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Toxo Exam I > Molds, Mycotoxins, and Ergots > Flashcards

Molds, Mycotoxins, and Ergots Flashcards

1
Q

What is a mycotoxin?

A

A secondary metabolite/chemical of a fungus producing toxins in other orgs. that are always immunosuppressive

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2
Q

What is the number one cause of diarrhea in animals? What about the second most common cause?

A

Diet; parasites

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3
Q

Two classifications of metabolites of fungi are:

A
  1. Field Fungi

2. Storage Fungi

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4
Q

Field fungi–>

A

growing in plant while out in a field before processing occurs. Grow BEFORE HARVEST

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5
Q

Storage fungi–>

A

Do not invade grain before harvest but rather in conditions that damage the seed coat thus predisposing to fungal growth

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6
Q

Mycotoxin is often causes what conditions?

A

Often cause vague, subacute or chronic conditions

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7
Q

ALL MYCOTOXINS ARE ______

A

IMMUNOSUPPRESSIVE

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8
Q

What are two ways in which we can test for mycotoxins?

A

Testing feeding suspected rations, ID known mycotoxins in diet or in bodily tissues

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9
Q

What conc. of mycotoxins are considered safe?

A

NONE!!! ALL are responsible for some aspect of immunosuppression!!!!**

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10
Q

What are the toxigenic molds and mycotoxins thought to be most prevalent and toxic to dairy cattle??? (three of them)

A

Fusarium, Aspergillus, Penicillium

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11
Q

Fusarium subspecies we must know:

A

Deoxynivalenol, Zearalenone, T2 toxins, Fumonisin

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12
Q

What is the one Aspergillus toxin subsp. we must know?

A

Aflatoxin

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13
Q

What is the one Penicillium toxins subsp. we must know?

A

PR toxin

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14
Q

Aflatoxin is a potential carcinogen in humans, what is the primary targeted organ? What does it lead to?

A

Liver; leads to loss of proteins, improper antibody formation, decreased clotting factors

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15
Q

Alfaltoxin- what animals are more susceptible? What animals seem to be the most resistant to the acute forms?

A

Younger animals; adult ruminants

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16
Q

Diagnosis in lab for aflatoxin:

A

Increased liver enzymes, hyperbilirubinemia, decreased albumin, decreased prothrombin, M1 marker in milk/urine, black light positive

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17
Q

Aflatoxin lesions of acute infection are found as….

A

hepatic necrosis, gall bladder edema, ascites

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18
Q

Aflatoxin tx—>

A

Hydrated sodium calcium aluminosilicate (HSCAS)- toxin binder and supplements with Vit E and Selenium

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19
Q

Prevention of Aflatoxin–>

A

Mold inhibitors, tx with grain and anhydrous NH4 (ammonia)

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20
Q

Public Heath concerns of Aflatoxin toxicity:

A

Aflatoxins are carcinogens, milk is monitored closely for M1 metabolites– legal limit is 0.5ppb. Milk from cows fed more than 20ppb (legal limit of grain for cows that are lactating) may contain milk residues that are over the legal limit

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21
Q

What is the ratio used to find conc in feed from how much is in the milk?

A

40:1 ratio is used between ppb residue in milk and how much is in the feed

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22
Q

Zearalenone causes…

A

Fungal infections “scabs”

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23
Q

What enviro. does Zearalenone prefer to grow?

A

High moisture and alternating high and low temps. Cooler morning followed by hotter afternoons

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24
Q

Zearalenone is absorbed in the ___ ____ and may be secreted in _____ without any regulatory restrictions

A

GI tract; milk

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25
Q

Mode of action of Zearalenone:

A

Binds to receptors of estradiol and functions as a weak estrogen, inhibiting secretion and release of GnRH which stimulates ovulation and is released from the hypothalamus.

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26
Q

What species are most affected by Zearalenone, what are the least susceptible species?

A

Most: swine
Least: Cattle

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27
Q

Zearalenone lab diagnosis:

A

Increased plasma progesterone

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28
Q

Zearalenone lesions in the body:

A

Ovarian atrophy and follicular atresia, follicular cysts, uterine edema and cystic appearance, proliferation of mammary tissues

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29
Q

Zearalenone tx and prevention includes…

A

TX–> removing source, bovine repro effects can last 2+ months, activated charcoal may help + GnRH or HCG/PGF2alpha
Prevention–> Betonite clay binder to contaminated diets

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30
Q

Trichothecenes (aka T2, DON, Vomitoxin) sources

A

Corn, milo, cereal, wheat

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31
Q

Conditions for Trichothecenes (aka T2, DON, Vomitoxin) to grow the most:

A

Alternating warm and cool and late harvested or overwintered grains

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32
Q

Trichothecenes (aka T2, DON, Vomitoxin) characteristics include what type of environment?

A

Stable environment, they are resistant to heat and pressure cooking/processing :((

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33
Q

Trichothecenes (aka T2, DON, Vomitoxin) Mode of Action–>

A

Highly toxic, inhibition of protein synthesis and inhibition of DNA and RNA nucleic synthesis. Directly cytotoxic to cells and produce DERMONECROTIC EFFECTS WITH IMMUNOSUPPRESSION!!!

34
Q

Trichothecenes (aka T2, DON, Vomitoxin) what animals are most suscpetible? Which are least susceptibe?

A

Cats (most susceptible); mice are least susceptible (most resistant!!!)

35
Q

Trichothecenes (aka T2, DON, Vomitoxin) clinical signs

A

GI signs WITH VOMITING, FEED REUSAL IS MOST COMMON SIGN.

36
Q

Trichothecenes (aka T2, DON, Vomitoxin) lab Diagnosis:

A

Anemia/leukopenia, bile is rapidly metabolized and may not be seen

37
Q

Trichothecenes (aka T2, DON, Vomitoxin) Tx:

A

Purgatives/laxatives and electrolytes/fluids + supportive care

38
Q

Public health relating to Trichothecenes (aka T2, DON, Vomitoxin) is not as issue bc its rapid meta. and excretion. T/F

A

True!! :)) :))

39
Q

Fumonisins sources and what environment do they prefer for growth?

A

White and yellow corns, drought followed by cool and wet conditions

40
Q

Fumonisins characteristics—>

A

Water soluble, heat stable, resistant to alkali tx and includes FB1, FB2, and FB3 (FB1 and FB2 BEING THE MOST TOXIC FORMS!!)

41
Q

Fumonisins mode of action:

A

Interference with sphingolipid synthesis (neutral tissue and plays impt role in signal transmission and cell to cell recognition). Can produce pulmonary toxicosis and hepatic toxicosis in swine

42
Q

Can produce _____ toxicosis and _____ toxicosis in what species?

A

Pulmonary; hepatic; swine

43
Q

What species are most affected to least affected by Fumonisins???

A

Horses (most affected)> ruminants> swine> poultry (least affected)

44
Q

Fumonisins levels in:

  1. Horses
  2. Swine
  3. Cattle
A
  1. less than 5 ppm
  2. 10 ppm for swine
  3. 50 ppm for Cattle
45
Q

Fumonisins causes _____ ________ in horses which is identical to sleepy foal sickness

A

Equine Leukoencephalomalacia

46
Q

Clinical signs of fumonisins in swine:

A

Resp. syndrome, death within four hrs and pulm. edema

47
Q

Clinical signs in swine but lower doses is just ___

A

ADR

48
Q

Clinical signs of fumonisins in:

  1. cattle
  2. poultry
A
  1. anorexia and wt loss

2. requires high doses to show clinical signs, but they are anorexia and skeletal muscle abn in growing chicks

49
Q

Lab findings/diagnosis of Fumonisins:

A

Evidence of hepatic dysfunction and softening of cerebral white matter in horses and pulmonary edema and hydrothorax in swine

50
Q

Tx and prevention of fumonisins

A

Supportive care and try to prevent by cleaning corn and screening

51
Q

Fumonisins public heath concerns:

A

Potential carcinogens, may be regulated in the future, Fumonsins are excreted rapidly in bile and urine

52
Q

Ergots aka “______ _____” attack the plant. What environment do they prefer to grow in?

A

“Parasitic fungus”, like warm, moist conditions

53
Q

What are the physiological effects of ergots?

A

Smooth muscle contractions and gangrene along with CNS derangement

54
Q

Sources of Ergotism:

A

Small grains (rye, barely, and oats), Forage plants (bromes, bluegrass, ryegrass), Warm and humid weather favors growth

55
Q

Ergotism mode of action:

A

Potent inhibition of contraction of smooth muscles causing VASOCONSTRICITON, RESULTS IN TERMINAL NECROSIS OF EXTREMITIES, inhibition of prolactin (decreases milk production), and mimic action of dopamine in CNS.

56
Q

Ergotism clinical signs and what species are affected?

A 
PSYCHOACTIVE SIGNS (convulsions, hallucinations, abortions), PARALYSIS, GI ISSUES, GANGRENE OF EXTREMETIES, DEATH;
Species affected include farm animals and horses
57
Q

What is the very first sign of Ergotism?

A

Lameness, standing in mud or water, then dry gangrene, then agalactia, hyperexcitability, hypermetric, tremors and heat intolerances

58
Q

Lab diagnosis of Ergotism:

A

Hard to do, analyze tissues or bodily fluids, thin layer chromatography of feed also done.

59
Q

Lesions associated with Ergotism:

A

Small, flaccid mammary glands without lacteal secretion, microscopic lesions of gangrene

60
Q

TX of Ergotism and prevention:

A

TX: no specific tx, remove source, provide supplemental feeding to babies
Prevention: Do not feed grain known with ergot to preg. or lactating sows. Dilute with non-infected feeds/

61
Q

Ergotism vs. Fescue foot:

A

Ergotism is prevalent in late summer and occurs in seed heads of grass with mature seeds.
Fescue foot is common in fall and winter and can occur from dried fescue free of seed heads

62
Q

Ryegrass staggers are caused by ____ _____ and assoc. with changes in the GABA neurotransmitters in the cerebellum.

A

Endophytic fungus

63
Q

What is the lesion assoc. with ryegrass? What animals does it affect? What are the clinical signs?

A

None; affects cattle, sheep, horses; causes muscle tremors and ataxia

64
Q

Though there are no physical lesions assoc. with ryegrass, there are clinical signs.. what are they???

A

Fine head tremors, nodding, more severe with heat stress, stress, exercise, noises. Signs develop gradually over a few days esp. on lush new ryegrass.

65
Q

What causes the death assoc. with ryegrass toxicity?

A

Acting a fool/hallucinations

66
Q

Dallisgrass (Paspalum d latatum) is found in the ____ regions and is heat tolerant

A

Southeast

67
Q

Dallisgrass Staggers/poisoning can occur after several days, after cattle ingest a signifcant amount of it. T/F

A

True!!

68
Q

When is dallisgrass most toxic?

A

When it turns that brown color, seedheads are usually infected with the fungus in the later summer and fall, as the seedheads age.

69
Q

The fungus only affects _____ and the other parts of the plant are nontoxic

A

Seedheads

70
Q

Dallisgrass cattle toxicity leads to ___ ____

A

Ergot alkaloids

71
Q

Clinical signs of dallisgrass

A

Early stages- muscle tremors a exercising, progresses to ataxia/incoordination, shaking or bobbing head, staggering, inability to stand, might bloat/die

72
Q

Tx of dallisgrass toxicity

A

No specific tx, remove source, clinical signs WILL resolve in 3-5 days. Clip pastures to remove the seed heads as needed. Dilute with noninfectious feeds to get it out of their system, leave p that was exposed for 2-3 weeks (do not mess or move them bc high stress will make them be neurologic and act crazy and prob try to kill you!!)

73
Q

What is an example of a field mold? Do they grow after harvested?

A

Fuscarium; no growth after harvested or while in storage

74
Q

What are examples of storage fungi which thrive after harvesting in storage?

A

Aspergillus and penicillium

75
Q

Can you assume you have other mycotoxins if just one is isolated?

A

ohhh yeaaaa

76
Q

Aspergillus prefers what climate unlike the others?

A

Hot and humid

77
Q

What glows glue/green under IV light?

A

Aflatoxin

78
Q

White and yellow corn causes….

A

Fumonisins

79
Q

Fumonisins species affected in order from most to least:

A

Horses>ruminants>swine>poultry

80
Q

Evidence of hepatic dysfunction and a potential carcinogen in humans is….

A

Fumonisins

Toxo Exam I (11 decks)

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