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Research Article Free access | 10.1172/JCI3065

Molecular analysis of the role of the group A streptococcal cysteine protease, hyaluronic acid capsule, and M protein in a murine model of human invasive soft-tissue infection.

C D Ashbaugh, H B Warren, V J Carey, and M R Wessels

Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. cashbaugh@channing.harvard.edu

Find articles by Ashbaugh, C. in: JCI | PubMed | Google Scholar

Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. cashbaugh@channing.harvard.edu

Find articles by Warren, H. in: JCI | PubMed | Google Scholar

Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. cashbaugh@channing.harvard.edu

Find articles by Carey, V. in: JCI | PubMed | Google Scholar

Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. cashbaugh@channing.harvard.edu

Find articles by Wessels, M. in: JCI | PubMed | Google Scholar

Published August 1, 1998 - More info

Published in Volume 102, Issue 3 on August 1, 1998
J Clin Invest. 1998;102(3):550–560. https://doi.org/10.1172/JCI3065.
© 1998 The American Society for Clinical Investigation
Published August 1, 1998 - Version history
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Abstract

Human invasive soft-tissue infections caused by group A Streptococcus are associated with significant morbidity and mortality. To investigate the pathogenesis of these serious infections, we characterized the host response to bacterial challenge with an M-type 3 isolate recovered from a patient with necrotizing fasciitis, or with isogenic gene replacement mutants deficient in cysteine protease, hyaluronic acid capsule, or M protein in a murine model of human invasive soft-tissue infection. Animals challenged with the wild-type or cysteine protease-deficient strain developed spreading tissue necrosis at the site of inoculation, became bacteremic, and subsequently died. Histopathologic examination of the necrotic lesion revealed bacteria throughout inflamed subcutaneous tissue. Arterioles and venules in the subcutaneous layer were thrombosed and the overlying tissue was infarcted. In contrast, animals challenged with either an acapsular or M protein-deficient mutant developed a focal area of tissue swelling at the site of inoculation without necrosis or subsequent systemic disease. Histopathologic examination of the soft-tissue lesion demonstrated bacteria confined within a well-formed subcutaneous abscess. We conclude that the group A streptococcal hyaluronic acid capsule and M protein, but not the cysteine protease, are critical for the development of tissue necrosis, secondary bacteremia, and lethal infection in a murine model of human necrotizing fasciitis.

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