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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