Morbidity is high in susceptible herds and flocks and increasing with degree of contact. Younger animals are more severely affected. Animals are febrile and appear to be in discomfort. They have a dull coat, dry muzzle, congested mucous membranes and depressed appetite. Early there is a serous nasal discharge; later, it becomes mucopurulent, and may cause the nares to become crusted shut. The conjunctiva is frequently congested, and some affected animals develop a profuse necrotic conjunctivitis with matting of the eyelids. Necrotic stomatitis affects the lower lip and gum and the gum line of the incisor teeth; in more severe cases, it may involve the dental pad, buccal mucosa and their papillae and the tongue. Diarrhea is fetid may be profuse and is accompanied by dehydration and emaciation, hypothermia and death follow, usually after a disease course of 5-10 days. Bronchopneumonia, characterized by coughing may develop at later stages of the disease. Pregnant animals may abort. Mortality is high, and can approach 100%, especially when there are other complicating factors such as parasitic infestation, poor nutrition, lack of shelter, and adverse climatic conditions. 6. Pathologic findings PPRV has a particular affinity for lymphoid tissues and epithelial tissue of the gastrointestinal and respiratory tracts, where it produces characteristic lesions. Lymphoid tissue is collapsed, so the lymph nodes are small and the spleen is flaccid. The virus replicates in epithelial cells and ruptures them, creating erosions and ulcerations, which then fill with exudates. These ulcerative and necrotizing lesions are seen at the nares, in the conjunctiva, and throughout the oral cavity. In the intestinal tract, there can be ulceration, 216
hemorrhage and necrosis in multiple areas, but especially over Peyers patches, and is often most severe at the ileo-ceco-colic junction. Zebra striping in the large intestine is common. Esophagus and forestomachs are spared. The pneumonia can be anteroventral or diffuse, and consists of foci of consolidation centered around the terminal bronchioles. 7. Diagnosis The clinical signs and pathologic lesions of PPR are highly characteristic. Definitive diagnosis requires laboratory confirmation that can be detection of virus by ELISA, AGID, and PCR or observation of typical microscopic lesions by histopathology. Differential diagnoses include: coccidiosis, contagious ecthyma, pasteurella pneumonia, CCPP, FMD. 8. Treatment There is no specific therapy; however treatment for bacterial and parasitic complications decreases mortality in affected flocks and herds. 9. Prevention and control Prevention of introduction into a herd or flock can best be achieved by segregating new animals for a short period of time to ensure freedom from active disease. A particular risk is unsold animals returning from market, where they may have picked up the virus. An attenuated vaccine has been prepared in embryonic caprine kidney cell culture; it affords protection from natural disease for at least one year. (photos, next page)
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PPR - Typical oral and nasal lesions seen in the acute disease
PPR - Profuse diarrhea
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9 ABORTION DISEASES
1. Definition The ewe and doe are both normally very fertile animals but may have a high incidence of abortions when compared to other farm animals. Infectious causes of abortion play an important role in this process and could be a major source of economic loss. Major infectious causes of abortion in sheep and goats are chlamydiosis [enzootic abortion of ewes (EAE)], toxoplasmosis, brucellosis, Q-fever, campylobacteriosis, and listeriosis. 2. Etiology Chlamydiosis is caused by Chlamydophila psittaci, a Gram negative, intracellular bacteria. Toxoplasmosis is caused by Toxoplasma gondii, an intracellular protozoan. Brucellosis is caused by Brucella melitensis, a small gram-negative coccobacillus, specific for goats; Brucella ovis, specific for sheep; and occasionally, Brucella abortus infection occurs in goats running with infected or vaccinated cattle. Although considered goat specific, B. melitensis may cause abortion in sheep. Q-fever is caused by Coxiella burnetii, an obligate intracellular rickettsial (bacterial) organism. 219
Campylobacteriosis is caused by Campylobacter Campylobacter fetus (formerly Vibrio fetus intestinalis)
jejuni
and
Listeriosis is caused by Listeria monocytogenes, a gram positive, nonacid fast bacteria. Abortion strains are often serotype 1. 3. Transmission Chlamydiosis: Pigeons and sparrows may serve as reservoirs for the organism, and it has been suggested that ticks or insects may play a role in transmission of the disease. Aborting females shed large numbers of organism from the uterine discharge, fetus and placenta, particularly in the first three weeks after abortion, which is ingested by other animals. Toxoplasmosis: Cats are pivotal in the transmission of Toxoplasma gondii. They become infected by ingestion of infected rodents and birds which can lead to excretion of large numbers of environmentally resistant oocytes. Cats often defecate and bury their feces in the hay and food bins of barns. Ewes and does become infected by ingestion of food or water contaminated with oocytes from feces of infected cats. The organism enters the blood and spreads to other tissues within two weeks of ingestion of oocytes. In the pregnant ewe or doe, Toxoplasma can invade and multiply in the placenta and then spread to the fetus causing abortion, fetal death, and resorption of the fetus, stillbirth, birth of live but weak lambs and kids, or the birth of a normal offspring depending on the stage of pregnancy. Brucellosis: The most common route of transmission is by the ingestion of contaminated food and water. The organism enters through mucous membranes and becomes localized in lymph nodes, udder, uterus, testes, and spleen. In pregnant animals, localization in the placenta leads to the development of placentitis with subsequent abortion. 220
Q-fever: Cattle, sheep, goats, and wildlife may carry the organism which is shed in large numbers in placentas, uterine fluids, colostrum, and milk. Therefore, cows and sheep may be a source of infection for goats when they share pasture. Animals and humans can be infected by inhaling contaminated dust. Tick bites and grazing contaminated pastures are other modes of transmission. Campylobacteriosis: The major source of infection is the placenta and the uterine discharge of aborting animals. The main route of transmission is through ingestion of organisms shed in vaginal fluid and placenta at the time of abortion or parturition, or through inhalation of aerosol. Listeriosis: Listeria monocytogenes may be found in soil, water, plant litter, silage, and the digestive tract of ruminants. The organism can survive in soil and feces for a very long time, and grows in poorly fermented silage (pH level greater than 5.5). On some farms abortion is contributed to silage feeding, while abortions have been reported on farms in which the sheep and goats were fed hay with the addition of concentrate, or were on woody browse. 4. Species affected Most of the diseases that cause abortion are zoonotic, including chlamydiosis, Q-fever, toxoplasmosis, campylobacteriosis, brucellosis and listeriosis. Owners should be advised to wear gloves when handling aborted fetuses and to burn or bury any placentas and fetuses not needed for diagnostic efforts. In addition pasteurization of milk for human consumption should be stressed. 5. Clinical signs Chlamydiosis: Abortions usually occur in the last month of gestation but can occur as early as day 100 of gestation. Does and ewes are not normally ill but may show a bloody vaginal discharge two to three days prior to abortion. The fetus may be autolyzed or fresh. Some weak 221
newborns may be seen, and a few females may retain the placenta. Occasionally there is concurrent respiratory disease, polyarthritis, conjunctivitis, and retained placentas in the flock. Toxoplasmosis: Goats appear to be more susceptible to Toxoplasma infection than sheep. Abortion can occur in does of all ages but primarily in does that acquire infection during pregnancy although abortion may be repeated in the next gestation. Ewes and does infected prior to breeding do not abort. Those infected 30 to 90 days after breeding usually have fetal resorption or mummification. Most observed abortions occur in the last trimester of gestation, 2 to 3 weeks before term, after occurrence of infection during the latter half of gestation. Ewes and does themselves are generally clinically normal at the time of abortion. Brucellosis: Infection occurs in both sheep and goats and produce abortion in late pregnancy. As in other species, there may be an abortion storm when the disease is introduced followed by a period of herd resistance during which abortions do not occur. A systemic reaction with fever, depression, loss of weight and sometimes diarrhea occurs and may be accompanied by mastitis, lameness, hygroma, and in males, orchitis. Q-fever: In livestock, the disease is usually inapparent. However, occasional abortion outbreaks due to Coxiella burnetii have been reported in sheep and goats. Clinical signs are infrequent but abortion or stillbirth usually occurs late in gestation due to severe damage to placenta and necrosis of cotyledons and thickening of the intercotyledonary areas. Some does abort without apparent clinical signs, while others show anorexia and depression 1 to 2 days before abortion. Campylobacteriosis: Clinical signs include late gestation abortions in does/ ewes and weak and/or stillborn lambs/ kids. Aborting animals may 222
or may not show signs of systemic illness. A mucopurulent or sanguinopurulent vaginal discharge is reported in all aborting animals. Listeriosis: Abortion results from infection early in gestation, but later infection results in stillborn or weak offspring. The abortion form and the encephalitic form of listeriosis do not usually occur simultaneously in a herd. Abortion occurs in the last 2 months of pregnancy and is preceded by septicemia. Signs of septicemia may include fever, decreased appetite and reduced milk production. 6. Pathologic findings The lesion common in all cases of infectious abortion is placentitis. From the placentitis, the fetus either dies due to inability to exchange nutrients through the placenta, or becomes infected itself and dies. A prolonged period of uterine disease and infertility may follow and in case of infectious abortion, the disease threatens the rest of the herd. Chlamydiosis: The fetus may be autolyzed or fresh. The placenta shows regional to generalized placentitis (white to yellow necrotic areas) involving the cotyledons and intercotyledonary space. Toxoplasmosis: Abortion occurs due to necrosis of the placenta, particularly the cotyledons. The intercotyledonary areas of the placenta are usually normal with the cotyledons having white to yellow focal areas of necrosis and calcification up to 1 cm in diameter. These lesions are clearly visible to the eye when the cotyledons are washed in saline. Brucellosis: On gross examination, the placenta is normal in B. melitensis infection in goats, whereas B. ovis infection of sheep result in thickened, necrotic placentitis. The aborted foetuses are often fresh but can be somewhat autolyzed. Often, the affected foetus has no gross lesions in affected organs. In Brucella ovis infections, calcified plaques 223
on the walls and soles of the hooves and accessory digits are considered a characteristic lesion. Q-fever: There is severe damage to placenta and necrosis of cotyledons and thickening of the intercotyledonary areas. Campylobacteriosis: The placenta is often edematous, with necrosis of cotyledons, and thickened brown intercotyledonary areas covered by exudate. Aborted fetuses have grossly visible liver necrosis. Listeriosis: There is some necrosis of cotyledons and the intercotyledonary areas, and the fetus is usually autolyzed. The fetal liver (and possibly lung) may have necrotic foci, 0.5-1 mm in diameter. 7. Diagnosis A systematic approach is essential for the diagnosis of abortions in sheep and goats. The investigator must obtain a good nutritional and clinical history, including possible exposure to carrier animals. Although history seldom provides information pointing directly to the cause of abortion, clues may be found that will indicate what needs to be done to determine the diagnosis. When abortion occurs, the animal should be isolated and any aborted fetus kept for further laboratory examination. In sheep and goats, the entire fetus, placenta, and paired serum samples from aborting dam should be submitted to the diagnostic laboratory. Without the placenta, identification of chlamydiosis and toxoplasmosis is unlikely. Chlamydiosis: Diagnosis is by history of abortion along with clinical signs and demonstration of the characteristic inclusion bodies in the impression smears of placenta, fetal tissue or uterine discharge. A definitive diagnosis is made by culturing the organism from the placenta or fetal tissue. Serological testing is also a valuable aid in diagnosis 224
Toxoplasmosis: A presumptive diagnosis can be made from placental lesions alone, if placenta is available. Presence of white to yellow focal areas of necrosis and calcification on the cotyledons is characteristic of only toxoplasmosis and can be used in the field as a diagnostic tool. On the other hand, Coxiella burnetii, Brucella spp. and Chlamydia spp. usually cause placentitis that include the intercotyledonary region. Positive diagnosis of toxoplasmosis requires isolation of the organism from placenta or fetal brain, lung and muscles. The samples for isolation studies should be shipped on ice but not frozen. Brucellosis: Identification of brucellosis as the cause of abortion is usually made by isolation of the organism from aborted fetus, placenta or vaginal discharge. Various agglutination, precipitation and complement fixation tests are used to detect carrier animals. Q-fever: Diagnosis is based on placental findings, serology and isolation of the organism. While isolation of Coxiella burnetii is the ideal means for diagnosis of the disease, it is usually not feasible due to the contagious and zoonotic potential of the organism. The Fluorescent Antibody (FA) Test can be used to identify organism in frozen section of placenta. Campylobacteriosis: Definitive diagnosis of campylobacter abortion is through isolation of the organism. Direct microscopic examination and isolation of Campylobacter spp. from placenta, fetal abomasal contents and maternal vaginal discharge is the preferred diagnostic procedure. Listeriosis: Diagnosis is by isolation of the organism from the placenta, abomasal contents, or uterine discharge. 8. Treatment: The diagnosis in the event of an abortion storm often is not available for several days. It is reasonable to begin treatment of remaining pregnant 225
animals with tetracycline, since most infectious agents causing abortion in sheep and goats are susceptible to tetracycline. One possible protocol is three injections of long-acting tetracycline at 20 mg/kg at 3-day intervals. Meat and fiber producing herds are commonly treated with oral tetracycline (400 to 500 mg per head per day) for two weeks. In dairy herds, it is more customary to treat individual non-lactating does or ewes by injection of long-acting oxytetracycline preparation at a dose of 20 mg/kg SC every 10 to 14 days. Withdrawal time in lactating animal should be observed. 9. Prevention and control There is no recommended vaccination for most of these diseases in Afghanistan. Fetal membranes and dead fetuses should be buried or incinerated to prevent infection of other animals. Control of toxoplasmosis is based on preventing exposure of pregnant females to cat feces. Cats should be prevented from defecating in feeders or hay. Fetal membranes and dead fetuses of sheep or goats that abort should be handled with caution by persons wearing gloves to prevent infection in humans. Goat and sheep milk should be pasteurized or boiled before human consumption.
(photos, next page)
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Multifocal necrosis of cotyledons, Toxoplasma abortion
Multifocal hepatic necrosis, characteristic of Listeria abortion
Circular zones of necrosis, liver, characteristic of Campylobacter abortion
Suppurative epididymitis, seen with Brucella ovis.
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10 SCRAPIE
1. Definition Scrapie is a fatal, transmissible, neurologic disease of sheep, and is considered in the family of diseases known as transmissible spongiform encephalopathies (TSEs). 2. Etiology The causative agent is a malformed version of a normal cell protein, called a prion. These malformed prions resist the normal process of cellular degradation, and also influence other normal prion proteins to undergo altered formation. The malformed prions all accumulate within the neurons in large vacuoles, inhibiting neuronal function and causing the brain to have a spongey appearance under the microscope. 3. Transmission Spread is by contact, and it is believed that placental tissue contains much more infectious material than any secretion or excretion. 4. Species affected Sheep are the principal victims of scrapie, although occasionally a goat will be infected also. There are some breed differences in susceptibility, with Suffolk sheep being the most at risk. There is no evidence that scrapie is transmissible to humans. 228
5. Clinical Disease Incubation period is 6 months to 5 years, during which time the animals may be shedding the prion protein in placental tissue. General signs of illness include ataxia and intense pruritis. The animal becomes preoccupied with biting its extremities and rubbing its body against posts, fences, trees, etc., so that wool is torn out leaving areas of raw wounds. These itching areas and lesions are characteristically bilaterally symmetrical. If the sheep's head is tilted sideways, nystagmus may be very marked. Other central nervous system clinical signs are excitability with fine head and neck tremors, dazed expression, high stepping gait, incoordination, prostration and epileptiform convulsions. These signs may be exacerbated by stimulation. The duration of signs of illness is usually one to two months but can range from two weeks to six months. The mortality rate in clinical scrapie is 100 per cent. There is no way at present in which subclinical cases of the disease can be recognized. 6. Pathological findings Gross findings are minimal. Loss of wool and superficial trauma caused by rubbing and biting may be seen. Pathologic lesions are restricted to microscopic changes in the CNS. 7. Diagnosis Diagnosis is based on typical clinical signs and microscopic examination of the CNS. Differential diagnoses include: any form of encephalitis, pregnancy toxemia, sheep scabies, maedi-visna, and poisoning. 8. Treatment There is no treatment. 9. Prevention and control Control programs focus on removing affected animals from the flock. It is especially important to keep susceptible animals away from placental tissues. There is no vaccine. 229
11 SHEEP POX AND GOAT POX

1. Definition Sheep pox and goat pox are contagious viral systemic diseases characterized predominantly by skin and pulmonary lesions. 2. Etiology Sheep pox and goat pox are separate viruses within the Genus Capripoxvirus, Family Poxviridae. 3. Transmission Transmission of disease can occur via aerosol or contact, with inhalation or mucous membrane contact with infected animals. 4. Species affected Most viruses are species-specific but there are a few strains which will infect both sheep and goats. 5. Clinical signs Incubation period is 1-2 weeks. Morbidity depends on degree of contact between animals and existing immunity, and so varies between 10 and 100%. First signs of clinical disease may be papules progressing to ulceration on the mucous membranes and skin. Skin lesions are most easily appreciated in areas of poorly haired or poorly wooled skin, such as axilla or inguinal region. Animals are febrile, depressed, and may 230
have some dyspnea or coughing. Illness may last 1-2 weeks followed by recovery or death. Mortality varies from 20 to 100%. 6. Pathologic findings The capripoxviruses differ from the other poxviruses in that the lesions are quite deep and ulcerative. Much of the damage occurs in the dermis, so the lesions will feel thick and when they ulcerate, can expose the subcutis. These ulcerations can be seen throughout the skin and certain mucous membranes, especially conjunctiva, nares, lips, and trachea. Lung is usually the only internal organ affected, and here the pattern is one of multifocal necrotizing to firm nodules scattered throughout. Occasionally, serosal nodules are present as well - often on intestinal serosa and tunica vaginalis. These nodules only rarely penetrate through to the mucosal surfaces. 7. Diagnosis Clinical disease is highly characteristic. Confirmation of diagnosis requires laboratory testing - histopathology, PCR, or virus isolation. Differential diagnoses include orf (contagious ecthyma), urticaria, and insect bites. 8. Treatment There is no treatment for sheep pox or goat pox. 9. Prevention and control The best prevention is to keep the disease out of flocks and herds by controlling introduction from infected animals. This is difficult in areas where there is extensive mixing of herds and flocks. Good vaccines exist for sheep pox and goat pox and a single vaccine is used for both diseases, providing immunity for at least two years. (photos, next page) 231
Developing papules on the underside of the tail, sheep pox
Deeply ulcerative lesions on the skin, typical of sheep and goat pox
Disseminated nodules in the lung, pneumonia due to sheep pox
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Illustrated Manual of Infectious Diseases of Livestock in Afghanistan
VETERINARIANS ON THE WRITING TEAM First row, left to right: Dr. Seyedmehdi Mobini, Dr. Abdul Qader Samsor, Dr. Abdulhabib Nawroz, Dr. Corrie Brown, Dr. Ezatullah Jaheed Second row, left to right: Dr. Said Gul Safi, Dr. Ghulam Mohammad Ziay, Dr. Lutfullah Rlung, Dr. Fridoon Oria Not pictured: Dr. Daad Mohammad Amir, Dr. Afzal Masoodi, Dr. Azizullah Osmani, Dr. Fatima Safi, Dr. Robert M. Smith
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Illustrated Manual of Infectious Diseases of Livestock in Afghanistan
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Illustrated Manual of Infectious Diseases of Livestock in Afghanistan

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ILLUSTRATED MANUAL OF INFECTIOUS DISEASES OF LIVESTOCK IN AFGHANISTAN

Fort Valley State University

Copyright 2008 Fort Valley State University

Library of Congress Catalogue Card Number: 2008935063 ISBN: 978-0-9659583-3-2

ILLUSTRATED MANUAL OF INFECTIOUS DISEASES OF LIVESTOCK IN AFGHANISTAN

Infectious Diseases of Livestock in Afghanistan

Infectious Diseases of Livestock in Afghanistan

the Plum Island Animal Disease Center Audiovisual Services,

Infectious Diseases of Livestock in Afghanistan

Infectious Diseases of Livestock in Afghanistan

Infectious Diseases of Livestock in Afghanistan

Infectious Diseases of Livestock in Afghanistan

Infectious Diseases of Livestock in Afghanistan

Infectious Diseases of Livestock in Afghanistan / General Topics

Infectious Diseases of Livestock in Afghanistan / General Topics

Infectious Diseases of Livestock in Afghanistan / General Topics

Limbs reflected and skin peeled back

Internal organs exposed

Infectious Diseases of Livestock in Afghanistan / General Topics

Infectious Diseases of Livestock in Afghanistan / General Topics

Infectious Diseases of Livestock in Afghanistan / General Topics

Spleen - Normal appearance

Heart - Open all the chambers and look at the valves

Kidneys - Cut open and look for streaks, or pallor

Infectious Diseases of Livestock in Afghanistan / General Topics

Female reproductive tract

Intestinal tract - Be sure to look at both serosal and mucosal surfaces.

Infectious Diseases of Livestock in Afghanistan / General Topics

Infectious Diseases of Livestock in Afghanistan / General Topics

Biosafety and Biosecurity

Infectious Diseases of Livestock in Afghanistan / General Topics

Removing keel bone to expose viscera and remove the keel.

Checking air sacs

Digestive system removed, in entirety

Infectious Diseases of Livestock in Afghanistan / General Topics

Infectious Diseases of Livestock in Afghanistan / General Topics

Infectious Diseases of Livestock in Afghanistan / General Topics

Report back to veterinarian

Visit by animal health professional

Samples Taken Laboratory testing Samples submitted to lab

Infectious Diseases of Livestock in Afghanistan / General Topics

Tissue collection tray which is useful during a necropsy procedure

Infectious Diseases of Livestock in Afghanistan / General Topics

Infectious Diseases of Livestock in Afghanistan / General Topics

Infectious Diseases of Livestock in Afghanistan / General Topics

Infectious Diseases of Livestock in Afghanistan / General Topics

Infectious Diseases of Livestock in Afghanistan / General Topics

Anthrax bacilli from a lymph node impression smear

Gram negative coccobacilli from an abscess

Whipworm egg in a stool sample

Trypanosomes in a blood smear

Growing the organism - bacterial culture

Samples are streaked onto agar and bacterial colonies grow

Specialized media can detect Salmonella

Antibiotic sensitivity of bacteria is determined

Biochemical reactions in panel form identify bacteria

Infectious Diseases of Livestock in Afghanistan / General Topics

Detecting the organism immunologically

Fluorescent antibody testing - labeled antibody highlights antigen in tissue or smear

Detecting nucleic acid of the organism Polymerase chain reaction (PCR)

Infectious Diseases of Livestock in Afghanistan / General Topics

Infectious Diseases of Livestock in Afghanistan / General Topics

Infectious Diseases of Livestock in Afghanistan / General Topics