Eimeria tenella Infection in Testosterone-Injected Chicks

Abstract

During the hemorrhagic stages of Eimeria tenella infection, the mean hematocrits of testosterone-injected male and female birds were significantly lower than those of uninfected testosteronetreated chicks but remained significantly greater than those of infected, oil-injected animals. In each of 3 experiments, testosterone-injected young male and female chicks showed significantly elevated mean hematocrits compared with oil-injected control fowl. Testosterone-treated chicks also showed somewhat reduced growth rates when compared to controls. By 9 days after E. tenella infection, the hematocrits of 19 oil-injected and 21 testosterone-injected chicks were not significantly different from those of uninfected, oil-injected controls. During the course of E. tenella infection in testosterone-injected and oil-injected chicks, there were no consistently significant differences in cecal lesion score, growth indexes, or mortality between these groups. The results of these experiments indicate that, although testosterone injection caused a significant increase in the hematocrit of young chicks, it offered no protection against the cecal pathology, weight loss, and mortality which occurred during cecal coccidiosis. Eimeria tenella (Railliet and Lucet, 1891) Fantham, 1909, infections in chickens are manifest by the characteristic symptoms of muscular weakness, loss of appetite, lowered body temperature, and bloody droppings. Cecal hemorrhage begins about 90 hr after infection and forms a major part of the cecal coccidiosis syndrome. Lowered hematocrit can first be detected 5 days after E. tenella infection and hematocrit determinations are a sensitive and convenient indicator of the severity of the disease (Natt and Herrick, 1955; Joyner and Davies, 1960). Both cecal coccidiosis and artificial bleeding of chickens by heart puncture produce similar packed red cell volume decreases (Natt and Herrick, 1955) and adrenal ascorbic acid depletions (Challey, 1960). Cecal hemorrhage has therefore been suggested as the most likely cause of mortality. However, Joyner and Davies (1960) found that, in light infections, significant hematocrit decrease occurs without mortality, and others have suggested that toxins produced by the coccidium may be the cause of death (Burns, 1959; Rikimaru, Galysh, and Shumard, 1961). Yet most mortality occurs during the period of acute hemorrhage, and dietary vitamin K significantly reduces this mortality (Joyner, 1963). If hemorrhage and its resultant adverse Received for publication 3 October 1972. * This study was supported by a Brown-Hazen Grant from Research Corporation and by the Foundation of the University of North Carolina at Charlotte. physiological effects (anemia, hemodilution, anoxia, hematopoietic stimulation) are the most important consequences of E. tenella infection, treatments to counteract these effects should be useful in protecting chickens from the cecal coccidiosis syndrome. Gorshein and Gardner (1970) suggest that steroid metabolites which have erythropoietic activity might prove clinically useful in treating anemia in man. Testosterone has been shown to stimulate erythropoiesis in the chicken, and packed red cell volume increased significantly 2 days after testosterone propionate injection (Glick, 1969). The present study was undertaken to determine if testosterone injections could protect chicks from the lethal consequences of E. tenella infections. The severity of the cecal coccidiosis syndrome was assessed by mortality, hematocrit, weight gain, and cecal lesion score. MATERIALS AND METHODS One-day-old White Rock chicks were obtained from a local hatchery (Holly Farms, Indian Trail, North Carolina). They were housed in electrically heated battery brooders, maintained on continuous artificial illumination, and fed an all-mash, unmedicated ration (CFR LAYER 17; Security Mills Inc., Knoxville, Tennessee). The sex of the chicks was determined at necropsy. The E. tenella oocysts were obtained from a pure strain maintained for many years in the laboratory of Dr. W. C. Burns, Department of Zoology, University of Wisconsin, and were kindly donated for this study. They were routinely harvested in this laboratory from donor birds 7 days after oral inoculation, sporulated, separated from host tissue and cecal debris by the method of Wagenbach, Challey, and Burns (1966), and