Yersinia pestis causes severe disease in natural rodent hosts but mild to inapparent disease in rodent predators such as dogs. Y. pestis initiates infection in susceptible hosts by parasitizing and multiplying intracellularly in local macrophages during the early stage of infection. Thus, we hypothesized that Y. pestis infection severity may depend on how well the intracellular bacterium overcomes the initial host macrophage associated stress. To test this hypothesis, Y. pestis infection progress was studied in mouse splenic and dog peripheral blood macrophages, and various parameters of this infection were measured in mouse and dog tissue culture macrophages RAW264.7 and DH82, respectively. The study showed that during the early stage of infection, intracellular Y. pestis assumed filamentous cellular morphology with multiple genomes per bacterium in both mouse and dog macrophages. Later, in mouse macrophages, these filamentous Y. pestis returned to coccobacilli with spacious vacuolar extension ofVeterinary Pathobiolog
