Exam 4: Biotoxins, Mycotoxins Flashcards
Why is aflatoxin toxicosis primarily hepatic whereas ochraotixn toxicosis is primarily renal?
aflatoxins are readily absorbed in the small intestine an the toxicity of Aflatoxins are due to metabolism to reactive metabolites that react with cellular macromolecules. ochratoxins are excreted in bile and reabsorbed (eneterohepatic recycling) and the substrate formed for organic anion transporters in the kidney contribute to relatively high renal concentrations.
Why are ruminants relatively immune to ochratoxin-induced toxicosis?
ruminal microorganisms ability to detoxify ochratoxin
What toxicities are associated with ergot toxicosis and via what primary mechanism of action?
cutaneous and gangrenous lesions of the tail and extremities
hyperthermia and production loss
reproductive failure
convulsive or nervous form
Complex pharmacological action that involves agonist and antagonist activity at tryptaminergic, dopaminergic and α-adrenergic receptors.
Serotonin (5-HT)
Dopamine
Norepinephrine
Why are trichothecenes also referred to as vomitoxin?
Poor metabolism of deoxy-nivalenol (DON, vomitoxin) in pigs accounts for their relative sensitivity to the effects of these toxins.
Toxicities of zearalenone are primarily associated with its activity as a weak ______?
estrogen
What are the primary toxicoses associated with fumonisin?
equine leukoencephalomalacia (ELEM) and as porcine pulmonary edema (PPE)
What is the name of the toxin associated with “slobber syndrome” and why does it cause slobbering?
slaframine
The ketoimine metabolite acts as a parasympathomimetic agent to stimulate exocrine and endocrine glands.
Atropine can block activity by pre-administration but does not reverse response once initiated.
Why are dogs more likely to have toxicoses associated with penitrm A and roquefortine exposure?
They like to eat out o the trash and get into things like moldy cheese.
How does botulism occur and what does it cause?
Causes flaccid paralysis and occurs when there is an anaerobic overgrowth of spores producing toxin is ingested (the spores or toxin) and when theres is contamination of the wound with spores. Acetylcholine release is blocked in the presynaptic neuron.
What are the best prevention strategies for botulism?
There’s a vaccine for cows. As for prevention, check your silage.
How is tetanus different from botulism?
Tetanus is known as lock jaw, instead of it being flaccid paralysis, it is rigid.
What clinical signs are indicative of tetanus and in what group of affected animals do they occur?
musculoskeletal stiffness, nictitating membrane is elevated and may have abnormal blinking response, contraction of the muscle of the lips (sardonic grin), sawhorse stance, convulsions, death…
Animals at greater risk include those that have had recent field surgeries, castrations, shearing, or retained placentas.
Horses and ruminants are more susceptible to tetanus that are cats and dogs.
It has been suggested that this is due to differences in the gangliosides on the neurons and thus entry of the toxin into neurons.
What are the best prevention strategies for tetanus?
Vaccination, husbandry practices
What are the general toxicities that can be associated with blue-green algae ingestion?
What are the treatments utilized for dogs that ingest blue green algae?
None. Supportive care for sludge and prevention.
