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4.2 Feed and Water Toxicants Flashcards

1
Q

where are ionophores produced

A

naturally by bacteria (also synthetic)

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2
Q

are ionophores lipid-soluble or water-soluble

A

lipid

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3
Q

what are ionophore MOA

A

bind and transport cations down their concentration gradients

in toxic states -> uncontrolled transport leading to electrolyte imbalances -> loss of ATP -> cell death -> necrosis

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4
Q

what are ionophores used for (2)

A
  • coccidiostats
  • enhanced feed efficiency and weight gain
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5
Q

what are 3 examples of ionophores

A

monensin, narasin, salinomycin

note: all are coccidiostats

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6
Q

how can ionophore toxicosis occur (3)

A

mixing errors, overfeeding, feeding to non-target species

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7
Q

T/F adult turkeys are more susceptible to ionophore toxicosis than young turkeys

A

T

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8
Q

how are ionophores metabolized and eliminated

A

rapidly metabolized and eliminated in bile

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9
Q

ionophore toxicosis leads to imbalances in what electrolytes (4)

A

Na, Ca, K, H

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10
Q

what parts of the cell do ionophores impact

A

intracellular, extracellular and organelles

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11
Q

what are the main organs impacted by ionophore toxicosis

A

muscles (cardiac and skeletal muscle necrosis)

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12
Q

what are the clinical signs of ionophore toxicosis in cattle (7)

A

anorexia, decreased production, diarrhea, depression, dyspnea, ataxia, cardiac failure

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13
Q

ionophores impact the following in what species:
1) heart
2) heart and skeletal muscle
3) skeletal muscle

A

1) heart: horses, donkeys
2) heart and skeletal mm: ruminants
3) skeletal mm: pigs, dogs

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14
Q

what are some clinical signs of ionophore toxicosis in chickens

A

feed refusal, anorexia, weakness, ataxia, diarrhea, depression, squatting, sternal recumbency, dropped head and wings, proprioceptive deficits, paralysis, death, decreased production, leg weakness

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15
Q

what are 4 signs on biochemistry of ionophore toxicosis

A
  • elevated CK, AST, LDH
  • hypocalcemia
  • K increased or decreased
  • elevated troponin
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16
Q

what are 2 differentials for ionophore toxicosis

A

1) white mm disease (selenium deficiency)
2) cardiotoxins (taxus, oleander)

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17
Q

skeletal muscle necrosis in sheep is commonly caused by ________ associated myopathy

A

monensin (an ionophore)

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18
Q

how do we treat ionophore toxicosis

A
  • feed change
  • supportive care
  • gastric decontamination
  • avoid cardiorespiratory exertion
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19
Q

what animals are most susceptible to nitrate toxicosis

A

ruminants

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20
Q

what is nitrate toxicosis associated with (what types of conditions and sources)

A

stressed crops (hail, drought, herbicides), nitrate-containing fertilizers, nitrogen-accumulating plants, water, food preservatives

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21
Q

what is the MOA of nitrate toxicosis

A

nitrate -> nitrite -> ammonia

nitrite converts Fe2+ -> Fe3+

Fe3+ converts hemoglobin to methemoglobin -> hypoxia

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22
Q

what are clinical signs of nitrate toxicosis

A

cyanosis, weakness, ataxia, exercise intolerance, tachycardia, tremors, convulsions, death, abortions

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23
Q

what are the results of the following concentrations of methemoglobin:

30%:

80%:

A

30% -> exercise intolerance
80% -> death

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24
Q

how do we diagnose nitrate toxicosis

A

history of exposure

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25
what are the PM lesions observed with nitrate toxicosis and why
there are none (Met-Hb spontaneously reverses of Hb)
26
how can we do chemical analysis for nitrate toxicosis: 1) antemortem 2) postmortem
1) serum, blood, plasma 2) ocular fluid, eyeball, fetal fluids
27
nitrate > ____ ppm and nitrite > ____ ppm is diagnostic for toxicosis
nitrate > 20 ppm nitrite > 0.5ppm
28
what is the antidote for nitrate toxicosis? what other way can we prevent toxicosis?
methylene blue; limit nitrate levels in forages
29
what are the 3 most common sources of non-protein nitrogen
1) urea 2) ammonia (NH3) 3) ammonium phosphate salts
30
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
31
what happens when there is non-protein nitrogen toxicosis (ex. urea overload)
urea -> ammonia too much ammonia -> neurologic signs
32
what are the clinical signs of non-protein nitrogen toxicosis
salivation, bruxism, muscle tremors, abdominal pain, ataxia, dyspnea, recumbency, death
33
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)
34
T/F rumen contents are good samples for nitrate toxicosis but not non-protein nitrogen toxicosis
F; other way around
35
how do we treat non-protein nitrogen toxicosis
- remove source - acetic acid (vinegar) to lower rumen pH - iced water to dilute rumen - supportive care
36
how can we prevent non-protein nitrogen toxicosis
limit concentrations in feed; feed progressively to allow rumen microorganisms to adapt
37
Na toxicosis can be caused by (2)
- too much salt intake - water deprivation
38
what are some sources of excessive salt intake
- whey - salty ground water - mixing errors
39
what are some causes of water deprivation
- failure of mechanical waterers - freezing - overcrowding - water palatability
40
what species are commonly affected by Na toxicity
pigs and poultry
41
recommend < ____% salt in drinking water for livestock
0.5%
42
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
43
what are some clinical signs of salt toxicosis
- feed refusal - gastroenteritis - ataxia - mm tremors - seizures - opisthotonus - walking backwards - death
44
how do we diagnose salt toxicosis (5)
- history - clinical signs - Na in brain > 2000 ppm - feed and water analysis - histopathology
45
what are two signs on histopath of salt toxicosis
- polioencepalomalacia - eosinophilic meningitis (pigs only)
46
what is polioencephalomalacia
grey matter necrosis in the brain
47
what are two sources of sulfur toxicosis
molasses, water
48
what is the MOA of sulfur toxicosis
rumenal organisms convert sulfur -> H2S -> inhibits cytochrome C oxidase -> ATP depletion -> polioencephalomalacia
49
what are some clinical signs of sulfur toxicosis
blindness, ataxia, seizures, recumbency, death
50
how do we diagnose sulfur toxicosis
1) determine intake in feed and water 2) lead acetate 3) measure H2S in rumen
51
how does lead acetate paper work for diagnosing sulfur toxicosis
it converts H2S -> PbS, which appears black
52
what are mycotoxins
toxic secondary metabolites of molds that are produced under special conditions (temperature, moisture)
53
what percentage of grain worldwide contains mycotoxins
25%
54
describe the following signs of mycotoxin toxicity - acute toxicity - chronic toxicity
acute toxicity: disease, death chronic toxicity: reduced production, reproductive problems, immune suppression
55
trichothecenes, zearalenon, fumonisin, ochratoxin, ergot, aflatoxins and tremorgens are examples of
mycotoxins
56
what are the major activities of trichothecenes (3)
irritant, feed refusal, emesis
57
what are the major activities of zearalenone
estrogenic
58
what are the major activities of fumonisin (2)
cardiotoxic, hepatotoxic
59
what are the major activities of ochratoxin/citrinin (2)
nephrotoxin, carcinogenic
60
what are the major activities of ergot (2)
vasoactive (ischemia), abortion
61
what are the major activities of aflatoxins (2)
hepatotoxin, carcinogenic
62
what are the major activities of tremorgens
excitotoxic - staggers
63
fusarium produces what 3 mycotoxins
zearalenone, trichothecenes, fumonisin
64
aspergillus produces what 2 mycotoxins
ochratoxin/citrinin and aflatoxins
65
claviceps produces what mycotoxin
ergot
66
penicillium produces what mycotoxin
tremorgens
67
what is the MOA of mycotoxins
inhibition of protein synthesis in most cases
68
what are 2 types of tricothecenes
DON - vomitoxin, T-2
69
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
70
what do fumonisins do
inhibit sphinolipid biosynthesis
71
moldy corn produces what mycotoxin
fumonisin
72
what are signs of fumonisin toxicity (3)
- leukoencephalomalacia in horses - liver disease - pulmonary edema in pigs
73
what species are affected by ergot
bovine, equine, swine, poultry
74
what is produced by the following: - ergot alkaloids - ergot bodies
ergot alkaloids: lysergic acid, ergotamine ergot bodies: sclerotia
75
what are signs of ergotism
- reduced weight gain and production - reproductive problems - vasoconstriction -> laminitis, necrosis of tail/feet/ears
76
T/F ergot can cause hyperthemia in warm weather
T; due to vasoconstriction and dec. heat dissipation
77
what species is most commonly affected by tremorgenic mycotoxins
dogs
78
tremorgenic mycotoxins: - lipophilic or hydrophilic - clinical signs (6) - MOA (2)
- lipophilic - vomiting, irritation, weakness, tremors, seizures, panting - inhibits glycine; stim presynaptic Ach release
79
what animals are most susceptible to ochratoxin
monogastric animals (it gets degraded in the rumen)
80
what does ochratoxin do
nephrotoxic, carcinogenic, teratogenic
81
what are signs of aflatoxin
hepatotoxicity, carginogen, immunosuppression hepatopathy and cirrhosis in dogs
82
acute aflatoxicity: chronic aflatoxicity:
acute: hepatic necrosis chronic: neoplasia

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