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PubMed1992

Mycotoxins and reproduction in domestic livestock.

Molds are parasitic plants that are ubiquitous in livestock feedstuffs. Even though molds themselves reduce the quality of grains, their synthesis of chemical substances termed mycotoxins causes the greatest monetary loss to the animal industry. Five major mycotoxins that impair growth and reproductive efficiency in North America are aflatoxins, zearalenone, deoxynivalenol, ochratoxin, and ergot. Aflatoxins are produced by Aspergillus flavus and Aspergillus parasiticus. Consumption of grains containing aflatoxins by swine affects reproduction indirectly by reducing feed intake and growth. In swine, aflatoxins impair liver and kidney function, delay blood clotting, increase susceptibility to bruising, and interfere with cellular humoral immune systems. Ruminants are comparatively resistant to aflatoxicosis, but presence of aflatoxins in milk of dairy cows is closely monitored for human safety. Depending on environmental conditions, Fusarium roseum can produce either zearalenone or deoxynivalenol. Days 7 to 10 postmating seem to be a critical period of gestation for zearalenone to exert its detrimental actions on early embryonic development. Presence of deoxynivalenol in swine feedstuffs decreases feed intake, causes feed refusal, and induces occasional vomiting. Several species of Penicillium and Aspergillus produce ochratoxin, a mycotoxin that causes necrosis of kidney tissue. Ergot alkaloids produced by Claviceps purpurea on wheat can cause reproductive problems and are associated with lactational failure in swine. Various methods have been developed to remove mycotoxins from infected feedstuffs. Chemical analyses in laboratories as well as diagnostic kits suitable for use at the elevator or farm can be used successfully to identify which mycotoxins are present in suspect feedstuffs.

Animals↗
PubMed1979

Refractory phagocytosis by chicken thrombocytes during aflatoxicosis.

The percentage phagocytosis of chicken thrombocytes was insensitive to dietary aflatoxin (10 microgram/g diet) while the mean phagocytosis was slightly but significantly (P less than .05) reduced by 5 or 10 microgram/g but not lower levels. Thrombocytic phagocytosis was dependent on a heat sensitive serum factor which is not affected during aflatoxicosis. These findings contrast with reports that other phagocytic types such as heterophils, macrophages, and monocytes are sensitive to low levels (e.g., .625 microgram/g) of dietary aflatoxin.

Animals↗
PubMed1979

Impairment of phagocytosis in chicken monocytes during aflatoxicosis.

Graded doses of dietary aflatoxin (0, .625, 1.25, 2.5, 5.0, and 10.0 microgram/g) were tested for their effect on the phagocytic and locomotive capacities of monocytes from chicken blood. The percentage and mean phagocytic activites were decreased significantly (P less than .05) at 2.5 microgram/g and above and at 1.25 microgram/g and above, respectively. Both the directed and undirected locomotion of monocytes were impaired significantly (P less than .05) at 2.5 microgram/g and above. A serum factor with the heat sensitivity of complement and which was required for optimal phagocytosis by monocytes also was reduced in activity during aflatoxicosis. Thus, the circulating element of the mononuclear phagocyte series has reduced capacity to perform its role in host defense during aflatoxicosis.

Animals↗
PubMed1981

Strain variation in 59Fe absorption during aflatoxicosis.

Strain variation of iron absorption in response to dietary aflatoxin was studied using two commercial broiler strains and a nonselected randombred strain. Aflatoxin depressed chick body weights and increased mortalities in each strain. Hematocrits were significantly reduced in the commercial broilers receiving the toxin, but not in the randombreds. Aflatoxin reduced iron absorption in each strain regardless of the presence of anemia.

Absorption↗
PubMed1983

Effects of low level chronic aflatoxicosis in broiler chickens.

A completely random design consisting of three replicates of 25 broiler chickens (Hubbard x Hubbard) at each of four treatments was used to evaluate the effects of low level, chronic aflatoxicosis on performance and various processing parameters. The treatments in Trial 1 were control, .075, .225, and .675 and in Trial 2 control, .3, .9, and 2.7 micrograms/g toxin in feed (ppm). The chickens were maintained on these treatments from day-old to 7 weeks of age with feed and water available ad libitum. All aflatoxin dose levels in Trial 1 significantly (P less than .05) decreased live, dressed, and chilled eviscerated weight, whereas only 2.7 ppm significantly (P less than .05) decreased live and dressed weight in Trial 2, with chilled eviscerated weight being significantly (P less than .05) decreased at .3 and 2.7 ppm in Trial 2. Parts weights and dimension measurements reflected the aflatoxin-induced decrease in dressed weight. Breast yield (%) was significantly (P less than .05) decreased by aflatoxin while back, wing, drum, and thigh yields were significantly increased by aflatoxin. No effect of aflatoxin was seen on the incidence of crooked keel, feather follicle infection, breast blisters, or conformation. A hypocarotenoidemia and hepatic hyperlipemia were clearly a result of chronic aflatoxicosis in these broiler chickens. These data demonstrate that the toxicity of aflatoxin is dependent on the environment in which broiler chickens are exposed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗