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Toxicology > Mycotoxins > Flashcards

Mycotoxins Flashcards

1
Q

What are mycotoxins?

A
  • Metabolites of fungi, recongized as toxic to other life forms
  • 400+ mycotoxins based on experimental or field conditions
  • relatively stble once formed
    *
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2
Q

How are mycotoxins formed?

A

environmental & crop stress + genetic effect turns basic nutrients into secondary metabolites for survival or defense

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3
Q

What are the major mycotoxins from grains in North America

A
  • Aflatoxins
  • Trichothecenes (DON)
  • Zearalenone
  • Ergot
  • Fumonisins
  • Ochratoxin
  • Citrinin
  • Penitrem A
  • Roquefortine
  • Patulin
  • Mycophernolic acid
  • Penicillic acid
  • Wortmannin
  • Gliotoxin
  • Sterigmatocystin
  • Verruculogen
  • Alternariol
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4
Q

What are the major mycotoxins from foragess in North America

A
  • Ergovaline (fescue)
  • dicoumarol (sweet clover)
  • Slaframine (red clover)
  • Paspalitrem (dallis grass)
  • lolitrem B (ryegrass)
  • Sporodesmin
  • 2-bromo-alpha-ergocryptine
  • Ergometrine/ergonovine
  • Ergotamine
  • Lysergol
  • Methylergonovine
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5
Q

What factors influence mycotoxin production?

A
  • Plant varieties
  • Climate and Wather
  • Crop monoculture
  • Seed coat damage
  • Insect transport
  • Storage quality
  • Milling practices
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6
Q

What are the mycotoxins of most concern?

A
  • Aflatoxin
  • Deoxynivalenol
  • T2
  • Ergot
  • Fumonisins
  • Ochratoxin
  • Zearalenone
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7
Q

Where does Aflatoxin come from?

A
  • Aspergillus flavus
  • A. parasiticus
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8
Q

What are the common substrates for aflatoxin?

A
  • Corn
  • milo
  • cotton seed
  • peanutes
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9
Q

What are the factors that favor aflatoxin formation?

A
  • Temperatures 78-90F
  • Drought stress, insect damage
  • High relative humidity or grain moisture
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10
Q

What is the MOA of Aflatoxin?

A
  • Metabolized to epoxide that binds to nucleic acids
  • Inhibit protein synthesis ⇢ liver damage
  • Carcinogen in laboratory animals
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11
Q

What is aflotoxin’s affect on immune function?

A
  • Both humoral and cell-mediated
  • Reduces resistance to several infectious diseases
    *
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12
Q

What are the effects of Aflatoxin?

A
  • Reduced growth & productivity
  • hepatic lipidosis & necrosis
  • chronic hepatic damage
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13
Q

What are Trichothecene mycotoxins?

A
  • Complex sesquiterpenes with an epoxide ring
  • Fusarium spp. produces 60 toxins, mainly T-2, diacetoxyscirpenol, deoxynivalenol (DON)
  • Favored by cool temperatures or alternating cool and warm temperatures, higher moisture
  • Fusaria in storage require >20% moisture for optimum growth and toxin formation
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14
Q

What are the effects of Trichothecene?

A
  • Radiomimetic Syndrome (pancytopenia, diarrhea)
  • Irritant and necrotizing to mucosae and skin
  • Lymphoid depletion - GI tract
  • Thymic involution/suppression
  • Some aspects of immunosuppression - mainly cell mediated immunity
  • Rapidly metabolized and excreted
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15
Q

What mycotoxins come from Fusarium spp?

A
  • Deoxynivalenol (DON) - F. graminearum and culmorum
  • Fumonisins
  • Zearalenone
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16
Q

What affect does Deoxynivalenol (DON) have?

A
  • Vomitoxin
  • Neurochemical effect (serotonin)
    • increased levels of serotonin are responsible for the anorexic effect
  • Swine most sensitive
  • Vomiting @ 5-8 ppm
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17
Q

What are the effects of Zearalenone?

A
  • F-2 toxin or Giberella Toxin
  • Hyperestrogenism @ > 1ppm
  • Anestrus - retained CL @ > 3ppm
  • Embryonic Loss by failed implantation
  • luteotropic - NOT abortive in sows
  • Decreased libido/fertility in boars
  • Infertility in heifers @ >12 ppm
  • negative effects on semen quality
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18
Q

What are Fumonisin Mycotoxins?

A
  • Recently discovered (1988)
  • FB1, FB2, FB3
  • Water soluble toxins
  • Swine and Horses most affected
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19
Q

What are the effects of Fumonisins?

A
  • Liver toxicosis is common lesion
  • Leukoencephalomalacia in horses
  • Pulmonary Edema in swine
  • Recently reported as carcinogens
20
Q

What are the clinical signs of Fumonisin mycotoxin in horses?

(moldy corn poisoning)

A
  • Stumbling
  • blind
  • ataxia
  • depression
  • anorexia
  • high mortality
21
Q

What are the clinical signs of Fumonisin mycotoxin in swine?

A
  • Dyspnea
  • Cyanosis
  • weakness
  • death in 3-4 hours
22
Q

What is the clinical chemistry associated with Fumisin mycotoxin in swine?

A
  • Increased Sphinganine
  • Increased Cholesterol
  • Elevated LDH
  • Increased AST
  • High GGT levels
  • Increased serum bilirubin
23
Q

What are sphingolipids

A
  • cell membrane lipids
24
Q

What molds produce Ochratoxin?

A
  • Aspergillus ochraceus
  • Penicillium viridicatum
25
Q

What are the effects of Ochratoxin and Citrinin?

A
  • Nephrotoxic
  • Often accompanied by gastric ulcers
  • Depression early
  • Urine - low specific gravity
  • PD/PU
  • Primary lesion - toxic tubular damage
  • Survivors may have chronic renal scars
26
Q

Why are monogastrics more sensitive to Ochratoxin

A

inactivated in the rumen

27
Q

What common substrates are sources of Ergot?

A
  • Caused by Claviceps purpurea
  • Rye
  • Barley
  • Wheat
  • Oats
  • Brome other grasses
28
Q

What factors favor the production of Ergot?

A
  • humidity
  • moderate temperatures
29
Q

What is the MOA of Ergot?

A
  • Sclerotia containt ergopeptide alkaloids
  • Similar in action to ergovaline from tall fescue
  • Alkaloids are related to LSD
30
Q

What affects does Ergot poisoning have?

A
  • Classic lesion - peripheral gangrene
    • Peripheral vasoconstriction with dry gangrene, sloughing of feet, tail, ears
  • Abortion unlikely
  • Inhibit Prolactin release
  • Non-inflammatory agalactia
    • Neonates starve
  • Hyperthermia, heat intolerance in cattle
  • Hyperexcitability tremors
31
Q

How is Ergot poisoning diagnosed?

A
  • Hx, clinical signs
  • Lesions
  • Examine hay/grain
    • sclerotia on wt/wt basis - 0.3% allowed
  • Assay for alkaloids in feeds or urine -
    • excreted rapidly -need samples within 48 hours after exposure stops
32
Q

What is Slaframine?

A
  • Formed by Rhizoctonia leguminicola infested Red clover
    • causes “black patch”
  • Favored by cool wet weather
  • Found on clover in fresh pasture, hay, silage
33
Q

What is the MOA of Slaframine?

A
  • Bio-activated by liver microsomes to a parasympathomimetic quaternary amine vary similar to acetylcholine
  • “slobber factor:
34
Q

What are the clinical affects of Slaframine?

A

Profuse salivation ~30min post ingestion

35
Q

What are the Tremorgenic Mycotoxins? sources?

A
  • Penitrem A
    • moldy cream cheese, bread, macaroni & cheese, walnutes
  • Roquefortine
    • Moldy blue cheese, cream cheese, decaying organic matter (compost)
  • From Penicillium fungi
36
Q

What is the MOA of Tremorgenic Mycotoxins

A
  • Indole structure similar to lysergic acid
37
Q

What are the clinical signs of Tremorgenic Mycotoxins?

A
  • Acute:
    • restlessness, panting, excessive salivation, vomiting
    • Progressive mild to whole body muscle tremors
  • Advanced:
    • looks like strychnine
    • Tremors more severe
    • Hyperresponsiveness to external stimuli
    • Seizures
    • Hyperthermia, exhaustion, dehydration
38
Q

How is Tremorgenic Mycotosis diagnosed

A
  • Hx of eating moldy foods
  • Compatible clinical signs
  • Chemical detection of penitrem A or roquefortine
    • vomitus, stomach content, suspect material
39
Q

How is Tremorgenic Mycotoxicosis treated?

A
  • Control agitation, tremors and seizures
    • Diazepam / methocarbamol
  • Decontamination with activated charcoal and saline cathartic
  • IV fluids
  • Revocer in 24-48 hours w/ aggressive treatment
40
Q

How is Mycotoxicosis diagnosed?

A
  • Circumstantial or hx information
  • Mold cultures and spore counts
  • Clinical signs
  • Lesions and clinical shemistry
  • Chemical detection of mycotoxins
  • Test feeding of suspect ration
41
Q

What is the Black light test? (Mycotoxins)

A
  • Visualize grain under UV light
  • Useful only for aflatoxin screening
  • Measure non-aflatoxin metabolite
    • kojic acid
  • Not quantitative
  • Best if grain is cracked
  • Firefly or bright green-yellow fluorescence (BGYF) is positive
42
Q

How can Mycotoxin formation be prevented?

A
  • Survey weather and crop conditions
  • Remove damage grain by screening
  • Keep storage facilities clean
  • Keep grain cool
  • Avoid moisture in storage
  • Use feed promptly after milling
  • Use mold inhibitors / adsorbents
43
Q

What are Mold inhibitors?

A
  • Primarily organic acids
  • Suppress mold growth
  • Do NOT destroy mycotoxins
  • Will NOT restore grain quality
44
Q

What are adsorbents for Mycotoxins?

A
  • Calcium Aluminosilicates are effective for aflatoxins
  • Mycosorb alternative adsorbent for aflatoxins and others
  • Bentonite is effective for AF
  • Sodium metabisulfite & diatomaceous earth limited effectiveness
  • Activated charcoal and 25% alfalfa meal effective for zearalenone
45
Q

What are mycotoxin binders?

A
  • Zeolites and clays
  • Cell-wall fraction B-glucan of yeasts
  • Glucomannans
  • Labels call them:
    • preservatives
    • Antioxidants
    • Amino Acid
    • Direct-fed microbials
46
Q

What are the strategies for preventing mycotoxins?

A
  • Know contaminant levels
  • Test suspect feeds
  • dilute damaged grain
  • Feed to alternative species
  • supplement with high quality nutrients

Toxicology (25 decks)

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