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The rickettsial agent Coxiella burneti was studied in cultured mouse L cells by use of the electron microscope. Rickettsiae gain entry to the host cell in an apparently passive manner through phagocytic activity by L cells. The L cells show a lysosomal response to the presence of rickettsiae, as determined by cytochemical tests for acid phosphatase and 5′-nucleotidase. Further, examination of C. burneti within lysosomes suggests that rickettsiae can be degraded by the host cell. Autoradiographic analyses using tritiated thymidine show that rickettsial DNA is largely restricted to the dense nucleoid region, and when such labeled rickettsiae are used to inoculate L cells, most of the label becomes localized in the host cell nucleus. The above information is discussed in terms of dynamic interactions between C. burneti and infected L cells.

Mouse fibroblasts (L-929) and Vero (green monkey kidney) cells were infected with the rickettsia Coxiella burnetii, and persistent infections developed and were studied over a 6to 10-month period. Ultrastructural comparisons were made between the two infected cell types, and both were tested cytochemically for the presence of acid phosphatase, a marker enzyme of lysozymes. Rickettsiae were always observed within vacuoles, and some infected L cells showed flattened endoplasmic reticulum as compared with uninfected cells. Rickettsiae in Vero cells were most often seen in vacuoles containing whorls of membranes ("myelin configurations") which were also seen in uninfected cells. Rickettsiae in Vero cells were pleomorphic, with acid phosphatase reaction product in their periplasmic space. This suggests either rickettsial degradation by lysosomal enzymes which penetrated the cell envelope or a penetration after the rickettsiae were dead. Vacuoles of infected Vero cells showed much more reaction product than that in infected L cells, and most rickettsiae in L cells had a normal appearance and showed no reaction product in their periplasmic space.

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PARETSKY, D. (University of Kansas, Lawrence), C. M. DOWNS, AND C. W. SALMON. Some biochemical changes in the guinea pig during infection with (Coxiella burnetii. J. Bacteriol. 88: 137-142. 1964.-Guinea pigs infected with Coxiella burnetii, the rickettsial agent of Q fever, were studied for 11 days postinfection. Maximal changes in liver lipids, liver phosphorylase, and uridine diphosphate glucose (UDPG)-glycogen glucosyltransferase activities occurred 3 to 4 days postinfection. In this period, total liver lipids increased from 1.26 to 5.46 mrg/mg of N, with the largest inerement in the glyceride fraction. Liver glycogen virtually disappeared by the second day, with no chemically detectable restoration until the eleventh day. A pattern of altered phosphorylase and UDPG-glycogen transglucosylase activities was observed, with maximal phosphorylase and minimal glucosyltransferase activities at the third and fourth days. Histochemical observations confirmed chemical analyses for lipids and glycogen.