Rickettsiae can cause life-threatening infections in humans. Macrophages are one of the initial targets for rickettsiae after inoculation by ticks. However, it remains poorly understood how rickettsiae remain free in macrophages prior to establishing their infection in microvascular endothelial cells. Here, we demonstrated that the concentration of Rickettsia australis was significantly greater in infected tissues of Atg5flox/flox mice compared to the counterparts of Atg5flox/flox Lyz-Cre mice, in association with a reduced level of IL-1β in serum. The greater concentration of R. australis in Atg5 flox/flox bone marrow-derived macrophages (BMMs) compared to Atg5 flox/flox Lyz-Cre BMMs in vitro was abolished by exogenous treatment with recombinant IL-1β. Rickettsia australis induced significantly increased levels of LC3-II and LC3 puncta in Atg5-competent BMMs, but not in Atg5- deficient BMMs, while no p62 turnover was observed. Further analysis found that the co-localization of LC3 with a small portion of R. australis and Rickettsia-containing double-membrane-bound vacuoles in BMMs of B6 mice. Moreover, treatment with rapamycin significantly increased the concentrations of R. australis in B6 BMMs compared to the untreated controls. Taken together, our results demonstrated that Atg5 favors R. australis infection in mouse macrophages in association with a suppressed production level of IL-1β but not active autophagy flux. These data highlight the contribution of Atg5 in macrophages to the pathogenesis of rickettsial diseases.