Exam 4 - Biotoxins & Mycotoxins Flashcards
How does botulism occur
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
what does botulism cause
limber neck in waterfowl
shaker foal syndrome in foals
flaccid paralysis
LMN paresis with parasympathetics signs appears in dogs
What are the best prevention strategies for botulism?
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)
How is tetanus different from botulism?
Neurotoxin tetanospasmin produced by Clostridium tetani prevents the release of inhibitory neurotransmitters like glycine from neurons in the CNS
What clinical signs are indicative of tetanus and in what group of affected animals do they occur?
generalized MSK stiffness may be convulsions
carnivores - “sardonic grin”
horses - “sawhorse stance” w fixed stare, erect ears, “locked jaw”, elevated tail and flared nostrils
What are the best prevention strategies for tetanus?
Vaccination
good husbandry (clean needles and blades for vx, tagging and cx)
What are the general toxicities that can be associated with blue-green algae ingestion?
name specific toxins and MOA
neurotoxicity
- anatoxin-a (depolarized nicotinic membranes)
- anatoxin-a(s) (inhibits AChE)
hepatotoxicity
- microcystin & nodularin (inhibit serine/threonine phosphatases type 1 and 2)
What are the treatments utilized for dogs that ingest blue green algae?
specifically for neurotoxicity, anatoxin-a(s) toxicity, and hepatotoxicity
symptomatic/supportive
GI decontam
dermal decontam
resp & seizure support for neurotox
atropine for anatoxin-a(s) tox
fluids, corticosteroids for hepatotox
Why is blister beetle toxicosis most often observed in horses?
horses fed lush alfalfa
adults beetles baled in hay, crushed, release cantharidin
What does cantharidin cause clinically?
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
What is the mechanism of action of toxins associated with toads?
Bufadienolides are cardiac glycosides – inhibit Na-K ATPase
What species is most likely to be affected by toad toxins? Why?
dogs - curious - mouth or bite the toad and toxin gets absorbed via buccal mucous membranes
clinical signs of toad toxicity
hypersalivation, vomiting, anxiety, neurologic abnormalities
treatment for toad toxicity
oral decontamination
diazepam
cardiac exam
atropine for bradycardia
beta-blockers for tachycardia
insulin/glucose/sodium bicarb for hyperkalemia
eastern tent caterpillars MOA and clinical sign
setae (hair) allow streptococci, actinobacilli and enterococci to invade fetus & placenta
mare reproductive loss syndrome (MRLS) - abortion
fireflies toxicity
lucibufagins - cardiotoxicity
similar to bufodienolides of toads and cardenolides of plants
Why is aflatoxin toxicosis primarily hepatic whereas ochratoxin toxicosis is primarily renal?
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
Why are ruminants relatively immune to ochratoxin-induced toxicosis?
Rumen microbes cleave ochratoxin into a non-toxic form
What toxicities are associated with ergot toxicosis
4 forms:
Cutaneous and gangrenous lesions of the tail and extremities
Hyperthermia and production
Reproductive failure
Convulsive and nervous form
primary MOA of ergot toxicosis
vasoconstriction &
mixed agonist and antagonist activity at tryptaminergic, dopaminergic and 𝛼-adrenergic receptors affecting serotonin (5-HT), dopamine and NE
Why are trichothecenes also referred to as vomitoxin?
Pigs have poor metabolism of doxy-nivalenol (DON) → vomitoxin → vomit & feed refusal
Toxicities of zearalenone are primarily associated with its activity as a weak ______?
what are the clinical signs?
Weak estrogens – bind to receptors for estradiol-17𝛽 → hyperestrogenism & hyperemia, swelling of vulva, mammary glands and uterus, ovarian atrophy
What is the MOA and what are the primary toxicoses associated with fumonisin?
Inhibition of sphinganine & sphingosine N-acyltransferase → equine leukoencephalomalacia (ELEM) & porcine pulmonary edema (PPE)
What is the name of the toxin associated with “slobber syndrome” and why does it cause slobbering?
Slaframine – parasympathomimetic agent that stimulates exocrine and endocrine glands
Why are dogs more likely to have toxicoses associated with penitrm A and roquefortine exposure?
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
what mycotoxin causes the disease syndrome “staggers”
clinical sign seen with this
MOA
tremorgenic mycotoxins
opisthotonus
prolonged depolarization (reduced CNS GABA and glutamate)
what does Oosporein cause
nephrotoxicity in chickens
disease caused by Citrinin & Ochratoxin
porcine mycotoxin nephropathy
what causes “lupinosis” in sheep
Phomopsins
what does Sporidesmin cause and its MOA
accumulation of phylloerythrin (photosensitizer)
facial eczema, pithomycotoxicosis, photodermatitis, hepatotoxicity
