Affiliation:
1. Department of Microbiology, The University of Alabama at Birmingham, Birmingham, Alabama 35294
Abstract
ABSTRACT
Previous studies suggested that PspC is important in adherence and colonization within the nasopharynx. In this study, we conducted mutational studies to further identify the role PspC plays in the pathogenesis of pneumococci.
pspC
and/or
pspA
was insertionally inactivated in a serotype 2
Streptococcus pneumoniae
strain and in a serotype 19
S. pneumoniae
strain. In the mouse colonization model, pneumococcal strains with mutations in
pspC
were significantly attenuated in their abilities to colonize. In a mouse pneumonia model, strains with mutations in
pspC
were unable to infect or multiply within the lung. Using reverse transcriptase PCR we were able to demonstrate that
pspC
is actively transcribed in vivo, when the bacteria are growing in the nasal cavity and in the lungs. In the bacteremia model, a strain mutated for
pspC
alone behaved like the wild type, but the absence of both
pspC
and
pspA
caused accelerated clearance of the bacteria. Intranasal immunization with PspC with cholera toxin subunit B as an adjuvant protected against intranasal challenge. Evidence was also obtained that revertants that spontaneously acquired PspC expression could multiply and colonize the nasal tissue. This latter finding strongly indicates that pneumococci are actively metabolizing and growing while in the nasopharynx.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Cited by
140 articles.
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