Previous Article | Next Article ![]()
Infection and Immunity, February 2001, p. 657-664, Vol. 69, No. 2
Division of Infectious Diseases, Department
of Internal Medicine Centre Hospitalier Universitaire Vaudois, 1011 Lausanne,1 and Division of Infectious
Diseases, Department of Internal Medicine, Centre Hospitalier
Universitaire de Genève, 1211 Geneva,2
Switzerland
Received 25 May 2000/Returned for modification 9 August
2000/Accepted 1 November 2000
Because Staphylococcus aureus strains contain multiple
virulence factors, studying their pathogenic role by single-gene
inactivation generated equivocal results. To circumvent this problem,
we have expressed specific S. aureus genes in the less
virulent organism Streptococcus gordonii and tested the
recombinants for a gain of function both in vitro and in vivo. Clumping
factor A (ClfA) and coagulase were investigated. Both gene products
were expressed functionally and with similar kinetics during growth by
streptococci and staphylococci. ClfA-positive S. gordonii
was more adherent to platelet-fibrin clots mimicking cardiac
vegetations in vitro and more infective in rats with experimental
endocarditis (P < 0.05). Moreover, deleting
clfA from clfA-positive streptococcal transformants restored both the low in vitro adherence and the low in
vivo infectivity of the parent. Coagulase-positive transformants, on
the other hand, were neither more adherent nor more infective than the
parent. Furthermore, coagulase did not increase the pathogenicity of
clfA-positive streptococci when both clfA and
coa genes were simultaneously expressed in an artificial
minioperon in streptococci. These results definitively attribute a role
for ClfA, but not coagulase, in S. aureus endovascular
infections. This gain-of-function strategy might help solve the role of
individual factors in the complex the S. aureus-host relationship.
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.2.657-664.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Study of Staphylococcus aureus
Pathogenic Genes by Transfer and Expression in the Less Virulent
Organism Streptococcus gordonii
*
Corresponding author. Mailing address: Division of
Infectious Diseases, CHUV-BH19, 1011 Lausanne, Switzerland. Phone:
41-21-314.10.25. Fax: 41-21-314.10.36. E-mail:
Philippe.Moreillon{at}chuv.hospvd.ch.
This article has been cited by other articles:
| J. Bacteriol. | J. Virol. | Eukaryot. Cell |
|---|
| Microbiol. Mol. Biol. Rev. | Clin. Vaccine Immunol. | All ASM Journals |
|---|