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Toxicology > Unit 2 - Mycotoxins > Flashcards

Unit 2 - Mycotoxins Flashcards

1
Q

What are mycotoxins?

A

Secondary metabolites of fungi

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2
Q

What influences mycotoxin production?

A

Plant varieties, climate and weather, crop monoculture, seed coat damage, insects damage, storage quality, milling practices

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3
Q

T/F: Optimal conditions for mycotoxin production vary.

A

True

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4
Q

What fungi creates aflatoxin?

A

Aspergillus flavus and A. Parasiticus

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5
Q

What are the sources of aflatoxin?

A

High energy grains

Corn, peanuts, milo, and cottonseed

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6
Q

What factors favor aflatoxin?

A 
Temp: 78-90F
Drought stress
Insect damage
High humidity
High moisture
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7
Q

What is the MOA of aflatoxin?

A
  1. AFB1 metabolized to epoxide
  2. Epoxide binds to nucleic acids
  3. Inhibition of protein synthesis
  4. Cell processes are disrupted
  5. Cell death
  6. Necrosis
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8
Q

What predisposes animals to aflatoxin?

A

Low protein diet, low antioxidants, low vitamin A, low choline/methionine

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9
Q

What acute clinical signs are associated with aflatoxin?

A 
Anorexia
Depression/weakness
Emesis
Bloody diarrhea
Hemorrhage
Icterus
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10
Q

What chronic clinical signs are associated with aflatoxin?

A 
Decreased weight gain/production
Immune suppression
Hepatic damage
Teratogenic
Carcinogenic
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11
Q

What acute gross lesions are associated with aflatoxin?

A

Liver- tan to yellow

Multi-organ hemorrhage

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12
Q

What acute microscopic lesions are associated with aflatoxin?

A

Hepatocellular vacuolization
Centrilobular congestion and necrosis
renal tubular necrosis

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13
Q

What chronic gross lesions are associated with aflatoxin?

A

Nutmeg liver

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14
Q

What chronic microscopic lesions are associated with aflatoxin?

A

Hepatocellular vacuolization
Hepatic fibrosis
Bile duct proliferation

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15
Q

Why is aflatoxin a human health concern?

A

It is considered carcinogenic

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16
Q

What are the favored conditions for tricothecene mycotoxin (T2)
production?

A

Cool temperatures OR

Alternating cool & warm temps and high moisture

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17
Q

What are the wide range of effects on the body that tricothecene mycotoxins cause?

A

Hematopoetic, dermal, lymphoid, GI

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18
Q

What syndrome does T2 toxin cause?

A

Radiomimetic syndrome - affects rapidly dividing cells

It is also a severe irritant and causes dermal and mucosal necrosis

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19
Q

T2 toxin causes immunosuppression, how does it show it in the lymphoid tissues?

A

Lymphoid depletion, thymic involution, and pancytopenia

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20
Q

What is the main source of the mycotoxin Deoxynivalenol?

A

Corn

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21
Q

What are the optimal conditions for deoxynivalenol?

A

Cool and wet

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22
Q

Deoxynivalenol is produced alongside what?

A

Zearalenone

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23
Q

What is the most sensitive species to deoxynivalenol?

A

Swine - specifically younger pigs

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24
Q

What clinical signs are associated with deoxynivalenol toxicosis in swine?

A

Feed aversion, vomiting, feed refusal

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25
Q

What species are resistant to deoxynivalenol?

A

Ruminant and horses

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26
Q

What is the main source of the mycotoxin zearlenone?

A

Corn

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27
Q

What are the optimal conditions for zearalenone production?

A

Cool and wet

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28
Q

What is zearalenone produced alongside with?

A

dexynivalenol

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29
Q

What type of compound is zearalenone?

A

Estrogenic

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30
Q

What compound is zearalenone typically found with?

A

Vomitoxin

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31
Q

What is the MOA for Zearalenone?

A
  1. Zearalenone binds to estradiol receptor
  2. Promotes signs of estrogenism
  3. Decreased follicular maturation and inhibition of ovulation
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32
Q

What clinical effects does zearalenone cause in females?

A 
Hyperestrogenism
Anestrus
Embryonic loss
Mammary gland development
Luteotripic
Heifers - infertility
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33
Q

What clinical effects does zearalenone cause in males?

A

Decreased lqibido and semen quality

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34
Q

What are the most affected species by fumonisin toxicosis?

A

Equine and swine

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35
Q

What is the MOA of fumonisin toxicosis?

A

Inhibits sphingolipid synthesis which are important components of cell membranes and nervous tissue

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36
Q

Fumonisin primarily causes ________ signs in swine, whereas it causes ______ signs in horses.

Looking for a body system here

A

Respiratory signs in swine

Neurologic signs in horses

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37
Q

What clinical signs are associated with fumonisin toxicosis in swine?

A

Dyspnea, cyanosis, weakness, and acute death

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38
Q

What clinical signs are associated with fumonisin toxicosis in equine?

A

Ataxia, blindness, and depression

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39
Q

What gross lesions are associated with fumonisin toxicosis in swine?

A

Wet heavy edematous lungs
Pulmonary edema
Tan friable liver

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40
Q

What microscopic lesions are associated with fumonisin toxicosis in swine?

A

Pulmonary edema, centrilobular necrosis, portal fibrosis, and fatty disposition

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41
Q

What gross lesions does fumonisin toxicosis cause in horses?

A

Leukoencephalomalacia (!!!)

Brown- yellow liver

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42
Q

What microscopic lesions does fumonisin toxicosis cause in horses?

A

Neuronal vacuolization - expansion and edema

43
Q

What clin path results are associated with fumonisin toxicosis in swine?

A

Elevated AST, GGT, ALT, and bilirubin

44
Q

What clin path results are associated with fumonisin toxicosis in equine?

A

Elevated AST, GGT, ALT, ALP, SDH, and bilirubin

45
Q

What fungi produce orchratoxin?

A

Aspergillus ochraceus and Penicillium viridicatum

46
Q

What are the sources of ochratoxin?

A

Small grains and crib stored ear corn

It is a storage mycotoxin

47
Q

What does ochratoxin do to corn kernels it infects?

A

It turns the center blue

48
Q

What is the MOA of ochratoxin?

A

Inhibition of protein synthesis

49
Q

What species are more sensitive to ochratoxin?

A

monogastrics

50
Q

Why are ruminants not sensitive to ochratoxin?

A

It is inactivated in the rumen

51
Q

What clinical effects does ochratoxin cause?

A

It is nephrotoxic - urine has a low USG and PU/PD

Depression

52
Q

What gross lesions does ochratoxin cause?

A

Enlarged and pale kidneys
Perirenal and mesenteric edema
Renal fibrosis and scarring

53
Q

What microscopic lesions does ochratoxin cause?

A

Renal tubular damage - necrosis of the brush border and interstitial and glomerular fibrosis

54
Q

What produces ergot?

A

Claviceps purpurea

55
Q

What is the infectious agent of the fungus that produces ergot?

56
Q

How are sclerotia formed?

A
  1. The fungi invades ovary in place of the seed head
  2. Filaments spread and prevent seed development
  3. Filaments harden = sclerotia
57
Q

What are the sources of ergot?

A

Rye, barley, wheat, brome, and oats

58
Q

What disease causing agents does sclerotia contain?

A

Ergopeptide alkaloids
Alpha adrenergic agonists
Lysergic acid

59
Q

What do alpha adrenergic agonists cause?

A

Vasoconstriction

60
Q

What does lysergic acid do?

A

It causes activation of serotonin receptors which results in neurologic effects

61
Q

What clinical effects does ergot cause?

A 
Peripheral vasoconstriction (winter)
Inability to dissipate heat (summer) - hyperthermia
Abortion
Lameness
Decreased production
Decreased reproduction 
Agalactia and prolonged gestation
Hyperexcitability and tremors
62
Q

What lesion does peripheral vasoconstriction result in?

A

The sloughing of extremities - tails, ears, and hooves

63
Q

How is ergot toxicosis diagnosed?

A

History of clinical signs
Lesions
Evaluation of grain and forage material
Analysis of feed for ergot alkaloids

64
Q

How is ergot toxicosis treated?

A

Remove offending feedstuff
Euthanasia in severe cases of lameness and sloughing
Provision of shade or other means of cooling down
Domperidone in horses

65
Q

How does domperidone work?

A

It blocks the action of alkaloids

66
Q

How is ergot toxicosis prevented?

A

Remove seed heads by cutting forage
Tilling and cultivation
Crop rotation

67
Q

What creates slaframine?

A

Rhizoctonia leguminicola

68
Q

What is the ideal temperature for slaframine production?

A

Cool/wet weather

69
Q

Slaframine is a _________ quaternary amine.

A

Parasympathomometic

70
Q

What clinical effects does slaframine cause?

A

slobbers - profuse salivation

71
Q

When does slobbers associated with slaframine toxicosis stop?

A

After exposure

72
Q

What species is most commonly affected by tremorgenic mycotoxins?

73
Q

What species produces tremorgenic mycotoxins?

A

Penicillium sp.

74
Q

What are the sources of tremorgenic mycotoxins?

A

Moldy cream cheese, bread, mac n’ cheese, moldy cheese, and decaying organic fmatter

75
Q

What is the suspected MOA of tremorgenic mycotoxins?

A

It is believed to antagonize glycine

76
Q

When is the onset of clinical signs for tremorgenic mycotoxin toxicosis?

A

30 minutes - hours

77
Q

What early clinical signs are associated with tremorgenic mycotoxin toxicosis?

A 
Restlessness
Panting
Excessive salivation
Vomiting
Progressive mild to whole body muscle tremors
78
Q

What advanced clinical signs are associated with tremorgenic mycotoxin toxicosis?

A

Severe tremors
Hyperexcitable to external stimuli
Seizures
Hyperthermia, exhaustion, and dehydration

79
Q

What toxicosis does advanced tremorgenic mycotoxin toxicosis resemble?

A

Strychnine

80
Q

How is tremorgenic mycotoxin toxicosis diagnosed?

A

History of eating moldy foods
Clinical signs
Detection of tremorgenic mycotoxins in vomitus, stomach contents, and suspect material

81
Q

How is tremorgenic mycotoxin toxicosis treated?

A

Control agitation, tremors, and seizures
Decontaminate - activated charcoal
IV fluids

82
Q

With aggressive treatment of tremorgenic mycotoxin toxicosis, when does recovery typically occur?

A

Within 24-48 hours

83
Q

Generally, how is mycotoxicosis diagnosed?

A 
Historical information of environment and exposure
Associated clinical signs
Lesions
Detection of mycotoxins
Test feeding of ration
84
Q

What diagnostic tests can be done to detect mycotoxins in samples?

A

Black light test
ELISA
Liquid chromatography/MS

85
Q

What is the gold standard diagnostic for mycotoxin detection?

A

Liquid chromatography/ MS

86
Q

Generally, what can be done to prevent mycotoxicosis?

A 
Survey weather and crop conditions
Remove damaged grain by screening
Storage facilities need to be clean, cool/ventilated, and low moisture
Prompt use of feed after milling
Use of mold inhibitors/absorbents
Testing
Dilute damaged/contaminated grain
Feed to alternative species
Provision of adequate supplementation
87
Q

What inhibitors can be used for mycotoxicosis?

A

Zeolites, clays, B-glucan of yeast, and glucomannans

88
Q

What adsorbents can be used for mycotoxicosis?

A 
Ca aluminosilicates
Mycosorb
Bentonite
Na metabisulfite
Diatomaceous earth
\+/- activated charcoal
89
Q

T/F: There is no limit to the amount of inhibitors and adsorbents that you can use in cases of mycotoxicosis because the damage is most likely already done and you need to get rid of the mycotoxin.

A

Incorrect - some products used in excess can impair mineral absorption

90
Q

What health concerns or problems are associated with distillers grains (DDGS)?

A 
Sulfur toxicity in ruminants
Elevated mycotoxin concentration
Antibiotic residues
Acute interstitial pneumonia
Antagonistic effects
91
Q

What is the typical lesion/condition is associated with sulfur toxicosis in ruminants?

92
Q

What is the MOA of sulfur toxicosis?

A
  1. Sulfur/sulfate is ingested
  2. Sulfur reducing bacteria - convert sulfate to sulfide
  3. Hydrogen attaches to sulfide - enters the rumen gas cap
  4. Eructation or ruminal absorption
  5. Brain damage
93
Q

What does rumen pH matter in cases of sulfur toxicosis?

A

When there is a low pH there is a lot of H so more H2S can be produced

When the rumen is at a pH of 5.5 95% of the rumen becomes hydrogen sulfide

94
Q

When are cattle at the greatest risk for sulfur toxicosis?

A

When they are on the first 30 days on a full finishing diet

95
Q

What clinical signs are associated with sulfur toxicosis?

A

Predominantly neurologic - head pressing, muscle tremors, hypersalivation, and convulsions

96
Q

What gross lesions are associated with sulfur toxicosis?

A

Flattened gyri, cerebellar coning, +/- fluorescence

97
Q

What microscopic lesions are associated with sulfur toxicosis?

A

neuronal necrosis

98
Q

How is sulfur toxicosis diagnosed?

A

Sulfur in ration
Sulfate in water
H2S in the rumen gas cap
Response to treatment

99
Q

How is sulfur toxicosis treated?

A

Thiamine hydrochloride

Dexamethasone

100
Q

What can increase mycotoxin concentration by 3x?

101
Q

What do ethanol co-products cause?

A

Acute interstitial pneumonia

102
Q

The acute interstitial pneumonia caused by ethanol co-products is similar to what other condition caused by mold?

A

Moldy sweet potatoes

103
Q

What ethanol co-product causes acute interstitial pneumonia?

A

4 ipomeanol

104
Q

What causes the damage in cases of acute interstitial pneumonia due to ethanol co-products?

A

Eructated H2S

Toxicology (32 decks)

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