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Species that are most susceptible to nitrate poisoning
Ruminants
Why do plants produce nitrate
Most important nitrogenous nutrient
How do plants uptake nitrate
Constitutively for maintenance with low affinity transport system (LATS) and rapidly during growing phases with high affinity transport system (HATS)
Nitrate transport system that is energy dependent
HATS
How do plants utilize nitrate
Converts it to ammonium via nitrate reductase for protein synthesis
When do plants have a toxic level of nitrate concentration
When they turn off the activity of nitrate reductase. The conversion stops, but uptake doesn’t
When do plants turn off nitrate reductase activity
Stress
Types of plants that tend to accumulate more nitrate
Plants with the genetic potential to grow rapidly
Risk factors for nitrate accumulation
Peak growing season
Presence of nitrate in the soil
Drought
Lack of light
Unseasonal temperatures
How do herbicides contribute to nitrate toxicity risk
They shut down growth and metabolism, and if a plant was sprayed when it had high concentrations it can’t convert the nitrate to ammonia → protein
Common sources of nitrate in water
Fertilizers
Septic tanks
Why are nitrates so dangerous to ruminants
Rumen microbes efficiently convert nitrate to nitrite but less efficiently convert the nitrite to ammonium. The nitrite can build up and get absorbed
Species that are much less susceptible to nitrate toxicity
Monogastrics
Nitrite toxicity mechanism of action
Oxidizes HgB to MgB
Animals that are more susceptible to nitrite toxicity
Animals with a high metabolic rate (swine, late gestation fetuses) tolerate MgB worse
CS associated with acute nitrite toxicity
Hypoxia
Tachypnea
Exercise intolerance
How is nitrite toxicity different from onion toxicity
Onions cause oxidative damage tot he RBCs, nitrite oxidizes the iron, which does not result in hemolysis or renal failure
CS associated with chronic nitrite toxicity
Abortions and decreased production parameters
Specific treatment for nitrite toxicity
Methylene blue
Cons of using methylene blue for nitrite toxicity
It is possibly a carcinogen and is ELDU → be careful in food animals
Postmortem samples that can be submitted for nitrate testing
Serum and aqueous humor in the eye
Purpose of NPN in the ruminant diet
Converted by microbes into MCP
What has to be matched with NPN intake
Quickly available source of CHO
Most common source of NPN
Urea
Mechanism of NPN poisoning
Overwhelming build up of ammonia (NH3) that reacts with water to form NH4OH
How does NH4OH result in poisoning
Can rapidly cause an extremely alkaline rumen environment → damage and necrosis → absorption of NH4OH into the blood → alkalhosis
Species that are susceptible to NPN poisoning
Ruminants and occasionally hindgut fermenters
How long should you take to convert your ruminants to a high NPN diet
2-3 days
CS associated with NPN toxicity
RAPID CNS signs with mild bloat and alkalosis
Best sample to test if you suspect NPN poisoning
Rumen fluid
Which animals should you treat first if you suspect/confirm NPN poisoning
Those that are still unaffected and where treatment is more likely to work
Treatment for NPN poisoning
Vinegar (lower pH)
Cold water (lowers pH)
Formaldehyde (kill microbes)
Prognosis for NPN
Not great, because even if you treat the rumen is damaged and the microbial population is destroyed
Post-mortem lesions associated with bloat
“Bloat line”: gas pressure pushes blood causing cranial congestion and caudal anemia
Risk factors for NPN poisoning
High levels of NPN
Abrupt diet shift
Poor adaptation or CHO matching
Fertilizer contamination
How much of the diet should be NPN
No more than 3% of the diet
How much of dietary nitrogen should be NPN
No more than 1/3
Why is ammonia toxicity a problem
You can increase the quality of low quality feed if you expose it to ammonia gas
Mechanism of ammonia toxicity
Converts sugars and proteins to toxic pyrazines and imidazoles
CS associated with ammonia toxicity
Episodic bouts of crazy behavior
Why are nursing animals more susceptible to ammonia toxicity
The toxic pyrazine and imidazoles are efficiently excreted in milk, which is protective for mom but not for baby
Treatment for ammonia poisoning
Remove feed
± Sedatives
Supportive treatment for any lasting trauma
Syndrome caused by sulfur toxicity
Polioencephalomalacia (PEM)
Damage caused by PEM
Multiple areas of softness in the brain
Supplemental feed that provides an increased risk of sulfur tox
Brewer’s grains
Natural conditions that increase the sulfur content in feed
Geological history of the area and sulfur containing salts
Common sources or sulfur risk
Brewer’s grains
Water contamination
Fertilizer
Ration mixing error
Fish die-offs
How does sulfur exist in the body
Converted to sulfide → H2S
Mechanism of sulfur toxicity
Interferes with E metabolism, interferes with blood flow, and causes oxidative damage
CS associated with sulfur toxicity
Various CNS signs depending on when you catch the poisoning
Apparent blindness
DDx for apparent blindness
Lead and rabies
Clin path abnormalities seen with sulfur toxicity
Metabolic acidosis
Hypokalemia
Hypochloremia
Post mortem lesions seen with sulfur toxicity
Gray/black sulfide deposits
Brain swelling ± brainstem prolapse
Brain necrosis, often in the cerebrum at the junction of the gray and white matter, potentially fluorescent!
Feed sulfur content that is considered a high risk
>0.4%