4.2 Feed and Water Toxicants Flashcards
where are ionophores produced
naturally by bacteria (also synthetic)
are ionophores lipid-soluble or water-soluble
lipid
what are ionophore MOA
bind and transport cations down their concentration gradients
in toxic states -> uncontrolled transport leading to electrolyte imbalances -> loss of ATP -> cell death -> necrosis
what are ionophores used for (2)
- coccidiostats
- enhanced feed efficiency and weight gain
what are 3 examples of ionophores
monensin, narasin, salinomycin
note: all are coccidiostats
how can ionophore toxicosis occur (3)
mixing errors, overfeeding, feeding to non-target species
T/F adult turkeys are more susceptible to ionophore toxicosis than young turkeys
T
how are ionophores metabolized and eliminated
rapidly metabolized and eliminated in bile
ionophore toxicosis leads to imbalances in what electrolytes (4)
Na, Ca, K, H
what parts of the cell do ionophores impact
intracellular, extracellular and organelles
what are the main organs impacted by ionophore toxicosis
muscles (cardiac and skeletal muscle necrosis)
what are the clinical signs of ionophore toxicosis in cattle (7)
anorexia, decreased production, diarrhea, depression, dyspnea, ataxia, cardiac failure
ionophores impact the following in what species:
1) heart
2) heart and skeletal muscle
3) skeletal muscle
1) heart: horses, donkeys
2) heart and skeletal mm: ruminants
3) skeletal mm: pigs, dogs
what are some clinical signs of ionophore toxicosis in chickens
feed refusal, anorexia, weakness, ataxia, diarrhea, depression, squatting, sternal recumbency, dropped head and wings, proprioceptive deficits, paralysis, death, decreased production, leg weakness
what are 4 signs on biochemistry of ionophore toxicosis
- elevated CK, AST, LDH
- hypocalcemia
- K increased or decreased
- elevated troponin
what are 2 differentials for ionophore toxicosis
1) white mm disease (selenium deficiency)
2) cardiotoxins (taxus, oleander)
skeletal muscle necrosis in sheep is commonly caused by ________ associated myopathy
monensin (an ionophore)
how do we treat ionophore toxicosis
- feed change
- supportive care
- gastric decontamination
- avoid cardiorespiratory exertion
what animals are most susceptible to nitrate toxicosis
ruminants
what is nitrate toxicosis associated with (what types of conditions and sources)
stressed crops (hail, drought, herbicides), nitrate-containing fertilizers, nitrogen-accumulating plants, water, food preservatives
what is the MOA of nitrate toxicosis
nitrate -> nitrite -> ammonia
nitrite converts Fe2+ -> Fe3+
Fe3+ converts hemoglobin to methemoglobin -> hypoxia
what are clinical signs of nitrate toxicosis
cyanosis, weakness, ataxia, exercise intolerance, tachycardia, tremors, convulsions, death, abortions
what are the results of the following concentrations of methemoglobin:
30%:
80%:
30% -> exercise intolerance
80% -> death
how do we diagnose nitrate toxicosis
history of exposure
what are the PM lesions observed with nitrate toxicosis and why
there are none (Met-Hb spontaneously reverses of Hb)
how can we do chemical analysis for nitrate toxicosis:
1) antemortem
2) postmortem
1) serum, blood, plasma
2) ocular fluid, eyeball, fetal fluids
nitrate > ____ ppm and nitrite > ____ ppm is diagnostic for toxicosis
nitrate > 20 ppm
nitrite > 0.5ppm
what is the antidote for nitrate toxicosis? what other way can we prevent toxicosis?
methylene blue; limit nitrate levels in forages
what are the 3 most common sources of non-protein nitrogen
1) urea
2) ammonia (NH3)
3) ammonium phosphate salts
why is non-protein nitrogen added to ruminant feed (how does it work under normal conditions)
urea -> ammonia
ammonia + ketoacids -> aa
aa used for protein synthesis
what happens when there is non-protein nitrogen toxicosis (ex. urea overload)
urea -> ammonia
too much ammonia -> neurologic signs
what are the clinical signs of non-protein nitrogen toxicosis
salivation, bruxism, muscle tremors, abdominal pain, ataxia, dyspnea, recumbency, death
how do we diagnosis non-protein nitrogen toxicosis
- rumen pH > 7.5 at time of death
- feed analysis
- biological sample analysis (ocular fluid, blood, serum, rumen content)
T/F rumen contents are good samples for nitrate toxicosis but not non-protein nitrogen toxicosis
F; other way around
how do we treat non-protein nitrogen toxicosis
- remove source
- acetic acid (vinegar) to lower rumen pH
- iced water to dilute rumen
- supportive care
how can we prevent non-protein nitrogen toxicosis
limit concentrations in feed; feed progressively to allow rumen microorganisms to adapt
Na toxicosis can be caused by (2)
- too much salt intake
- water deprivation
what are some sources of excessive salt intake
- whey
- salty ground water
- mixing errors
what are some causes of water deprivation
- failure of mechanical waterers
- freezing
- overcrowding
- water palatability
what species are commonly affected by Na toxicity
pigs and poultry
recommend < ____% salt in drinking water for livestock
0.5%
what is the MOA of salt toxicosis
brain dehydration and hemorrhage
after rapid rehydration: brain edema -> increased intracranial pressure -> decreased perfusion -> ischemia and necrosis -> polioencephalomalacia
what are some clinical signs of salt toxicosis
- feed refusal
- gastroenteritis
- ataxia
- mm tremors
- seizures
- opisthotonus
- walking backwards
- death
how do we diagnose salt toxicosis (5)
- history
- clinical signs
- Na in brain > 2000 ppm
- feed and water analysis
- histopathology
what are two signs on histopath of salt toxicosis
- polioencepalomalacia
- eosinophilic meningitis (pigs only)
what is polioencephalomalacia
grey matter necrosis in the brain
what are two sources of sulfur toxicosis
molasses, water
what is the MOA of sulfur toxicosis
rumenal organisms convert sulfur -> H2S -> inhibits cytochrome C oxidase -> ATP depletion -> polioencephalomalacia
what are some clinical signs of sulfur toxicosis
blindness, ataxia, seizures, recumbency, death
how do we diagnose sulfur toxicosis
1) determine intake in feed and water
2) lead acetate
3) measure H2S in rumen
how does lead acetate paper work for diagnosing sulfur toxicosis
it converts H2S -> PbS, which appears black
what are mycotoxins
toxic secondary metabolites of molds that are produced under special conditions (temperature, moisture)
what percentage of grain worldwide contains mycotoxins
25%
describe the following signs of mycotoxin toxicity
- acute toxicity
- chronic toxicity
acute toxicity: disease, death
chronic toxicity: reduced production, reproductive problems, immune suppression
trichothecenes, zearalenon, fumonisin, ochratoxin, ergot, aflatoxins and tremorgens are examples of
mycotoxins
what are the major activities of trichothecenes (3)
irritant, feed refusal, emesis
what are the major activities of zearalenone
estrogenic
what are the major activities of fumonisin (2)
cardiotoxic, hepatotoxic
what are the major activities of ochratoxin/citrinin (2)
nephrotoxin, carcinogenic
what are the major activities of ergot (2)
vasoactive (ischemia), abortion
what are the major activities of aflatoxins (2)
hepatotoxin, carcinogenic
what are the major activities of tremorgens
excitotoxic - staggers
fusarium produces what 3 mycotoxins
zearalenone, trichothecenes, fumonisin
aspergillus produces what 2 mycotoxins
ochratoxin/citrinin and aflatoxins
claviceps produces what mycotoxin
ergot
penicillium produces what mycotoxin
tremorgens
what is the MOA of mycotoxins
inhibition of protein synthesis in most cases
what are 2 types of tricothecenes
DON - vomitoxin, T-2
what are some signs of zearalenone toxicity in:
- pre-puberal gilts
- sows
- pregnant sows
- boars
- cattle
pre-pubertal gilts: vulvar swelling, rectal/vaginal prolapse
sows: pseudopregnancy
pregnant sows: embryonic death
boars: feminization, preputial edema, infertility, reduced libido
cattle: infertility
what do fumonisins do
inhibit sphinolipid biosynthesis
moldy corn produces what mycotoxin
fumonisin
what are signs of fumonisin toxicity (3)
- leukoencephalomalacia in horses
- liver disease
- pulmonary edema in pigs
what species are affected by ergot
bovine, equine, swine, poultry
what is produced by the following:
- ergot alkaloids
- ergot bodies
ergot alkaloids: lysergic acid, ergotamine
ergot bodies: sclerotia
what are signs of ergotism
- reduced weight gain and production
- reproductive problems
- vasoconstriction -> laminitis, necrosis of tail/feet/ears
T/F ergot can cause hyperthemia in warm weather
T; due to vasoconstriction and dec. heat dissipation
what species is most commonly affected by tremorgenic mycotoxins
dogs
tremorgenic mycotoxins:
- lipophilic or hydrophilic
- clinical signs (6)
- MOA (2)
- lipophilic
- vomiting, irritation, weakness, tremors, seizures, panting
- inhibits glycine; stim presynaptic Ach release
what animals are most susceptible to ochratoxin
monogastric animals (it gets degraded in the rumen)
what does ochratoxin do
nephrotoxic, carcinogenic, teratogenic
what are signs of aflatoxin
hepatotoxicity, carginogen, immunosuppression
hepatopathy and cirrhosis in dogs
acute aflatoxicity:
chronic aflatoxicity:
acute: hepatic necrosis
chronic: neoplasia
