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 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
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
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, 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 1: Mycotoxicoses in Domestic Animals).
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Managing a Suspected Mycotoxicosis
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). 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
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.
Last full review/revision December 2014 by Gary D. Osweiler, DVM, MS, PhD