MycotoxinsRobert H. Poppenga

CHAPTER 206 Mycotoxins



Robert H. Poppenga


Mycotoxins are metabolic products of molds growing in or on grains and forages. Although the terms mold and fungus are often used interchangeably, the fungi include molds, yeasts, rusts, smuts, mushrooms, and mildews. Molds are filamentous organisms that produce spores that can be air, water, or insect borne; molds are responsible for producing most of the mycotoxins of relevance for horses. However, for the purposes of the following discussion, the broader term, fungus, will be used. The diseases caused by mycotoxins are called mycotoxicoses. The term toxigenic refers to fungi that are capable of producing mycotoxins.


Mycotoxins are not essential for fungal survival and are produced only sporadically in response to adverse plant and environmental conditions that are often specific for each toxigenic fungus. Such conditions include plant damage secondary to insect infestations or mechanical harvesting, drought, periods of unusual temperature and humidity, or improper storage. Mycotoxin occurrence tends to be sporadic and geographically restricted. However, the widespread movement of grains and forages can result in mycotoxicoses in unexpected areas.


Although fungal growth is a prerequisite for mycotoxin production, such growth is not always visually apparent on affected grains and forages or on culture media.Several relevant toxigenic forage fungi, such as Neotyphodium coenophialum, which is found in tall fescue (Festuca arundinacea Schreber), are endophytic, meaning that they live within plant tissue for all or part of their life cycle and cannot be identified by simple visual inspection of the plant.


Fungi can be classified as either field or storage fungi. Field fungi develop before harvest and include common toxigenic Fusarium spp. Field fungi grow poorly after harvest if the moisture content of the feed is kept below about 22%. Storage fungi such as Aspergillus spp. and Penicillium spp. can grow and produce mycotoxins at relatively low feed moisture content and within temperature ranges of 10° to 50° C.


There is little correlation between the degree of fungal contamination and growth and the concentrations of mycotoxins present. Mycotoxins can persist in fungus-free feeds because most mycotoxins in North America are resistant to degradation by factors that destroy or prevent fungal growth, including low moisture content, high-temperature drying, high temperature and pressure applied during feed processing, or chemical treatment of feeds with propionic acid to prevent fungal growth.


Mycotoxins found in feed grains in North America that are of concern for horses include aflatoxins and fumonisins. Forage-associated mycotoxins of relevance include slaframine and swainsonine (red clover), paspalitrems (dallis and bahia grasses), lolitrems (perennial ryegrass), and ergot alkaloids (especially ergovaline, found in tall fescue). Whereas other mycotoxins, such as zearalenone, deoxynivalenol (DON), T-2 toxin, ochratoxin, and citrinin, are identified in feedstuffs (primarily grains) in North America, they are not associated with significant morbidity in horses.



GRAIN-ASSOCIATED MYCOTOXICOSES



Aflatoxicosis


Aflatoxins (B1, B2, G1, and G2) are found in grains such as corn, milo, cottonseed, and peanuts. They are produced by Aspergillus flavus and A parasiticus, which are most commonly found in warm, humid regions. Aflatoxin B1 is of most toxicologic concern. It is metabolized in the liver to a reactive epoxide that binds covalently to nucleic acids and proteins in hepatocytes, producing characteristic liver lesions of fatty change and necrosis. Although natural cases of aflatoxicosis in horses are infrequently reported, the risk for exposure is certainly present. Acute or chronic intoxication can occur, depending on the degree and length of exposure. Experimentally, dietary concentrations of approximately 3.8 parts per million (ppm) cause death in ponies dosed for 37 to 39 days. A single oral dose of aflatoxin B1 as low as 2 mg/kg can cause death. Dietary concentrations of total aflatoxins of 0.5 to 1.0 ppm can cause weight loss and liver damage. Chronic exposure to dietary concentrations of total aflatoxins greater than 200 parts per billion (ppb) is likely to be associated with adverse effects.


Clinical signs of aflatoxicosis are dependent on whether acute or chronic liver disease is induced. Acute liver damage is associated with fever, anorexia, ataxia, colic, tachycardia, seizures, icterus, hematochezia, and tenesmus. Hepatic encephalopathy, manifested as belligerence, somnolence or depression, circling, blindness, and head pressing, is more likely to be associated with chronic aflatoxicosis.


A diagnosis of aflatoxicosis depends on the presence of hepatic disease and detection of potentially toxic concentrations of aflatoxins in representative feed samples. Unfortunately, as with other mycotoxins, failure to detect aflatoxins in a feed sample does not rule out animal exposure because the offending feed may have already been consumed or nonrepresentative samples may have been collected for analysis. Histologic evaluation of a liver biopsy specimen may be highly suggestive of aflatoxin exposure.


Differential diagnoses for acute liver disease include iron and fumonisin mycotoxin intoxications, drug-induced hepatopathy, Theiler’s disease, Tyzzer’s disease, hyperlipemia, infectious necrotic hepatitis, cholangiohepatitis, acute biliary obstruction, and parasitic or virus-induced hepatitis. Differential diagnoses for chronic aflatoxicosis include pyrrolizidine alkaloid intoxication, pasture-associated hepatopathy (alsike clover or Klein grass intoxication), chronic active hepatitis, cholelithiasis, neoplasia, amyloidosis, and chronic hepatic hypoxia.

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May 28, 2016 | Posted by in EQUINE MEDICINE | Comments Off on MycotoxinsRobert H. Poppenga

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