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POD > 4.2 Feed and Water Toxicants > Flashcards

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
Q

what are the PM lesions observed with nitrate toxicosis and why

A

there are none (Met-Hb spontaneously reverses of Hb)

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26
Q

how can we do chemical analysis for nitrate toxicosis:
1) antemortem
2) postmortem

A

1) serum, blood, plasma
2) ocular fluid, eyeball, fetal fluids

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27
Q

nitrate > ____ ppm and nitrite > ____ ppm is diagnostic for toxicosis

A

nitrate > 20 ppm
nitrite > 0.5ppm

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28
Q

what is the antidote for nitrate toxicosis? what other way can we prevent toxicosis?

A

methylene blue; limit nitrate levels in forages

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29
Q

what are the 3 most common sources of non-protein nitrogen

A

1) urea
2) ammonia (NH3)
3) ammonium phosphate salts

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30
Q

why is non-protein nitrogen added to ruminant feed (how does it work under normal conditions)

A

urea -> ammonia

ammonia + ketoacids -> aa

aa used for protein synthesis

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31
Q

what happens when there is non-protein nitrogen toxicosis (ex. urea overload)

A

urea -> ammonia

too much ammonia -> neurologic signs

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32
Q

what are the clinical signs of non-protein nitrogen toxicosis

A

salivation, bruxism, muscle tremors, abdominal pain, ataxia, dyspnea, recumbency, death

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33
Q

how do we diagnosis non-protein nitrogen toxicosis

A
  • rumen pH > 7.5 at time of death
  • feed analysis
  • biological sample analysis (ocular fluid, blood, serum, rumen content)
34
Q

T/F rumen contents are good samples for nitrate toxicosis but not non-protein nitrogen toxicosis

A

F; other way around

35
Q

how do we treat non-protein nitrogen toxicosis

A
  • remove source
  • acetic acid (vinegar) to lower rumen pH
  • iced water to dilute rumen
  • supportive care
36
Q

how can we prevent non-protein nitrogen toxicosis

A

limit concentrations in feed; feed progressively to allow rumen microorganisms to adapt

37
Q

Na toxicosis can be caused by (2)

A
  • too much salt intake
  • water deprivation
38
Q

what are some sources of excessive salt intake

A
  • whey
  • salty ground water
  • mixing errors
39
Q

what are some causes of water deprivation

A
  • failure of mechanical waterers
  • freezing
  • overcrowding
  • water palatability
40
Q

what species are commonly affected by Na toxicity

A

pigs and poultry

41
Q

recommend < ____% salt in drinking water for livestock

A

0.5%

42
Q

what is the MOA of salt toxicosis

A

brain dehydration and hemorrhage

after rapid rehydration: brain edema -> increased intracranial pressure -> decreased perfusion -> ischemia and necrosis -> polioencephalomalacia

43
Q

what are some clinical signs of salt toxicosis

A
  • feed refusal
  • gastroenteritis
  • ataxia
  • mm tremors
  • seizures
  • opisthotonus
  • walking backwards
  • death
44
Q

how do we diagnose salt toxicosis (5)

A
  • history
  • clinical signs
  • Na in brain > 2000 ppm
  • feed and water analysis
  • histopathology
45
Q

what are two signs on histopath of salt toxicosis

A
  • polioencepalomalacia
  • eosinophilic meningitis (pigs only)
46
Q

what is polioencephalomalacia

A

grey matter necrosis in the brain

47
Q

what are two sources of sulfur toxicosis

A

molasses, water

48
Q

what is the MOA of sulfur toxicosis

A

rumenal organisms convert sulfur -> H2S -> inhibits cytochrome C oxidase -> ATP depletion -> polioencephalomalacia

49
Q

what are some clinical signs of sulfur toxicosis

A

blindness, ataxia, seizures, recumbency, death

50
Q

how do we diagnose sulfur toxicosis

A

1) determine intake in feed and water
2) lead acetate
3) measure H2S in rumen

51
Q

how does lead acetate paper work for diagnosing sulfur toxicosis

A

it converts H2S -> PbS, which appears black

52
Q

what are mycotoxins

A

toxic secondary metabolites of molds that are produced under special conditions (temperature, moisture)

53
Q

what percentage of grain worldwide contains mycotoxins

A

25%

54
Q

describe the following signs of mycotoxin toxicity

  • acute toxicity
  • chronic toxicity
A

acute toxicity: disease, death

chronic toxicity: reduced production, reproductive problems, immune suppression

55
Q

trichothecenes, zearalenon, fumonisin, ochratoxin, ergot, aflatoxins and tremorgens are examples of

A

mycotoxins

56
Q

what are the major activities of trichothecenes (3)

A

irritant, feed refusal, emesis

57
Q

what are the major activities of zearalenone

A

estrogenic

58
Q

what are the major activities of fumonisin (2)

A

cardiotoxic, hepatotoxic

59
Q

what are the major activities of ochratoxin/citrinin (2)

A

nephrotoxin, carcinogenic

60
Q

what are the major activities of ergot (2)

A

vasoactive (ischemia), abortion

61
Q

what are the major activities of aflatoxins (2)

A

hepatotoxin, carcinogenic

62
Q

what are the major activities of tremorgens

A

excitotoxic - staggers

63
Q

fusarium produces what 3 mycotoxins

A

zearalenone, trichothecenes, fumonisin

64
Q

aspergillus produces what 2 mycotoxins

A

ochratoxin/citrinin and aflatoxins

65
Q

claviceps produces what mycotoxin

A

ergot

66
Q

penicillium produces what mycotoxin

A

tremorgens

67
Q

what is the MOA of mycotoxins

A

inhibition of protein synthesis in most cases

68
Q

what are 2 types of tricothecenes

A

DON - vomitoxin, T-2

69
Q

what are some signs of zearalenone toxicity in:
- pre-puberal gilts
- sows
- pregnant sows
- boars
- cattle

A

pre-pubertal gilts: vulvar swelling, rectal/vaginal prolapse

sows: pseudopregnancy

pregnant sows: embryonic death

boars: feminization, preputial edema, infertility, reduced libido

cattle: infertility

70
Q

what do fumonisins do

A

inhibit sphinolipid biosynthesis

71
Q

moldy corn produces what mycotoxin

A

fumonisin

72
Q

what are signs of fumonisin toxicity (3)

A
  • leukoencephalomalacia in horses
  • liver disease
  • pulmonary edema in pigs
73
Q

what species are affected by ergot

A

bovine, equine, swine, poultry

74
Q

what is produced by the following:
- ergot alkaloids
- ergot bodies

A

ergot alkaloids: lysergic acid, ergotamine
ergot bodies: sclerotia

75
Q

what are signs of ergotism

A
  • reduced weight gain and production
  • reproductive problems
  • vasoconstriction -> laminitis, necrosis of tail/feet/ears
76
Q

T/F ergot can cause hyperthemia in warm weather

A

T; due to vasoconstriction and dec. heat dissipation

77
Q

what species is most commonly affected by tremorgenic mycotoxins

A

dogs

78
Q

tremorgenic mycotoxins:
- lipophilic or hydrophilic
- clinical signs (6)
- MOA (2)

A
  • lipophilic
  • vomiting, irritation, weakness, tremors, seizures, panting
  • inhibits glycine; stim presynaptic Ach release
79
Q

what animals are most susceptible to ochratoxin

A

monogastric animals (it gets degraded in the rumen)

80
Q

what does ochratoxin do

A

nephrotoxic, carcinogenic, teratogenic

81
Q

what are signs of aflatoxin

A

hepatotoxicity, carginogen, immunosuppression

hepatopathy and cirrhosis in dogs

82
Q

acute aflatoxicity:
chronic aflatoxicity:

A

acute: hepatic necrosis
chronic: neoplasia

POD (18 decks)

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