Exam 4 - Biotoxins & Mycotoxins

Question 1

How does botulism occur

Answer 1

Clostridium botulinum toxin is ingested as a preformed toxin or spore or a wound is contaminated with spores

cleaves SNAP-25, synaptobrevin, and syntaxin to block the release of ACh in the presynaptic neuron

Question 2

what does botulism cause

Answer 2

limber neck in waterfowl
shaker foal syndrome in foals
flaccid paralysis
LMN paresis with parasympathetics signs appears in dogs

Question 3

What are the best prevention strategies for botulism?

Answer 3

Vaccination in horses and cattle
proper ensiling of poultry litter
examine feed for evidence of decaying carcasses
rodent control
proper disposal of any dead animals (deep burial)

Question 4

How is tetanus different from botulism?

Answer 4

Neurotoxin tetanospasmin produced by Clostridium tetani prevents the release of inhibitory neurotransmitters like glycine from neurons in the CNS

Question 5

What clinical signs are indicative of tetanus and in what group of affected animals do they occur?

Answer 5

generalized MSK stiffness may be convulsions

carnivores - “sardonic grin”

horses - “sawhorse stance” w fixed stare, erect ears, “locked jaw”, elevated tail and flared nostrils

Question 6

What are the best prevention strategies for tetanus?

Answer 6

Vaccination
good husbandry (clean needles and blades for vx, tagging and cx)

Question 7

What are the general toxicities that can be associated with blue-green algae ingestion?

name specific toxins and MOA

Answer 7

neurotoxicity
- anatoxin-a (depolarized nicotinic membranes)
- anatoxin-a(s) (inhibits AChE)

hepatotoxicity
- microcystin & nodularin (inhibit serine/threonine phosphatases type 1 and 2)

Question 8

What are the treatments utilized for dogs that ingest blue green algae?

specifically for neurotoxicity, anatoxin-a(s) toxicity, and hepatotoxicity

Answer 8

symptomatic/supportive
GI decontam
dermal decontam
resp & seizure support for neurotox
atropine for anatoxin-a(s) tox
fluids, corticosteroids for hepatotox

Question 9

Why is blister beetle toxicosis most often observed in horses?

Answer 9

horses fed lush alfalfa
adults beetles baled in hay, crushed, release cantharidin

Question 10

What does cantharidin cause clinically?

Answer 10

vesicles, ulcers, erosion
depression, discomfort, colic
gross lesions in esophagus, stomach and intestines
classic lesion consist of areas of ulceration or erosion

horses with gastric lesions may submerge their muzzles or play in water

Question 11

What is the mechanism of action of toxins associated with toads?

Answer 11

Bufadienolides are cardiac glycosides – inhibit Na-K ATPase

Question 12

What species is most likely to be affected by toad toxins? Why?

Answer 12

dogs - curious - mouth or bite the toad and toxin gets absorbed via buccal mucous membranes

Question 13

clinical signs of toad toxicity

Answer 13

hypersalivation, vomiting, anxiety, neurologic abnormalities

Question 14

treatment for toad toxicity

Answer 14

oral decontamination
diazepam
cardiac exam
atropine for bradycardia
beta-blockers for tachycardia
insulin/glucose/sodium bicarb for hyperkalemia

Question 15

eastern tent caterpillars MOA and clinical sign

Answer 15

setae (hair) allow streptococci, actinobacilli and enterococci to invade fetus & placenta

mare reproductive loss syndrome (MRLS) - abortion

Question 16

fireflies toxicity

Answer 16

lucibufagins - cardiotoxicity
similar to bufodienolides of toads and cardenolides of plants

Question 17

Why is aflatoxin toxicosis primarily hepatic whereas ochratoxin toxicosis is primarily renal?

Answer 17

Aflatoxins are metabolized to reactive metabolites (epoxide of AB1) and can react with DNA, RNA and proteins → liver disease/hepatic toxicosis

Ochratoxin is a substrate for organic anion transporters in the kidney → high renal accumulation

Question 18

Why are ruminants relatively immune to ochratoxin-induced toxicosis?

Answer 18

Rumen microbes cleave ochratoxin into a non-toxic form

Question 19

What toxicities are associated with ergot toxicosis

Answer 19

4 forms:
Cutaneous and gangrenous lesions of the tail and extremities
Hyperthermia and production
Reproductive failure
Convulsive and nervous form

Question 20

primary MOA of ergot toxicosis

Answer 20

vasoconstriction &
mixed agonist and antagonist activity at tryptaminergic, dopaminergic and 𝛼-adrenergic receptors affecting serotonin (5-HT), dopamine and NE

Question 21

Why are trichothecenes also referred to as vomitoxin?

Answer 21

Pigs have poor metabolism of doxy-nivalenol (DON) → vomitoxin → vomit & feed refusal

Question 22

Toxicities of zearalenone are primarily associated with its activity as a weak ______?

what are the clinical signs?

Answer 22

Weak estrogens – bind to receptors for estradiol-17𝛽 → hyperestrogenism & hyperemia, swelling of vulva, mammary glands and uterus, ovarian atrophy

Question 23

What is the MOA and what are the primary toxicoses associated with fumonisin?

Answer 23

Inhibition of sphinganine & sphingosine N-acyltransferase → equine leukoencephalomalacia (ELEM) & porcine pulmonary edema (PPE)

Question 24

What is the name of the toxin associated with “slobber syndrome” and why does it cause slobbering?

Answer 24

Slaframine – parasympathomimetic agent that stimulates exocrine and endocrine glands

Question 25

Why are dogs more likely to have toxicoses associated with penitrm A and roquefortine exposure?

Answer 25

CNS toxin found in blue cheese, moldy cheese, bread and walnuts – dogs are more likely to go into the garbage where these things are thrown away

Question 26

what mycotoxin causes the disease syndrome “staggers”

clinical sign seen with this

MOA

Answer 26

tremorgenic mycotoxins

opisthotonus

prolonged depolarization (reduced CNS GABA and glutamate)

Question 27

what does Oosporein cause

Answer 27

nephrotoxicity in chickens

Question 28

disease caused by Citrinin & Ochratoxin

Answer 28

porcine mycotoxin nephropathy

Question 29

what causes “lupinosis” in sheep

Answer 29

Phomopsins

Question 30

what does Sporidesmin cause and its MOA

Answer 30

accumulation of phylloerythrin (photosensitizer)
facial eczema, pithomycotoxicosis, photodermatitis, hepatotoxicity