A histologic study was performed on the livers of wild-type (WT), severe co
mbined immunodeficient (SCID), hydrocortisone acetate (HC)-treated WT and H
C-treated SCID mice infected intravenously with 10(5) CFU of Mycobacterium
bovis BCG. It mas found that infection progressed faster in SCID mice than
in WT mice and that HC treatment caused exacerbation of infection in both t
ypes of mite. In all cases infection in the liver was confined to granuloma
s that were populated predominantly by macrophages, Higher levels of infect
ion in HC-treated SCID mice, bat not HC-treated WT mice, were associated wi
th extensive infection and destruction of parenchymal cells at the margins
of granulomas. The results indicate that in the absence of T-cell-mediated
immunity and of HC-sensitive T-tell-independent defense mechanisms, macroph
ages are incapable of restricting BCG growth and of confining infection to
their cytoplasm. Consequently, BCG bacilli are released into the extracellu
lar environment, where they are ingested by; neighboring parenchymal cells.