Characteristics of Rickettsia mooseri infection of normal and immune mice

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Abstract
R. mooseri infection initiated by s.c. injection was studied in BALB/c mice with the objective of developing a model for the study of immune mechanisms. Characterization of infection included the following: measurement of the replication, dissemination and clearance of rickettsiae; measurement of correlates of the immune response, including humoral antibody, hypersensitivity to s.c. inoculated rickettsial antigen and activation of nonspecific macrophage microbicidal capacity; and measurement of resistance to a 2nd homologous challenge. Local infection at the site of s.c. injection progressed through day 5 and was controlled by day 7. Systemic infection as determined by the presence of rickettsiae in spleen was first detected on day 7 and progressed through day 14; rickettsiae persisted in this organ at reduced numbers through at least day 28. Control of the local infection at the site of s.c. injection occurred at about the time humoral antibodies and hypersensitivity reactions to s.c. injected rickettsial antigens became demonstrable and was paralleled by a capacity to resist homologous s.c. challenge at a site distant from that of the primary infection. Systemic infection progressed in spite of this acquired immune capacity and was controlled in the spleen in parallel with the development of enhanced macrophage microbicidal capacity in the liver. Thus, an acquired immunity is capable of restricting rickettsial growth at s.c sites at a time when rickettsiae are increasing in titer in deep organs.