Anthrax & Toxins Flashcards

1
Q

what causes anthrax, who is at risk, and when does this disease normally occur?

A

bacillus anthracis
herbivores most at risk
in summer, periods of hot and dry or hot and wet weather

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2
Q

what is the classic presentation of anthrax?

A

blood tinged fluid coming from all orifices and then dies suddenly

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3
Q

you go out to a farm to investiate a cow that suddenly died last night. When you get there, the cow is on the ground, appears bloated, and has blood coming from it’s mouth, ears, nose, and anus. What is your next step?

A

no NOT do a necropsy or cut into the animal and do NOT move the carcass

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4
Q

describe the life cycle of anthrax

A

when a cow with it dies, their tissues are full of bacteria, and if the carcass is opened and exposed to oxygen, these bacteria form indistructible spores. these spores are produced when the bacteria sense an environmental change, they can survive for decades, can be spread by scavengers, and are hydrophobic. Ultimately, the organism survives in the soil for years.

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5
Q

how do we think cows get exposed to anthrax?

A

anything that causes surface soil disturbance like construction or cattle walking into receeding water holes. they ingest the spores and they reactivate in the gut. potent toxins kill the animal within hours.

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6
Q

what is the ideal anthrax environment?

A

likes alkaline soil >6 pH, likes warm temps >15.5, and it likes receding flood waters

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7
Q

how do you diagnose anthrax?

A

do not open the carcass! sample the blood, look at it under the microscope, look for trains or organisms, and do a SNAP test

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8
Q

how are anthrax carcasses disposed of?

A

incineration or deep burial if no other option

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9
Q

when should you suspect a toxicosis?

A

acute illness in group of animals, similar signs of similar severity with all animals, signs appearing after a shared event (such as medication, feed change, or location change)

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10
Q

T or T: if you suspect a toxicosis, you can submit a poison screen test

A

false! there is no such thing

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11
Q

if you suspect a toxicosis, what kinds of samples are useful to collect?

A

feed, bedding, water

serum, whole blood, urine, ocular fluid
liver, kidney, brain, spinal cord, lungs, heart, spleen, intestines, bone

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12
Q

the 3 organs most commonly affected by organs are

A

brain, liver, kidney

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13
Q

name the antidotes for the following toxins:
lead, nitrate, organophosphate, cyanide, botulism/snake bitea

A

lead: EDTA and thiamine
nitrate: methylene blue
organophosphate: atropine
cyanide: sodium thiosulfate
botulism/snake bites: anti-toxin

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14
Q

mechanism of lead toxicity

A

decreased heme synthesis, interfere with GABA, calcium, and Na/K ATPase pumps all leading to altered nerve and muscle transmission

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15
Q

you are presented with a group of calves that are ataxic, teeth grinding, muscle tremors, and appear blind. when you walk the property there is an old car in the pasture. how will you confirm your top differential?

A

lead toxicosis

for a live calf: whole blood EDTA tube to check lead levels

for dead calves: liver, kidney, and brain (fixed and fresh)

feed or suspected source samples

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16
Q

how can you treat calves showing signs of lead toxicosis?

A

thiamine SQ alone or + Ca-EDTA

rumenotomy to remove lead source

17
Q

who gets copper toxicosis and what is the method of toxicity?

A

sheep get this, usually over supplemented or contaminated feed

sudden release of chronically built up copper causes intravascular hemolysis

18
Q

mechanism of selenium toxicosis?

A

either acute iatrogenic (overdose) or chronic from plants like locoweed, golden weed, etc.

19
Q

clinical signs of selenium toxicosis

A

weak with rapid progression to cardiogenic shock, abdominal pain, pulmonary edema

20
Q

mechanism of nitrate toxicosis

A

either from plants or water–>plants increase their nitrates in times of steess, or when fertilized or herbicides applied. nitrate in the rumen gets converted to nitrite and oxidizes the iron in hemoglobin causing methemoglobinemia=anoxia

21
Q

mechanism of urea/NPN toxicosis

A

excessive supplementation, barn break ins, or contaminated feed/water. urrea gets converted to ammonia in the rumen and it enters the blood and causes neurologic signs

22
Q

what diagnostic sample do you need for urea/NPN toxicosis?

A

ocular fluid FROZEN

23
Q

mechanism of ionophore toxicosis

A

increases sodium and calcium influx, causes lipid peroxidation and muscle necrosis–>exercise intolerance

24
Q

mechanism of salt toxicosis/water deprivation

A

no water–>sodium is pumped into the brain tissues causing CNS edema!

25
Q

mechanism of mycotoxin toxicosis

A

ergotism! causes vasoconstriction=gangrene

26
Q

mechanism of organophosphate toxicosis

A

acetylcholinesterase inhibitors