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Mycotoxicosis

ISSN 2398-2977


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

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.

Presenting signs

  • Depends on toxin involved. Many possible effects, either acute or chronic.
  • Hepatotoxicosis (acute or chronic), eg aflatoxins and phomopsins (lapinosis).
  • Acute: jaundice, anemia, hemorrhages; chronic: poor performance.
  • Nephrotoxicosis, eg citrinin: polyuria, polydipsia.
  • Hematopoietic changes and coagulopathies, eg aflatoxins.
  • Irritation → dermatonecrosis, gastrointestinal ulceration, eg trichothecenes.
  • Endocrine and reproductive problems, eg ergoline alkaloids.
  • Feed refusal - trichothecene ergoline alkaloids and indole tremorgens.
  • Central nervous system effects, eg fumonisins → equine leukoencephalomalacia.
  • Immune system effects, eg aflatoxins and trichothecenes.

Acute presentation

  • May cause acute liver failure, renal failure or central nervous system disease.

Geographic incidence

  • USA.
  • Europe.
  • Southern Africa.
  • Australia.
  • New Zealand.

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

Presenting problems

  • Jaundice.
  • Anemia.
  • Petechiae.
  • Anorexia.
  • Exercise intolerance.
  • Polyuria.
  • Polydipsia.
  • Alimentary tract ulceration.
  • Dermal necrosis.
  • Diarrhea.
  • Hypersalivation.
  • Ataxia.
  • Tremors.
  • Seizures.

Client history

  • Refusal of food.
  • Exercise intolerance or poor performance.
  • Tremors.
  • Ataxia.
  • Jaundice.
  • Polyuria and polydipsia.
  • Weakness.
  • Skin lesions.
  • Oral ulcers.
  • Hypersalivation.
  • Diarrhea.
  • Hematuria.
  • Seizures.

Clinical signs

  • Anemia Oral mucosa: pallor 01Conjunctiva: pallor 01.
  • Petechiation Oral mucosa: petechiation.
  • Icterus Sclera: icterusMouth: icterus - gums.
  • Ataxia.
  • Tremors, hyperexcitability.
  • Weakness.
  • Excessive salivation (slaframine).

Diagnostic investigation

Other

  • Examination of feed reveals signs of fungal activity.
  • Isolation of mycotoxin from feed.
  • Test feeding of suspect feed.

Hematology

Biochemistry

Confirmation of diagnosis

Discriminatory diagnostic features

  • Clinical signs.
  • History.
  • Hematology.
  • Biochemistry.

Definitive diagnostic features

  • Identification of toxin in feed.

Gross autopsy findings

  • Depends on toxin and organ involved.
  • Liver is swollen in actue aflatoxicxosis but smaller than normal if chronic.
  • Kidneys may be pale in ochratoxicosis.

Differential diagnosis

  • Depends on particular toxin and manifestation.

Hepatic disease

Renal failure

Treatment

Initial symptomatic treatment

  • Removal of source of toxin.
  • Supportive therapy depending on clinical signs.

Standard treatment

  • Removal of source of toxin, ie change feed.

Monitoring

  • Clinical signs.
  • Development of renal or hepatic disease.
  • Serum chemistry profile.
  • Urinalysis.

Subsequent management

Treatment

  • Symptomatic therapy.

Monitoring

  • Clinical signs.
  • Hematology.
  • Biochemistry, especially renal and hepatic function.

Prevention

Control

  • Avoid feeding contaminated materials.
  • Storage in dry, enclosed containers.
  • Avoid long-term storage of feedstuffs.
  • Analyze feedstuffs before feeding.

Group eradication

  • Removal of contaminated feed.

Outcomes

Prognosis

  • Depends on dose, type of mycotoxin and clinical manifestations.

Expected response to treatment

  • Clinical signs.
  • Hepatic and renal function.

Reasons for treatment failure

  • Large ingested dose.
  • Acute hepatic or renal failure.
  • Severe nervous system involvement.

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.