Some major mycotoxins and their mycotoxicoses—An overview
John L. Richard⁎
Romer Labs, Inc., 34423 N. Wilderness Trail, Cave Creek, AZ 85331, United States
Abstract
Mycotoxins likely have existed for as long as crops have been grown but recognition of the true chemical nature of such entities of fungal
metabolism was not known until recent times. Conjecturally, there is historical evidence of their presence back as far as the time reported in the Dead
Sea Scrolls. Evidence of their periodic, historical occurrence exists until the recognition of aflatoxins in the early 1960s. At that time mycotoxins were
considered as a storage phenomenon whereby grains becoming moldy during storage allowed for the production of these secondary metabolites
proven to be toxic when consumed by man and other animals. Subsequently, aflatoxins and mycotoxins of several kinds were found to be formed
during development of crop plants in the field. The determination of which of the many known mycotoxins are significant can be based upon their
frequency of occurrence and/or the severity of the disease that they produce, especially if they are known to be carcinogenic. Among the mycotoxins
fitting into this major group would be the aflatoxins, deoxynivalenol, fumonisins, zearalenone, T-2 toxin, ochratoxin and certain ergot alkaloids. The
diseases (mycotoxicoses) caused by these mycotoxins are quite varied and involve a wide range of susceptible animal species including humans.
Most of these diseases occur after consumption of mycotoxin contaminated grain or products made from such grains but other routes of exposure
exist. The diagnosis of mycotoxicoses may prove to be difficult because of the similarity of signs of disease to those caused by other agents.
Therefore, diagnosis of a mycotoxicoses is dependent upon adequate testing for mycotoxins involving sampling, sample preparation and analysis.
© 2007 Elsevier B.V. All rights reserved.
Keywords: Mycotoxins; Mycotoxicoses; Aflatoxin(s); Deoxynivalenol; Fumonisins; T-2 toxins; Trichothecenes; Zearalenone; Ergot; Ochratoxin
1. Historical aspects
The toxic secondary metabolites of fungi that we call
mycotoxins, have been conjecturally associated with disease, by
modern day investigators, and go back to times included in the
writings of the Dead Sea Scrolls (noting destruction of “houses
of mildew”). They also have been included as the cause of the
last of the Ten Plagues of Egypt whereby it was suggested that
the oldest son, his family and animals succumbed following the
opening of the grain storage facilities whose contents were
contaminated by toxic fungi (Marr and Malloy, 1996).
While ergot alkaloids were used as Chinese medicinal
preparations over 500 years ago, the accounts of the Middle
Ages included descriptions of “St. Anthony's Fire” which was
attributed to the human consumption of foods prepared from
ergot-contaminated grain. Ergot alkaloids, with both gangrenous
and convulsive effects, likely were involved in the “bewitchments”
(possession of some evil spirits) leading to the Salem
Witchcraft Trials in Salem, Massachusetts.
During the late 1800s and early 1900s there was considerable
recognition of the ability of fungi to carry out fermentations and
a number of investigators recognized the myriad of “secondary
metabolites” produced by fungi in both solid state and liquid
fermentations. Because a few of the products of such
fermentations were consumed by humans, some interest in the
toxicity of these products was developed. DeBary in 1879 noted
that when two organisms were grown side by side, one inhibited
the growth of the other (Skinner et al., 1947). Other workers
followed up with these investigations and Alexander Fleming's
discovery of penicillin was a monument to the entire field of
antibiosis. Once this discovery was determined to be important,
due to the curative effect delivered by this antibiotic for some
devastating diseases, the antibiotic industry rapidly developed.
Some investigators included studies of animal toxicity during
development of antibiotics. Noting that some of these fungal
metabolites indeed were toxic to animals was the first clue to
many in the scientific community that fungi could produce
toxins that could cause disease in humans and other animals.
Available online at www.sciencedirect.com
International Journal of Food Microbiology 119 (2007) 3–10
www.elsevier.com/locate/ijfoodmicro
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doi:10.1016/j.ijfoodmicro.2007.07.019
Concomitant with the studies of grain storage, which included
interest in the deterioration of grains by fungi, there became a
better understanding of the potential for fungi to be both
deleterious to grains in storage and to be agents of toxic
problems in livestock and human consumers (Richard, 2000).
During the 1940s and 1950s, episodes of lethal disease in
humans in Russia occurred during the early years of the Second
World War. This situation was well-documented and referred to
as “Alimentary Toxic Aleukia” (ATA). This devastating disease
with its necrotizing, hemorrhagic and central nervous system
effects, resulting often in death, was recognized as a toxic
manifestation of mold contamination of harvested grains
(Richard, 2003). However, the true causative toxic compounds
were not found at that time and it has retrospectively been
considered to be caused by T-2 toxins attributed to the
production of this metabolite by Fusarium sporotrichioides,
the most common fungal isolate from the contaminated grains
incriminated in ATA. Simultaneously, the Russians were dealing
with another serious disease occurring in both horses and
humans. In the 1930s, this disease resulted in the death of
thousands of horses. The causative fungus was finally
determined to be Stachybotrys atra, (now known as S.
chartarum) but confusion existed due to the similarity of signs
of disease to that of ATA. Subsequently, it was found that the
chemical nature of the causative compounds of the two diseases
is similar and they are known today as members of the class of
mycotoxins called trichothecenes. Forgacs and Carll (1962),
being convinced that similar diseases occurred in the United
States, considered them toxic diseases and began a systematic
approach to the study of mycotoxins and mycotoxicoses such as
Moldy Corn Toxicosis and Stachybotryotoxicosis (Forgacs,
1962). Also, during this time another disease called facial
eczema had plagued the New Zealand sheep industry and was
determined to be caused by a toxic component eventually called
sporodesmin. It was produced in the conidia of a fungus growing
on ryegrass pastures known, at that time, as Sporodesmium
bakeri (now known as Pithomyces chartarum).
Modern mycotoxicology began with the discovery of
aflatoxins after losses of a large number of animals in England
in 1961 was attributed to consumption of peanut meal
incorporated in the diets. Subsequent to the finding of the
carcinogenicity of the aflatoxins, the immunosuppressive nature
of the aflatoxins and the discovery that the aflatoxins were not
only a storage problem in grains but actually contaminated certain
crops pre-harvest, the total mycotoxin problem became a
multidisciplinary issue involving analytical chemists, microbiologists,
agronomists, agricultural engineers, entomologists, plant
pathologists, crop breeders, geneticists, medical and veterinary
practitioners and producers (farmers/ranchers). The combined
efforts of interactions of these groups led to the discovery of many
new mycotoxins and their involvement in diseases of animals.
2. Mycotoxin/mycotoxicoses overviews
2.1. Aflatoxins
The major aflatoxins consist of aflatoxins B1, B2, G1 and G2
produced by selected isolates (not all isolates are toxigenic) of
either Aspergillus flavus or A. parasiticus (Fig. 1). However,
aflatoxin M1, a hydroxylated metabolite, found primarily in
animal tissues and fluids (milk and urine) as a metabolic product
of aflatoxin B1 should be noted in any discussion of these
mycotoxins. Aflatoxin M1 is not a contaminant of feed grains.
When grain such as corn is growing and there is warm
ambient temperature, especially noted during drought conditions,
the grain becomes more susceptible to aflatoxin
formation. These stresses are more prevalent in the southern
United States but they can occur in occasional years in the
Midwest (Corn Belt). The saprophytic organism is disseminated
via their conidia (asexual spores) carried by wind or insects to
the growing crop. Any condition that provides a portal of entry
into the host plant tissue or interferes with the integrity of the
seed coat allows the organism to enter and grow on the living
tissue of the host including the ears or kernels of the developing
grain. Insects, such as sap beetles, corn earworms and the
European corn borer can provide transmission and portals of
entry into the host plant. Corn, peanuts, certain tree nuts and
cottonseed are the major U.S. crops affected.
In severely affected crops, yellow–green masses of conidia
may be visible at sites of kernel damage or along insect feeding
paths. Individual kernels of corn may contain as high as
400,000 μg/kg of aflatoxin (Shotwell et al., 1974), therefore
sampling is very important in the testing for levels of
contamination in bulk grain lots.
Grains stored under high moisture/humidity (N14%) at warm
temperatures (N20 °C) and/or inadequately dried can potentially
become contaminated (Ominski et al., 1994). Grains must be
kept dry, free of damage and free of insects. These conditions
allow mold “hot spots” to occur in the stored grain. Initial growth
of fungi in grains can form sufficient moisture from metabolism
to allow for further growth and mycotoxin formation.Fig. 1. Structure of aflatoxin B1 as a representative of the aflatoxins.
Table 1
U.S. Food and Drug Administration action levels for total aflatoxins in food and
feed (μg/kg)
Commodity Concentration
Cottonseed meal as a feed ingredient 300
Corn and peanut products for finishing beef cattle 300
Corn and peanut products for finishing swine 200
Corn and peanut products for breeding beef cattle, swine and
mature poultry
100
Corn for immature animals and dairy cattle 20
All products, except milk, designated for humans 20
All other feedstuffs 20
Milk 0.5
4 J.L. Richard / International Journal of Food Microbiology 119 (2007) 3–10
The aflatoxins are primarily hepatotoxic or cause liver
damage in animals; aflatoxin B1 is the most potent. Susceptibility
varies with breed, species, age, dose, length of exposure
and nutritional status. Aflatoxins may cause decreased production
(milk, eggs, weight gains, etc.), are immunosuppressive,
carcinogenic, teratogenic and mutagenic (Miller and Wilson,
1994). Aflatoxins can be present in milk of dairy cows, meat of
swine or chicken eggs if the animals consume sufficient
amounts in their feed. Aflatoxin B1 is a human carcinogen but
may be only part of the total answer to human liver cancer
(Robens and Richard, 1992). Pet foods contaminated with
aflatoxins have been involved in disease and death of animals
consuming sufficiently contaminated food (Garland and
Reagor, 2007). Ammoniation and certain adsorbents are
effective in reducing or eliminating the effects of aflatoxins in
animals (Park et al., 1988). The FDA has action levels for
aflatoxins regulating the levels and species to which contaminated
feeds may be fed (CAST, 2003) (Table 1). The European
Community levels are more restrictive (FAO Food and
Nutrition Paper No. 81, 2004) (Tables 2 and 3).
2.2. Deoxynivalenol
Deoxynivalenol (Fig. 2), also known as vomitoxin or DON,
is produced principally by Fusarium graminearum and in some
geographical areas by F. culmorum (Richard, 2000). DON may
co-exist with zearalenone, another mycotoxin produced by
these organisms. DON belongs to the class of mycotoxins called
trichothecenes of the Type B group and it is non-fluorescent.
Corn and small grains such as wheat, oats, and barley are the
major crops affected but DON can be found in corn as well
(CAST, 2003). The organisms survive on residue left on the
field from the previous season's crop, providing an inoculum
source for the new crop. The organisms do well in cool, moist
conditions with contamination of the crop occurring when
conidia of the organism are windblown to the corn silks or in
small grains to the anthers which emerge outside the floret
during anthesis. The fungus penetrates the host ear or floret and
produces the disease which may be ear rot in corn or head blight
in small grains. Certain environmental conditions may allow for
late growing season development of DON in crops. Apparently,
DON production is necessary for the organism to produce
disease in some crops.
In corn, the ear rot produced by F. graminearum may appear.
Wheat heads may appear prematurely and unevenly ripe and the
kernels will have a blanched appearance (tombstone kernels) at
harvest and may have pink staining present as well. In those
commodities where there is pink staining the disease may be
referred to as pink scab.
Storage under good conditions (b14% moisture), including
control of insect pests, will minimize further elaboration of the
toxin by these toxigenic fungi. Again, if grains have matured
and are stored under appropriate conditions, DON does not
further accumulate in storage.
Swine are the animals most usually affected by this toxin and
exhibit reduced intake of contaminated grain; if they do eat it
they may vomit. Levels above 1 μg/g are considered potentially
harmful to these animals (Richard, 1998). Pet foods prepared
with wheat contaminated with this toxin have been involved in
acute toxicities. DON is immunosuppressive and may cause
kidney problems in animals (Pestka and Bondy, 1994). Humans
are thought to exhibit a similar vomition syndrome when
consuming DON-contaminated grain (Bhat et al., 1989). DON
does not appear to be significantly carried over into tissues or
fluids of animals consuming toxic levels (Prelusky, 1994).
Baking and malting using contaminated wheat and barley are
adversely affected (Richard, 2000).
The FDA had issued “Advisory Levels” for the industry
(Chesemore, 1993) (Table 4). Again, the European community
has more stringent regulations for DON (FAO Food and
Nutrition Paper No. 81, 2004) (Table 5).
2.3. Fumonisins
The fumonisins are a group of non-fluorescent mycotoxins
(FB1, FB2 and FB3 being the major entities) (Fig. 3) produced
primarily by Fusarium verticillioides and F. proliferatum
(CAST, 2003). Strains vary in toxin-producing ability.
Corn is the major commodity affected by this group of toxins
although some occurrence has been found in sorghum and rice
Table 2
European Union regulations for aflatoxins (μg/kg)
Human food AfB1 AfB1, B2, B3, B4 M1
Groundnuts, dried fruit and processed
products thereof
2 4 –
Groundnuts subjected to
sorting or phys. treating
8 15 –
As above but for nuts and dried fruits 5 10 –
Cereals (including maize) and
processed products thereof
2 4 –
Milk – – 0.05
Table 3
European Union regulations for aflatoxins (μg/kg)
Feed AfB1 Feed AfB1
Feed (exceptions below) 50 Complete feedstuff for
pigs and poultry
20
Groundnuts, copra, palm kernel,
cottonseed, babasu, maize
and products derived from
processing thereof
20 Other complete feedstuffs 10
Complementary feedstuffs
for cattle, sheep, goats
(except dairy, calves
and lambs)
50
Complete dairy feed 5 Complementary feedstuffs
for pigs
and poultry (except for young
animals)
30
Complete feed for lambs
and calves
10
Fig. 2. Structure of deoxynivalenol.
5J.L. Richard / International Journal of Food Microbiology 119 (2007) 3–10
(CAST, 2003). The exact conditions for disease are not known
but drought stress followed by warm, wet weather later in the
growing season seems to be important. Insect damage to
maturing corn ears allows for environmentally present strains of
the organism to enter the ear and kernels. However, the organism
is present in virtually every seed and is present in the corn plant
throughout its growth and therefore is present in the ears and
kernels. Sometimes there is considerable amount of fumonisins
present in kernels of corn with no symptoms of disease.
While some kernels may have no evidence of infection, other
kernels or areas on an ear may exhibit “pink kernel rot”
(sometimes may appear white) with closely adhering organism
on the kernels. Kernels with insect or bird damage or other
broken kernels will often contain the highest levels of toxin.
Thus, corn screenings will contain the highest levels of toxins
and have been the cause of severe animal disease.
Increase in concentrations of fumonisins during storage does
not appear to be a major problem, however, grains should be
harvested without additional kernel damage, screened to
remove broken kernels and stored dried and maintained at
moisture concentrations b14%.
A major disease of horses that includes a softening of the
white matter in the brains (leukoencephalomalacia) is caused by
the fumonisins (Marasas et al., 1988). Swine lung edema is also
produced by the fumonisins (Colvin and Harrison, 1992). Other
maladies such as liver disease, including tumors of the liver and
kidney, have been noted in studies using rodents. The
fumonisins are suspect in the cause of esophageal tumors in
certain human populations (Marasas, 1993, 1996). Regardless
of the effects on animals, the fumonisins are often involved in
liver toxicity and their major mode of action is that they
interfere with sphingolipid metabolism. There is no carryover of
fumonisins into milk in cattle and there appears to be little
absorption of them in tissues (Richard et al., 1996). Because of
the lack of toxicity information due to fumonisins in some
animal species, disease diagnosis can be difficult.
The guidance levels for fumonisins (total including FB1, FB2
and FB3) in human foods and animal feed proposed by the FDA
and European Community are shown in Tables 6 and 7,
respectively (FAO Food and Nutrition Paper No. 81, 2004).
2.4. Zearalenone
This mycotoxin was mentioned earlier in that it may co-exist
with DON as the same organisms, F. graminearum or F.
culmorum (CAST, 2003), may produce both compounds.
Chemically, it is a phenolic resorcyclic acid lactone (Fig. 4)
that is estrogenic when consumed by animals, primarily swine
(Hidy et al., 1977). Grains infected with the above organism
may exhibit the pink color associated with the production of a
pink pigment simultaneously produced with the zearalenone.
Most often this mycotoxin is found in corn. However, it is
found also in other important crops such as wheat, barley,
sorghum and rye throughout various countries of the world
(CAST, 2003). In wheat the conditions for the occurrence of
zearalenone would be essentially the same as for the occurrence
of DON since the organism gains entry into the host plant in the
same manner. Generally, the Fusarium species grow in moist
cool conditions and similarly invade crops under these more
favorable conditions. In wheat, sorghum and corn, zearaleone
occurs in pre-harvest grain but in other commodities the surveys
are insufficient to determine if zearalenone occurred pre-or postharvest
(WHO Food Additives Series: 44, 2000). Variations in
the incidence of zearalenone occur with different crop years,
cereal crop and geographical areas.
Again, adequately storing grain to avoid fungal growth is
important. However, zearalenone can be formed at relatively
cool temperatures and have led to increased levels of this
mycotoxin during storage where conditions for fungal growth
and mycotoxin formation were favorable.
The most notable effect of zearalenone is that it causes
precocious development of mammae and other estrogenic
effects in young gilts as well as prepucial enlargement in young
barrows. Swine are the most significantly affected species and
are considerably more sensitive to zearalenone than, for
example, rodents and other species such as cattle and poultry.
Weak piglets and small litter size have been attributed to the
effects of zearalenone when fed to sows during gestation.
Levels of 0.5 to 1.0 μg/g of dietary zearalenone have been
associated with the latter effects while hyperestrogenism in
swine was associated with dietary levels of 1.5 to 5 μg/g
(Prelusky et al., 1994). Zearalenone appears to bind to estrogen
receptors and can result in hormonal changes. Mortalities are
not a concern due to zearalenone.
Table 4
U.S. Food and Drug Administration advisory levels for deoxynivalenol in wheat
and derived products and other grains (μg/g)
Product Concentration
Finished wheat products for human consumption 1
Grain and grain by products destined for swine and other
animals (except cattle and chickens), not to exceed 20% of
diet for swine (40% for other species)
5
Grain and grain byproducts for beef, feedlot cattle older than
4 months and chickens; not to exceed 50% of the diet.
10
Fig. 3. Structure of fumonisin B1 as a representative of the fumonisins.
Table 5
European Union regulations for deoxynivalenol (μg/kg)
Product Concentration
Cereal products as consumed and other products at retail stage 500
Flour used as raw material in food products 750
6 J.L. Richard / International Journal of Food Microbiology 119 (2007) 3–10
There are no U.S. regulations imposed on the occurrence of
this mycotoxin however, the European Union has regulations
for this mycotoxin (FAO Food and Nutrition Paper No. 81,
2004) (Table 8).
2.5. T-2 toxin
This mycotoxin is a representative of a large group of
mycotoxins called trichothecenes (Fig. 5). It belongs to the Type
A chemical class of non-macrocyclic trichothecenes while
DON, as mentioned earlier, belongs to the Type B nonmacrocyclic
trichothecenes. The principle fungus responsible
for the production of T-2 toxin is F. sporotrichioides (CAST,
2003). Some strains of this fungus also produce some closely
related mycotoxins (HT-2 toxin and diacetoxyscirpenol)
belonging to the same chemical class.
Corn, wheat, barley, oats, rice, rye and other crops have been
reported to contain T-2 toxin (CAST, 2003). Natural occurrence
has been reported in Asia, Africa, South America, Europe and
North America. Natural levels range from near zero to 10 μg/g
with few exceptions up to levels of 40 μg/g. Toxin production is
greatest with moisture and temperatures ranging from 6 to
24 °C. Visible evidence of the producing fungus may appear on
corn as white mold growth which, in some instances, may
appear pink to reddish, often beginning at the tip of the ear.
Adequate storage with low moisture and insect control will
minimize further fungal growth and T-2 toxin production. In the
United States, T-2 toxin is infrequently found and, if found,
likely results from inadequate storage of products.
The major effect of T-2 toxin and other trichothecenes is that
they inhibit protein synthesis which is followed by a secondary
disruption of DNA and RNA synthesis. It affects the actively
dividing cells such as those lining the gastrointestinal tract, skin,
lymphoid and erythroid cells. It can decrease antibody levels,
immunoglobulins and certain other humoral factors such as
cytokines (Niyo et al., 1988; Richard, 1991). The manifestations
of disease include signs of weight loss or poor weight
gains, bloody diarrhea, dermal necrosis or beak and mouth
lesions, hemorrhage and decreased production of milk and eggs.
The Type A trichothecenes are more toxic to poultry species
than the Type B trichothecenes. Yellow caseous plaques,
occurring at the margin of the beak, mucosa of the hard palate,
angle of the mouth and tongue, characterize typical oral lesions
in poultry. These lesions can occur at dietary levels of 4 mg/kg
after one week, 0.4 mg/kg after seven weeks, and with 1–4 mg/
kg, beak or oral lesions occurred with concomitant decreased
weight and feed intake after three weeks.
No regulations are present for T-2 toxin in commodities or
any other products.
2.6. Ochratoxin
Ochratoxin A (Fig. 6) is the major mycotoxin of this group
and it is an innately fluorescent compound produced primarily
by Aspergillus ochraceus and Penicillium verrucosum (CAST,
2003). Other fungi such as members of the Aspergillus niger
group may be important in some commodities or geographic
areas (Tjamos et al., 2004).
Little is known of the conditions necessary for involvement
of the producing fungi in grains during development in the field.
Except for its occurrence in some crops such as grapes,
ochratoxin has been regarded as being produced in storage
conditions which favor mold growth and toxin production.
Because of the diverse commodities on which the producing
organisms and ochratoxin are found, it is difficult to describe the
visible presence of the fungus on them. However, visible mold
from the major species producing ochratoxin varies from
yellowish-tan with A. ochraceus to blue–green with Penicillium
species and black with A. niger. Visible mold may not be present
for ochratoxin to occur in grains and other commodities. Grain that
has a “musty” odor should be suspect for mycotoxins and
ochratoxin would be included in the suspect list. Any time the
Table 7
European Union regulations for fumonisins (μg/kg)
Product Concentration
Unprocessed maize 2000
Maize grits, meal and flour 1000
Maize-based food for direct consumption except maize grits,
meal, flour and processed maize-based foods for infants and
young children and baby food
400
Processed maize-based foods for infants and young children and
baby food
200
Table 6
U.S. Food and Drug Administration guidelines for fumonisins in human foods
and animal feeds (μg/g)
Concentration total
fumonisins
(FB1, FB2, FB3)
Human foods
Degermed dry milled corn products 2
Whole/partially degermed dry milled corn product 4
Dry milled corn bran 4
Cleaned corn intended for mass production 4
Cleaned corn intended for popcorn 3
Corn and corn byproducts for animals
Equids and rabbits 5 b20% diet
Swine and catfish 20 b50% diet
Breeding ruminants, poultry, mink, dairy cattle, laying
hens
30 b50% diet
Ruminants N3 mos. before slaughter and mink for pelts 60 b50% diet
Poultry for slaughter 100 b50% diet
All other livestock and pet animals species 10 b50% diet
Fig. 4. Structure of zearalenone.
7J.L. Richard / International Journal of Food Microbiology 119 (2007) 3–10
integrity of the seed coat has been compromised there is potential
for invasion by ochratoxin-producing fungi. Appropriate sampling
for testing is important as “hot spots” can occur in storage. The
ubiquitous fungi can contaminate grains stored under high
moisture/humidity and warm temperatures. Therefore, grains
should be adequately dried and stored where insects are controlled.
Ochratoxin is primarily a kidney toxin but in sufficiently high
concentrations it can damage the liver as well. Ochratoxin is a
carcinogen in rats and mice and is suspect as the causative agent of
human disease. Balkan Endemic Nephropathy is one such kidney
disease, often with associated tumors, of humans that is
considered by some to be caused by ochratoxin (PfohlLeszkowicz
et al., 2002). A significant feature of ochratoxin is
that it occurs in a wide variety of commodities such as raisins,
barley, soy products and coffee in varying amounts but at
relatively low levels (CAST, 2003). However, the levels may
accumulate in body tissues and fluids of either humans or animals
consuming contaminated food because ochratoxin appears to be
slowly eliminated from the body. Its occurrence in house dust and
other airborne particulates may be of significance in human
disease by this mycotoxin (Richard et al., 1999; Skaug et al.,
2001). Regulations for ochratoxin A are present in the European
Community (FAO Food and Nutrition Paper No. 81, 2004)
(Table 9) but none have been established in the United States.
2.7. Ergot
Ergot is often used as a name for any condition which causes
for the production or accumulation of ergot alkaloids either in
hardened masses of fungal tissue (sclerotia), the most typical
association, or liberated into host plant tissue by endophytic
fungi. Ergot alkaloids are a large group of compounds produced
by fungi that attack a wide variety of grass species, including
small grains, during the growing season. They are divided into
the clavine alkaloids, lysergic acids, simple lysergic acid amides
and peptide alkaloids (Fig. 7).
The major ergot fungus is Claviceps which produces
sclerotia in several grass species with C. purpurea being the
most commonly found species, however, C. fusiformis has
produced ergot in pearl millet and C. paspali has been
associated with problems in dallis grass poisonings (CAST,
2003). The endophytic fungi, Neotyphodium or Epichloe
produce ergotpeptines such as ergovaline in tissues of selected
grasses such as fescue. In the United States, Neotyphodium
ceonophialum inhabits tall fescue and produces ergovaline
which is implicated in an ergot-like toxicosis in animals grazing
on this grass (CAST, 2003).
The entire life cycle of the organism Claviceps is quite
complex, but for simplicity, species of this genus replace the
developing ovaries of the seed with masses of fungal tissue
which harden into sclerotia (sometimes called “ergots”). The
sclerotia are brown to purple–black in color and contain the
ergot alkaloids. The fungus gains entry into the host plant from
sclerotia that have been in the soil. The infecting fungal
elements (ascospores) are ejected forcibly but also are assisted
by wind and splashing rain in gaining access to the host plant
where the florets are invaded with subsequent sclerotial
development. The sclerotia are harvested with the grain and if
not eliminated by screening or some other process they can end
up in feed or food made from the contaminated grain.
Noted earlier, ergotism is one of the oldest mycotoxicoses
with ancient records of its occurrence. In these cases, signs of
gangrene, central nervous system and gastrointestinal effects
were observed. Animals are affected similarly. In swine,
agalactia has been attributed to ergot alkaloids. The loss of
ears and other appendages is a common effect of ergot in
animals. Two types of ergotism have been described; gangrenous
and convulsive. The differences may be due to the
different kinds of alkaloids present in the ergot as variations in
amount and kinds of alkaloids can occur in the sclerotia. In
more recent years, outbreaks have occurred in human populations
and the effects included gangrene and loss of limbs and
nervous signs including giddiness, drowsiness, nausea and
vomiting (Demeke et al., 1979; Krishnamachari and Bhat,
Table 8
European Union regulations for zearalenone (μg/kg)
Product Concentration
Unprocessed cereals other than maize 100
Unprocessed maize 200
Cereal flour except maize flour 75
Maize flour, meal, grits and refined maize oil 200
Bread, pastries, biscuits, other cereal snacks and breakfast
cereals
50
Maize snacks and maize-based breakfast cereals 50
Processed maize-based foods for infants and young children 20
Other processed cereal-based foods for infants and young
children and baby food
20
Fig. 5. Structure of T-2 toxin.
Fig. 6. Structure of ochratoxin A.
Table 9
European Union regulations for ochratoxin (μg/kg)
Product Concentration
Raw cereal grains 5
All products derived from cereals intended for direct human
consumption
3
Dried vine fruit (currants, raisins and sultanas) 10
8 J.L. Richard / International Journal of Food Microbiology 119 (2007) 3–10
1976). Several different alkaloids were found in these outbreaks.
Because some of the ergot alkaloids are vasoconstrictive
and have beneficial pharmacological properties, they have been
used therapeutically. Fescue toxicity caused by mycotoxins,
produced by N. coenophialum in the United States, has caused
severe economic losses in the beef cattle industry as well as in
the dairy and equine industries.
There are no regulatory actions for ergot in grain but the
USDA grain grading agency, GIPSA, classifies grain containing
0.05% or more sclerotia as “ergoty.”
2.8. Other important mycotoxins
Other mycotoxins such as penitrem (a tremorgenic mycotoxin),
patulin, cyclopiazonic acid and citrinin should be classified as
important producers of disease in recipient animals including
man. They have been found in foods or feeds and have the
potential for causing severe disease in animal species. Neither
time nor space allows for sufficient discussion of these potential
agents of disease. Therefore, the reader is referred to the CAST
report (CAST, 2003) for discussions of these mycotoxins.
2.9. Control
A control program for mycotoxins from field to table should
involve the criteria of an HACCP approach which will require an
understanding of the important aspects of the interactions of the
toxigenic fungi with crop plants, the on-farm production and
harvest methods for crops, the production of livestock using grains
and processed feeds, including diagnostic capabilities for mycotoxicoses,
and to the development of processed foods for human
consumption as well as understanding the marketing and trade
channels including storage and delivery of foods to the consumer's
table. A good testing protocol for mycotoxins is necessary to
manage all of the control points for finally being able to ensure a
food supply free of toxic levels of mycotoxins for the consumer.
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