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
In general, how can wildlife toxicoses be prevented?
Mitigation of exposure by risk assessment Improve detection and diagnostics Education of clients and general public Involve naturalists in habitat management
26
What is the main mycotoxin of concern to our wildlife species?
Aflatoxin
27
What are the sources of mycotoxin toxicosis to wildlife?
High energy grains, **corn, peanuts**, milo, cotton seed
28
T/F: Wildlife are not susceptible to algal blooms and cyanobacteria because they are frequently exposed to them.
False - NO ONE IS SAFE
29
What bacteria is the etiologic agent of botulism?
Clostridium botulinum
30
What are the sources of botulism?
Ingestion of preformed toxin - dead animal in feed, spoiled silage, rotten vegetation, larvae, bones Anaerobic wound contamination Colonization in the GI tract
31
What is the MOA of botulism?
Presynaptic neuromuscular blockade **Release of acetylcholine is inhibited resulting in paralysis**
32
When is the onset of clinical signs due to botulism?
Hours to days after exposure
33
What non-specific clinical signs are associated with botulism?
Vomiting Salivation Dry eyes Rear limb weakness Gagging Depressed pupillary reflexes Death (respiratory paralysis)
34
What specific clinical signs are associated with botulism in dogs?
Megaesophagus - regurgitation, aspiration Progressive ascending paralysis, keratoconjunctivitis sica, neuronal degeneration in autonomic ganglia
35
What specific clinical signs are associated with botulism in birds?
Progressive ascending paralysis Paralysis of the neck Paralysis of the eyelids Vultures have preexisting Ab
36
What specific clinical signs are associated with botulism in cows and horses?
Dysphagia **↓ Tongue & jaw tone** Depression Mydriasis **Decreased tail tone** GI atony/ colic **Recumbency**
37
How is botulism diagnosed?
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
How is botulism treated?
Remove suspect feedstuffs Wound cleaning Antibiotics - penicillin Antitoxin administration - only good for circulating toxins
39
What antibiotics do you want to avoid using when treating botulism?