Etiology

• Mycotoxins are diverse, secondary toxic metabolites produced by molds, especially Aspergillus spp Aspergillus spp, Penicillium spp (aflatoxins, ochratoxins) and Fusarium spp (fumonisins) Sweet potato poisoning.
• Clinical signs are due to the action of these mycotoxins and not fungal growth or allergic reactions to foreign proteins within the affected animal.

Predisposing factors

General

• Spoilage of feedstuff by fungi.
• Depends on moisture content, viability, physical state of grain and insect activity.
• Seasonal.
• Climatic conditions.
• TMR feeding may precipitate mycotoxins being widely disseminated to a greater number of animals.

Specific

• Field fungi: grow under conditions prior to harvest, eg Fusarium spp, require relative humidity above 90%.
• Storage fungi, eg Aspergillus spp, especially in leaky containers or after long periods of storage.
• Note that this division of field and storage molds is not distinct, and some fungal species can affect feed under both field and storage conditions.

Pathophysiology

• Ruminants are relatively resistant to mycotoxins but detoxification by rumen bacteria may be overwhelmed, and the risk of toxic effects is increased if multiple mycotoxins with synergistic effects are involved.
• 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.

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.

Affect on carbohydrate metabolism

• Aflatoxins, ochratoxin A, rubratoxin B, cyclochlorotine and citreoviridin.
• Inhibit biosynthetic enzymes such as glycogen synthetase and increasing the activity of enzymes metabolizing glycogen precursors resulting in reduced hepatic glycogen and increased blood glucose concentrations.

Other mechanisms

• Ergotism Ergotism and fescue foot Distal limb necrosis: the ergopeptine alkaloids inhibit D1-dopaminergic receptors and are partial agonists of alpha-1 adrenergic and serotonin receptors, resulting in vasoconstriction.
• Slaframine: acts as a parasympathomimetic agent and stimulates exocrine and endocrine glands, particularly the salivary glands and pancreas.
• Sporidesmin: undergoes cyclic reduction/auto-oxidation to produce superoxide radicals which cause tissue damage.

Timecourse

• May be acute or chronic.

Epidemiology

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