Wildlife Disease 2
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Wildlife Disease 2
Study Guide txt
Part 2 of Wildlife Disease Notes
What is wildlife rehabilitation?
It involvies caring for injured, ill and orphaned wild animals with the goal of releasing each into its natural habitat
Wildlife rehabilitation is also used for?
What else are wildlife rehabilitators involved in?
biological and ecological concepts
writing new laws
What you need to become a wildlife rehabilitator?
complete and submit a form
pass wildlife rehabilitator exam with 80% or higher
exam consist of 100 multiple choice questions
offered state wide in the spring and fall
study guide costs $15 check or money order stating request
2 letters of recommendation
interview with regional wildlife office
liscense expires annually on Dec 31st
NO fee for the liscense
Wildlife rehabilitators rules are?
native wildlife may NOT be kept as pets in NYS
must obtain liscense to collect or possess
must be certified by vets as permanently disabled and/or non releasable
What are the synonyms for rabies?
What is the history of rabies?
rabies is one of the oldest recorded infectious dieseases
What is the etiology of rabies?
acute, infectious disease of the central nervous system
rabies is caused by?
a virus that generally persists in nature as a salivary gland infection of carnivorous animals
Hosts of rabies?
: raccoons, skunks, foxes, coyotes, bats. all species of mammals susceptible, small
rodents (squirrels, rats, mice, hamsters, guinea pigs, gerbils, chipmunks) and rabbits almost never
found to be infected with rabies. Opossum are highly resistant.
Distribution of rabies?
rabies is enzootic (naturally found endemic) throughout the world. Hawaii is the only state that is rabies free. anids are the most important vectors of rabies.
transmission of rabies?
contamination of a bite wound, virus in biting animals saliva, also from ingestion
mucosal contact, aerosol of urine from infected bats.
Incubation of rabies?
incubation of the disease is highly variable, average is usually 2-12 weeks in carnivorous animals
and bats rarely greater than 10 days or less than 6 months
what are the 4 possible stages of rabies an animal goes through?
: NO symtoms
: early signs are subtle, animal acts strange
: Very aggressive (the saliva contains the greatest amount of the virus)
: in-coordination, tremors, convulsions, loss of the swallowing reflex, paralysis, death
clinical course of rabies?
in animals 2-10 days, in humans 2-8 days
Pathogenesis of rabies?
believed to travel from the site of the wound centripetally (towards the CNS) and then centrifugally
(away from the CNS) to the salivary gland and other tissues.
Adrenal glands and lungs most common
ovaries or testes
once symtoms occur almost always fatal!
Pathology of rabies?
NO gross lesions seen at necropsy
some inflammation of the CNS
damage to parts of the brain
What are negri bodies?
are inclusion bodies specific to the rabies virus, particles in the nucleus and cytoplasm of cells
that result from viral infections (negri bodies are specific inclusion bodies of that virus rabies)
3 types of lab tests used for rabies?
Direct microscopic method (histology)
Fluorescent rabies antibody method (FRA)
Mouse inoculation method
What are the human anti-rabies treatment?
Local wound treatment (washing with soap and water)
Rabies immune globulin (human origin)
Describe how rabies immune globulin works?
it takes antibodies from someone exposed to rabies and giving the antibodies to someone else after they have been exposed. It is recommended for all exposures and bites
Managment and Control of rabies?
controlled through vaccination in domestic animals
reduction of stray animals
wildlife more difficult
: population control and oral vaccinaions with use of bait
Transmission of rabies to humans?
contamination of mucous membranes
Incubation of rabies in humans?
days to years
symtoms of rabies in humans?
flu like signs
discomfort or tingeling at site of exposure
Diagnosis of rabies in humans?
virus detection in saliva
antibody tests on serum and spinal fluid
antigen detection in skin biopsy
Treatement of rabies in humans?
what are the synonyms of hemorrhagic disease?
epizootic hemorrhagic disease
history of hemorrhagic disease?
BLU was first recognized in South Africa in the early 1870's, it caused high
morbidity and mortality in introduced European breeds of sheep, it also caused
clinical disease in cattle, in 1944 arthropods were determined to be the
vectors of this disease
distribution of hemorrhagic disease?
BLU has a wide distribution that followed the international trade in cattle, EHD
has been in white-tailed deer in the U.S. since 1890's, its found throughout
much of the US. In white-tailed deer, BLU and EHD can be active concurrently in
the same deer population
etiology of hemorrhagic disease?
BLU and EHD are closely related infectious, often fatal, viral diseases of wild
ruminants (hooved animals with a four chamber stomach), the viruses are
classified as orbiviruses, which are RNA viruses
species affected with BLU?
Big horn sheep
species affected with EHD?
How is hemorrhagic disease transmitted?
Arthropods in the genus Culicoides are vectors of the diseases, common names
: biting nat or midges
They are common in hot, wet, low lying areas which are often chosen as breeding
areas by affected animals, the midge must harbor the virus for 10-20 days
before it can pass it to its host
field signs of hemorrhagic disease?
sudden onset of disease
loss of appetite
loss of wariness
edema of head and neck
often salivate excessively
hyperemia- presence of excess blood in the vessels specifically the mucosa of orbital and oral regions = a rosy or
blue appearance = blue tongue
pathogenesis of hemorrhagic disease?
Multiplication of virus
Formation of cytoplasmic inclusion bodies
Erythrocytic viremia (The virus in the blood) follows, transported in the blood
Virus numbers and body temperature peak at the same time
Prime pathogenic mechanism (what leads to all the damage in the animals body) or intravascular coagulation
Necrosis of blood vessel walls
Hemorrhaging occurs from clotted vessels as well as widespread diapedesis (blood cells are escaping
out of the vascular system)
Plural, pulmonary,pericardial, and retroperitoneal edema occurs (refers to different parts of the
There is a widespread interference with normal blood circulation and leukopenia (decrease
in white blood cells)
pathology of hemorrhagic disease?
Extensive hemorrhaging- commonly in heart, liver, spleen, kidney, lungs and intestinal tract
And the tongue muscles! Liver, spleen and lymph nodes are large and congested
Wide spread edema
Erosion of portions of the epithelium of the lips, tongue and buccal surfaces
In pronghorn and bighorn sheep, lesions similar to those in acute pneumonia may occur
how to diagnosis hemorrhagic disease?
Isolation and identification of virus
EHD and BLU cannot be differentiated by lesions alone
Dual infections can occur
Submit blood, lung, liver, spleen, and kidneys
treatment and control of hemorrhagic disease?
Animals are not treatable once infected
Pre-exposure vaccination is possible for captive animals & domestics
The midge vectors cannot be eliminated
Some domestics are long term carriers
There is NO human health risk with this disease- can handle animals and eat the meat
People not affected by midges
chronic wasting disease or (CWD) is caused by?
proteinaceous agents called "prions" that are devoid of nucleic acids no genetic identity
-In animals, TSE's are infectious
-Prions are produced in lymphoid and CNS tissues
-Prior to 1980, TSE'S were only documented in four species
: domestic sheep and goats
-Transmissible mink encephalopathy (TME)
: Creutzfeldt-Jakob disease, Gerstmann-Straussler-Scheinker syndrome and Kuru
what is the distribution of CWD?
First recognized in 1967 in captive mule deer in Colorado, diagnosed in 1978 as a
spongiform encephalopathy, Recent updates
: Jan 16th 2010 16 new cases in West
Virginia, Feb 4th 2010 38 new cases confirmed in Saskatchewan, March 11th 2010
first case in first Utah elk, March 14th 2010 Missouri first case of CWD
species affected by CWD?
Only 3 species of Cervidae are known to be naturally susceptible
rocky mountain elk
transmission and study of CWD in populations?
Mode of transmission
NO evidence that CWD is a food-borne disease (BSE- food borne)- mad cow disease
Strong evidence that transmission is lateral-meaning animal to animal, and maternal transmission MAY also occur.
Incubation period- unknown
youngest wild animal 17 months who received CWD Alimentary tract shedding
TSE agents extremely resistant in environment
Captivity or artificial feeding may increase likelihood of transmission
: epizootiology in free ranging cervids
clinical signs of CWD are?
Loss of body condition and change in behavior
May increase or decrease interactions with other members of the herd or a handler Repetitive behaviors
in set patterns
Somnolence- drowsiness or depression, are easily roused
Carry head and ears lowered
Continue to eat, but reduced amounts
Gradual loss of body condition
May display polydipsia- means in increase in drinking, and polyuria- means increased or frequent urination
Increased salivation may result in slobbering or drooling
In-coordination particularly posterior ataxia- means hind end in-coordination
Fine head tremors Esophageal dilation- means the esophagus becomes more dilated,
hyper excitability and syncope- means fainting which is rarely seen.
Death is inevitable Clinical course a few days to a year
Most animals a few weeks to 3 or 4 months
Probably shorter in free ranging cervids
In captive herds, death from aspiration pneumonia common misdiagnosed easily
what is the pathology in CWD?
Gross lesions non-specific
Carcass may be in poor nutritional or emaciated state
Can be in fair condition if died of aspiration pneumonia or had a short lived clinical course Rumen- largest chamber in the
4 chambered stomach, rumen contents contain excessive water in those animals displaying polydipsia, sometimes contents appear frothy Sand and gravel abundant in fore-stomachs
Lesions in the brain (more specific way to tell disease)
Spongiform changes (more specific way to tell disease)
what is the diagnosis for CWD?
Examination of the brain for spongiform lesions and/or accumulation of prions
Most important section of brain to examine is the obex
Submit the whole head or brain
Recently biopsy tonsil tissues in live deer doesn't work for elk
control and treatment for CWD are?
There is NO known control or treatment
Considered 100% fatal once clinical signs develop
Control is extremely difficult because so much is unknown about disease
Long term surveillance of populations is important to determine distribution
Translocation and artificial feeding in endemic areas has been banned
Population control is being considered in areas of high CWD prevalence
public health concerns for CWD?
No cases of human disease have been associated with CWD
There is a long history of human contact with scrapie, with no known effects
In endemic areas, hunters should be careful, don't take sick looking animals
Wear rubber gloves when dressing the animal
Discard brain, spinal cord, lymph nodes, spleen, tonsils and eyes
Remove the bones from the meat
what caused the sylvatic plague?
Yersinia pestis, is a bacterial disease transmitted by fleas that afflicts many mammalian species, including humans
introduced into N. America in early 1900's
species affected by the slvatic plague?
Most-species little or no immunity - succumb quickly to the disease
Prairie dogs particularly susceptible - suffer high mortality rates (90% or more) during outbreaks,
often resulting in local or even regional extinctions
Black-footed ferrets also highly susceptible, contracting the disease by ingestion of infected prey or via infected flea- bite
distribution of the sylvatic plague?
Plague now throughout the western states
Newly discovered in the Conata Basin, South Dakota, in May 2008
how to control the sylvatic plague?
Vaccination of ferrets against plague successful
All captive born ferrets vaccinated before release
Wild animals as well, but difficult - $, time, capturing, handling, etc.
Ultimately must protect prairie dogs
Dusting individual prairie dog burrows with pesticides that kill plague - infected fleas
Plague vaccine for prairie dogs delivered by oral bait
Work in progress - develop bait for delivering vaccine to prairie dogs that can be dispersed from a
plane or vehicle
This is the first time the vaccine has been used during a major plague epizootic
Strategies to control the outbreak include applying insecticide to over 300,000 burrows to reduce
the flea populations in prairie dog colonies that support black-footed ferrets, but that have not yet experienced plague die-offs
what is pododermatitis or bumble foot?
Inflammatory condition of the feet
Local abrasion to the foot pad
Ulceration and swelling and erythema (flushed or pink looking) of one or more of the digital or metatarsal pads
what are the predisposing factors of bumble foot?
Trauma (self-inflicted talon puncture, bite wounds or fighting)
Inappropriate perch size or substrate
Poor environmental hygiene
clinical signs of bumble foot?
Infectious/inflammatory disease which may involve skin, underlying soft tissues, and even bone
Swelling, inflammation and pain are the hallmark of pod dermatitis
Clinically the raptor will favor one leg over the other
Lay down in sternal recumbence (lying down on its belly and sit with their head up) if the pain is severe
how to treat bumblefoot?
Reduce swelling and inflammation
Surgically removing dying tissue
Draining and removing abscesses
Identifying and eliminating the underlying cause (pathogens and husbandry (properly taking care of)
Protecting the wound Antibiotics
What is West Nile Virus?
Flavivirus (family Flaviviridae)
Many species of birds can be infected and affected with WNV
American crow and other corvids commonly suffer high morbidity and mortality
Transmission of WNV occurs primarily through C. Pipiens (common house mosquito)
Ingestion of infected prey species (house sparrows and pigeons) may also serve as a means of
acquiring the WNV
what are the clinical signs involved with West Nile?
Clinical signs are variable
Sometimes dependent upon the age of the raptor
Signs ranging from
: slight depression and weight loss
: marked depression
seizures sudden death
what are the 3 phases of West Nile?
Phase 1: depression, anorexia, weight loss sleeping, elevated white cell count
: In addition to the above, head tremors, green urates (more green in waste product), mental
dullness/central blindness, general lack of awareness of
surroundings,ataxia, weakness in the legs
: more severe tremors
what is the diagnosis for West Nile?
Ante mortem (before death) diagnosis of WNV infection can be difficult
Clinical signs, antibody levels may allow for a more definitive diagnosis
Unfortunately, most cases are confirmed through post-mortem examination
Kidney and brain are good samples to submit for histopathologic evaluation
Most common lesions In raptors include myocarditis (heart inflammation) and encephalitis
(inflammation of the brain)
whats the treatment for West Nile?
There is no specific treatment available for WNV
Treatment is often unrewarding
Preventative measures (vaccinations) involve the use of a vaccine available for equids
There is no definitive data
evaluating the long term efficacy of this vaccine in birds