Mycotoxins Flashcards

1
Q

Mycotoxins Characteristis

A

Non-antigenic, heat-stable metabolites of filamentous fungi [plant pathogens]
Produced by fungi growing on crops or in stored feed

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2
Q

Mycotoxins

Predisposing factors

A

Availability of usable substrate
Ambient temperature [20oC to 30oC]
Moisture
Damage by insects and harvesting machines

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3
Q

Mycotoxicoses

A

Diseases associated with fungal toxin
Acciddental or ingestion of toxic fungi
Their metabolites

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4
Q

Mycotoxins Obersvations

A
  • Not all moldy feeds/foods contain Mycotoxins
  • Not all feeds/foods containing Mycotoxins are toxic
  • Feed/food does not have to look moldy to be contaminated
  • May not be uniformly distributed
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5
Q

Toxic Mold Disease Endpoints

A

Allergy: Sensitization to mold or mold products
Mycosis: Direct infection by fungi
Irritation: Mechanical effects pf spores, mycelia debris
Mycotoxicosis: Response to toxins

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6
Q

Mycotoxins

Transmission

A

Ingestion of contaminated plant material or feed

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7
Q

Mycotoxins

Susceptibility

A

Species, age, and sex

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8
Q

Mycotoxins

Clinical Findings

A

Acute or chronic; rapid death to tumor formation

Immunosuppression, organ degeneration, endo-crine disturbances, neoplasms, etc

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9
Q

Mycotoxins

Diagnosis

A

History, clinical signs, and lesions

Detection of toxic levels of mycotoxin in the animal and/or feed

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10
Q

Mycotoxins

Treatment

A

Remove source of toxin

Symptomatic

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11
Q

Aflatoxicosis

A

Produced mostly by Aspergillus flavus and Aspergillus parasiticus

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12
Q

Aflartoxicosis

Sources

A

Peanuts, corn, cottonseed, etc

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13
Q

Aflatoxicosis

Specie Susceptibility

A

Poultry are more susceptible than mammals

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14
Q

Aspergillus (AFLATOXINS)

Characterisitic

A

Dietary carcinogen
From Aspergillus flavus
Universal food contaminant
- Corn peanuts and wheat rice

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15
Q

Types of Aflatoxins

A

B [blue fluorescence] group: B1 [most abundant] and B2
G [green fluorescence] group: G1 and G2
M: Found in milk

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16
Q

Aflatoxicosis

Pathogenesis

A

-Primary target organ: Liver—hepatocellular necrosis, fatty degeneration, hepatoma, etc
Carcinogenesis—Activation of proto-oncogenes
-Immunosuppression
Depressed activity of phagocytes

17
Q

Diseases of Alfatoxicosis

A
Turkey X disease (birds)
Cancer in humans 
Pharmacological and clinical syndroms 
Anorexia and muscle weakness
Spasm and death
hemorrhage and necrosis of liver
18
Q

Aflatoxicosis

Clinical Findings

A

Acute—rapid death; hepatic necrosis, etc

Chronic—reduced weight gain, icterus, hepatic cirr-hosis, hepatoma or hepatocellular carcinoma, etc

19
Q

Alfatoxicosis

Diagnosis

A

Clinical signs and lesions
Detection of aflatoxins in feed, urine, milk, etc
Characteristic blue or green fluorescence of feed
Liver function tests

20
Q

Ergot alkaloids (Claviceps)

A
Bacteria: Claviceps purpurea 
Grows in wet and over wintered 
grains: rye, barle, wheat 
Sclerotia oor ergots 
      - Hard-packed mycelium
Ergotism
Gangrene and/or convulsions and gastrointestinal symptoms
Livestock: decreased weight gains, milk production, and reproductive efficiency
21
Q

Ergotism

A

Following ingestion of sclerotia [ergots] of Claviceps purpurea
Ergots replace the seed heads of wheat, rye-grass, barley, etc
Species affected
Mainly cattle, swine, sheep, and poultr

22
Q

Ergotism

Alkaloids

A

Ergotamine, ergometrine, ergocristine, etc

23
Q

Ergotism

Pathogenesis

A

Constriction of smooth muscles
Vasoconstriction—blood stasis and gangrene
Oxytocic action—abortion
CNS signs

24
Q

Ergotism

Clinical Findings

A
Gangrenous ergotism
Peripheral vasoconstriction
Convulsive ergotism
Abortion—cattle and swine
Agalactia
Prolactin inhibitor
25
Q

How Ergot Exposure Occurs

A

Claviceps purpure - spoil
Spores released when grain flowers
Land on stigma: germinate: hyphae extend into the ovary
Replaces the ovary - harden ergot body or sclerotium, recyle
- Seeds and sclerotida harvested together
- Screening techniques to remove the ergot based on size and weight
- Exposure occurs by ingesting grain/food