Wildlife Diseases
Are you prepared to be grossed out?
Disease:
Any departure from health
Classification
•
•
•
•
•
•
•
Infectious
Parasitic
Toxic
Physiological
Nutritional
Congenital
Degenerative
Infectious
Caused by pathogens
• Bacteria
• Viruses
• Rikettsiasa
• Parasites
• Fungi
Bacterial Diseases
Avian Botulism
Clostridium botulinum, an anaerobic bacterium
Major Botulism Outbreaks in N.A.
Avian Botulism
1. Inability to fly—’steaming’
2. Paralyzed nictitating membrane
3. Paralysis of neck muscles; can’t
hold head erect; drowning
Rickettsia
• Bacterial, intracellular parasites
• All transmitted by arthropod vectors
• Humans are accidental/incidental hosts
Rickettsiae
Disease
Organism
Vector
Reservoir
Rocky Mountain
spotted fever
Rickettsia rickettsii
Ehrlichiosis
Ehrlichia chaffeensis
E. erwingii
Tick
Anaplasma
phagocytophilium
Deer
Deer
Small mammals
Rickettsialpox
R. akari
Mite
Mites, wild rodents
Scrub typhus
R. tsutsugamushi
Mite
Mites, wild rodents
Epidemic typhus
R. Prowazekii
Louse
Murine typhus
R. typhi
Flea
Wild rodents
Q fever
Coxiella Burnetii
None
Cattle, sheep,
goats, cats
Tick
Ticks, wild rodents
Humans, squirrel
fleas, flying
squirrels
Rocky Mountain Spotted Fever
American dog tick
(Dermacentor
variabilis)
Rocky Mountain Spotted Fever
•Most common rickettsial disease in US
•Principal reservoir is a hard tick
•Most cases April-September
•Inactive rickettsia are warmed by
blood meal, get into saliva; hence,
prolonged bite increases transmission
likelihood
•Wild rodents infected, but not main
reservoir host
The ‘spots’
•Symptoms: abrupt onset of fever,
chills headache and myalgia usually 212 days after the bite
•Mortality rate in untreated patients is
20%
Parasitic Diseases
Parasitic Life Cycles
• Several different kinds of hosts
– Definitive
– Intermediate
• Reservoir
• Dead end
• May be endo- or ectoparasites
Ichthyophthirius
A ciliated protozoan
Black Spot/Black Grub
•complex life cycle requires fish-eating birds or mammals,
snails, and fish at different stages
•encysted larval stage of one of several flukes
•even heavy infestation do relatively little damage unless on
gills, eyes, or very young fish
Botfly life cycle
Tapeworm
Taenia pisiformis
Taenia pisiformis
Cysticercosis
• In rabbits, appears as conspicuous spots on the liver (sometimes
confused with tularemia)
• Dogs and related carnivores are host to the adult tapeworm.
• Eggs are passed out of the body in the feces.
• Rabbits are the major intermediate host; become infected when the
eat vegetation contaminated with the eggs.
• In digestive tract eggs develop into tiny free-moving parasites that
penetrate the gut wall and enter the blood stream where they are
carried to the liver. After traveling through the liver tissue for a
number of days, they break through the liver wall and enter the
abdominal cavity. There they attach to the surface of various
abdominal organs and complete development into cysts.
• The cyst stage is as far as these tapeworms develop in rabbits. If
eaten by a dog or other suitable carnivore, the tapeworms will then
continue their development to maturity.
Sarcoptic
Mange
Sarcoptes scabiei
•mite parasites of
squirrels, rabbits, foxes,
dogs, humans, and many
other mammals
•larvae and adult mites eat
skin cells from their hosts
•mate on the surface of
the host's skin
•cause allergic reaction
w/intense itching and often
bald spots
•often leads to secondary
infections
Deer Liver Fluke
Fascioloides magna
•Often fatal in sheep
•In cervids, are encapsulated,
thus restricting migration
•Usually fairly well tolerated in
deer
Whirling Disease
•
•
•
•
introduced from Europe
serious problem in hatcheries
pathogen is Myxobolus cerebralis, a metazoan parasite
penetrates the head and spinal cartilage of fingerling
trout where it multiplies very rapidly, putting pressure on
the organ of equilibrium
• causes the fish to swim erratically (whirl), and have
difficulty feeding and avoiding predators
Gapeworm
Syngamus trachea
•Inhabit trachea of wild and domesticated birds
•Infection can be direct (eggs or larvae) or by eating a
host (earthworms, snails, slugs, flies)
•Not a problem of confined birds, but can be serious in
free ranging birds (so much for free range chicken!)
Male and female
gapeworms entwined in
tracheal lumen
Toxic Substances
• Pesticides
– Chlorinated hydrocarbons a.k.a. organochlorines
• Lipophilic, attack CNS, persistent, mobile, biomagnify; some may mimic
action of sex hormones
• Examples: DDT (banned), aldrin, dieldrin, endrin, chlordane, heptachlor,
toxaphene (banned)
– Organophosphates
• Less persistent than organochlorines
• Associated with secondary poisoning, e.g., hawks die after eating poisoned
grasshoppers (the target species)
• Examples: malathion, parathion; inhibit acetylcholinesterase
– Carbamates
• Less persistent, hence less biomagnification; also inhibit Ach-ase
• Example: Fenoxycarb-inhibits insect metamorphosis; Temic. Sevin. Furadan
– Bacillus thuringiensis (Bt)-not toxic to animals, but may affect their prey,
e.g. silkworm moths and Whip-poor-wills
Toxic Substances
• Herbicides
– Of course, animals are non-target species;
may have direct toxicity or indirect effects
such as defoliation
– Examples:
• Trifluralin (mallards)
• 2, 4-5 T-little effect on mallards
• Paraquat-very significant effects
Mercury Poisoning
• used in the past as the active ingredient in ointments, parasiticidals,
antiseptics, disinfectants, diuretics and fungicides
• A current major source is coal-burning power plant emissions
• accumulates in fish and fish-eating animals. Inorganic mercury
which enters a water source is readily converted to methyl mercury
by aquatic microorganisms and accumulates in the tissues of fish.
The common loon, mink and otter have been poisoned by mercury
as a result of ingestion of mercury contaminated fish.
• reported to cause abnormal egg laying behavior, impaired
reproduction, slowed duckling growth, and altered duckling behavior
in mallard ducks. Occasionally seed eating birds are affected by
mercury toxicity after feeding on mercury fungicide treated seed.
Lead Poisoning
•
•
•
•
•
•
•
•
Today is the result of ingestion of spent lead shot or
fishing sinkers and jig heads during normal feeding
activities.
When the lead reaches the acidic environment of the
gizzard (ducks, geese and swans) or the ventriculus
(loons), it is worn down, dissolved, and absorbed into
body tissues.
Also been noted in small mammals (raccoon) and
raptors, presumably from the ingestion of lead
contaminated prey.
Once the lead reaches toxic levels in the tissues, muscle
paralysis and associated complications result in death.
Mimics the movement of calcium.
Signs include lowered food intake, weakness, weight
loss, drooping wings, inability to fly, and green watery
diarrhea.
mortality directly due to lead poisoning may be
secondary to the losses due to "non-lethal" effects of
lead such as reproductive problems, increased
susceptibility to disease and infection, and increased
predation due to anemia and weakened muscles.
The switch from lead to non-toxic shot has significantly
reduced the number of birds dying from lead poisoning in
the U.S.
Others of Interest
• Brucellosis in bison
• Epizootic hemorrhagic disease
• Tuberculosis
“New” Diseases
•
•
•
•
Conjunctivitis
West Nile Virus
Lyme Disease
Spongiform encephalopathies
– Mad Cow Disease
– Chronic Wasting Disease
Transmission to Humans
•
•
•
•
Lyme Disease
Sylvatic (bubonic) Plague
Tularemia
Rabies