For discussion of mycotoxicoses in poultry, see Mycotoxicoses in Poultry.
Acute or chronic toxicoses in animals 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.
Some principles that characterize mycotoxic disease include:
The cause of mycotoxic disease may not be immediately identified.
Mycotoxins are not transmissible from one animal to another. Often, young, immature animals are more at risk.
Treatment with drugs or antimicrobials has little effect on the course of the disease. The first course of action is to stop the exposure to contaminated feed.
Outbreaks are often seasonal, because particular climatic sequences may favor fungal growth and toxin production.
Investigation of the outbreak indicates specific association with a particular feed.
Large numbers of fungi or their spores found on examination of feedstuffs does not necessarily indicate that toxin production has occurred. Absence of fungi or their spores does not exclude mycotoxicosis (eg, feed storage or preparation conditions, such as acid treatment or pelleting, can destroy fungi while the heat-tolerant mycotoxin persists).
Most veterinary mycotoxicoses occur 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, multiple mycotoxins may be present in feedstuffs, and their different toxicological properties may cause clinical signs and lesions inconsistent with those evident when animals are dosed experimentally with pure, single mycotoxins. Some mycotoxins are immunosuppressive, increasing susceptibility to secondary infections that are more obvious than the primary disease. 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 after diagnosis. A preventive approach with recognition of risk factors and avoidance or reduction of 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; metabolism of some mycotoxins, especially in ruminant animals, can be supported by use of feed ingredients of good nutritional quality. 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. Alternatively, feed with known mycotoxin concentrations can be fed to less susceptible species, with the caveat that some mycotoxins such as aflatoxin could result in violative residues in food in the absence of illness. When contaminated feed is blended with uncontaminated 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 ().
Mycotoxicoses in Domestic Animals
Disease | Toxins (When Known) | Fungi or Molds | Regions Where Reported | Contaminated Toxic Foodstuff | Animals Affected | Signs and Lesions |
|---|---|---|---|---|---|---|
Aflatoxicosis | Aflatoxins | Aspergillus flavus, A parasiticus | Widespread (warmer climatic zones) | Moldy peanuts, soybeans, cottonseeds, rice, sorghum, corn (maize), other cereals | All poultry, pigs, cattle, sheep, dogs | Major effects in all species are slow growth and hepatotoxicosis. Also see Aflatoxicosis in Animals and see Mycotoxicoses in Poultry. |
Diplodiosis | Unknown | Diplodia zeae | South Africa | Moldy corn (maize) | Cattle, sheep | Nervous system disorders, cold and insensitive limbs. Recovery usual on removal of source. |
Ergotism | Ergot alkaloids | Claviceps purpurea | Widespread | Seed heads of many grasses, grains | Cattle, horses, pigs, poultry | Peripheral gangrene, late gestation suppression of lactation initiation. See page Ergotism in Animals. |
Paspalinine and paspalitrems, tremorgens | C paspali, C cinerea | Widespread | Seed heads of paspalum grasses | Cattle, horses, sheep | Acute tremors and ataxia. See page Paspalum Staggers in Animals. | |
Estrogenism and vulvovaginitis | Zearalenone | Fusarium graminearum Perfect state: Gibberella zeae | Widespread | Moldy corn (maize) and pelleted cereal feeds, standing corn, corn silage, other grains | Pigs, cattle, sheep, poultry | Vulvovaginitis in pigs, anestrus or pseudopregnancy in mature sows, early embryonic death of swine embryos, estrogenism in cattle and sheep, reduced egg production in poultry. Also see Mycotoxin-Associated Estrogenism and Vulvovaginitis in Animals. |
Facial eczema (Pithomycotoxicosis) | Sporidesmins | Pithomyces chartarum | Widespread | Toxic spores on pasture litter | Sheep, cattle, farmed deer | Also see Facial Eczema in Animals. |
Fescue foot | Ergovaline | Neotyphodium coenophialum | USA, Australia, New Zealand, Italy | Tall fescue grass (Lolium arundinacea) | Cattle, horses | Lameness, weight loss, hyperthermia, heat intolerance, dry gangrene of extremities, agalactia, thickened fetal membranes. Also see Fescue Poisoning in Animals. |
Fusariotoxicosis, vomiting and feed refusal in pigs | Nonmacrocyclic trichothecenes (deoxynivalenol, T-2 toxin, diacetoxyscirpenol [DAS], many other trichothecenes) | Fusarium sporotrichioides, F culmorum, F graminearum, F nivale; other fungal species | Widespread (except for deoxynivalenol, more likely in temperate to colder climates) | Cereal crops, moldy roughage | Pigs, cattle, horses, poultry | Vomiting and feed refusal (deoxynivalenol), loss of appetite and milk production, diarrhea, staggers, skin irritation, immunosuppression; recovery (from T-2, DAS) on removal of contaminated feed. Also see Trichothecene Toxicosis in Animals. |
Leukoencephalomalacia | Fumonisin B1 | Fusarium verticilloides | Egypt, USA, South Africa, Greece | Moldy corn (maize) | Horses, other Equidae, pigs | Depends on degree and specific site of brain lesion. Also see Fumonisin Toxicosis in Animals. |
Mycotoxic lupinosis (as distinct from alkaloid poisoning) | Phomopsins | Phomopsis leptostromiformis | Widespread | Moldy seed, pods, stubble, and haulm of several Lupinus spp affected by Phomopsis stem blight | Sheep, occasionally cattle, horses, pigs | Lassitude, inappetence, stupor, icterus, marked liver injury. Usually fatal. Also see Mycotoxic Lupinosis in Animals. |
Myrotheciotoxicosis, dendrodochiotoxicosis | Macrocyclic trichothecenes (verrucarins, roridins, etc) | Myrothecium verrucaria, M roridum | Southeast Europe, former USSR | Moldy rye stubble, straw | Sheep, cattle, horses | Acute—diarrhea, respiratory distress, hemorrhagic gastroenteritis, immunosuppression, death. Chronic—ulceration of GI tract, unthriftiness, gradual recovery. Also see Trichothecene Toxicosis in Animals. |
Macrocyclic trichothecenes (baccharinoids) | M verrucaria | Brazil | Plants of Baccharis spp that contain the toxins | Cattle, other herbivores | Epithelial necrosis of GI tract. Also see Trichothecene Toxicosis in Animals. | |
Ochratoxicosis | Ochratoxin, also citrinin | Aspergillus ochraceus and others, Penicillium viridicatum, P citrinum | Widespread | Moldy barley, corn (maize), wheat | Pigs, poultry | Perirenal edema, enlarged pale kidneys with cortical cysts, and tubular degeneration and fibrosis; immunosuppression, polyuria and polydipsia. |
Penicillium-associated tremorgens | Penitrem A | P crustosum, P cyclopium, P commune | Widespread | Cereal grains, cheese, fruit, meats, nuts, refrigerated foods; compost | Cattle, dogs, horses, sheep | Neurotoxic signs, including continual tremors, seizures, hyperexcitability, ataxia. Vomiting and CNS signs in dogs. |
Roquefortine | P roqueforti | As above, and in silage | ||||
Perennial ryegrass staggers | Lolitrems | Lolium perenne,Neotyphodium lolii, an endophyte fungus confined to L perenne | Australia, New Zealand, Europe, USA | Endophyte-infected ryegrass pastures | Sheep, cattle, horses, deer | Tremors, incoordination, collapse, convulsive spasms. Also see Annual Ryegrass Toxicosis. |
Poultry hemorrhagic syndrome | Probably aflatoxins and rubratoxins | Probably Aspergillus flavus, A clavatus, Penicillium purpurogenum, Alternaria sp | USA | Moldy grain and meal | Growing chickens | Depression, anorexia, no weight gain, widespread internal hemorrhages, sometimes aplastic anemia, death. See chapter Mycotoxicoses in Poultry. |
Pulmonary edema, emphysema | 4-Ipomeanol | Fusarium solani | USA | Moldy sweet potatoes | Cattle | Acute pulmonary edema, leading to interstitial pneumonia and emphysema. |
Porcine pulmonary edema | Fumonisin B1 and Fumonisin B2 | Fusarium verticilloides | USA, South Africa | Corn | Swine | Acute interlobular pulmonary edema and hydrothorax cause anoxia and cyanosis. Survivors may develop icterus and chronic hepatotoxicosis. |
Slobbers syndrome | Slaframine (and swainsonine) | Rhizoctonia leguminicola | USA | Black patch disease, legumes (notably red clover) eaten as forage or hay | Sheep, cattle, horses | Salivation, bloat, diarrhea, sometimes death. Recovery usual when removed from clover. Also see Slaframine Toxicosis in Animals. |
Stachybotryotoxicosis | Macrocyclic trichothecenes (satratoxin, roridin, verrucarin) | Stachybotrys atra (S alternans) | Former USSR, southeast Europe | Moldy roughage, other contaminated feed | Horses, cattle, sheep, pigs | Stomatitis and ulceration, anorexia, leukopenia, extensive hemorrhages in many organs, inflammation and necrosis in the gut, immunosuppression. Also see Trichothecene Toxicosis in Animals. |
Sweet clover poisoning | Dicumarol | Penicillium spp, Mucor spp, Aspergillus spp | North America | Sweet clover (Melilotus spp) | Cattle, horses, sheep | Vitamin K antagonism with coagulopathy and hemorrhage. Also see Sweet Clover Poisoning. |
Tremorgen ataxia syndrome | Penitrems, verruculogen, paxilline, fumitremorgens, aflatrems, roquefortine | Penicillium crustosum, P puberulum, P verruculosum, P roqueforti, Aspergillus flavus, A fumigatus, A clavatus, and others | USA, South Africa, probably worldwide | Moldy feed; high-protein food products, even under refrigeration, eg, cream cheese, walnuts | All species, but dogs are quite susceptible | Tremors, polypnea, ataxia, collapse, convulsive spasms. |
Managing a Suspected Mycotoxicosis
When mycotoxicosis is suspected, corrective actions could include the following:
Change the feed even when a specific mycotoxin is not identified.
Thoroughly inspect storage bins, mixing equipment, and feeders for caking, molding, or musty odors.
Remove contaminated feed and clean equipment and sanitize with hypochlorite (laundry bleach) to reduce contaminating fungi.
Analyze for known mycotoxins.
Use spore counts or fungal cultures for some indication of potential mycotoxin production.
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).
Use a mycotoxin adsorbent if appropriate for the mycotoxin suspected.
Save a representative sample of each diet mixed until animals are at 1 month beyond when the feed was consumed.
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 hours to reduce moisture to 12%–13%. If mold studies are to be done, dry at 140°F (60°C) for 6–12 hours to preserve fungal activity.
Mycotoxin Adsorbents
Adsorption of mycotoxins in contaminated feeds is an area of active research. Aflatoxins are effectively adsorbed by the aluminosilicate feed additives. 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, glucomannan adsorbents reduces the number of stillborn piglets. Glucomannan 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 US.
For More Information
Also see pet health content regarding fungal poisoning in animals.
