Acute or chronic toxicoses can result from exposure to feed or bedding contaminated with toxins produced during growth of various saprophytic or phytopathogenic fungi or molds on cereals, hay, straw, pastures, or any other fodder. These toxins are not consistently produced by specific molds and are known as secondary (not essential) metabolites that are formed under conditions of stress to the fungus or its plant host.
A few principles characterize mycotoxic diseases: 1) The cause may not be immediately identified. 2) They are not transmissible from one animal to another. 3) Treatment with drugs or antibiotics has little effect on the course of the disease. 4) Outbreaks are often seasonal, because particular climatic sequences may favor fungal growth and toxin production. 5) Study indicates specific association with a particular feed. 6) Large numbers of fungi or their spores found on examination of feedstuffs does not necessarily indicate that toxin production has occurred. However, absence of molds does not exclude mycotoxicosis, because feed storage or preparation conditions, eg, acid treatment or high pelleting, can destroy molds while the heat-tolerant mycotoxin persists.
Diagnosis of mycotoxic disease requires a combination of information. Most veterinary mycotoxicoses are found in large animal species, but important outbreaks can happen in pets and exotic animals. Especially important in diagnosis is the presence of a disease documented to be caused by a known mycotoxin, combined with detection of the mycotoxin in either feedstuffs or animal tissues.
Sometimes more than one mycotoxin may be present in feedstuffs, and their different toxicologic properties may cause clinical signs and lesions inconsistent with those seen when animals are dosed experimentally with pure, single mycotoxins. Some mycotoxins are immunosuppressive, which may allow viruses, bacteria, or parasites to create a secondary disease that is more obvious than the primary. When immunosuppression by a mycotoxin is suspected, differential diagnoses must be carefully established by thorough clinical and historical evaluation, examination of production records, and appropriate diagnostic testing.
Mycotoxicoses are generally not successfully treated with medical therapy after diagnosis. A preventive approach with recognition of risk factors and avoiding or reducing exposure is preferred. Best management practices are aimed at prevention of the occurrence of mycotoxins, inactivation of the preformed toxin in grain or feed, and adsorption or inactivation of the toxin in the GI tract. Testing of suspect grain at harvest, maintaining clean and dry storage facilities, using acid additives (eg, propionic acid) to control mold growth in storage, ensuring effective air exclusion in silage storage, and reducing storage time of prepared feeds are established procedures to prevent mycotoxin formation. Acidic additives control mold growth but do not destroy preformed toxins.
There are no specific antidotes for mycotoxins; removal of the source of the toxin (ie, the moldy feedstuff) eliminates further exposure. The absorption of some mycotoxins (eg, aflatoxin) has been effectively prevented by aluminosilicates. If financial circumstances do not allow for disposal of the moldy feed, it can be blended with unspoiled feed just before feeding to reduce the toxin concentration. This approach should be monitored by follow-up toxin analysis and may not be acceptable to regulatory agencies. Alternatively, feed with known mycotoxin concentrations can be fed to less susceptible species, remembering that some mycotoxins such as aflatoxin could result in violative food residues in the absence of illness. When contaminated feed is blended with good feed, care must be taken to prevent further mold growth by the toxigenic contaminants. This may be accomplished by thorough drying or by addition of organic acids (eg, propionic acid).
Important mycotoxic diseases occur in domestic animals worldwide (see Table: Mycotoxicoses in Domestic Animals Mycotoxicoses in Domestic Animals For discussion of mycotoxicoses in poultry, see Mycotoxicoses. Acute or chronic toxicoses can result from exposure to feed or bedding contaminated with toxins produced during growth of various... read more ).
When mycotoxicosis is suspected, corrective actions could include the following: 1) Change the feed even when a specific mycotoxin is not identified. 2) Thoroughly inspect storage bins, mixing equipment, and feeders for caking, molding, or musty odors. 3) Remove contaminated feed and clean equipment and sanitize with hypochlorite (laundry bleach) to reduce contaminating fungi. 4) Analyze for known mycotoxins. 5) Use spore counts or fungal cultures for some indication of potential mycotoxin production. 6) If storage conditions or grain moisture are adverse, use a mold inhibitor to reduce or delay mold growth. Remember, mold inhibitors do not destroy preformed toxins. 7) Use a mycotoxin adsorbent if appropriate for the mycotoxin suspected. 8) Save a representative sample of each diet mixed until animals are at 1 mo beyond when the feed was consumed. 9) Take a representative sample of suspect feed after milling by passing a cup through a moving auger stream at frequent intervals, mixing samples thoroughly, and saving a 4.5-kg (10-lb) sample for analysis. Alternatively, use probe sampling of recently blended grain in bins or trucks at five locations in each structure for each 6 feet of depth. Freeze or dry samples, and submit for analysis in a paper bag (not plastic). Dry samples are preferable in a paper bag to prevent condensation during transport and storage. Samples should be dried at 176°–194°F (80°–90°C) for ~3 hr to reduce moisture to 12%–13%. If mold studies are to be done, dry at 140°F (60°C) for 6–12 hr to preserve fungal activity.
Adsorption of mycotoxins in contaminated feeds is an area of active research. Aflatoxins are effectively adsorbed by the aluminosilicate feed additives (see Aflatoxicosis Aflatoxicosis Aflatoxins are produced by toxigenic strains of Aspergillus flavus and A parasiticus on peanuts, soybeans, corn (maize), and other cereals either in the field or during storage when moisture... read more ). However, this group of adsorbents are of little or limited use for other mycototoxins. Trichothecene mycotoxins, including deoxynivalenol, are not readily adsorbed by common feed additives. The aluminosilicate adsorbents that are effective against aflatoxins have limited or no benefits against trichothecenes. Sodium bentonite is an effective adsorbent for aflatoxins in cattle and poultry but appears ineffective for trichothecenes and zearalenone. The polymeric glucomannan adsorbents (GM) are useful for poultry growth and feed consumption with low natural concentrations of aflatoxin, ochratoxin, T-2 toxin, and zearalenone. When added to Fusarium-contaminated diets, GM reduced the number of stillborn piglets compared with controls. GM adsorbent efficacy for ruminants has been variable in different studies. Cholestyramine has been an effective binder of fumonisins and zearalenone in vitro and for fumonisins in animal experiments, but response in cattle is unknown. Although various adsorbents are allowed for animal feed in various countries, none is FDA approved in the USA.