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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. Myco­toxin­ 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 like­lihood of a mycotoxicosis
Diseases called mycotoxicoses and mycoses are is reduced.
sometimes­confused. 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 consum­ing 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 myco­toxins 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 M1 present in milk or urine;
in feed, the disease it causes should match the clinical syn-
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 by aflatoxins, 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 B1, Ergot toxicosis is a disease caused by the ingestion of ergot
B2, G1, G2, and M1. Aflatoxin M1 is a metabolite of aflatoxin alkaloids contained in the sclerotia of Claviceps spp. They are
B1 found in milk and urine. It is formed after aflatoxin B1 commonly found in cereal grains, especially rye. Tall fescue
enters the body. It is not found in feed. Aflatoxin B1 is found (Festuca arundinaceae) may contain the endophytic fungus
most frequently and in the highest concentrations in naturally Neotyphodium coenophialumin (Acre­monium 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
Chronic exposure, poultry: Decreased growth rate, reduced­ arterioles. Uterine contractions may be stimulated.
feed efficiency, steatorrhea (fat in feces), bruising.
Chronic exposure, swine: Anorexia, unthriftiness, slow growth, Clinical signs of ergot toxicosis:
icterus, mild anemia, ascites, increased susceptibility to Peripheral vascular syndrome: Lameness, swelling of feet and
infection. fetlocks; sharply demarcated necrosis of feet, ears or tail.
Chronic exposure, cattle: May slow rumen motility for 24 In severe cases, hooves or feet, or tail may slough. Dry
to 48 hours. gangrene. These effects are due to ischemia resulting from
constriction of arterioles in peripheral vascular beds.
Lesions of aflatoxicosis: Lactating females: Cessation of milk production; agalactia in
Acute exposure: Hemorrhage, ascites. post-partum females.
Chronic exposure: Pale, soft, clay-colored liver, mild anemia, Central nervous system syndrome: Hyperexcitability, hyper-
icterus, ascites. metria, tremors; heat intolerance in cattle.
Histopathological: Hepatocyte degeneration and necrosis;
centrilobular hemorrhagic hepatic necrosis, fatty changes
Lesions of ergot toxicosis: scopically, liquefaction and proliferation of macrophages
Described above under clinical signs for peripheral vascu- in response to necrosis.
lar syndrome. Additionally, small and flaccid mammary glands
Diagnostic aids for fumonisin toxicosis:
of females in late pregnancy, with no evidence of secretions,
Blood workup: Evidence of hepatic dysfunction.
are indications of probable agalactia.
Tissue analysis: Sphinganine:sphingosine ratio is increased.
Histopathological: Endothelial damage, thrombosis, coagula-
Analysis of tissues for sphinganine and sphingosine is
tive necrosis.
not readily available.
Diagnostic aids for ergot toxicosis: Analysis of corn or corn-containing feed for fumonisins:
Analysis of stomach or rumen content for ergot alkaloids. Concentrations in excess of 3 ppm fumonisin may be
Detection of ergot alkaloids in stomach or rumen content significant for horses. Concentrations above 5 ppm may
is evidence of exposure. be significant for pigs.
Analysis of feed or grains for ergot alkaloids ingested by af-
fected animals. Sclerotia may be visible if the feed has Treatment for fumonisin toxicosis:
not been ground. Stop exposure. Remove contaminated feed from ration. Be-
cause of the long time between consumption of feed and
Treatment for ergot toxicosis: onset of signs, oral detoxification is not recommended.
Stop exposure. Remove contaminated grain or feed from ration. Supportive treatment – prognosis for horses and pigs suffering
Lactation may commence 5 to 7 days afterwards. from advanced stages of the disease is poor.
Control secondary infections in limbs suffering from dry
gangrene. Vomitoxin (Deoxynivalenol, DON) Toxicosis
Place animals in a warm, clean, stress-free environment.
Vomitoxin is produced by Fusarium roseum (F. graminear-
Fumonisin Toxicosis um) and F. moniliforme. It is found in corn, wheat, barley, milo
and occasionally in oats. It is rarely found in hay or forages.
Fumonisins are produced by Fusarium moniliforme and F. Roseum also produces zearalenone, so DON may also be
F. proliferatum, and is found primarily in white and yellow found with zearalenone.
corn. There are three kinds, called fumonisins B1, B2, and B3. Vomitoxin is a chemical that belongs to a group of myco-
Fumonisin B1 is most prevalent in naturally contaminated corn toxins called tricothecenes. There are at least 140 chemicals in
and it is the most toxic. that class, including T-2 toxin and diacetoxyscripenol (DAS).
Horses and pigs are the most sensitive species. Equine Trichothecenes other than vomitoxin are rarely, if ever, found
leukoencephalomalacia (ELE) is a fatal disease of horses in grain grown in Nebraska.
caused by fumonisins. Porcine pulmonary syndrome is the form Vomitoxin is not very toxic, but it is associated with feed
of the disease in swine. The mechanism of action is believed refusal and decreased feed consumption, which can affect
to be the inhibition of enzymes involved in the production of animal performance. Concentrations ranging from 5 to 10
sphingosine from sphinganine. Sphingosine is an important ppm are associated with vomiting in pigs, hence its name.
component of cell membranes, especially for neurons. Thresholds for decreased feed intake are about 1 ppm in swine
Clinical signs of fumonisin toxicosis: and 10 to 20 ppm in ruminants.
Swine: Dyspnea, cyanosis, and weakness, which develop 4-7 The mechanism by which vomitoxin acts has not been
days after fumonisin-contaminated feed begins. Death may elucidated. Other trichothecenes inhibit protein and nucleic
occur withing a few hours of onset of the syndrome. acid synthesis.
Horses: Depression, blindness, ataxia, aimless wandering, Cattle are very resistant to the effects of vomitoxin.
facial paralysis, which may rapidly progress to coma and Pigs are more sensitive. There have been reports of health
death. Death may occur 1 to 7 days after onset of signs. effects in dogs from pet foods contaminated with vomitoxin-
Ruminants: May develop anorexia and suffer mild weight containing grains.
loss if fumonisin concentrations approach 200 ppm. Few Clinical signs of vomitoxin toxicosis:
other significant or persistent signs. Swine, dogs, cats – feed refusal, vomiting; cattle – usually
Poultry: Appear to be more resistant than other species. none, however some reports of feed refusal may by found
Inappetence and skeletal abnormalities may develop in the scientific literature; poultry – usually none.
at concentrations of 200 - 400 ppm.
Lesions of vomitoxin toxicosis:
Lesions of fumonisin toxicosis: No gross or histopathological lesions have been reported in
Swine: Acute pulmonary edema characterized by marked animals consuming vomitoxin-contaminated feed.
to massive intralobular pulmonary edema and marked
hydrothorax. Lungs are distended and turgid. Thoracic Diagnostic aids for vomitoxin toxicosis:
cavity is filled with straw-colored proteinaceous fluid. Analysis of grains or feeds. Forages are seldom, if ever, con-
Microscopically, interstitial and interlobular edema. May taminated with vomitoxin.
include multiple areas of focal pancreatic necrosis and Analysis of tissues from affected animals: Not available.
hepatic lesions characterized by disorganized hepatocytes, Treatment for vomitoxin toxicosis:
increased mitotic figures, necrosis of single hepatocytes Remove vomitoxin-contaminated grain/feed from ration­.
and mild bile retention. Icterus.
Horses: Leukoencephalomalacia – massive softening and liq- Zearalenone Toxicosis
uefaction of cerebral white matter, ranging from discrete
focal areas to large cavitations and inward collapse of the Zearalenone is produced by Fusarium roseum (F.
cortical gray matter. Hemorrhage is prominent. Micro- graminearum) and F. moniliforme. It is found in corn, wheat,
barley, milo and occasionally in oats. F. Roseum also produces estrogenic activity of the feed. That assay detects any
vomitoxin (deoxynivalenol, DON), so vomitoxin may also be chemical with estrogenic activity that might be present
found with zearalenone. in the feed.
Zearalenone is a chemical that can act similarly to the
Treatment for zearalenone toxicosis:
female sex hormone estrogen. Excessive exposure does not
Stop exposure. Remove contaminated feed and replace with
cause death or abortions, but it can disrupt the estrus cycle
un-contaminated feed. Signs may persist for several days
in females, cause infertility and feminization in males, and
afterwards.
precocious puberty in sexually immature females. Zearalenone
Decrease zearalenone absorption: Activated charcoal
content typically found in Nebraska grains is usually not enough
may help limit absorption of ingested zearalenone by
to adversely affect animals, but unusual environmental condi-
individual animals. Several commercially available
tions during the growing season, or insufficiently dried grain
feed additives are advertized to bind zearalenone and
put up for storage may increase zearalenone production.
help prevent excessive exposure. The efficacy of such
Clinical signs of zearalenone toxicosis: additives may not have been adequately assessed. Thor-
Clinical signs vary with species, sex and age of the oughly assess the evidence offered by manu­facturers be-
animal. fore using them. Such use may require approval by federal
Swine, sexually immature gilts: Behavioral estrus, swollen and regulatory agencies before it can be used legally.
edematous vulva, enlarged mammary glands, tenesmus
(spasmodic contraction of anal or bladder sphincter), Prevention of Mycotoxicoses
sometimes vaginal or rectal prolapse; clinical signs ap-
pear 2-7 days after exposure begins and subsides 4 to 10 Purchase grain or feed that are free of mycotoxins.
days after exposure ends. Have feed analyzed for mycotoxins before purchase
Swine, mature sows: Exposure early in estrus cycle – sup- or use. Make mycotoxin analysis a condition of sale. Re-
pression of ovulation and signs of estrus that are severe quire that the seller have the feed analyzed by a suitable
and prolonged; exposure mid-cycle – pseudopregnancy, laboratory before you accept delivery. However, it may be
anestrus which may persist for 40 to 60 days after ex- difficult to find feed free of mycotoxins sometimes because
posure stops. they occur naturally.
Swine, castrated boars: Enlarged prepuce and nipples.
Remove grain or feed contaminated with mycotoxins.
Swine, immature boars: Reduced libido, retarded testicular
Substitute grain or feed known not to be contaminated.
development.
Swine, mature boars: Not effected unless dietary concentra-
Use of feed additives to bind mycotoxins.
tions reach 200 ppm or higher. Such concentrations are
Mycotoxin binders are commercially available, but
rarely encountered in U.S. grains.
before purchase, determine if the product can be legally
Lesions of zearalenone toxicosis: used for such purposes. Ask the seller if the product is
Lesions are present only in the reproductive system. approved under federal law or regulations for use as
Prepubertal gilts: Swollen and edematous vulva; enlarged mycotoxin binder. If the seller claims such approval is not
mammary glands; enlarged, hypertrophic and edematous necessary, or if the seller cannot document approval, consult
uterus. Histopathologically, uterine and vaginal metaplasia with staff at the Center for Veterinary Medicine (CVM) of
and follicular atresia. the U.S. Food and Drug Agency. Its Web site address at the
Mature sows: Retained and functional corpora lutea with time this NebGuide was published is www.fda.gov/cvm/. Or,
anestrus. Mammary alveolar development and ductular contact the regional office listed below:
sqamous metaplasia.
MINNEAPOLIS DISTRICT
Diagnostic aids for zearalenone toxicosis: 240 Hennepin Avenue
Blood workup: Serum analysis for estrogen can help rule out Minneapolis, MN 55401
an organic hormonal problem. (612) 334-4100
Tissue or fluid analysis: Not available.
Feed or grain analysis: Since clinical effects are delayed sev- This publication has been peer reviewed.
eral days after ingestion, feed analysis may be of limited
value. A specimen collected after the problem is noticed
may not contain detectable amounts of zearalenone. UNL Extension publications are available online
Planned retention and dating of feed specimens aids in at http://extension.unl.edu/publications.
the identification of zearalenone-contaminated feed.
Differential considerations for zearalenone toxicosis:
Other estrogenic chemicals from plants (phyto­estrogens) or
Index: Plant Diseases
other sources could also produce some of the signs of
Field Crops
zearalenone toxicosis. An expensive, but possibly valu- Issued June 2003
able estrogenic assay of feed is available to help assess

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