R.D. Wyatt, R.O. Manning, R.A. Pegram and H.L. Marks


The detrimental effects of aflatoxicosis in poultry are well documented and include growth depression (Smith and Hamilton, 1970), anemia (Tung et al., 1975a), increased susceptibility to bruising (Tung et al., 1971) and inhibition of protein synthesis (Tung et al., 1975b). Inhibition of protein synthesis is thought to be responsible, in part, for other effects of aflatoxicosis, such as immunosuppression (Thaxton et al., 1974), poor digestion (Osborne et al., 1982), and coagulopathies (Doert et al., 1976; Doerr and Hamilton, 1981). The liver is the target organ in chickens, characterized by severe enlargement and fatty infiltration (Smith and Hamilton, 1970). Renal pathology and changes in function are also characteristic of aflatoxicosis in chickens; however, these changes are less severe than those noted in the liver (Tung et al., 1973).

It is well documented that aflatoxin is widely distributed in nature, is carcinogenic in laboratory animals, is highly toxic, affects numerous organ systems in chickens, and results in high economic losses within the poultry industry. Unfortunately, the poultry industry cannot prevent aflatoxin contamination in commodities used in the formulation of poultry feeds. In spite of rigorous quality control measures, the purchase of aflatoxin-contaminated feedstuffs can and does occur. Aflatoxin formation subsequent to feed manufacture is also well documented. Thus, several approaches aimed at ameliorating aflatoxicosis in chickens have been investigated. These include dietary modifications, environmental modifications, and genetic selection.

Dietary Modifications

Changes in the composition of poultry diets alleviate some of the adverse effects attributed to the consumption of aflatoxin. Dietary fortification with certain vitamins (Hamilton et al., 1974), protein (Smith et al., 1971), fat (Hamilton et al., 1972), and fatty acids (Lanza et al., 1981) have shown promise to lessen the effect of aflatoxin on the performance of poultry, as have modifications of a non-nutritive nature. One of the latter, dietary hydrated sodium calcium aluminosilicate, was highly effective in alleviating aflatoxicosis in broiler chickens (Phillips et al., 1988). Its effect appears to result from non-reversible binding of the dietary additive to aflatoxin, thereby minimizing absorption of the aflatoxin from the intestinal tract.

Environmental Modifications

Acclimation of chickens to a low environmental temperature minimizes many of the acute (oral dosing) effects of aflatoxicosis (Wyatt et ai., 1977; Manning and Wyatt, 1990). Acclimation-induced resistance was related to the acclimation temperature (i.e., the lower the acclimation temperature, the more resistance) and the length of acclimation (chicks acclimated for 20 days were more resistant than chicks acclimated for 10 days). The cold-induced resistance was temporarily lost when acclimated chicks were housed in a warmer environment) and could be overcome by administration of relatively high levels of aflatoxin. Decreased pentobarbital sleeping times and increased hepatic cytochrome PA50 in cold acclimated (resistant) chicks suggested that changes in the hepatic metabolism of aflatoxin B1 were responsible.

Genetic Selection

Following the observation of differing mortality patterns from acute aflatoxicosis in various growth-selected lines of Japanese quail (Marks and Wyatt, 1979a), a specific effort was made to genetically select Japanese quail for resistance to acute aflatoxicosis (Marks and Wyatt, 1979b). After only 5 generations of selection, an 11-fold increase in resistance to acute aflatoxicosis was accomplished. Lanza et al. (1983) noted genetic variation in a nonselected population of chickens in regard to aflatoxin resistance. In view of the rapid and substantial progress accomplished in Japanese quail for resistance to aflatoxin and the genetic variability of aflatoxin resistance in chickens, we investigated whether chickens could be selected for resistance to aflatoxin and the basis for this resistance.

The technique of selection for aflatoxin resistance in chickens was similar to that used by Marks and Wyatt (1979b) in Japanese quail, that is, a nonselected (NS) line of chickens was maintained at the same time as the survivors from a similar population of chickens that had been administered an LD50 dose of aflatoxin. Survivors were utilized as the breeding stock for each subsequent generation. The resulting line of chickens is designated as the aflatoxin resistant (AR) line.

Two original populations of chickens were used: one, a commercial broiler stock and the other nonselected random-bred population (Athens-Canadian) of chickens maintained for experimental purposes (Wyatt et al., 1987). After each generation of selection, progress in selection for aflatoxin resistance was assessed by administering both the NS (control) and AR lines identical oral doses of aflatoxin capable of causing high mortality.

After 4 generations of selection in the Athens-Canadian population, administration of an oral dose of aflatoxin (20 mg/kg) resulted in 76% mortality in the NS line but only 18% mortality in the AR line. In the two lines derived from the commercial broiler stock, differences were present, but the magnitude was less. In both cases, sensitive indicators of aflatoxicosis, including plasma total protein, albumin, cholesterol concentrations, and gamma glutamyl transferase, were significantly altered in the NS chicks but not in the AR chicks fed aflatoxin. This selection for resistance to acute aflatoxicosis in chickens was rapid and substantial; also the resistance was maintained during more chronic exposure of chicks to aflatoxin.

In vitro microsomal metabolism of aflatoxin B1 was investigated in the NS and AR lines derived from the Athens-Canadian population of chickens. The rate of aflatoxin B1 metabolism was greater with microsomes from AR chicks than with microsomes from NS chicks. Additionally, in vivo pretreatment with sodium phenobarbital increased aflatoxin B1 metabolism with NS microsomes but decreased aflatoxin B1 metabolism with AR microsomes. In vivo pretreatment with beta-nathoflavone (a microsomal enzyme inducer) enhanced the metabolism of aflatoxin B, by AR microsomes compared to NS microsomes. Aflatoxin B1-dihydrodiol was the major metabolite produced by both lines, and aflatoxin M1 and Q1 were produced in small quantities from beta-naphthoflavone pretreated AR microsomal incubations only. The data indicated that increased in vivo resistance of the AR line to acute aflatoxicosis may be related to increased hepatic aflatoxin B1 metabolism. Thus, it can be concluded that genetic selection alters in vitro metabolism (both quantitative and qualitative) of aflatoxin B1.

The significance of this project lies in the potential use of these lines (NS and AR) for comparative studies of aflatoxin toxicity and metabolism in the broiler chicken. Additional research is needed to investigate the metabolism of aflatoxin, including the metabolic profiles and clearance rates in poultry before genetic selection can be a viable means to assist in successful management of aflatoxicosis in chickens. Nevertheless, the present knowledge of genetic selection for aflatoxin resistance, coupled with dietary and environmental modifications may help the commercial poultry industry successfully cope with aflatoxicosis.


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