Exam 4: Feed and Water Contaminants Flashcards
What are the sources of food contaminants? How do they get there?
Glossypol, Ionophores, Sulfur, Ammoniation of feed, Nonprotein Nitrogen. It is added or can occur naturally.
Why is melamine relatively non-toxic when given as a single agent but shows toxicity when combined with cyanuric acid?
The structure has a lot of nitrogen so made it look like it was high in protein when it was just a filler… when combined with cyanuric acid, creates crystalline lattices in the kidneys and can cause renal failure (and stone formation).
What major subclass of ionophore is used as a food additive?
There are two major subclasses: neutral and carboxylic. There are seven corboxylic ionophores approved for control of coccidosis and promotion of growth and feed efficiency in several animals of economic importance.
What is the proposed mechanism of action associated with ionophore toxicosis and what are the primary clinical signs?
safe in appropriate species and dose. the MOA transport ions across biologic membranes leading to net cellular imbalance (of sodium, potassium, calcium, hydrogen) and loss of ATP production in mitochondria.
clinical signs are: feed refusal/decreased intake, weakness/ataxia/incoordination, tachycardia/hypotension, dyspnea/hyperpnea, recumbency/death.
cardiac lesions in cow hearts.
What treatment options are available for ionophore toxicosis?
GI decontamination, vitamin e and selenium, supportive care
What are the primary organ systems and processes affected by gossypol?
heart, liver, kidney, muscles, and testes
What animals are more or less susceptible to gossypol poisoning and why?
ruminants are less susceptible because gossypol binds to proteins in the urine.
What form of sulfur is responsible for the toxicosis and where does it come from?
sulfur toxicosis develops due to the overproduction of sulfide. sulfur intake in monogastrics is via amino acids and vitamins.
What is the primary toxicosis associated with sulfur exposure in ruminants?
sulfur toxicosis develops due to the overproduction of sulfide by ruminal microflora and the primary manifestation is polioencephalomalacia (PEM)
Why is feed ammoniated and what type of feed poses the biggest danger from ammoniation?
Ammoniation of low-quality feed substantially improves the nutrient characteristics of these roughages.
What product of ammoniation is thought to be responsible for toxicosis and when is it formed?
pyridines and imidazoles are formed by maillard reaction when high quality forages with more reducing sugar content are ammoniated.
Why are nursing calves and lambs susceptible to toxicosis associated with ammoniated feed?
4-mel is a potent convulsant but a mixture of imidazoles probably play a role due to low levels of 4-mel in milk and the ability of the syndrome to be passed on to nursing calves or lambs. They may be more sensitive or receiving a higher dose.
How is NPN processed in the rumen and what is the toxic component that is generated? What role does pH play in this process?
NPN increased NH3. Rumen pH increases. Increased NH3 transit to liver. Ability for liver to convert NH3 to urea is saturated. Excess NH3 enters the circulation leading to toxicosis.
What role does the liver play in NPN toxicosis?
Can’t convert NH3 to urea if saturated and pushes excess NH3 into circulation.
What risk factors are associated with potential NPN toxicosis?
lack of acclimation of individual to urea
increasing the alkalinity of the rumen
rations high in roughage and low in carbs
animals with poor BCS
poorly mixed rations
unrestricted acces to palatable supplements
