Abstract

Isolator-reared, uninfected, bacteria-free chicks appeared active and healthy and grew slightly faster than uninfected conventional controls in commercial brooders. Differences between the 2 groups were observed in cecal histology and color and consistency of the cecal contents. Fourteen- day-old and 40-day-old bacteria-free chicks were more resistant than conventional controls to cecal coccidiosis as assessed by the development of clinical signs and cecal pathology and the extent of weight loss and mortality. This indicates that the presence of the flora is involved in the manifestation of clini- cal coccidiosis. The same results were obtained with 2 different diets and a total of 139 of 229 conven- tionals died of coccidiosis whereas none of 89 bacteria-free chicks succumbed. Increasing the oocyst dose increased the severity of the clinical signs in bacteria-free chicks and demonstrated that the flora was not alone responsible for the manifestation of ceoal coccidiosis. Histological observations, oocyst production determinations, and oocyst viability tests showed that the presence of the intestinal flora was not essential for the development of E. tenella. Since fewer first- and second-generation schizonts were observed in bacteria-free fowl, it appears that the presence of the flora favorably affected the early stages of the parasite. Oocyst production, however, was similar in both bacteria-free and con- ventional chicks. Bacteria-free chicks infected with E. tenella produced serum lysins against second- generation merozoites and resisted challenge after conventionalization (placement of bacteria-free chicks into conventional animal housing facilities) as well as conventional controls. Experiments with con- ventionalized chicks indicate that mortality, cecal pathology, and clinical signs, but probably not oocyst production, were related to the presence of the flora during E. tenella infection. The earlier in infection the flora was established in bacteria-free fowl the more similar to the conventional syndrome the disease became.

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