Lungs and spleens of white mice were examined after intranasal and intraperitoneal challenge with Coxiellae burnetii, respectively. As a rule, these organisms inhabit lung alveolar macrophages and spleen reticular cells’ vacuoles and are surrounded with a three-layered wall. The vacuoles seem to be formed from phagolysosomes. They are stable structures. When lodged within vacuoles for a long time, Coxiellae preserve viability. Due to the capacity of Coxiellae to parasitize in cellular phagolysosomes, one might consider Q-rickettsiosis as an ‘exoplasmic parasitosis’.

Two phase I strains of Coxiella burnetii of different virulence were injected into the yolk sacs of chicken embryos, and the yolk sacs and livers were examined at intervals by light, fluorescent, and electron microscopy. The high absorptive and digestive capacities of the yolk endoderm contributed to he entrance of the organisms into endodermal epithelial cells where C. burnetii multiplied. Organisms multiplied not only inside specific vacuoles originating from phagolysosomes but also in the cytoplasm itself. Lysis of the limiting membrane of some phagolysosomes, a normal function of endodermal cells, as well as rupture of vacuoles, provided the release of C. burnetii into the cytoplasm. The C. burnetii strain of greater virulence infected 100% of the endodermal cells, whereas the strain of lesser virulence infected only 60%. Budding of very small particles from the C. burnetii bodies was demonstrated. The particles were regarded as filterable forms of the organism. Despite the enormous multiplication of C. burnetii in the endodermal cells, organisms were only rarely detected in the vitelline blood vessels and liver sinusoids of the embryos. Peculiarities of the infectious process of C. burnetii in chicken embryos and possible mechanisms of limitation of spread of the infection are discussed.

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