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Toxicology > Unit 3 - Common Toxicants in Wildlife > Flashcards

Unit 3 - Common Toxicants in Wildlife Flashcards

1
Q

A large majority of wildlife poisonings involve _____.

A

Birds

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2
Q

What are the common sources of toxicosis in wildlife species?

A

Non-target species - Rodenticides, insecticides, varmint control

Malicious poisonings of predatory species or homemade pests - OP/Carbamates and methylxanthines

Natural -mycotoxins, cyanotoxins, botulism

Environmentla pollution - metals, chemicals

Mistakes/negligence - barbituates

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3
Q

What are the sub-clinical resulting effects of wildlife toxicosis (general)?

A

Chronic, usually not detected, decreased reproductive capability, +/- death

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4
Q

What diagnostic difficulties are associated with wildlife toxicosis?

A

Detection of incidents is challenging

Rapid disappearance of affected animals - scavenged and predators

Fast and reliable diagnosis is missing

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5
Q

What is the leading cause of wildlife intoxication worldwide?

A

Organophosphates and carbamates

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6
Q

How do organochlorines/chlorinated hydrocarbons act in the environment?

A

They accumulate in fatty tissue and are toxic to wildlife - there are reproductive concerns

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7
Q

Tell me the difference between 1st gen and 2nd gen anticoagulatnts in regards to toxicity level and exposure. Which has a higher potential for relay toxicosis?

A

1st gen: intermediate toxicity, repeated exposure necessary

2nd gen: high toxicity, single dose exposure, strong potential for relay toxicosis

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8
Q

How do anticoagulants get introduced into the environment/ to wildlife?

A

They are used to control feral hogs - scavengers can eat the dead feral hogs

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9
Q

What are the sources of lead toxicosis in the environment?

A

Fishing tackle, lead shot, industrial waste

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10
Q

What is the 1/2 life of lead in the environment?

A

300 years

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11
Q

What species is mainly effected by lead toxicosis?

A

Birds

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12
Q

What clinical effects does lead toxicosis cause in birds?

A

Depression
Ataxia
Weight Loss
Wing Droop
Loss of thermoregulation

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13
Q

What is the source of mercury in the environment that leads to toxicosis cases? How does it act?

A

Methyl mercury - it is a carcinogen that forms in aquatic systems and bioaccumulates

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14
Q

What clinical effects are associated with methyl mercury toxicosis in the environment?

A

Immunosuppression

Embryo toxic

Endocrine disruptor

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15
Q

High concentrations of mercury are found in what animals?

A

Stranded marine mammals

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16
Q

How does selenium become a problem to wildlife?

A

There is bioaccumulation and biomagnification in the food chain

17
Q

What clinical effects are associated with wildlife selenium toxicosis?

A

Embryo toxic - teratogen, ↑ mortalit, ↓ development
↓ growth
Feather loss
Death

18
Q

How do polychlorinated biphenyls act?

A

They are highly lipophilic compounds that are persistent, bio accumulative, and biomagnified

19
Q

What clinical effects are associated with PCB toxicosis?

A

↓ Reproduction
↓ Blood Thyroxine
Negative effects on nesting behavior

20
Q

What do polybrominated diphenyl esters do to birds?

A

Immunosuppressive and decreased reproduction

21
Q

What are perfluorinated compounds commonly found in?

A

Fire retardents

22
Q

What clinical effects do PFCs have?

A

Avian - decreased hatachbility, developmental defects

Human health affects

23
Q

Why is pentobarbital, a euthanasia solution, problematic if found in the wild?

A

It is extremely stable and can be eaten by predators and scavengers

24
Q

What is vital to the prevention of barbituate exposure/toxicosis to our wildlife species?

A

Educate clients - proper carcass disposal and explain legal ramifications

Protect yourself from liabilities too

25
Q

In general, how can wildlife toxicoses be prevented?

A

Mitigation of exposure by risk assessment

Improve detection and diagnostics

Education of clients and general public

Involve naturalists in habitat management

26
Q

What is the main mycotoxin of concern to our wildlife species?

A

Aflatoxin

27
Q

What are the sources of mycotoxin toxicosis to wildlife?

A

High energy grains, corn, peanuts, milo, cotton seed

28
Q

T/F: Wildlife are not susceptible to algal blooms and cyanobacteria because they are frequently exposed to them.

A

False - NO ONE IS SAFE

29
Q

What bacteria is the etiologic agent of botulism?

A

Clostridium botulinum

30
Q

What are the sources of botulism?

A

Ingestion of preformed toxin - dead animal in feed, spoiled silage, rotten vegetation, larvae, bones
Anaerobic wound contamination
Colonization in the GI tract

31
Q

What is the MOA of botulism?

A

Presynaptic neuromuscular blockade
Release of acetylcholine is inhibited resulting in paralysis

32
Q

When is the onset of clinical signs due to botulism?

A

Hours to days after exposure

33
Q

What non-specific clinical signs are associated with botulism?

A

Vomiting
Salivation
Dry eyes
Rear limb weakness
Gagging
Depressed pupillary reflexes
Death (respiratory paralysis)

34
Q

What specific clinical signs are associated with botulism in dogs?

A

Megaesophagus - regurgitation, aspiration
Progressive ascending paralysis, keratoconjunctivitis sica, neuronal degeneration in autonomic ganglia

35
Q

What specific clinical signs are associated with botulism in birds?

A

Progressive ascending paralysis
Paralysis of the neck
Paralysis of the eyelids
Vultures have preexisting Ab

36
Q

What specific clinical signs are associated with botulism in cows and horses?

A

Dysphagia
↓ Tongue & jaw tone
Depression
Mydriasis
Decreased tail tone
GI atony/ colic
Recumbency

37
Q

How is botulism diagnosed?

A

New Bolton Center - National Botulism Reference Lab:
PCR
Samples - stomach/rumen contents, GI contents, feces, suspect forage, dead animals in soil

NVSL (Ames, IA):
Mouse bioassay (toxin typing)
38
Q

How is botulism treated?

A

Remove suspect feedstuffs

Wound cleaning

Antibiotics - penicillin

Antitoxin administration - only good for circulating toxins

39
Q

What antibiotics do you want to avoid using when treating botulism?

A

Toxicology (32 decks)

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