Wildlife Disease 2

  1. What is wildlife rehabilitation?
    It involvies caring for injured, ill and orphaned wild animals with the goal of releasing each into its natural habitat
  2. Wildlife rehabilitation is also used for?
    • research
    • captive propagation
    • reintroduction projects
  3. What else are wildlife rehabilitators involved in?
    • public education
    • biological and ecological concepts
    • writing new laws
    • enforecement
    • population management
    • habitat preservation
  4. 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
  5. 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
  6. What are the synonyms for rabies?
    • hydrophobia
    • rage
    • rabia
  7. What is the history of rabies?
    rabies is one of the oldest recorded infectious dieseases
  8. What is the etiology of rabies?
    acute, infectious disease of the central nervous system
  9. rabies is caused by?
    a virus that generally persists in nature as a salivary gland infection of carnivorous animals
  10. Hosts of rabies?
    • reservoir hosts: 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.
  11. 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.
  12. transmission of rabies?
    • contamination of a bite wound, virus in biting animals saliva, also from ingestion
    • mucosal contact, aerosol of urine from infected bats.
  13. 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
  14. what are the 4 possible stages of rabies an animal goes through?
    • Asymptomatic: NO symtoms
    • Prodromal: early signs are subtle, animal acts strange
    • Furious: Very aggressive (the saliva contains the greatest amount of the virus)
    • Dumb: in-coordination, tremors, convulsions, loss of the swallowing reflex, paralysis, death
  15. clinical course of rabies?
    in animals 2-10 days, in humans 2-8 days
  16. 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
    • kidneys
    • bladder
    • ovaries or testes

    once symtoms occur almost always fatal!
  17. Pathology of rabies?
    • NO gross lesions seen at necropsy
    • some inflammation of the CNS
    • damage to parts of the brain
  18. 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)
  19. 3 types of lab tests used for rabies?
    • Direct microscopic method (histology)
    • Fluorescent rabies antibody method (FRA)
    • Mouse inoculation method
  20. What are the human anti-rabies treatment?
    • Local wound treatment (washing with soap and water)
    • Rabies immune globulin (human origin)
    • Vaccination
  21. 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
  22. Managment and Control of rabies?
    • controlled through vaccination in domestic animals
    • reduction of stray animals
    • rabies education
    • wildlife more difficult: population control and oral vaccinaions with use of bait
  23. Transmission of rabies to humans?
    • bite wounds
    • contamination of mucous membranes
    • aerosol transmission
    • corneal transplants
  24. Incubation of rabies in humans?
    days to years
  25. symtoms of rabies in humans?
    • flu like signs
    • hydrophobia
    • discomfort or tingeling at site of exposure
    • cerebral dysfunction
    • hyper salivation
  26. Diagnosis of rabies in humans?
    • virus detection in saliva
    • antibody tests on serum and spinal fluid
    • antigen detection in skin biopsy
  27. Treatement of rabies in humans?
    • wound care
    • post-exposure prophylaxis
  28. what are the synonyms of hemorrhagic disease?
    • blue tongue
    • epizootic hemorrhagic disease
    • sore muzzle
    • hemorrhagic septicemia
  29. 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
  30. 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
  31. 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
  32. species affected with BLU?
    • Big horn sheep
    • elk
    • white-tailed deer
    • pronghorn
    • mule deer
  33. species affected with EHD?
    • mule deer
    • pronghorn
    • elk
  34. 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
  35. field signs of hemorrhagic disease?
    • sudden onset of disease
    • pyrexia (fever)
    • loss of appetite
    • loss of wariness
    • edema of head and neck
    • dehydration
    • progressive weakness
    • increased respiration
    • 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
  36. 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
    • body cavity)
    • There is a widespread interference with normal blood circulation and leukopenia (decrease
    • in white blood cells)
  37. 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
  38. how to diagnosis hemorrhagic disease?
    • Clinical signs
    • Lesions
    • 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
  39. 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
  40. 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
    • -Scrapie: domestic sheep and goats
    • -Transmissible mink encephalopathy (TME)
    • -In humans: Creutzfeldt-Jakob disease, Gerstmann-Straussler-Scheinker syndrome and Kuru
  41. 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
  42. species affected by CWD?
    • Only 3 species of Cervidae are known to be naturally susceptible
    • mule deer
    • white-tailed deer
    • rocky mountain elk
  43. transmission and study of CWD in populations?
    • Mode of transmission: unknown
    • 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
    • (digestive tract)
    • TSE agents extremely resistant in environment
    • Captivity or artificial feeding may increase likelihood of transmission
    • Many unknowns: epizootiology in free ranging cervids
  44. 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: walking
    • 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
  45. 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)
  46. 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
  47. 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
  48. 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
  49. 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
  50. 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
  51. distribution of the sylvatic plague?
    • Plague now throughout the western states
    • Newly discovered in the Conata Basin, South Dakota, in May 2008
  52. 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
  53. 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
  54. what are the predisposing factors of bumble foot?
    • Trauma (self-inflicted talon puncture, bite wounds or fighting)
    • Inappropriate perch size or substrate
    • Obesity
    • Sedentary lifestyle
    • Poor environmental hygiene
    • Nutritional deficiencies
  55. 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
  56. 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)
    • related etiologies)
    • Protecting the wound Antibiotics
  57. 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
  58. 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
    • To: marked depression
    • anorexia
    • blindness
    • ataxia (in-coordination)
    • head tremors
    • seizures sudden death
  59. what are the 3 phases of West Nile?
    Phase 1: depression, anorexia, weight loss sleeping, elevated white cell count

    • Phase 2: 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

    • Phase 3: more severe tremors
    • and seizures
  60. 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)
  61. 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
Card Set
Wildlife Disease 2
Part 2 of Wildlife Disease Notes