 |
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 occur 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 usually seasonal because particular climatic sequences may favor fungal growth and toxin production; 5) study indicates specific association with a particular feed; and 6) although large numbers of fungi found on examination of feedstuff does not necessarily indicate that toxin production has occurred.
Confirmation of diagnosis of mycotoxic disease requires a combination of information. Detection of fungal spores alone, even at high concentrations, is not sufficient for diagnosis; fungal spores or even mold growth may be present without formation of mycotoxins. 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 more than one mycotoxin may be present in feedstuffs, and their different toxicologic properties may cause clinical signs and lesions that are not consistent with those seen when animals are dosed experimentally with pure, single mycotoxins. Several mycotoxins are immunosuppressive, which may allow viruses, bacteria, or parasites to create a secondary disease that is more obvious than the primary.
In reaching a diagnosis of mycotoxicosis characterized by reduced feed intake, reproductive failure, or increased infectious disease due to immunosuppression, differential diagnoses must be carefully established and eliminated by a combination of thorough clinical and historical evaluation, examination of production records, and close attention to appropriate diagnostic testing.
Current technology is aimed at l) prevention of the occurrence of mycotoxins, 2) inactivation of the preformed toxin in grain or feed, and 3) adsorption or inactivation of the toxin in the GI tract. Testing of suspect grain at harvest, maintaining clean and dry storage facilities, use of acid additives (eg, propionic acid) to control mold growth in storage, effective air exclusion in silage storage and shorter 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 aluminosilicate. 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 followup toxin analysis and may not be acceptable to governmental 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) to prevent mold growth.
Important mycotoxic diseases occur in domestic animals worldwide (see Mycotoxicoses: Mycotoxicoses in Domestic Animals ).
|
Table 1
|
PrintOpen table in new window  |
 |  |  |
|
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. See also see Mycotoxicoses: Aflatoxicosis, and poultry mycotoxicoses, see Mycotoxicoses.
|
|
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
|
Seedheads of many grasses, grains
|
Cattle, horses, pigs, poultry
|
Peripheral gangrene, late gestation suppression of lactation initiation. See see Mycotoxicoses: Ergotism.
|
|
|
Paspalinine and paspalitrems, tremorgens
|
C paspali, C cinerea
|
Widespread
|
Seedheads of paspalum grasses
|
Cattle, horses, sheep
|
Acute tremors and ataxia. See paspalum staggers, see Mycotoxicoses: Paspalum Staggers.
|
|
Estrogenism and vulvo-vaginitis
|
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. See also see Mycotoxicoses: Estrogenism and Vulvovaginitis.
|
|
Facial eczema (Pithomycotoxicosis)
|
Sporidesmins
|
Pithomyces chartarum
|
Widespread
|
Toxic spores on pasture litter
|
Sheep, cattle, farmed deer
|
See also see Mycotoxicoses: Facial Eczema.
|
|
Fescue foot
|
Ergovaline
|
Neotyphodium coenophialum
|
USA, Australia, New Zealand, Italy
|
Tall fescue grass (Festuca arundinacea)
|
Cattle, horses
|
Lameness, weight loss, hyperthermia, heat intolerance, dry gangrene of extremities, agalactia, thickened fetal membranes. See also see Mycotoxicoses: Fescue Poisoning.
|
|
Fusariotoxicosis, vomiting and feed refusal in pigs
|
Nonmacrocyclic trichothecenes (deoxy-nivalenol, T-2 toxin, diacetoxyscirpenol, many other trichothecenes)
|
Fusarium sporotrichioides, F culmorum, F graminearum, F nivale; other fungal species
|
Widespread (except for deoxy-nivalenol, more likely in temperate to colder climates)
|
Cereal crops, moldy roughage
|
Pigs, cattle, horses, poultry
|
Vomiting, feed refusal (deoxynivalenol), loss of appetite and milk production, diarrhea, staggers, skin irritation, immunosuppression; recovery on (from T-2, DAS); removal of contaminated feed. See also see Mycotoxicoses: Trichothecene Toxicosis.
|
|
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. See also see Mycotoxicoses: Fumonisin Toxicosis.
|
|
Mold nephrosis
|
See ochratoxicosis (below)
|
|
|
|
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. See also see Mycotoxicoses: Mycotoxic Lupinosis.
|
|
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. See also see Mycotoxicoses: Trichothecene Toxicosis.
|
|
|
Macrocyclic trichothecenes (baccharinoids)
|
Myrothecium verrucaria
|
Brazil
|
Plants of Baccharis spp that contain the toxins
|
Cattle, other herbivores
|
Epithelial necrosis of GI tract. See also see Mycotoxicoses: Trichothecene Toxicosis.
|
|
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
|
Penicillium crustosum, P cyclopium, P commune
|
Widespread
|
Cereal grains, cheese, fruit, meats, nuts, refrigerated foods; compost
|
Cattle, dogs, horses, sheep
|
Neurotoxic signs including continuous 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
|
Australia, New Zealand, Europe, USA
|
Endophyte-infected ryegrass pastures
|
Sheep, cattle, horses, deer
|
Tremors, incoordination, collapse, convulsive spasms. See
ryegrass staggers, see Ryegrass Toxicity.
|
|
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 poultry mycotoxicoses, see Mycotoxicoses.
|
|
Pulmonary edema, emphysema
|
4-Ipomeanol
|
Fusarium solani
|
USA
|
Moldy sweet potatoes
|
Cattle
|
Acute pulmonary edema, leading to interstitial pneumonia and emphysema.
|
|
Porcine pul-monary edema
|
Fumonisin B1 and Fumonisin B2
|
Fusarium verticilloides and F proliferatum
|
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
|
Blackpatch-diseased legumes (notably red clover) eaten as forage or hay
|
Sheep, cattle
|
Salivation, bloat, diarrhea, sometimes death. Recovery usual when removed from clover. See see Mycotoxicoses: Slaframine Toxicosis.
|
|
Stachybotryotoxicosis
|
Macrocyclic tricho-thecenes (satratoxin, roridin, verrucarin)
|
Stachybotrys atra (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. See also see Mycotoxicoses: Trichothecene Toxicosis.
|
|
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. See 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
|
All species
|
Tremors, polypnea, ataxia, collapse, convulsive spasms.
|
|
Sampling and Submitting Feeds for Laboratory Analysis
Much of the error in detecting mycotoxins in feed results from sampling (or subsampling) rather than from analytical methodology. Samples can be taken at various stages—from growing crops or during transport or storage. Whenever possible, samples should be taken after particulate size has been reduced (eg, by shelling or grinding) and soon after blending has occurred (as in harvesting, loading, or grinding). Sampling is most effective if small samples are taken at periodic, predetermined intervals from a moving stream of grain or feed. These individual stream samples should be combined and mixed thoroughly, after which a subsample of 10 lb (4.5 kg) should be taken.
Probe sampling is acceptable when grain has been recently blended but is less reliable because different microenvironments within the storage facility may cause areas of mold or mycotoxin concentration. A suggested method of probe sampling is to sample at 5 locations, each 1 ft (30 cm) from the periphery of a bin, plus once in the center. This should be done for each 6 ft (2 m) of bin depth. Thus, taller bins would require more samples, and the total weight submitted for analysis should be >10 lb.
Dry samples are preferable for 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, drying at 140°F (60°C) for 6–12 hr should preserve fungal activity.
Containers should be appropriate for the nature of the sample. For dried samples, paper or cloth bags are recommended. Plastic bags should be avoided unless grain is dried thoroughly. Plastic bags are useful for high-moisture samples only if refrigeration, freezing, or chemicals are used to retard mold growth during transport and storage. Once a sample has been cooled or frozen, warming may induce condensation and allow mold growth.
Mycotoxin Adsorbents
Adsorption of mycotoxins in contaminated feeds is an area of active research. Aflatoxins are effectively adsorbed by the aluminosilicate feed additives (see Mycotoxicoses: 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 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) were protective for poultry growth and feed consumption with low natural concentrations of aflatoxin, ochratoxin, T-2 toxin, and zearalenone. When added to Fusarium-contaminated diets, GM reduced the number of stillborn piglets compared to controls. GM adsorbent efficacy for ruminants has not been demonstrated. Cholestyramine has been an effective binder of fumonisins and zearalenone in vitro and for fumonisins in animal experiments, but response in cattle is unknown.
Last full review/revision March 2012 by Gary D. Osweiler, DVM, MS, PhD, DABVT
|  |
|