Mycotoxins (Mycotoxicosis)
Etiology
Mycotoxicosis is a general term that applies to a broad range of clinical syndromes, caused by the ingestion of feed contaminated with toxic metabolites produced by several species of fungi commonly found in grain. The severity of the disease condition varies with the concentration of toxin ingested. There are many types of mycotoxins recognized. However, the ones most commonly associated with disease in poultry include aflatoxins (produced by Aspergillus flavus, Aspergillus parasiticus and Penicillium puberulum), fusarium toxins (produced by Fusarium spp.) and ochratoxins (primarily produced by Aspergillus ochraceus and Penicillium viridicatum).
Host Range
Mycotoxins are capable of causing disease in many species of birds, as well as non-avian species, and humans. The following avian species may be affected, in decreasing order of susceptibility: ducks, turkeys, geese, pheasants, and chickens.
Epidemiology
In poultry, mycotoxicosis occurs when birds ingest feed contaminated with fungal toxins. Molds can grow and mycotoxins can be produced pre-harvest or during storage, transport, processing or feeding. The improper storage of grains at high temperatures and humidity, as well as insect damage, predisposes feed to fungal growth and toxin contamination. These spores and toxins are generally highly resistant to environmental conditions. Problems with mycotoxicosis occur worldwide, but are especially problematic in climates with high temperatures and humidity. In these countries, the economic impact of mycotoxicosis can be significant.
Clinical Signs
Clinical signs of mycotoxicosis vary significantly with the avian species, type of mycotoxin, dose ingested, and the duration of toxin exposure.
Fusarium toxins, such as trichothecenes (e.g. T-2 toxins, DAS and DON), fumonisins, and moniliformin, are found worldwide. These three groups of toxins are associated with a wide range of clinical signs. Early signs may include refusal to eat, depression, and severe ulceration, crusting and necrosis of any epithelium that comes into contact with the toxin; most commonly the oral mucosa but sometimes the feet and legs. In cases of long-term ingestion, reduced growth, decreased egg production, thin-shelled eggs, abnormal feathering, and skin pigmentation defects may be present. Other possible signs may include edema of head and neck, hemorrhages of the skin, digestive disturbances, slow heart rate, loss of motor control, abnormalities of the legs, rickets, dyspnea, cyanosis of the comb and wattles, diarrhea, and oral plaques. Some toxins in this group can cause sudden death within a poultry flock.
Aflatoxins are present worldwide and are highly toxic. Aflatoxins are primarily associated with liver disease and immunotoxicity. Chronic aflatoxin ingestion can also lead to neoplasia. Clinical signs may include inappetence, decrease body weight gain and impaired feed utilization, passage of indigested feed particles can be found in the stools, increase carcass condemnations; drop in egg production, reduce egg size, poor feather growth and feather picking, pigmentation abnormalities of the feet and legs, and lameness. In addition, mature broiler breeders aflatoxins decrease fertility, increase percentage of early- dead and late-dead embryos, and severely decline hatchability. Poor progeny performance has been reported in chicks from eggs laid by hens exposed to dietary aflatoxins. Aflatoxicosis may also be associated with an increased susceptibility to infectious diseases and can increase mortality rate.
Serious ochratoxin intoxication causes reduced activity, huddling, hypothermia, diarrhea, weight loss, and death. Sublethal intoxication can seriously impair feed conversion resulting in failure to gain weight, loss of pigmentation, a delay in sexual maturity, decreased egg production, fertility and hatchability.
Post-mortem Lesions
On post-mortem examination, Fusarium toxins may be associated with acute and chronic digestive disease including a reddened gastrointestinal mucosa, inflammation and ulcers of the crop, a thickened and roughened ventricular lining, digestive ulcers, and necrosis anywhere along the gastrointestinal tract. Other findings may include hemorrhages of the viscera, ascites, enlarged heart, abnormal bone marrow, rickets, tibial dyschondroplasia, enlargement of the proventriculus and ventriculus, enlarged and friable liver, swollen kidneys and the presence of excessive urates.
On the other hand, aflatoxicosis may produce lesions in the liver and kidneys. In acute cases, the liver may be enlarged, friable and discolored, while chronic cases may be associated with a small, firm, nodular liver and distended gallbladder. Lymphoid tissues undergo atrophy with small bursas and regression of the thymus glands. Additionally, hemorrhages may be present in these organs as well as an increased susceptibility to bruising resulting from capillary fragility and by inadequate synthesis of blood clotting factors. This effect is manifested by an increased incidence of petechial hemorrhages of the musculature of young animals.
The target organ of ochratoxins is the kidneys. Kidneys of affected birds exhibit acute nephrosis, with swelling of the tubular epithelial cells. The kidneys are severely swollen and pale in color, with market accumulation of urates. The ureteres can also show marked accumulation of urates. The livers of affected birds will be often enlarged and pale but not yellowish as observed with aflatoxicosis. One of the most distinctive changes associated with the liver is accumulation of glycogen. This effect can be used to confirm field diagnosis. Ochratoxins may be associated with small bursas, decreased bone strength, and enlarged pale kidneys.
Differential Diagnosis
In general, mycotoxicosis must be differentiated from poor nutrition, poor management, physical damage to tissues, and infectious diseases. Aflatoxicosis mimics infectious bursal disease, fatty liver syndrome, deficiency of linoleic acid, and malabsorption syndrome. Fusarium toxins produce disease similar to avian pox (wet form), vitamin A deficiency, thrush, trichomoniasis, ochratoxicosis, aflatoxicosis, infectious bursal disease, and visceral gout. Oral lesions in poultry are commonly attributed to trichothecene mycotoxins. However other agents associated with oral lesions include copper sulfate toxicity, quaternary ammonium disinfectant toxicity, deficiency of pantothenic acid, biotin and vitamin A, infectious diseases (such as avian pox, trichomoniasis, candidiasis, etc.), trauma and mash feed in laying hens and broiler breeder hens. Regarding a reduction in egg production, changes in the egg characteristics (egg shell quality and internal egg quality) a differential diagnosis should be made between fusarium toxins and other etiologies such as heat stress, excess of sulphonamides, nicarbazin, vanadium, DDT (dichlorodiphenyltrichloroethane) insecticide, infectious diseases (avian influenza, infectious bronchitis, new castle, EDS76, TRT) Ochratoxicosis produces disease similar to aflatoxicosis, visceral gout, infectious bronchitis, infectious bursal disease, citrinin toxicity, sodium intoxication or "salt poisoning", calcium nephropathy, water deprivation, vitamin A deficiency, and malabsorption syndrome.
Diagnosis
If mycotoxicosis is suspected, a complete diagnostic evaluation should be performed including obtaining a thorough feeding history, observation of clinical signs, necropsy exam, tissue collection for histopathology, bacterial and viral cultures, and serology. These tests will help to rule out other diseases. Birds that have died recently and those that are obviously sick should be selected for submission. An ultraviolet (black) light (long wavelength 360 nm) can be used to test corn for the presence of kojic acid-producing fungi, associated with blue-green fluorescence. This can be helpful in making a presumptive field diagnosis. However, a laboratory feed analysis will also be required. Multiple feed samples from different sites (feeder, storage, transport bins, manufacturer) should be properly collected into clean, non-air tight, labeled bags and promptly submitted for analysis. Feed and grain can now be rapidly screened in some laboratories for several mycotoxins including, aflatoxin B1, T-2 toxin, ochratoxins, zearalenone, using monoclonal antibody detection (ELISA) kits. Many poultry companies routinely test grain for aflatoxin contamination by column chromatography. The use of thin layer chromatography (TLC) and high performance liquid chromatography (HPLC) is also recommended for the identification and quantification of mycotoxins in grains and feeds.
Prevention and Control
Prevention is based on detection of contaminated ingredients and the exclusion from rations if this is practical or justified financially
Pre-harvest control has involved using agronomic practices, which minimize plant stress, fungal invasion, and thus mycotoxin accumulation in the field. These include proper irrigation, insect control and pesticide application, proper fertilization, timely planting and avoiding delayed harvest.
The best strategy for the post-harvest control of mycotoxins is proper storage and handling of feedstuffs to prevent conditions conductive to fungal growth. Controlling temperature, moisture, and insects are the factors most closely associated with mycotoxin formation in storage. Management strategies also include: mycotoxin analysis of feedstuffs, rejection of contaminated lots of grain or feed, diversion of contaminated lots, routine inspection and cleaning of all feed handling equipment (trucks, bins, feeders, etc), routine inspection of proper feed manufacturing equipment (silos, cleaning and drying grain, mills, mixers, pellet coolers, etc) and treatment to reduce mold growth. Antifungal agents can be added to the feed but this will have no effect on pre-formed toxins.
Above all, the best recommendation is buying and maintaining good quality grains with low moisture. Under field conditions removing or diluting contaminated feed helps with the control of the disease. Supportive nutritional care might also help in the complete recovery of the flock.
Selected References
- Charlton, B. R. (ed). 2006. Avian Disease Manual, 6th ed. American Association of Avian Pathologists (AAAP), 953 College Station Road, Athens, Georgia 30602-4875.
- Hoerr, F.J. 2008. Mycotoxicoses. In Diseases of Poultry, 12th ed. Y.M. Saif. et al. (ed.). Blackwell Publishing, Ames, Iowa.
- Robens, J.F. and J.L. Richard. 1992. Aflatoxins in animal and human health. Rev Environ Contam Toxicol 127:69-94. Review.
- World Organization for Animal Health (OIE) website. 2008. www.oie.int
- Wyatt, R.D. 2008. Mycoses and Mycotoxicoses. In A Laboratory Manual for the Isolation and Identification of Avian Pathogens, 5th edition. L. Dufour-Zavala Louise et al. (ed.) OmniPress, Inc., Madison, Wisconsin.
Thank you to the following individuals for reviewing these materials:
Orlando Osuna
Jaime Ruiz
Jose Bruzual
