ISSN 2398-2977      

Mycotoxicosis

pequis

Synonym(s): Mycotoxin poisoning, Ryegrass staggers, aflatoxicosis, leukoencephalomalacia, lapinosis, gangrenous and tremorgenics ergotism, slobbers

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Introduction

  • Mycotoxicoses are poisonings caused by secondary toxic metabolites produced by molds.
  • Cause: important mycotoxin-producing, include Penicillium spp, Claviceps spp, Phomopsis leptostromiformis, Rhizoctonia leguminicola.
  • Signs: vary depending on toxin and species. Mycotoxins affect almost all organ systems. Ergot and some Penicillium spp produce indole tremorgens which affect the nervous system.
  • Diagnosis: difficult. Mycotoxin isolation from feed, clinical signs and history, feeding trials.
  • Treatment: removal of toxin source; supportive therapy.
  • Prognosis: depends on toxin, dose and clinical course.

Pathogenesis

Etiology

  • Mycotoxins are secondary toxic metabolites produced by molds, especially Aspergillus spp Aspergillus spp, Penicillium spp (aflatoxins, ochratoxins) and Fusarium spp (fumonisins).

Predisposing factors

General

  • Spoilage of feedstuff by fungi.
  • Depends on moisture content, viability, physical state of grain and insect activity.
  • Seasonal.
  • Climatic conditions.

Specific

  • Field fungi: grow under conditions prior to harvest, egFusariumspp, require relative humidity above 90%.
  • Storage fungi, eg Aspergillus spp, especially in leaky containers or after long periods of storage.

Pathophysiology

  • Mycotoxins affect metabolic and anabolic processes in various organ systems.
  • Four general mechanisms affect carbohydrate metabolism, mitochondrial function, lipid metabolism or nucleic acid function and protein biosynthesis.
  • Mycotoxins may affect a variety of cellular processes.
  • May require activation by biotransformation.

Effects on carbohydrate metabolism

  • Aflatoxins, ochratoxins, rubratoxin, cyclochlorotine.
  • Reduced glycogen synthesis.

Disruption of mitochondrial function

  • Aflatoxins, ochratoxins, rubratoxin.
  • Inhibit electron transport and uncouple oxidative phosphorylation.

Altered lipid metabolism

  • Reduced fatty acid and cholesterol biosynthesis.
  • Impaired lipid transport.
  • Disruption of sphingolipid metabolism (fumonisins).

Altered nucleic acid function and protein synthesis

  • Aflatoxin, trichothecenes.
  • Modification of DNA, inhibition of RNA polymerase, increased RNA breakdown.

Timecourse

  • May be acute or chronic.

Epidemiology

  • Not transmissible between animals.
  • Common source outbreaks.
  • Association with particular feedstuff.
  • Field outbreaks seasonal and associated with particular climatic patterns.
  • May be difficult or impossible to identify cause.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Johnstone L K, Mayhew I G & Fletcher L R (2012) Clinical expression of loitrem B (perennieal rygrass) intoxication in horses. Equine Vet J 44 (3), 304-309 PubMed.
  • Hasso S A (2003) Non-fatal aflatoxicosis in Arabian horses in Iraq. Vet Rec 24 (152), 657-658 PubMed.
  • Lebars J & Lebars P (1996) Recent acute and subacute mycotoxicoses recognized in France. Vet Res 27 (4-5), 383-394 PubMed.
  • Diaz G J & Boermans H J (1994) Fumonisin toxicosis in domestic animals - a review. Vet Human Toxicol 36 (6), 548-555 PubMed.

Other sources of information

  • Plumlee K H (1997) Mycotoxins. In: Current Therapy in Equine Medicine IV. Ed: N E Robinson. W B Saunders, UK. pp 668-670.

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