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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
What species are resistant to deoxynivalenol?
Ruminant and horses
26
What is the main source of the mycotoxin zearlenone?
Corn
27
What are the optimal conditions for zearalenone production?
Cool and wet
28
What is zearalenone produced alongside with?
dexynivalenol
29
What type of compound is zearalenone?
Estrogenic
30
What compound is zearalenone typically found with?
Vomitoxin
31
What is the MOA for Zearalenone?
1. Zearalenone binds to estradiol receptor 2. Promotes signs of estrogenism 3. Decreased follicular maturation and inhibition of ovulation
32
What clinical effects does zearalenone cause in females?
``` Hyperestrogenism Anestrus Embryonic loss Mammary gland development Luteotripic Heifers - infertility ```
33
What clinical effects does zearalenone cause in males?
Decreased lqibido and semen quality
34
What are the most affected species by fumonisin toxicosis?
Equine and swine
35
What is the MOA of fumonisin toxicosis?
Inhibits sphingolipid synthesis which are important components of cell membranes and nervous tissue
36
Fumonisin primarily causes ________ signs in swine, whereas it causes ______ signs in horses. Looking for a body system here
Respiratory signs in swine | Neurologic signs in horses
37
What clinical signs are associated with fumonisin toxicosis in swine?
Dyspnea, cyanosis, weakness, and acute death
38
What clinical signs are associated with fumonisin toxicosis in equine?
Ataxia, blindness, and depression
39
What gross lesions are associated with fumonisin toxicosis in swine?
Wet heavy edematous lungs Pulmonary edema Tan friable liver
40
What microscopic lesions are associated with fumonisin toxicosis in swine?
Pulmonary edema, centrilobular necrosis, portal fibrosis, and fatty disposition
41
What gross lesions does fumonisin toxicosis cause in horses?
Leukoencephalomalacia (!!!) | Brown- yellow liver
42
What microscopic lesions does fumonisin toxicosis cause in horses?
Neuronal vacuolization - expansion and edema
43
What clin path results are associated with fumonisin toxicosis in swine?
Elevated AST, GGT, ALT, and bilirubin
44
What clin path results are associated with fumonisin toxicosis in equine?
Elevated AST, GGT, ALT, ALP, SDH, and bilirubin
45
What fungi produce orchratoxin?
Aspergillus ochraceus and Penicillium viridicatum
46
What are the sources of ochratoxin?
Small grains and crib stored ear corn It is a storage mycotoxin
47
What does ochratoxin do to corn kernels it infects?
It turns the center blue
48
What is the MOA of ochratoxin?
Inhibition of protein synthesis
49
What species are more sensitive to ochratoxin?
monogastrics
50
Why are ruminants not sensitive to ochratoxin?
It is inactivated in the rumen
51
What clinical effects does ochratoxin cause?
It is nephrotoxic - urine has a low USG and PU/PD | Depression
52
What gross lesions does ochratoxin cause?
Enlarged and pale kidneys Perirenal and mesenteric edema Renal fibrosis and scarring
53
What microscopic lesions does ochratoxin cause?
Renal tubular damage - necrosis of the brush border and interstitial and glomerular fibrosis
54
What produces ergot?
Claviceps purpurea
55
What is the infectious agent of the fungus that produces ergot?
Sclerotia
56
How are sclerotia formed?
1. The fungi invades ovary in place of the seed head 2. Filaments spread and prevent seed development 3. Filaments harden = sclerotia
57
What are the sources of ergot?
Rye, barley, wheat, brome, and oats
58
What disease causing agents does sclerotia contain?
Ergopeptide alkaloids Alpha adrenergic agonists Lysergic acid
59
What do alpha adrenergic agonists cause?
Vasoconstriction
60
What does lysergic acid do?
It causes activation of serotonin receptors which results in neurologic effects
61
What clinical effects does ergot cause?
``` Peripheral vasoconstriction (winter) Inability to dissipate heat (summer) - hyperthermia Abortion Lameness Decreased production Decreased reproduction Agalactia and prolonged gestation Hyperexcitability and tremors ```
62
What lesion does peripheral vasoconstriction result in?
The sloughing of extremities - tails, ears, and hooves
63
How is ergot toxicosis diagnosed?
History of clinical signs Lesions Evaluation of grain and forage material Analysis of feed for ergot alkaloids
64
How is ergot toxicosis treated?
Remove offending feedstuff Euthanasia in severe cases of lameness and sloughing Provision of shade or other means of cooling down Domperidone in horses
65
How does domperidone work?
It blocks the action of alkaloids
66
How is ergot toxicosis prevented?
Remove seed heads by cutting forage Tilling and cultivation Crop rotation
67
What creates slaframine?
Rhizoctonia leguminicola
68
What is the ideal temperature for slaframine production?
Cool/wet weather
69
Slaframine is a _________ quaternary amine.
Parasympathomometic
70
What clinical effects does slaframine cause?
slobbers - profuse salivation
71
When does slobbers associated with slaframine toxicosis stop?
After exposure
72
What species is most commonly affected by tremorgenic mycotoxins?
Dogs
73
What species produces tremorgenic mycotoxins?
Penicillium sp.
74
What are the sources of tremorgenic mycotoxins?
Moldy cream cheese, bread, mac n' cheese, moldy cheese, and decaying organic fmatter
75
What is the suspected MOA of tremorgenic mycotoxins?
It is believed to antagonize glycine
76
When is the onset of clinical signs for tremorgenic mycotoxin toxicosis?
30 minutes - hours
77
What early clinical signs are associated with tremorgenic mycotoxin toxicosis?
``` Restlessness Panting Excessive salivation Vomiting Progressive mild to whole body muscle tremors ```
78
What advanced clinical signs are associated with tremorgenic mycotoxin toxicosis?
Severe tremors Hyperexcitable to external stimuli Seizures Hyperthermia, exhaustion, and dehydration
79
What toxicosis does advanced tremorgenic mycotoxin toxicosis resemble?
Strychnine
80
How is tremorgenic mycotoxin toxicosis diagnosed?
History of eating moldy foods Clinical signs Detection of tremorgenic mycotoxins in vomitus, stomach contents, and suspect material
81
How is tremorgenic mycotoxin toxicosis treated?
Control agitation, tremors, and seizures Decontaminate - activated charcoal IV fluids
82
With aggressive treatment of tremorgenic mycotoxin toxicosis, when does recovery typically occur?
Within 24-48 hours
83
Generally, how is mycotoxicosis diagnosed?
``` Historical information of environment and exposure Associated clinical signs Lesions Detection of mycotoxins Test feeding of ration ```
84
What diagnostic tests can be done to detect mycotoxins in samples?
Black light test ELISA Liquid chromatography/MS
85
What is the gold standard diagnostic for mycotoxin detection?
Liquid chromatography/ MS
86
Generally, what can be done to prevent mycotoxicosis?
``` 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
What inhibitors can be used for mycotoxicosis?
Zeolites, clays, B-glucan of yeast, and glucomannans
88
What adsorbents can be used for mycotoxicosis?
``` Ca aluminosilicates Mycosorb Bentonite Na metabisulfite Diatomaceous earth +/- activated charcoal ```
89
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.
Incorrect - some products used in excess can impair mineral absorption
90
What health concerns or problems are associated with distillers grains (DDGS)?
``` Sulfur toxicity in ruminants Elevated mycotoxin concentration Antibiotic residues Acute interstitial pneumonia Antagonistic effects ```
91
What is the typical lesion/condition is associated with sulfur toxicosis in ruminants?
Polio
92
What is the MOA of sulfur toxicosis?
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
What does rumen pH matter in cases of sulfur toxicosis?
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
When are cattle at the greatest risk for sulfur toxicosis?
When they are on the first 30 days on a full finishing diet
95
What clinical signs are associated with sulfur toxicosis?
Predominantly neurologic - head pressing, muscle tremors, hypersalivation, and convulsions
96
What gross lesions are associated with sulfur toxicosis?
Flattened gyri, cerebellar coning, +/- fluorescence
97
What microscopic lesions are associated with sulfur toxicosis?
neuronal necrosis
98
How is sulfur toxicosis diagnosed?
Sulfur in ration Sulfate in water H2S in the rumen gas cap Response to treatment
99
How is sulfur toxicosis treated?
Thiamine hydrochloride | Dexamethasone
100
What can increase mycotoxin concentration by 3x?
ethanol
101
What do ethanol co-products cause?
Acute interstitial pneumonia
102
The acute interstitial pneumonia caused by ethanol co-products is similar to what other condition caused by mold?
Moldy sweet potatoes
103
What ethanol co-product causes acute interstitial pneumonia?
4 ipomeanol
104
What causes the damage in cases of acute interstitial pneumonia due to ethanol co-products?
Eructated H2S

Toxicology (32 decks)

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