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Infection and Immunity, February 2004, p. 623-628, Vol. 72, No. 2
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.2.623-628.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Contribution of CsrR-Regulated Virulence Factors to the Progress and Outcome of Murine Skin Infections by Streptococcus pyogenes

N. Cary Engleberg,1,2* Andrew Heath,1 Kristal Vardaman,1 and Victor J. DiRita2,3

Departments of Internal Medicine,1 Microbiology and Immunology,2 Laboratory Animal Medicine, University of Michigan Medical School, Ann Arbor, Michigan 48109-03783

Received 16 January 2003/ Returned for modification 25 February 2003/ Accepted 7 November 2003

Streptococcus pyogenes with null mutations in the csrRS regulatory locus are highly virulent in mice due to derepression of hyaluronic acid capsule synthesis and exotoxins, e.g., streptolysin S (SLS) and pyrogenic exotoxin B (SpeB). We generated derivatives of a {Delta}csrRS strain that also carry deletions in hasAB (leading to an acapsular phenotype) or in sagA (phenotypically SLS-) or an interruption of speB (SpeB-) to test the relative contributions of these factors to the development of necrotic skin lesions. Inoculation of 2 x 106 to 4 x 106 CFU of either acapsular or SLS- strains into hairless mice resulted in lesions ~70% smaller than those of the {Delta}csrRS parent strain. Elimination of SLS also reduced lethality from 100% to 0% at this inoculum (P < 10-7; Fisher exact test). In contrast, SLS+ SpeB- mutants yielded lesions that were only 41% smaller than the parent strain (t = 2.2; P = 0.04), but only 3 the 17 lesions had dermal sloughing (P = 10-5). The nonulcerative lesions associated with SpeB- strains appeared pale with surrounding erythema. We conclude that capsule and SLS contribute to the subcutaneous spread of S. pyogenes and to a fatal outcome of infection. SpeB facilitates early dermal ulceration but has minor influence on lesion size and mortality. Large ulcerative lesions are observed only when both toxins are present.

* Corresponding author. Mailing address: 3116B Taubman Center box 0378, University of Michigan Hospitals, Ann Arbor, MI 48109. Phone: (734) 936-5205. Fax: (734) 936-2737. E-mail: cengleb{at}umich.edu.

Editor: D. L. Burns

Infection and Immunity, February 2004, p. 623-628, Vol. 72, No. 2
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.2.623-628.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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