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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: [email protected]
Copyright © 2008
by
Fort Valley State University
ALL RIGHTS RESERVED
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: [email protected]
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.
Infectious Diseases of Livestock in Afghanistan
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,
the Plum Island Animal Disease Center Audiovisual Services,
Drew Adams, and, LTC Richard Probst.
Infectious Diseases of Livestock in Afghanistan
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
1
12
18
22
25
28
CH. 2/ DISEASES OF MULTIPLE SPECIES
1 Anthrax
2 Clostridial Diseases
3 Crimean Congo Hemorrhagic Fever
4 Echinococcosis
5 Foot-and-Mouth Disease
6 Johne’s Disease
7 Rabies
35
39
46
49
52
56
60
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
65
67
69
72
75
78
81
84
87
90
Infectious Diseases of Livestock in Afghanistan
11 External Parasites of Cattle
12 Internal Parasites of Cattle
13. Abortion Diseases of Cattle
14 Rinderpest
15 Theileriosis
93
97
101
106
109
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
115
118
120
123
126
128
130
133
136
140
143
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 Marek’s Disease
13 Newcastle Disease
147
151
154
157
160
162
165
168
171
174
176
179
181
Infectious Diseases of Livestock in Afghanistan
14 Pullorum Disease
15 Tuberculosis, Avian
184
187
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
191
194
198
200
203
206
209
215
219
228
230
Infectious Diseases of Livestock in Afghanistan
CHAPTER
1
GENERAL TOPICS
Infectious Diseases of Livestock in Afghanistan
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.
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Infectious Diseases of Livestock in Afghanistan / General Topics
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.
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Infectious Diseases of Livestock in Afghanistan / General Topics
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.
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Infectious Diseases of Livestock in Afghanistan / General Topics
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.
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Infectious Diseases of Livestock in Afghanistan / General Topics
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.
5
Infectious Diseases of Livestock in Afghanistan / General Topics
Lungs - Should be pink and well
aerated. Cut down the trachea
and bronchi to look at mucosal
airway surfaces.
Spleen - Normal appearance
Heart - Open all the chambers and
look at the valves
6
Kidneys - Cut open and look for
streaks, or pallor
Infectious Diseases of Livestock in Afghanistan / General Topics
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.
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Infectious Diseases of Livestock in Afghanistan / General Topics
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
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Infectious Diseases of Livestock in Afghanistan / General Topics
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.
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Infectious Diseases of Livestock in Afghanistan / General Topics
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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Infectious Diseases of Livestock in Afghanistan / General Topics
Kidneys, also apposed closely
to the body wall, but in the
abdomen.
Lungs removed - these need
to be dissected away from the
thoracic body wall as they are
closely adherent.
5. Examine and sample the organs - Similar to the procedure for
mammals.
6. Write the report - Same as for mammals.
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Infectious Diseases of Livestock in Afghanistan / General Topics
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 doesn’t 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
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Infectious Diseases of Livestock in Afghanistan / General Topics
enteritis, submit a fecal sample also. If internal or external parasites are
noted, collect those as well into separate vials.
Treatment
Sick animal
Visit by animal
health
professional
Report
back to
veterinarian
Samples
Taken
Laboratory
testing
Samples
submitted
to lab
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Infectious Diseases of Livestock in Afghanistan / General Topics
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
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Infectious Diseases of Livestock in Afghanistan / General Topics
− 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
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Infectious Diseases of Livestock in Afghanistan / General Topics
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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Infectious Diseases of Livestock in Afghanistan / General Topics
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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Infectious Diseases of Livestock in Afghanistan / General Topics
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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Infectious Diseases of Livestock in Afghanistan / General Topics
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
19
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
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
Infectious Diseases of Livestock in Afghanistan / General Topics
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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Infectious Diseases of Livestock in Afghanistan / General Topics
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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Infectious Diseases of Livestock in Afghanistan / General Topics
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
Infectious Diseases of Livestock in Afghanistan / General Topics
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
24
Infectious Diseases of Livestock in Afghanistan / General Topics
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.
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Infectious Diseases of Livestock in Afghanistan / General Topics
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
Advantages
5% Bleach,
iodine,
Virkon,
hydrogen
peroxide
Kills most
viruses and
bacteria
Alkalis
Caustic
soda, lime
Acids
2% Vinegar,
citric acid
Kill most
viruses and
bacteria
Work even in
the presence
of organic
matter
Excellent for
foot-andmouth
disease
Disadvantages
Poor activity
in the
presence of
organic
material
Irritating to
respiratory
membranes
and skin
Do not work
well for many
agents
Main use
Decontaminate
surfaces
that may
have virus
or bacteria
To cover
carcasses
or pathways
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
Infectious Diseases of Livestock in Afghanistan / General Topics
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.
27
Infectious Diseases of Livestock in Afghanistan / General Topics
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
Infectious Diseases of Livestock in Afghanistan / General Topics
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
Species
Advantages
Disadvantages
Exsanguination
(Halal
slaughter in
Moslem
countries)
All
livestock
and poultry
Meat can be
consumed, but
only if animal was
not physically ill
No necessity for
disposal of
carcasses if meat
is consumed
May not work for
diseases with zoonotic
potential
Often requires transport
to slaughtering facility
Blood exposure can
spread disease
Free bullet
All
livestock
Good for animals
that are difficult to
restrain, or are
agitated, or in
open fields
Dangerous for people in
the area
Can spread bodily fluids
Requires considerable
operator skill to kill
humanely
Brain not available for
examination
29
Infectious Diseases of Livestock in Afghanistan / General Topics
Captive bolt
Electro-cution
Gases
(CO2, CO)
Injectable
chemicals,
such as
barbiturates,
magnesium
sulfate,
chloral
hydrate,
strychnine
Cervical
dislocation manual or
with
burdizzos
All
livestock
No need to move
large animals off
of premises
Calves,
sheep,
goats,
poultry
Poultry,
neonatal
sheep and
goats
No tissue or body
fluid exposure
All
livestock
Poultry
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
30
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
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
Infectious Diseases of Livestock in Afghanistan / General Topics
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
31
Infectious Diseases of Livestock in Afghanistan / General Topics
32
CHAPTER
2
DISEASES OF
MULTIPLE SPECIES
33
Infectious Diseases of Livestock in Afghanistan / Multi-Species
34
Infectious Diseases of Livestock in Afghanistan / Multi-Species
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
Infectious Diseases of Livestock in Afghanistan / Multi-Species
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 1−14 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 41.5°C, 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
Infectious Diseases of Livestock in Afghanistan / Multi-Species
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
Infectious Diseases of Livestock in Afghanistan / Multi-Species
Taking blood from animal suspected of dying of
anthrax, to check for the bacteria in a smear.
38
Infectious Diseases of Livestock in Afghanistan / Multi-Species
2
CLOSTRIDIAL DISEASES
This disease
is known to
occur in
Afghanistan.
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
Infectious Diseases of Livestock in Afghanistan / Multi-Species
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
Infectious Diseases of Livestock in Afghanistan / Multi-Species
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
Infectious Diseases of Livestock in Afghanistan / Multi-Species
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
Infectious Diseases of Livestock in Afghanistan / Multi-Species
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 Diseases of Livestock in Afghanistan / Multi-Species
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
Infectious Diseases of Livestock in Afghanistan / Multi-Species
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.
45
Infectious Diseases of Livestock in Afghanistan / Multi-Species
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
Infectious Diseases of Livestock in Afghanistan / Multi-Species
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
Infectious Diseases of Livestock in Afghanistan / Multi-Species
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.
48
Infectious Diseases of Livestock in Afghanistan / Multi-Species
4
ECHINOCOCCOSIS
This disease
is known to
occur in
Afghanistan.
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
Infectious Diseases of Livestock in Afghanistan / Multi-Species
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
Infectious Diseases of Livestock in Afghanistan / Multi-Species
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 dog’s 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
51
Infectious Diseases of Livestock in Afghanistan / Multi-Species
5
FOOT-AND-MOUTH DISEASE
This disease
is known to
occur in
Afghanistan.
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
Infectious Diseases of Livestock in Afghanistan / Multi-Species
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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Infectious Diseases of Livestock in Afghanistan / Multi-Species
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)
54
Infectious Diseases of Livestock in Afghanistan / Multi-Species
Vesicle forming in interdigital
cleft, bovine
Ruptured vesicle on
tongue, bovine
Vesicle forming along coronary
band, sheep
Ruptured vesicle, dental pad,
sheep
55
Infectious Diseases of Livestock in Afghanistan / Multi-Species
6
JOHNE’S DISEASE
This disease
is known to
occur in
Afghanistan.
1. Definition
Johne’s 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 Johne’s disease is zoonotic. There is however, some
scientific evidence to suggest that people who drink milk from cows
56
Infectious Diseases of Livestock in Afghanistan / Multi-Species
infected with Map, might also become infected, and that Crohn’s
disease, a chronic granulomatous inflammation of the ileum, is actually
caused by Map.
There is incomplete evidence that the
agent of Johne’s disease might also
cause Crohn’s 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 Johne’s 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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Infectious Diseases of Livestock in Afghanistan / Multi-Species
7. Diagnosis
Clinical signs and the gross appearance of the intestine is highly
characteristic of Johne’s 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 Johne’s disease.
9. Prevention and Control
The only way to control Johne’s 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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Infectious Diseases of Livestock in Afghanistan / Multi-Species
Johne’s disease enlarged mesenteric
lymph node.
Johne’s disease mucosa of ileum is
thickened and
corrugated; also cecocolic lymph node is
markedly enlarged.
Fluid feces, from a cow
with Johne’s disease
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Infectious Diseases of Livestock in Afghanistan / Multi-Species
7
This disease
is known to
occur in
Afghanistan.
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.
3. Transmission
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.
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Infectious Diseases of Livestock in Afghanistan / Multi-Species
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.
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Infectious Diseases of Livestock in Afghanistan / Multi-Species
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.
8. Treatment
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.
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.
62
CHAPTER
3
DISEASES OF
CATTLE
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Infectious Diseases of Livestock in Afghanistan / Cattle
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Infectious Diseases of Livestock in Afghanistan / Cattle
1
ACTINOBACILLOSIS
This disease
is known to
occur in
Afghanistan.
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
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Infectious Diseases of Livestock in Afghanistan / Cattle
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.
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Infectious Diseases of Livestock in Afghanistan / Cattle
2
ACTINOMYCOSIS
This disease
is known to
occur in
Afghanistan.
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
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Infectious Diseases of Livestock in Afghanistan / Cattle
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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Infectious Diseases of Livestock in Afghanistan / Cattle
3
ANAPLASMOSIS
This disease
is known to
occur in
Afghanistan.
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
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Infectious Diseases of Livestock in Afghanistan / Cattle
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 (41°C), 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.
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Infectious Diseases of Livestock in Afghanistan / Cattle
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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Infectious Diseases of Livestock in Afghanistan / Cattle
4
BABESIOSIS
(Red Water, Piroplasmosis, Tick Fever)
This disease
is known to
occur in
Afghanistan.
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.
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Infectious Diseases of Livestock in Afghanistan / Cattle
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 (41-42°C), 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.
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Infectious Diseases of Livestock in Afghanistan / Cattle
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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Infectious Diseases of Livestock in Afghanistan / Cattle
5
BOVINE SPONGIFORM ENCEPHALOPATHY
This disease has not
been diagnosed in
Afghanistan.
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.
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Infectious Diseases of Livestock in Afghanistan / Cattle
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.
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Infectious Diseases of Livestock in Afghanistan / Cattle
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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Infectious Diseases of Livestock in Afghanistan / Cattle
6
BOVINE TUBERCULOSIS
This disease
is known to
occur in
Afghanistan.
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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Infectious Diseases of Livestock in Afghanistan / Cattle
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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Infectious Diseases of Livestock in Afghanistan / Cattle
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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Infectious Diseases of Livestock in Afghanistan / Cattle
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 10–70%. 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
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Infectious Diseases of Livestock in Afghanistan / Cattle
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.
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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
This disease
is known to
occur in
Afghanistan.
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.
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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
This disease
is known to
occur in
Afghanistan.
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
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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 40.5-41°C. 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.
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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
This disease
is known to
occur in
Afghanistan.
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.
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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.
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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.
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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
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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
These parasites
are known to
occur in
Afghanistan.
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.
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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.
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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 (Bang’s 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 bull’s 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
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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
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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.
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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.
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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
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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 Peyer’s 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.
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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.
Rinderpest - Feces, showing
mucus, blood
“Shooting” diarrhea
characteristic of rinderpest
Rinderpest - ulceration of
Peyer’s patch, small intestine
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15
THEILERIOSIS
This disease
is known to
occur in
Afghanistan.
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.
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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.
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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 naïve 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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112
CHAPTER
4
DISEASES OF
HORSES
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1
EPIZOOTIC LYMPHANGITIS
This disease
has not been
diagnosed in
Afghanistan.
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 animal’s skin to an open
wound on a susceptible animal’s 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
This disease has
not been diagnosed
in Afghanistan.
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
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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.
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3
EQUINE INFLUENZA
This disease has
not been
diagnosed in
Afghanistan.
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 41.1°C),
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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 40°C.
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
This disease
is known to
occur in
Afghanistan.
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 (40ºC), 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 orange–brown. 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 enzyme–linked 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
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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 tick–borne infections. However, preventing the transfer of blood from
one animal to another is vital.
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5
EQUINE RHINOPNEUMONITIS
This disease
has not been
diagnosed in
Afghanistan.
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.
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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
This disease has not
been diagnosed in
Afghanistan.
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
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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
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EXTERNAL PARASITES OF HORSES
These
parasites
are known
to occur in
Afghanistan.
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
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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
This disease
is known to
occur in
Afghanistan.
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!
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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.
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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
These
diseases are
known to
occur in
Afghanistan.
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.
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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.
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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
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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
This disease has not
been diagnosed in
Afghanistan.
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 (39.4-41.1°C), 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
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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
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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
This disease
is known to
occur in
Afghanistan.
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.
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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.
144
CHAPTER
5
DISEASES OF
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.
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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.
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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)
This disease
is known to
occur in
Afghanistan.
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.
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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
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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
This disease
has not been
diagnosed in
Afghanistan.
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
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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 naïve.
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.
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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
This disease
is known to
occur in
Afghanistan.
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
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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
This disease
is known to
occur in
Afghanistan.
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.
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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.
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6
COLIBACILLOSIS, AVIAN
This disease
is known to
occur in
Afghanistan.
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,
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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.
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Good sanitation and adequate nutrition will prevent many cases of
colibacillosis. Hygiene in the hatchery is especially important for
preventing navel infections.
Colibacillosis - fibrin and caseous
exudates on the surface of the
lungs, and fibrin covering the
spleen
Colibacillosis - with fibrin covering
the surface of the liver
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7
FOWL CHOLERA
This disease
is known to
occur in
Afghanistan.
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
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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.
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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
This disease
is known to
occur in
Afghanistan.
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
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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
This disease
is known to
occur in
Afghanistan.
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.
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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
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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
This disease
is known to
occur in
Afghanistan.
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,
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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, Marek’s 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.
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11
INFECTIOUS LARYNGOTRACHEITIS
This disease
has not been
diagnosed in
Afghanistan.
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.
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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
MAREK’S DISEASE
This disease
has not been
diagnosed in
Afghanistan.
1. Definition
Marek’s 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 Marek’s 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
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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.
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13
NEWCASTLE DISEASE
This disease
is known to
occur in
Afghanistan.
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
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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
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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
This disease
is known to
occur in
Afghanistan.
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.
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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
This disease
is known to
occur in
Afghanistan.
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
6
DISEASES OF
SHEEP AND GOATS
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Infectious Diseases of Livestock in Afghanistan / Sheep and Goats
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Infectious Diseases of Livestock in Afghanistan / Sheep and Goats
1
BLUETONGUE
This disease
is known to
occur in
Afghanistan.
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
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Infectious Diseases of Livestock in Afghanistan / Sheep and Goats
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.
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Infectious Diseases of Livestock in Afghanistan / Sheep and Goats
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
This disease
has not been
diagnosed in
Afghanistan.
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.
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Infectious Diseases of Livestock in Afghanistan / Sheep and Goats
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
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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 (56°C 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
This disease
has not been
diagnosed in
Afghanistan.
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
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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.
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4
CONTAGIOUS CAPRINE PLEUROPNEUMONIA
This disease
is known to
occur in
Afghanistan.
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.
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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 (41°C) 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
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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
This disease
is known to
occur in
Afghanistan.
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.
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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
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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
These
diseases are
known to
occur in
Afghanistan.
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.
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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.
Sheep with nosebot infestation
Hair loss in sheep due to
external parasites
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7
INTERNAL PARASITES OF SHEEP AND GOATS
These
diseases are
known to
occur in
Afghanistan.
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
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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
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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
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Infectious Diseases of Livestock in Afghanistan / Sheep and Goats
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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Infectious Diseases of Livestock in Afghanistan / Sheep and Goats
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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Infectious Diseases of Livestock in Afghanistan / Sheep and Goats
8
PESTE DES PETITS RUMINANTS
This disease
is known to
occur in
Afghanistan.
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.
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Infectious Diseases of Livestock in Afghanistan / Sheep and Goats
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,
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Infectious Diseases of Livestock in Afghanistan / Sheep and Goats
hemorrhage and necrosis in multiple areas, but especially over Peyer’s
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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Infectious Diseases of Livestock in Afghanistan / Sheep and Goats
PPR - Profuse diarrhea
PPR - Typical oral and nasal
lesions seen in the acute disease
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Infectious Diseases of Livestock in Afghanistan / Sheep and Goats
9
ABORTION DISEASES
These
diseases are
known to
occur in
Afghanistan.
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.
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Infectious Diseases of Livestock in Afghanistan / Sheep and Goats
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.
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Infectious Diseases of Livestock in Afghanistan / Sheep and Goats
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
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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
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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
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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
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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
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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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Infectious Diseases of Livestock in Afghanistan / Sheep and Goats
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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Infectious Diseases of Livestock in Afghanistan / Sheep and Goats
10
SCRAPIE
This disease
has not been
diagnosed in
Afghanistan.
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.
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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.
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11
SHEEP POX AND GOAT POX
These
diseases are
known to
occur in
Afghanistan.
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
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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)
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Infectious Diseases of Livestock in Afghanistan / Sheep and Goats
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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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
234