Molecular, serological, and clinical features of 16 consecutive cases of invasive streptococcal disease

F. R. Cockerill, R. L. Thompson, J. M. Musser, P. M. Schlievert, J. Talbot, K. E. Holley, W. S. Harmsen, D. M. Ilstrup, P. C. Kohner, M. H. Kim, B. Frankfort, J. M. Manahan, J. M. Steckelberg, F. Roberson, W. R. Wilson

Research output: Contribution to journalArticlepeer-review

51 Scopus citations

Abstract

We performed a comprehensive analysis of the molecular, serological, and clinical features of 16 consecutive cases of invasive streptococcal disease (ISD). The majority of cases were linked to two group A streptococcus (GAS) clones closely related by pulsed-field gel electrophoresis (PFGE) and designated as PFGF-1 and PFGE-1.1. These clones, serotyped as M-3, T-3/B3264, carried an allelic variant of the gene that encodes pyrogenic exotoxin A (speA3) and the gene that encodes streptococcal superantigen (SSA) but different emm alleles that encode M-protein. The characteristics and clinical features of patients were similar to those described in previous reports, regardless of the responsible GAS clone. However, worse clinical outcomes (shock and death) were more frequent when patients infected with PFGE1/1.1 clones were considered as a group and compared with all other patients as a group. One striking feature in some patients with deep tissue infection was a lack of inflammatory cells despite the presence of numerous streptococci. An evaluation of PFGE profiles of GAS isolated elsewhere demonstrated that the PFGE-1 clone has caused invasive disease in other locations in the United States and in Japan.

Original languageEnglish (US)
Pages (from-to)1448-1458
Number of pages11
JournalClinical Infectious Diseases
Volume26
Issue number6
DOIs
StatePublished - 1998

Bibliographical note

Funding Information:
Received 9 September 1997; revised 17 February 1998. Grant support: J. M. M. was supported in part by a grant from the U.S. Public Health Service (AI-33119) and the Texas Advanced Technology Program. P. M. S. was supported by a grant from the National Heart, Lung, and Blood Institute (HL 36611). *Members are listed at the end of text. Reprints or correspondence: Dr. F. R. Cockerill, Clinical Microbiology, Mayo Clinic, Hilton 4, Rochester, Minnesota 55905.

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