Exam 4: Feed and Water Contaminants Flashcards
What are the sources of food contaminants? How do they get there?
Melamine - added to falsely increase protein content
Ionophores - control of coccidiosis, growth promotion (mixing errors/wrong species major cause)
Gossypol - cottonseed fed to livestock as high protein source
Sulfur - essential nutrient
Ammonia - increase roughage digestibility, intake, protein content
Why is melamine relatively non-toxic when given as a single agent but shows toxicity when combined with cyanuric acid?
Bacterial enzymes can convert melamine to cyanuric acid and bacterial GI can do this –> may be nontoxic due to low concentrations or specific animal microbiota
When combined with cyanuric acid, melamine forms a crystalline lattice under acidic conditions leading to renal toxicosis and renal failure
What major subclass of ionophore is used as a food additive?
Carboxylic Ionophores
What is the proposed mechanism of action associated with ionophore toxicosis?
Transport of ions across biologic membranes leading to net cellular imbalance (sodium, potassium, calcium, hydrogen)
Loss of ATP production in mitochondria –> uncoupling of ox phos + loss of mitochondrial integrity
What are the primary clinical signs of ionophore toxicosis?
Feed refusal/decreased intake
Weakness, ataxia, incoordination
Tachycardia, hypotension
Dyspnea, hyperpnea
Recumbency, death
cellular and subcellular ion imbalalnces causing deficits in the function of excitable tissues - neurologic, musculoskeletal, cardia, smooth muscle
What treatment options are available for ionophore toxicosis?
No antidote
GI decontamination w recent ingestions - emesis, activated charcoal, cathartic
Vit E or selenium - antioxidants
Supportive care - fluids, quiet, nutritional support
Only give ionophores to species they are formulated for
What are the primary organ systems and processes affected by gossypol?
Heart, liver, kidney, muscles, testes
Accumulates in these tissues
Little/no excreted in milk
What animals are more or less susceptible to gossypol poisoning and why?
Binds to proteins in the rumen - so ruminants more resistant to toxicity than monogastrics
Young ruminants are more susceptible than adults
What form of sulfur is responsible for the toxicosis and where does it come from?
Sulfur toxicosis develops due to overproduction of sulfide H2S by ruminal microflora
Caused by rumen metabolism
What is the primary toxicosis associated with sulfur exposure in ruminants?
Polioencephalomalacia (PEM)
Excess dietary sulfur may contribute to copper deficiency
Why is feed ammoniated and what type of feed poses the biggest danger from ammoniation?
Increases roughage digestibility, increases roughage intake, increases crude protein intake, allows storage of higher moisture roughage by inhibiting mold development
Biggest danger = higher quality forages, with more reducing sugar content
What product of ammoniation is thought to be responsible for toxicosis and when is it formed?
Pyridines and imidazoles formed by the Maillard reaction are found in toxic hay
Rxn caused by the condensation of an amino acid group with a reducing sugar –> occurs more frequently when higher quality forages, with more reducing sugar content, are ammoniated
Why are nursing calves and lambs susceptible to toxicosis associated with ammoniated feed?
Low levels of 4-mel in milk, so ammoniated feed syndrome can be passed on to nursing calves or lambs through milk
More sensitive + higher dose
How is NPN processed in the rumen?
Excess NPN increases NH3 –> increased rumen pH –> increased NH3 transit to liver –> ability of liver to convert NH3 to urea is saturated –> excess NH3 enters the systemic circulation leading to toxicosis
What is the toxic component that is generated with NPN? What role does pH play in this process?
Ammonia
Leads to alkalinization of rumen and systemic ammonia goes to brain - urea cycle saturated
