' Bacillus piliformis ’ (Tyzzer) and Tyzzer's disease of the laboratory mouse II. Mouse pathogenicity of B . piliformis grown in embryonated eggs

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Abstract
Hitherto the only sources of ''B. piliformis'' available for experimental study of Tyzzer''s disease have been infected mouse liver and brain and the sole evidence that this organism is the etiologicalagenthas been its constant association with the typical liver lesions of the disease. The isolation and serial propagation of B. piliformis in embryonated eggs is described in the preceding paper (Craigie 1966) and this communication reports results of obtained when infected yolk sac and chick embryo liver were injected into mice. B. piliformis did not lose its capacity to infect hepatic cells of the mouse and produce typical liver lesions when subjected to serial passage in embryonated eggs. A non-sporing variant proved as pathogenic as the parent sporing strain and produced hepatic lesions in rats and hamsters. In general, suspensions prepared from infected yolk sac and chick embryo liver were sufficiently potent to produce liver infection when injected intraperitoneally and with a number of preparations fatal infection was obtained by intraperitoneal injection of adult mice not treated with cortisone. With active preparations the enhancing effect of cortisone was confirmed. Penicillin was found effective in checking experimental and naturally occurring infection. An increase in the severity of infection was demonstrated in mice implanted with a transplantable sarcoma, in which the organism multiplied. B. piliformis was also found to survive in the Krebs 2 ascites tumour preserved at -75[degree]C.