MORPHOMETRIC AND HISTOPATHOLOGIC ANALYSIS OF LYMPHOID DEPLETION IN MURINE SPLEENS FOLLOWING INFECTION WITH BRUCELLA-ABORTUS STRAIN-2308 OR STRAIN-RB51 OR AN HTRA DELETION MUTANT

BALB/C mice were inoculated intraperitoneally with suspensions of Bruc ella abortus strains 2308 or RB51 or an htrA mutant. Spleens were exam ined on postinoculation day (PID) 2, 4, 7, 10, 15, 21, 30, and 60. Bru cellae were cultured in high numbers from the spleens of mice infected with strains 2308 or htrA through PID 60; however, mice infected with strain RB51 cleared the infection between PID 30 and PID 60. Histopat hologic changes in spleens from 2308-infected mice were characterized by marked accumulations of macrophages, which expanded marginal zones beginning as early as PID 7 and persisting through PID 60. Morphometri c analysis showed a decrease in splenic white pulp in 2308-infected mi ce at PID 10, which correlated with the peak of bacterial infection. A lthough this decrease was significant (P < 0.05) when compared with va lues at the previous (PID 7) and the following(PID 15) time periods, i t was not significantly different from white pulp values noted at PID 2 or PID 4 or the values for control spleens. Spleens from RB51-infect ed mice showed only mild to moderate accumulations of macrophages in m arginal zone areas during the peak of RB51 infection (PID 7-10). Morph ometric analysis of RB51-infected spleens showed a decrease in white p ulp area, which coincided with peak bacterial numbers. However, this d ecrease was not significant (P > 0.05). Spleens from mice infected wit h the htrA mutant showed moderate to marked accumulations of macrophag es in marginal zone areas, which persisted through PID 60. Multifocal necrosis in lymphoid follides as early as PID 4 was seen in both htrA and 2308 infection. Morphometric analysis of htrA-infected spleens rev ealed no significant decrease in white pulp and no obvious correlation with bacterial numbers in the spleen. These results suggest that viru lent B. abortus does not induce lymphoid depletion significantly below those values seen in noninfected mice; thus, the possible role of lym phoid depletion in the pathogenesis of brucellosis remains questionabl e.