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What botulinum toxins are cattle susceptible to, and where do they become exposed to them?
Cattle A, B, C, D; soil and forage
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What forages are often associated with botulism? (4)
hay cubes (horses), contaminated wheat, oatlage (baled wet in plastic bags), feed contaminated with "animal parts"
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What is type D botulinum toxin associated with?
phosphorous deficient soils/ pica (South Africa, South America)
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What is the mechanism of action of botulinum toxin?
blocks the release of acetylcholine, inhibiting muscle contraction--> flaccid paralysis
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What are the 3 forms of botulism?
- consumption of pre-formed toxin: toxin elaborated in feed prior to ingestion (protoxin converted to toxin in the GI tract)
- toxicoinfectious botulism: ingestion of BACTERIA (elaboration of toxin in gut)
- wound associated botulism: wound infected w/ bacteria then toxin production and absorbed systemically
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Clinical signs of botulism. (6)
progressive muscle weakness, drooping head carriage, tongue paralysis, dysphagia, increasing respiratory difficulty--> death
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What is the treatment for botulism? (4)
confinement, limit organism growth, antitoxin, supportive (ventilation)
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How does urea toxicity arise?
- common to add urea to feed to increase nitrogen content--> rumen microflora use N to synthesize protein, controls feed spoilage
- poisoning occurs when animals gain access to large amounts/fed too much too rapidly
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Describe the pathogenesis of urea toxicity.
protein production from urea--> microbe assimilate NH3 and release amino acids-->rumen urease hydrolyzes urea to free NH3--> rapidity of NH3 released and rumen pH determines toxicity (gradually increasing urea may be tolerated)
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Describe the pathologic mechanism of urea.
normally urea converted to AA by microbes; release of NH3 and NH4+, rapid breakdown of urea--> rumen becomes alkaline--> animal not acclimated, leads to high levels of free NH3--> readily absorbed from alkaline rumen--> NH in liver re-converted to urea (usually urinated, saliva,etc); when overwhelmed, inc blood NH3, systemic lactic acidosis
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pKa=
pH where 50% is ionized
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As far as urea metabolism, __________ is absorbed systemically, while __________ is retained in the rumen.
NH3; NH4+
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Excess NH3 in blood leads to... (2)
lactic acidosis, hyperkalemia
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Clinical signs of urea toxicity. (8)
bloating, odontoprisis/ bruxism (grinding teeth), weakness/ recumbency, salivation, hypersensitivity, aggression, labored respiration, convulsions/ tetany, death
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A sublethal dose of urea causes... (3)
indigestion, diarrhea, splashy rumen
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How is urea toxicity diagnosed? (6)
- hx of NPN (nonprotein nitrogen) feed supplement, rumen pH > 8 suggestive, compatible history/ signs, systemic metabolic acidosis, blood ammonia >2mg/dL
- save sample of offending feed for analysis
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What is the treatment for urea toxicity? (4)
- lower rumen pH- VINEGAR
- cool rumen- COLD WATER
- rumen lavage +/- rumenotomy
- treat metabolic acidosis- SODIUM BICARB
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What is "Bonkers"?
ammoniated feed toxicity
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Clinical signs of bonkers. (6)
trembling, muscle twitching, wild stampeding, salivation, convulsions, death
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Describe the pathophysiology of bovine bonkers.
in cattle fed ammoniated high-quality hay, silage, molasses, and protein blocks is thought to be caused by formation of 4-methylimidazole (4-MI) through the action of NH3 on soluble carbohydrates (reducing sugars) in these feedstuffs. Cattle fed dietary components containing 4-MI develop a syndrome known as the “bovine bonkers syndrome". Because nursing calves are affected, the toxic principle apparently is excreted in milk
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Why do only mature cattle get urea toxicity, while any aged cattle can be affected by bovine bonkers?
urease is normally present in the functional rumen after 50 days of age
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Treatment for bovine bonkers. (4)
remove ammoniated feed, add grain/molasses, laxatives, anti-seizure drugs
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Describe the pathogenesis of Na+ toxicity.
high sodium diet (feed or water)--> sodium accumulation intracellularly in brain--> decreased Na+ transport and glycolysis--> CNS depression, encephalopathy
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Describe the pathogenesis of water intoxication.
hypernatremia--> intracellular Na+ accumulation in brain--> thirst--> unlimited access to fresh water--> intracellular water accumulation--> CNS edema, increased intracellular pressure--> acute encephalopathy
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Why does sodium toxicity have a more chronic/slow onset than water intoxication?
Na+ion not rapidly equilibrated b/w blood and CSF, increases over time (days), but when re-exposed to H2O, CNS gradient rapidly draws water into the cells
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What are clinical signs of salt poisoning/ water intoxication? (10)
muco-hemorrhagic diarrhea, colic, grinding teeth (bruxism), nystagmus, aggression, blindness, star gazing, seizures, head pressing, death
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What does salt intoxication cause in swine?
eosinophilic meningoencephalitis, cerebrocortical necrosis, polioencephalomalacia
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How is salt poisoning/ water intoxication diagnosed? (4)
- CSF and Serum Na+ >160mEq/L
- CSF: Serum Na+ > 1
- hemolysis, hemoglbinuria
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How is salt intoxication treated? (2)
restrict water intake to 50% or less of normal for several days, slow IV infusion of normal or hypertonic saline (oral rehydration is possible, but it is slow and labor intensive)
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What are the normal uses of ionophore in ruminants? (4)
improved feed efficiency, control coccidiosis, growth promotion, Johne's dz treatment/ prevention
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In what species are ionophores not tolerated at all?
horses
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What are clinical signs of monensin toxicity in cattle? (13)
- acute: diarrhea, depression, anorexia, apprehensiveness, dyspnea, rear limb ataxia, death
- sublethal or chronic: decreased appetite, heart failure, jugular pulses, murmurs, tachycardia, elevated cTnI
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What is the toxic mechanism of ionophores?
cause altered balance of Na+, K+, and Ca2+, in cells, leading to death of myofibers
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Describe the gross pathological findings with monensin toxicity. (4)
edematous lungs, pleural effusion, cardiac and skeletal muscle necrosis (white areas), skeletal muscle may appear normal acutely
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What are the microscopic pathological findings with monensin toxicity? (2)
- vacuolar degeneration of myocardium
- focal areas of skeletal muscle degeneration and fibrosis
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With monensin toxicity, __________ accumulates in the heart, which causes lack of __________ and subsequently, __________.
calcium phosphate; blood flow; anaerobic infection
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Differential diagnoses for decreased appetite, signs of heart failure (jugular pulses, murmurs, tachycardia), and elevated cTnI? (5)
monensin toxicity, nutritional myopathy (selenium), Cassia occidentalis (senna), white snakeroot, Vetch
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What is the treatment for monensin toxicity? (5)
remove incriminating feed, administer activated charcoal, laxatives, supplemental vit E and selenium
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What conditions favor nitrate accumulation in plants?
conditions that stress the plant, esp drought [most nitrate accumulation is in the stem or lower parts of plant]
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Clinical signs of nitrate poisoning. (7)
[30min-4hr post-ingestion] anxiety, polypnea, dyspnea, rapid weak pulse, exercise intolerance, cyanotic MMs, death in <24hr
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How is nitrate poisoning diagnosed? (2)
- appearance of "chocolate blood"- methemoglobinuria
- clinical signs
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What is the treatment for nitrate poisoning?
methylene blue- reduces Fe3+ to Fe2+
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What plants accumulate cyanide/ prussic acid? (3)
sorghum, sudan grass, birdfoot trefoil [leaves and stems!] [more with high nitrogen fertilizers!]
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What is the mechanism of action of cyanide poisoning?
cyanide interferes with cellular cytochrome oxidase, shutting down electron transport--> oxygen use by cell is inhibited--> cells become anoxic (even tho blood has oxygen)--> cells with great conc of cytochrome oxidase (cardiac muscles and brain) are rapidly affected
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What are clinical signs of cyanide poisoning? (10)
found dead, excitement/ muscle tremors, bright red MMs, polypnea, dyspnea, lacrimation, salivation, defecation, urination, convulsions
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How is cyanide poisoning diagnosed? (3)
smell of bitter almond in rumen+ Hx of sudden death and exposure to CN containing plants
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What is the treatment for CN poisoning?
usually they're dead BUT supply thiosulfate (body forms thiocyanate, which is excreted by kidney)
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What is the most common metal intoxication, and where does it usually come from?
lead poisoning; batteries, caulking, solder, linoleum, bird shot, oil
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Is lead poisoning acute or chronic and why?
chronic- lead is accumulated over time, animals need not ingest a toxic dose to develop clinical signs
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Ingested lead is incorporated into __(3)__, which has implications for __________.
RBCs, muscle, bone; food safety
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What is the mechanism of lead poisoning?
lead inhibits delta-aminolevulinic acid dehydrase, causing increased levels of trans-ALA--> interferes with many enzyme systems---> increased RBC fragility--> decreased energy metabolism by brain--> encephalopathy
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Clinical signs of lead poisoning in cattle. (9)
DORSOMEDIAL STRABISMUS, anorexia, depression, rumen stasis, grinding teeth, head pressing, central blindness, spastic eyelids, convulsions
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Necropsy findings with lead poisoning. (3)
cerebral edema, polioencephalomalacia, damage to cerebral microvasculature
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What is the treatment of lead poisoning? (4)
- calcium EDTA "Versenate"- lead chelator
- DMSA
- thiamine
- +/- rumenotomy
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What are differentials for dorsomedial striabismus, anorexia, depression, rumen stasis, grinding teeth, central blindness, convulsions in cattle? (4)
lead poisoning, Vit A deficiency, polioencephalomalacia/ cerebrocortical necrosis, Na+ toxicity/ water intox
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With copper in feed, the ratio of __________ is critical in determining potential problems.
Cu: Molybdenum
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What animals have the lowest tolerance for copper?
sheep
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Clinical signs of copper poisoning or molybdenum deficiency. (8)
anemia, lethargy, anorexia, weakness, trembling, icterus, hemoglobinuria, death
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Necropsy findings with copper toxicity. (8)
- blood fails to clot, hemolytic plasma, yellow friable liver, dark kidneys, enlarged spleen, icterus, dark urine in bladder
- rhodamine, Rubeanic acid + stains of liver
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What is the treatment for copper poisoning? (6)
ammonium molybdate, sodium thiosulfate, ammonium tetrathiol molybdate, new methylene blue, D-penacillamine, supportive care
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2 differentials for hemoglobinuria.
copper poisoning, salt poisoning/water intoxication
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