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Infection and Immunity, May 2001, p. 3175-3180, Vol. 69, No. 5
The Trudeau Institute, Saranac Lake, New York
12983
Received 8 December 2000/Returned for modification 3 January
2001/Accepted 29 January 2001
A histologic study was performed on the livers of wild-type (WT),
severe combined immunodeficient (SCID), hydrocortisone acetate (HC)-treated WT, and HC-treated SCID mice infected intravenously with
105 CFU of Mycobacterium bovis BCG. It was
found that infection progressed faster in SCID mice than in WT mice and
that HC treatment caused exacerbation of infection in both types of
mice. In all cases infection in the liver was confined to granulomas
that were populated predominantly by macrophages. Higher levels of
infection in HC-treated SCID mice, but not HC-treated WT mice, were
associated with 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-cell-independent defense mechanisms, macrophages are incapable of
restricting BCG growth and of confining infection to their cytoplasm.
Consequently, BCG bacilli are released into the extracellular
environment, where they are ingested by neighboring parenchymal cells.
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.5.3175-3180.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Extensive Mycobacterium bovis BCG
Infection of Liver Parenchymal Cells in Immunocompromised
Mice

*
Corresponding author. Mailing address: Trudeau
Institute, 100 Algonquin Ave., Saranac Lake, NY 12983. Phone: (518)
891-3080. Fax: (518) 891-5126. E-mail: rjnorth{at}northnet.org
Present address: Paul Smith's College of Arts and Sciences, Paul
Smiths, NY 12970.
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