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109 Cards in this Set
- Front
- Back
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When do GI micro-organisms convert NPN to protein
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-if pH is in an acceptable range (5.5-7)
-digestible carbohydrates are available -time to adapt |
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Why should NPN be used?
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-boosts the protein content of feed
-helps to maintain a more neutral rumen pH with a high-grain diet -improves rumen microbial growth efficiency -improves hindgut fiber digestion |
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Sources of NPN
-which is most common |
-Urea (most common)
-biuret -ammonium sulfate -mono ammonium phosphate |
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Describe the mechanism of converting NPN to protein
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-NPN first converted to ammonia via a first order process
-Ammonia is then converted to protein via a zero order process |
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First order process
-define |
-the more of the substrate that is present, the more of the product that will form
-No top out |
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Zero order process
-define |
-process with a maximum top out of product formation
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How can the rate of conversion of NPN to ammonia be slowed down?
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-low temperature and pH
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Describe what happens when there is excess Ammonia formation from NPN
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-excessive free gas from ammonia causes bloat
-ammonia reacts with water to form ammonium hydroxide (extremely basic and corrosive) -increased rumen pH promotes absorption of ammonium |
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How does an increased rumen pH lead to CNS effects?
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-increased pH promotes ammonium absorption
-physiological ammonium uptake by the urea cycle is overwhelmed -inc. in blood ammonium -CNS effects |
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Animals most susceptible to NPN toxicity
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-adult ruminants
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Animals resistant to NPN toxicity
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-non-fermenting monogastrics
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Animals with a high capacity for NPN
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-hindgut fermenters
-need 3-4x NPN for poisoning |
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What promotes NPN conversion to protein?
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-adequate feeding of microbes (carbohydrate, minerals)
-takes at least 2-3 days -requires consistent NPN feeding (acclimation lost 1-2 days of low NPN) |
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Signs of NPN toxicity
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-First signs: uneasiness, bloat, excessive salivation
-Next signs: muscle tremors, tachypnea, tachycardia, urination, stiffness -Final signs: collapse, lateral prostration, bloat, regurgitation, tetanus-like spasms, convulsions, death |
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Sample to use to diagnose an increased pH from NPN
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-rumen contents
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Effect of Ammonium on blood pH
-progression |
-initial inc. blood pH (alkalosis)
-alkalosis casuses reduced ATP production -cells produce lactate for energy needs -lactate drops blood pH back to normal |
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NPN toxicity treatment
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-treat animals that are still standing (often futile if dose is high and there is already involvement of the nervous system)
Early, aggressive intervention -lots of cold water and vinegar into the rumen -broad spectrum antibiotics into the rumen -.5 L 10% formaldehyde into the rumen -rumenotomy |
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NPN toxicity
-antemortem diagnosis |
-characteristic signs
-history of NPN in the diet -high rumen pH -ammonia smell |
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NPN toxicity
-postmortem diagnosis |
-rumen content assay for ammonia (place in a sealed container and freeze)
-Feed assay for high NPN content -bloat lesions (bloat line) -pulmonary edema and froth/fluid in trachea |
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NPN toxicity
-risk factors |
-high levels of NPN
-abrupt/periodic NPN intake -inadequate feed mixing -poor adaptation -high levels of soluble protein -open feed troughs -poorly maintained fertilizer storage containers |
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How are high levels of soluble protein a risk factor for NPN toxicity?
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-protein gets rapidly hydrolyzed in the rumen and leads to the ammonium burden
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NPN feeding recommendations
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-slowly acclimatize to NPN over 2-3 days (acclimatize again if a day of NPN feeding is skipped)
-feed no more than 3% NPN -NPN should be no more than 1/3 of total feed nitrogen |
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What is the effect of exposing poor quality roughage to high levels of anhydrous ammonia gas?
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-inc. digestibility
-inc. crude protein -inc. palatability |
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What is the effect of exposing high quality material with sugars, or protein blocks with urea and molasses to high levels of anhydrous ammonia gas?
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-amino acids from ammonization react with sugars to form toxic pyrazines and imidazoles
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Effects of toxic pyrazines and imidazoles
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-intermittent abnormal nerve function
-convulsions |
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Ammonization of high grade materials
-clinical effects |
Animals go "bonkers" for brief periods
-spontaneous trembling -rapid blinking -ataxia -apparent blindness -tachypnea -mouth frothing Nursing animals affected through milk but mothers may seem fine |
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Bonkers
-recovery period |
-1-3 days after toxic feed removal
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Bonkers
-diagnosis |
-clinical signs
-history of feeding ammoniated feed -recovery upon feed removal |
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Bonkers
-treatment |
-remove txic feed
-prevent injury (escape proof paddock without sharp objects) -prevent nursing from infected animals -discard milk from affected cows |
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Forms of nitrogen absorbed by plants
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-nitrate
-nitrite, urea, ammonia -gaseous N2 if a nitrogen fixing system is present (legumes with mycorrhizal fungi) |
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Most common way plats take up nitrogen
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-Nitrate
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2 systems that control nitrate uptake in plants
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-constitutive, low affinity transport system (LATS)
-inducible, high affinity transport system (HATS) |
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LATS
-function |
Low affinity transport system
-provide just enough nitrate to the plant for maintenance |
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Nitrate use by plant
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-reduced to ammonium by nitrate reductase
-ammonium incorporated into amino acids and proteins -excess ammonium converted to ammonia and released to air |
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Nitrate Reductase control
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-production suppressed with reduced protein production
-affected by environmental conditions |
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Soil nitrate
-sources |
-soil microbes
-fertilizer and organic matter |
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Risk factors of nitrate accumulation
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-plant species (plants that can grow very fast have best potential for poisoning)
-time of year (shut down nitrogen uptake at end of season) -high soil nitrogen (highly fertilized fields, enclosures that had high animal densities) -environmental conditions that reduce/stop plant growth (drought, shade, unseasonal weather) -contaminated water (fertilizer, septic tank, some soils) -fertilizer spill/inappropriate amount/storage -herbicides |
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What happens to Nitrate in animals?
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Ruminants:
-nitrate reduced to nitrite by rumen microbes (rapid, high capacity process) -nitrite reduced to ammonia and eructated into air (less efficient) -high nitrite production causes it to accumulate and get absorbed Fermenting monogastrics and non-fermenting monogastrics: low nitrate reduction capacity |
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Nitrate salt toxic effects
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-mild irritation
-GI irritation (dominant effect when rumen microbial activity is low) |
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GI irritation
-signs |
-salivation
-colic -diarrhea -vomiting |
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Nitrite toxic effects
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-oxidize hemoglobin to methemoglobin (can overwhelm MetHb reductase capacity)
-inc. MetHb reduces oxygen carrying capacity of blood -fetus and neonates most sensitive -low, level persistent exposure --> impaired Vit A function, endocrine abnormalities |
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Nitrate toxicity
-acute syndrome |
-hypoxia
-weakness, exercise intolerance, tachypnea, collapse, convulsion, death |
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Nitrate toxicity
-subacute and chronic syndromes |
-abortions in 3-7 dyas
-weak calves -dec. milk production -dec. feed conversion rates -inc. susceptibility in feed |
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Nitrate toxicity
-acute treatment |
-remove suspect feed/water source
-methylene blue (repeat if necessary) |
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Nitrate toxicity
-subacute treatment |
-injectable/oral Vit. A, D, E
-Iodized salt -feed high quality protein and abundant carbs |
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Methylene blue
-withdrawal time |
-180 days
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Nitrate toxicity
-postmortem signs |
-brown discoloration (methemoglobinemia) of blood and tissues (takes 2-10 minutes to develop on an opened carcass surface)
-GIT inflammation (non-specific signs) -rumen contains nitrogen-accumulating plants -late term abortions with placental necrosis from hypoxia |
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Nitrate toxicity
-antemortem diagnostic sample |
-serum
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Nitrate toxicity
-postmortem diagnostic sample |
-eyeball or aqueous humor
-high nitrate stability in aqueous humor |
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Nitrate toxicity
-when is the normal level of nitrate concentration highest |
-neonate eye ball
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Feed levels of nitrate that can cause effects
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Nitrate is additive
Based on dry weight - >3,000-5,000 ppm (pregnancy and lactation) - >10,000 ppm (acute poisoning) -levels 10x less in water |
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Nitrate poisoning management
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-test suspected feed before use
-mix high nitrate feed with low nitrate feed -feed high quality protein and abundant carbs -adaptation to moderate nitrate levels (gradual nitrate feed introduction) -propionibacteria (Bovapro) inoculations into rumen 3 wks prior to exposure (not protective with extremely high concentrations) |
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Sulfate
-common in |
-great plains ground water
-feed supplements (molasses) -manure waste |
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Sulfate toxicity
-risk factors |
-water contamination with industrial waste
-naturally high sulfate in drinking water -sulfur-containing fertilizers -excessive use of sulfur in feed additives -algal blooms |
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Reasons sulfur is used in feed additives
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-ammonium sulfate to prevent urinary calculi
-dosing sulfur tonic to horses |
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Sulfate toxicity mechanism
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-converted to sulfite by rumen and cecum microbes
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Sulfide toxicity
-effects |
-blocks neuronal energy metabolism
-interferes with cerebrum blood flow -generates reactive oxygen species -induces poliencephalomalacia |
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Sulfide toxicity
-clinical signs |
-weight loss
-rotten egg smelling breath -diarrhea -rumen stasis -dehydration -tachycardia -blindness -convulsions -death |
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Sulfide toxicity
-signs similar to |
-lead poisoning
-rabies |
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Sulfide toxicity
-treatment |
-no effective treatment for cerebral necrosis
-remove suspected source -corticosteroids, oral fluids, nutrition |
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Sulfide toxicity
-postmortem diagnosis |
-gray/black sulfide deposits in GI tract
-swelling, flattening of cerebral gyri -focal malacia or cavitation in midbrain and thalamus (fluoresce in UV light) -possible cerebral herniation |
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Sulfide toxicity
-diagnose |
-measure sulfur levels in feed and water
-hydrogen sulfide in rumen > 2,000 ppm |
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Sulfide toxicity
-confirmation diagnosis |
-PEM confirmation
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Cotton
-derived protein supplements |
-whole cottonseed
-cottonseed meal and hulls |
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Chemical produced by cotton
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-gossypol
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Why does cotton produce gossypol?
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-protects plant from insect attack
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Where is gossypol found in the cotton plant?
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-lysigenous cavities in all parts of the plant
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Organs effected by gossypol
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-heart
-reproductive system -liver -membrane function |
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Gossypol
-3 toxic effects |
-reactive oxygen species formation
-suppression of cellular redox cycling -DNA scission |
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DNA scission
-definition |
-breakage in DNA strands
-induces cell cycle arrest and apoptosis |
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DNA scission
-cells affects |
-cells that are actively deviding
-suppress sperm production in males -abortion and progesterone suppression in females |
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Gossypol
-where are the most toxic effects |
-heart
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How can gossypol be made less toxic?
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-provide high quality excess protein to the diet for it to bind to in the rumen
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Animals more susceptible to gossypol poisoning
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-young ruminants
-monogastrics |
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Gossypol
-clinical syndromes |
Acute syndrome:
-acute heart failure from exertion or stress Chronic syndrome: -unthrifty, rough haircoat, ascites, edema -death following excitement or exertion |
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Gossypol
-postmortem diagnosis |
-no lesions in rapidly lethal cases
-signs of acute or chronic heart failure (congestion, fluid in body cavities, enlarged heart, nutmeg liver) |
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Gossypol poisoning
-diagnosis |
-acute/chronic heart failure
-postmortem lesions -history of cottonseed based feed |
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Gossypol poisoning
-treatment |
-change feed
-avoid excitement/stress -good nursing care to mildly affected animals |
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Selenium poisoning
-causes |
-ingestion of plants/water with high Se content
-iatrogenic poisoning from excessive supplementation *Essential to the diet |
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Forms of Selenium
-where are they found |
-Selenate (well absorbed by plants in well aerated alkaline soils)
-Selenite (poorly absorbed by plants; acidic soils) -Selenide (uncommon) -Elemental selenium (rare) |
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Key of selenium accumulating plants (obligate, facultative)
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-unpalatable
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Plants responsible for selenium poisoning
-why |
-grasses and grains
-remain palatable -selenium level high enough for poisoning, but not high enough to make unpalatable |
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Selenium toxicity
-mechanism of action |
-non-specific incorporation of Se into proteins in the form of Se-methionine
-mimics sulfur-containing analogue -abnormalities due to sulfur-dependent structural and functional proteins (hooves, skin, hair) |
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Selenium toxicity
-acute syndrome |
-iatrogenic
-progressive weakness, ataxia, dyspniea -vomiting -death in 48 hrs with signs of heart failure |
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Selenium toxicity
-subchronic syndrome |
-pigs fed high selenium diets
-hindlimb ataxia -progressive paralysis -hoof separation -animal remains alert |
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Selenium toxicity
-chronic syndrome |
-requires long term exposure to grains and forages
-weight loss -alopecia -lameness -hoof separation/deformation -immunosuppression -dec. fertility -DJD -anemia |
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Selenium toxicity
-diagnosis |
-Se in diet (> 5 ppm)
-symptoms and lesions -Se in blood (1-4 ppm chronic; >4 acute) -Se in liver and kidney (10-20 ppm chronic; >4 acute) |
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Selenium toxicity
-acute treatment |
-poor prognosis
-supportive treatment -Vit E can possibly reduce free radicals |
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Selenium toxicity
-chronic treatment |
-arsenic may protect proteins from non-specific selenium incorporation
-eliminate source -provide selenium deficient diet with protein and sulfur -therapeutic hoof trimming and special shoes -NSAIDS |
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Selenium toxicity
-prevention |
-avoid Se supplement error
-runoff from seleniferous soil -low protein/sulfur diet will potentiate toxicity -low copper can increase Se deficiency -fence off high Se areas -test forage seasonally |
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Ionophores
-original purpose |
-developed as coccidiostatic antibiotics
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Ionophores
-other uses |
-enhance growth and feed conversion rates
-increase milk production efficiency |
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Most common ionophore
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-Monensin
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Ionophore
-mechanism of action |
-assists transmembrane exchange of Na+, H+, and other ions
-shifts microbial fermentation from acetic and butyric acid production to propionic acid production in the rumen -interferes with transmembrane ion balance in muscle tissue |
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Ionophore
-risk factors |
-exposure to high doses
-repeated exposure -low quality diet -poor body condition -compromised liver condition due to P450 enzyme suppression |
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Ionophore
-most sensitive animal |
-horses
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Ionophore
-most to least sensitive animals |
-horses
-dogs -sheep -pigs -cattle -poultry |
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Ionophore poisoning
-clinical signs 24-48 hrs - > 48 hrs |
24-48:
-animals not cleaning out the feed bunks as they use to -anorexa -diarrhea -sudden death with stress, forced exercise, high temps > 48: -difficulty rising -collapse -CHF -death |
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Ionophore poisoning
-clin path |
-inc. CPK and AP
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Ionophore poisoning
-gross lesions |
-hemorrhage of heart muscle
-pale streaking of ventricular myocardium -fluid accumulation in body cavities -edema May not be present with acute death |
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Ionophore poisoning
-histo lesions |
-muscle degeneration and necrosis
-liver and renal necrosis |
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Ionophore poisoning
-treatment |
-remove source
-avoid stress -activated charcoal and cathartics (interrupt enterohepatic cycling) -high rate IV fluid to support renal function -Injectable vitamin E and Se (reduce muscle damage) -colic treatment |
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Ionophore poisoning
-management |
-adequately maintain feed mixers
-avoid inappropriate feeding practices -don't let horses into poultry/catt;e feed |
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Fluoride
-sources |
-mining deposits
-rock phosphates -water from deep wells -industrial pollution |
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Fluoride
-kinetics |
-rapidly absorbed
-excreted in urine -some excretion in milk -50% absorbed dose sequestered in bone (developing bone, teeth) |
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Fluoride
-clinical signs |
-Acute: GI irritation, kidney damage
-Chronic: affects bones and developing teeth (halted osteogenesis, spurring around joints) |
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Fluoride
-effect on teeth |
-incorporates in enamel matrix
-hypoplasia, weakening -pain with chewing and cold water -lesions only occur while the enamel is formed |
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Fluoride toxicity
-diagnosis |
-analysis of feed, mineral, water
-biopsy of coccygeal vetebrae or ribs -urine fluoride w/n 1-3 wks of exposure -kidney and liver test Postmortem |
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Fluoride toxicity
-treatment/management |
-poor prognosis
-no specific treatment -pain management -avoid exposure -give aluminum or calcium carbonate in diet to reduce absorption |
