wildlife disease

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klokot
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12311
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wildlife disease
Updated:
2010-03-29 21:16:23
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wildlife disease midterm
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  1. ZOONOTIC
    A disease that is transmitted between wildlife and humans
  2. DISEASE
    Any impairement that interferes or modifies the performance of normal functions
  3. EPIZOOTIC
    An epidemic in wildlife
  4. MORBIDITY
    Refers to an illness or sickness
  5. MORTALITY
    Refers to death
  6. RATE
    Refers to time
  7. WHAT TO LOOK FOR WHEN COMING ACROSS A DISEASE
    • Time & Date
    • Species Affected
    • Age
    • Sex
    • Number of Individuals Affected
  8. ACUTE
    Fast acting
  9. CHRONIC
    Long lasting
  10. PROPER PROTECTION IN THE FIELD
    • Goggles
    • Coveralls
    • Face mask
    • Eye protection
    • Rubber gloves
  11. PROSECTOR
    The person performing the necropsy (AKA pathologist)
  12. POST MORTEM
    After death
  13. PATHOLOGY
    The science dealing with the nature of the disease
  14. PURPOSE OF PERFORMING A NECROPSY
    • To determine the cause of death
    • To find out what normal looks like
    • Collect info.
  15. WHY DO WE MANAGE FOR DISEASE?
    • Because some diseases are zoonotic
    • Some diseases affect domestic animals
    • Some diseases affect other wildlife species
  16. OBJECTIVES FOR MANAGEMENT
    • Prevent
    • Control
    • Eradicate
  17. IMMUNOLOGY
    Science of the immune system and making vaccines to protect against fatal diseases.
  18. IMMUNITY
    Condition of being non-susceptible to a disease causing agent
  19. INNATE RESISTANCE
    humans not susceptible to certain diseases like canine parvo
  20. IMMUNE SYSTEM
    A recognition system that distinguishes between self and non-self
  21. ANTIGEN
    foreign substances that elicits a specific immune response
  22. ANTIBODY
    A protein thats capable of reacting with a specific antigen
  23. PRIMARY IMMUNE RESPONSE
    • Antibodies produced in the blood within 2-4 days
    • By day 4-5 several antibodies in bloodstream & peak by day 14
    • By day 30-40 almost gone from bloodstream
  24. SECONDARY IMMUNE RESPONSE
    • Antibody production is accelerated
    • Antibody synthesis is greater & more produced than the first time
    • Peak level is higher and faster
    • Antibodies disappear less rapidly and can remain in the blood for years
  25. HUMORAL IMMUNITY
    Antibodies in blood plasma and lymph fluids, act on free bacteria
  26. CELL MEDIATED IMMUNITY
    Specialized cells acting on bacteria, viruses that have already been infected with host cells
  27. LYMPHICYTES
    • B cells- secrete antibodies
    • T cells- attach cells
  28. LEAD POSIONING (Pb)
    Intoxication from hazardous levels of lead in the body
  29. ETIOLOGY
    Study of the cause of disease
  30. SOURCES OF LEAD
    • Mining waste
    • Batteries
    • Leaded gasoline
    • Paints
  31. AFFECTED SPECIES OF LEAD POSIONING
    • Waterfowl
    • Upland birds
    • Eagles
    • Swans
    • Loons
    • Pelican
    • Canada Geese
  32. FIELD SIGNS OF LEAD POSIONING
    • Reluctance to fly
    • Run to escape
    • Wing droop
    • Tendency to hide under vegatation
  33. NECROPSY FINDINGS FOR LEAD POSIONING
    • Hatchette Breast
    • Emaciated
    • Impaction in esophagous
    • Gall Bladder filled with bile
  34. ENVIRONMENTAL FACTORS FOR LEAD POSIONING
    • Depth of water
    • Type of underlying soil or mud
    • Species attracted to site
    • Last use of lead shot at site
  35. PRESUMPTIVE DIAGNOSIS
    "best guess" based on clinical signs and lesions
  36. DEFINITIVE DIAGNOSIS
    "based on data" final diagnosis based on pathological and toxicological findings
  37. TREATMENT & CONTROL FOR LEAD POSIONING
    • Metal chelating agents
    • Gastric lavage
    • Endoscopy
    • Surgical removal
  38. CONTROL FOR LEAD POSIONING
    • Invert or cultivate soil
    • Dredge wetlands
    • Excavate shot from shooting ranges
  39. MANAGEMENT FOR LEAD POSIONING
    • Deny use of problem areas
    • Rigorous pickup and disposal of dead birds
  40. HUMAN HEALTH CONSIDERATIONS FOR LEAD POSIONING
    • Flesh from lead posioned birds is edible
    • Lead posioning from flesh is rare
    • Lead eaten can become lodged in appendix causing appendicitis
  41. AFLATOXIN POSIONING
    Toxic compounds produced by fungi (aspergillus flavus, aspergillus parasiticus)
  42. AFLATOXINS FOUND IN?
    • Ground nuts like peanuts
    • Corn
    • Other grains
  43. CONDITIONS FOR GROWTH IN AFLATOXINS
    • Relative humidity greater than 70%
    • Temps above 70 degrees
    • Moisture content greater than 14%
    • Occurs in field and storage
  44. SPECIES AFFECTED IN AFLATOXIN POSIONING
    • Humans
    • Domestic animals
    • Wildlife
    • Birds more susceptible than mammels
    • Ducks, geese and sandhill cranes
  45. FEILD SIGNS AFLATOXIN POSIONING
    • Depression/lethargy
    • Blindness
    • Lack of awareness
    • Inability to fly
    • Tremors and wing flapping
  46. NECROPSY FINDINGS FOR AFLATOXIN POSIONING
    • Enlarged swollen & pale liver
    • Hemorrhages
  47. CONTROL & MANAGEMENT AFLATOXIN POSIONING
    • Do not feed grain with aflatoxin levels greater than 20ppb
    • Deep plowing of grains to make unavailable
    • Haze wildlife from area
  48. REGULATIONS OF AFLATOXINS
    • Milk
    • Meat
    • Grains
  49. SCREENING FOR AFLATOXINS
    • Ultraviolet light used
    • Green & yellow florescense test
  50. SYNONYMS FOR CAPTURE MYOPATHY
    • Excertional myopathy
    • Transport myopathy
    • Degenerative myopathy
    • White muscle disease
  51. MYOGLOBIN
    A protein thats associated with muscle breakdown
  52. ENDEMA
    Build up of fluid (aka: congestion)
  53. CAPTURE MYOPATHY
    • Non-infectious disease of domestic and wild animals
    • Characterized by damage to skeletal and cardiac muscles
  54. SPECIES AFFECTED BY CAPTURE MYOPATHY
    • Occurs in any vertebrate species
    • Most noted in ungulates
    • Long legged birds
    • Raptors
  55. WHEN DOES CAPTURE MYOPATHY OCCUR?
    Occurs in recently immobilized, captured and transported wild animals
  56. FIELD SIGNS FOR CAPTURE MYOPATHY
    • Vary greatly
    • All ages and sexes are susceptible
    • Warm environmental conditions predispose animals
    • Hyperthermia
    • Trouble breathing
    • Weakness/muscle stiffness
    • Hyperacute- very sudden death often occuring
    • Acute- Dead heart muscle occurs in 2-4 days
    • Subacute- kidney failure releases myoglobin
    • Chronic- Die over 2-4 weeks from heart failure or paralysis
  57. MANAGEMENT & PREVENTION FOR CAPTURE MYOPATHY
    Danger & cost to animals should be weighed against scientific or management benefits
  58. THINGS TO CONSIDER FOR CAPTURE MYOPATHY
    • Species
    • Season & Temp
    • Capture Technique
  59. WHEN HANDLING ANIMALS IN CAPTURE MYOPATHY
    • Keep nosie down
    • Cover animal evyes
    • Keep animal from overheating
  60. DRUG THERAPIES FOR CAPTURE MYOPATHY
    • Prevenitive: Antibiotics
    • Balanced electrolyte solution
    • Sodium bicarbonate
    • Selenium preperations

    Treatment: fluids to treat kidney failure and acidosis
  61. AVIAN CHOLERA (#1 DISEASE THREAT IN MIGRATORY WATERFOWL)
    SYNONYMS?
    • Fowl Cholera
    • Avian Pasteurellosis
  62. WHAT IS AVIAN CHOLERA?
    • Highly infectious disease death with 6-12 hrs
    • Disease caused by bacteria: pasteurella multocida
  63. TRANSMISSION OF AVIAN CHOLERA
    • Bird to bird contact
    • Ingestion of contaminated food or water
    • Biting insects
    • Ingestion most common
  64. SPECIES AFFECTED WITH AVIAN CHOLERA
    Most species of birds and mammels can become affected
  65. VIRULENT STRAINS
    Ability of a pathogen to cause disease
  66. DISTRIBUTION OF AVIAN CHOLERA
    • Unreported before 1944
    • Now found throughout the entire US
    • Follow normal movement of birds
  67. SEASONALITY FOR AVIAN CHOLERA
    • Dieoffs occur anytime of the year
    • Outbreaks are predictible in these areas where avian cholera is well established
  68. CLINICAL SIGNS OF AVIAN CHOLERA
    • Birds lethargic & drowsy
    • Approachable
    • Die quickly when captured
    • Convulsions
    • Swim in circles
    • Throw head back between wings & die
    • Flight is eradic
    • Mucous discharge from mouth
  69. PATHOLOGY FOR AVIAN CHOLERA
    • Visceral & subcutaneous fat
    • Various size hemorrahages
    • Small white or yellow spots
    • Thick yellow fluid in digestive tract
  70. DIAGNOSIS IN AVIAN CHOLERA
    • Isolation of bacteria is required
    • Submit entire carcass or if decomposed submit wings
    • Persists for weeks in bone marrow
  71. MANAGEMENT & CONTROL FOR AVIAN CHOLERA
    • Timely submission of carcass important
    • Collect and incinerate carcasses ASAP otherwise fluid escape
  72. HABITAT MANAGEMENT FOR AVIAN CHOLERA
    • Drain
    • Enhance another area
    • Add lots of water to an area to dillute bacteria
    • Scare birds from site with planes
  73. TREATMENT FOR AVIAN CHOLERA
    • There is no practical method of immunizing wild birds
    • Vaccines and post exposure treatment used only for threatened and endangered species
  74. HUMAN HEALTH CONSIDERATIONS FOR AVIAN CHOLERA
    • Infections in people are not common
    • Maybe infected by an animal bite or scratch
    • Avoid exposure to smoke from carcass fires
  75. RESEARCH FOR AVIAN CHOLERA
    • Bacteria doesnt last long enough in the environment to cause major outbreaks
    • Birds are the most likely carriers
    • Ecology of the disease still being studied
  76. AVAIN BOTULISM (#1 THREAT WORLDWIDE)
    SYNONYMS?
    • Limber neck
    • Western duck sickness
    • Duck disease
  77. WHAT IS AVIAN BOTULISM?
    Its a bacterium which produces toxins that lead to paralysis, often fatal disease
  78. WHAT HAPPENS
    IN A BOTULISM OUTBREAK?
    • The bacterium persists in wetland sediments in a spore dorment form
    • Resistent to heat and drying
    • Viable for many seasons-yrs
    • Toxin formed when bacteria germinates and multiplies
  79. CONDITIONS FOR GROWTH IN AVIAN BOTULISM
    • Dead organic material
    • Complete lack of oxygen
    • Optimum Temp of 77 degrees
  80. CONDITIONS LEADING TO TOXIN PRODUCTION IN AVIAN BOTULISM
    • Changes in water depth
    • Fertilization of marshes with sewage or run-off
    • Warm temps dead carcasses attract flies=maggots
  81. SPECIES AFFECTED IN AVIAN BOTULISM
    • Many species of birds and mammals (mink)
    • Water birds suffer greatest loss
    • Vultures are resistant
  82. FIELD SIGNS ASSOCIATED WITH AVIAN BOTULISM
    • Lines of carcasses appearing along waters edge
    • Healthy, sick & dead birds all found together
    • Paralysis of muscles occur
    • Death from drowning is typical
  83. DIAGNOSIS IN AVIAN BOTULISM
    • Presumptive- symtoms in sick birds, no lesions on dead birds
    • Definitive- Mouse test used for toxin, ELISA
  84. MANAGEMENT IN AVIAN BOTULISM
    Remove carcasses and burn them, kills maggots

    • Migratory waterfowl- Avoid re-flooding of dry land in summer, avoid draw downs
    • Shorebirds- drawn down water
  85. TREATMENT IN AVIAN BOTULISM
    • Waterfowl need fresh water and shade
    • Inject with antitoxin
    • Shorebirds few survive even with treatment prevention is better
  86. HUMAN HEALTH CONSIDERATIONS WITH AVIAN BOTULISM
    • Humans are affected with type A or B from improperly canned foods
    • Humans are fairely resistant to type C
    • Thorough cooking destroys botulism in food
  87. AVIAN POX SYNONYMS?
    • Fowl Pox
    • Avian diptheria
    • Contagious epithelioma
    • Poxvirus infection
  88. CAUSE OF AVIAN POX
    • The virus can be mild to severe and is slow developing
    • Some are host specific & Some affect several species
  89. TRANSMISSION OF AVIAN POX
    • By mosquitoes
    • Contact with virus-food & water
    • On contaminated surfaces through abraded skin
  90. SPECIES AFFECTED IN AVIAN POX
    • Waterfowl
    • Upland birds
    • Songbirds
    • Raptors
    • Marine birds
  91. DISTRIBUTION OF AVIAN POX
    • Worldwide
    • Little known in wild birds
    • Conditions that inhibit flies or mosquitoes can influence occurance
  92. SEASONALITY OF AVIAN POX
    • Occurs all seasons of the yr
    • Emergence of vector populations important
  93. FIELD SIGNS WITH AVIAN POX
    Wart like growths on feet, legs, base of beak, eye margin
  94. LESIONS WITH AVIAN POX
    • Cutaneous pox
    • diphtheric or wet pox
  95. DIAGNOSIS OF AVIAN POX
    • Presumotive- appearence
    • Definitive- examination of tissues, isolation of virus, submit whole carcass, keep cool
  96. TREATMENT FOR AVIAN POX
    • Lesions are self limiting
    • Keep proper nutrition
  97. MANAGEMENT & CONTROL WITH AVIAN POX
    • Eliminate vector breeding and resting sites
    • Remove heavily affected birds
    • Decontaminate food, water, perches, clothes etc.
    • Live vaccines in poultry operations
  98. DUCK PLAGUE SYNONYMS?
    Duck virus enteritis, DVE
  99. CAUSE IN DUCK PLAGUE
    is an acute, contagious, & often fatal disease caused by a herpes virus
  100. TRANSMISSION IN DUCK PLAGUE
    • bird to bird contact
    • contaminated environment
    • food or water contaminated by virus in feces
    • inhalation of the virus by splashing of water & from female to egg
  101. SPECIES AFFECTED IN DUCK PLAGUE
    • susceptibility varies greatly among ducks, geese, and swans.
    • Ex- blue-winged teal are most susceptible, pintails are least susceptible
  102. DISTRIBUTION IN DUCK PLAGUE
    • was not detected in the US until 1967
    • Outbreaks of DVE in the US have only been documented in Lake Andes, S. Dakota in 1973 & in the Finger Lakes region of NY in 1993.
  103. SEASONALITY IN DUCK PLAGUE
    can occur at any time of the yr, most common in April, May & June
  104. FIELD SIGNS IN DUCK PLAGUE
    • no prolonged illness
    • sick birds are seldom seen
    • time frame: incubation exposure death captive birds 3-7 days
    • free living up to 14 days
    • Hypersensitivity to light
    • extreme thirst
    • droopy head & wing
    • bloody discharge from vent & bill
    • ulcerative cold sore under tongue in some
    • inability to fly
    • convulsions
    • prolapsed of the penis
    • swimming in circles
  105. LESIONS IN DUCK PLAGUE
    duck plague virus attacks the vascular system, resulting in hemorrhaging and free blood throughout the gastrointestinal tract. Organs affected by hemorrhagic or necrotic bands include: intestine, esophagus, proventriculus (beginning of birds stomach) liver, heart, button like soars on intestinal wall, not all lesions occur in all birds.
  106. DIAGNOSIS IN DUCK PLAGUE
    • Presumptive characteristic lesions
    • Definitive isolation & identification of the virusWhole carcass should be submitted or just the liver- should be frozen
  107. CONTROL MANAGEMENT IN DUCK PLAGUE
    control is difficult because carriers show no signs, sick birds spread virus through fecal material & other oral discharges, this contaminates food & water, and the environment, carcasses also release the virus
  108. LAND MANAGEMENT IN DUCK PLAGUE
    chlorinate water which increases pH, burn soil & litter
  109. ASPERGILLOSIS (FUNGUS THAT GROWS INSIDE THE BODY) SYNONYMS?
    asper, brooder pneumonia (incubation) chicks & ducklings
  110. CAUSE OF ASPERGILLOSIS
    asper is an infection of the respiratory tract, it is caused by fungi in the genus aspergillus, aspergillus fumigatus is the species most commonly involved, inhalation of aspergillus spores
  111. SPECIES AFFECTED WITH ASPERGILLOSIS
    • all birds probably susceptible
    • mammals
    • loons
    • waterfowl
    • raptors
    • penguins
  112. DISTRIBUTION IN ASPERGILLOSIS
    is worldwide
  113. SEASONALITY OF ASPERGILLOSIS
    winter and fall in waterfowl, otherwise anytime
  114. FIELD SIGNS IN ASPERGILLOSIS
    • emaciated
    • severe & progressive difficulty in breathing
    • unthrifty appearance
    • wing droop
    • weakness
    • no escape response
    • if reaches brain: loss of muscular coordination, twisting of head & neck into unnatural position, epizootic aspergillus’s possible
  115. LESIONS IN ASPERGILLOSIS
    • various sized lesions in lungs & air sacs
    • flattened yellow plaques with a cheesy appearance & consistency
    • can have extensive growth of fungus on plaques and tissues.
    • Acute: air sacs usually thickened
    • one striking lesion
    • dark red firm lungs studded with small yellow nodules
  116. DIAGNOSIS OF ASPERGILLOSIS
    characteristic lesions, isolation of fungus
  117. CONTROL IN ASPERGILLOSIS
    sources of spores: moldy feed, dirty brooders & incubators, moldy straw, rotting agricultural waste. Conditions for fungus growth: decomposing organic matter, warm, moist, dark environment. Other sites for growth: fields previously covered by moldy corn silage, moldy waste grain, dusty straw hay, a concern in duck boxes
  118. HUMAN HEALTH WITH ASPERGILLOSIS
    those who should be careful: severe, pre-existing lung damage, cancer, anyone allergic to molds, severe reactions occur

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