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Understanding Fungal (Mold) Toxins (Mycotoxins) Michael P

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Understanding Fungal (Mold) Toxins (Mycotoxins) Michael P ® ® KFSBOPFQVLCB?O>PH>¨ FK@LIKUQBKPFLK KPQFQRQBLCDOF@RIQROB>KA>QRO>IBPLRO@BP KLTELT KLTKLT G1513 Understanding Fungal (Mold) Toxins (Mycotoxins) Michael P. Carlson, Diagnostic Toxicologist/Analytical Chemist; and Steve M. Ensley, Veterinary Toxicologist of the immune system. Common mycoses include athlete’s This NebGuide briefly discusses mycotoxins commonly foot and ringworm. encountered in grains and feeds used in Nebraska and the mycotoxicoses they cause. Myco toxin sources and clini- Diagnosis and Treatment of Mycotoxicoses cal signs, lesions, diagnostic aids and treatment for each mycotoxicosis are listed. Different mycotoxins cause different diseases. Although they all are called mycotoxicoses, they are very different from Mycotoxins are chemicals produced by fungi (molds) each other. under certain conditions. They are not essential for fungal Modern agricultural practices make acute mycotoxicoses growth or reproduction, and are toxic to animals or humans. with high death loss (mortality) rare. Chronic mycotoxicoses Scientists do not yet know how many mycotoxins may ex- are often suspected when clinical signs include poor perfor- ist, even though more than 250 have been detected. They mance, ill thrift, or increased incidence of infectious diseases. represent many different kinds of chemicals. For many, if Establishing cause and effect relationships between consump- not most, their toxicological characteristics have not been tion of mycotoxin-contaminated feed and vague chronic fully determined. conditions is very difficult. Diseases in animals caused by mycotoxins are called my- Diagnosis of mycotoxicoses is usually not very easy. cotoxicoses. There are many different kinds of mycotoxicoses Exposure cannot be established by detection of mycotoxins in because there are many different kinds of mycotoxins. tissues from animals suspected of being poisoned by mycotox- This NebGuide is not intended to allow animal owners ins because analytical services for detection of mycotoxins in to diagnose cases of mycotoxicoses without consulting a animal tissues are not commonly available. We must rely on veterinarian. Diagnosing mycotoxicoses is not easy. Other the detection of mycotoxins in grain or feed to help establish diseases besides mycotoxicoses can cause similar clinical the diagnosis. signs or lesions, and the expertise of a veterinarian is vital Investigation of suspected mycotoxicoses should to accurate diagnoses. Otherwise, valuable resources may be begin by obtaining thorough histories. Clinical signs are worthlessly expended treating wrong diseases. very important because they can be used to select ap- The medical vocabulary used here may not be familiar propriate diagnostic tests to help confirm or refute myco­ to some readers. Those words are used to minimize the size toxicoses. Investigation of suspected mycotoxicoses of this NebGuide. Definitions of unfamiliar words may be should include histopathological examination of tissues from found in medical dictionaries. affected animals whenever possible. Specific histopathologi- cal lesions may be evidence of mycotoxicoses. If there are Mycotoxicoses and Mycoses no lesions in or evidence of pathology in organs known to be effected by mycotoxins, then like lihood of a mycotoxicosis Diseases called mycotoxicoses and mycoses are is reduced. sometimes confused. They are not the same. Diseases caused Confirmation of suspected mycotoxicoses is assisted by by mycotoxins are called mycotoxicoses. Diseases caused by either reproducing the clinical disease during a feeding trial mold infections are called mycoses. using the suspected ration, or by detection of a known myco- Mycotoxicoses occur when mycotoxins enter the body, toxin in the ration or tissues of animals consum ing the ration. usually by consumption of contaminated feed. Ill health is Feeding trials are not routinely performed because they are caused by actions of mycotoxins on cells in the body. Myco- difficult to conduct, expensive, and slow to provide results. toxicoses are not contagious, nor is there significant stimulation Detection of known myco toxins in feeds is relatively easy of the immune system. with modern analytical chemical methods. Mycoses occur when molds infect tissues of the body. One of the most challenging aspects of diagnosing cases They can be contagious. Molds begin to grow in or on the body of suspected mycotoxicoses is collecting a feed sample that after the infections are established. There may be stimulation adequately represents the feed suspected of being contami- nated. Mycotoxins are not evenly distributed in feeds, so and regeneration of hepatocytes; bile duct epithelial the contaminated part of the feed may be consumed before proliferation progressing to interlobular fibroplasia and disease is evident. Collection of meaningful feed specimens extensive proliferation; Karyomegaly, atypical nuclei, under such conditions is very difficult. More information hepatocytic vacuolization, bile retention. about feed specimen collection and analysis for mycotoxins Diagnostic aids for aflatoxicosis: may be found in NebGuide G1515, Sampling and Analyzing Blood workup: Check for anemia, elevated liver enzymes, Feed for Fungal (Mold) Toxins (Mycotoxins). serum bile acids, albumin:globulin ratio; prothrombin Interpreting the significance of finding mycotoxins activity. present in the ration is difficult. If a mycotoxin is detected Tissue or fluid analysis: Aflatoxin M present in milk or urine; in feed, the disease it causes should match the clinical syn- 1 parent compound may be present in kidney or liver. drome observed for the case and its concentrations should be Grain or feed analysis: Aflatoxins are most likely to be sufficient to cause a mycotoxicosis. If not, it is unlikely that present in corn, peanuts or cotton seed. They are not the presence of the mycotoxin in the feed is significant. likely to be present in forages or silage at significant Treatment of animals suffering from mycotoxicoses concentrations. Dietary aflatoxin concentrations at usually is supportive and often not very effective. Antidotes which performance or clinical effects become notice- for mycotoxins are generally not available. Stopping and able depends upon species and effect. Decreased preventing further exposure by removing contaminated feed per -formance may occur at concentrations as low as is important. 200 ppb in young, sensitive species. Immunity may It is not uncommon for animals to improve after they become impaired at concentrations of about 200 ppb. quit eating feed suspected or known to be contaminated with Hepatic lesions may become noticeable at 200 to 400 mycotoxins. Such an occurrence supports the suspicion of the ppb. Clinical illness may become obvious at about 400 feed as a causal factor, but does not prove that the animals ppb. Generally, ruminants are most resistant and swine suffered from a mycotoxicosis. and avian specimens least resistant to adverse effects. Health effects, clinical signs, lesions and treatment for Violative residues in milk can occur at concentrations at selected mycotoxicoses. (Reference: Osweiler, G.D. (1996) or near 50 ppb aflatoxin1. Toxicology, William & Wilkins, Media, PA: 416-432.) Treatment for aflatoxicosis: Aflatoxicosis Stop exposure. Stop feeding contaminated ration and replace with noncontaminated ration. Aflatoxicosis is caused byaflatoxins , produced by Asper- Supportive treatment. Provide supportive treatment as clinical gillus flavus and Aspergillus parasiticus. Aflatoxins are com- situation dictates. monly found in corn, milo, cottonseed and peanuts. Aflatoxin concentrations in grains produced in Nebraska rarely contain Ergot Toxicosis enough aflatoxin to cause acute aflatoxicosis. There are five important aflatoxins, called aflatoxin B Ergot toxicosis is a disease caused by the ingestion of ergot 1, alkaloids contained in the sclerotia of Claviceps spp. They are B2, G1, G2, and M1. Aflatoxin M1 is a metabolite of aflatoxin B found in milk and urine. It is formed after aflatoxin B commonly found in cereal grains, especially rye. Tall fescue 1 1 (Festuca arundinaceae) may contain the endophytic fungus enters the body. It is not found in feed. Aflatoxin B1 is found most frequently and in the highest concentrations in naturally Neotyphodium coenophialumin (Acre monium coenophialum), contaminated feed. which can also make ergot alkaloids. Aflatoxin is a liver poison (hepatotoxin) in all species Sclerotia are dark brown, brownish-purple or black that consume it, however, ruminants tolerate it better than colored bodies that stick out from the seed heads of infected do monogastrics or poultry. It causes liver damage at higher plants. They are visible to the naked eye and look similar to doses and liver cancer at lower doses. Aflatoxin exposure can rodent droppings when removed from the seed heads. They depress the immune system. It may cause abortions in some may become quite large, up to an inch in length. instances, however the circumstances necessary for abortions Several different ergot alkaloids may be present in scle- to occur are not well defined. rotia. They cause two syndromes: a central nervous system disorder and a peripheral vascular disorder. They can cause Clinical signs of aflatoxicoses: agalactia in lactating females. Acute exposure, all species: Depression, anorexia, reduced Ergot alkaloids are potent smooth muscle stimulants. Any gain or milk production, subnormal body temperature. organ with smooth muscle in it may be affected, especially
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