Abstract

PURPOSE: To determine the incidence of group A streptococcal necrotizing fasciitis in Ontario, Canada, and to describe the clinical features, outcome, and microbiologic characteristics of this infection.PATIENTS AND METHODS: Prospective, population-based surveillance for invasive group A streptococcal infections was conducted in Ontario from November 1991 to May 1995. All 77 patients meeting clinical and/or histopathologic criteria for streptococcal necrotizing fasciitis were included. Demographic and clinical information was obtained by patient interviews and chart review. Group A streptococci were characterized by M-protein and T-agglutination typing, and polymerase chain reaction (PCR) detection of streptococcal pyrogenic exotoxin genes A and C (speA; speC).RESULTS: The incidence of group A streptococcal necrotizing fasciitis increased during the study from 0.085 per 100,000 population in the first year to 0.40 per 100,000 population in the last year (P <0.001). The median age of cases was 57.5 years and the rate of disease increased with increasing age. Seventy-nine percent of cases were community-acquired, 11% were nosocomial, and 10% were acquired in a nursing home. Forty-seven percent of cases were associated with the presence of streptococcal toxic shock syndrome (Strep TSS) and 46% were bacteremic. Thirty-four percent of cases died and mortality was correlated with increasing age (P = 0.006), presence of hypotension (P = 0.01), and bacteremia (P = 0.03). The most common streptococcal serotypes were M1 (35%) and M3 (25%). Forty-one percent of strains possessed the speA gene and 30% the speC gene. Outcome was not correlated with M-type or the presence of spe genes.CONCLUSIONS: The incidence of necrotizing fasciitis caused by group A streptococcus increased in Ontario between 1992 and 1995. Elderly individuals were more likely to acquire the disease and to die from it. Mortality because of streptococcal necrotizing fasciitis was also associated with the presence of hypotension, Strep TSS, or bacteremia, but not with M-type or the presence of pyrogenic exotoxin genes.

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