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Invasive Group A Streptococcal Disease: Risk Factors for Adults

Year: 2003

Type: article

Abstract: We conducted a case-control study to identify risk factors for invasive group A streptococcal (GAS) infections, which can be fatal.Case-patients were identified when Streptococcus pyogenes was isolated from a normally sterile site and control subjects (two or more) were identified and matched to case-patients by using sequential-digit telephone dialing.All participants were noninstitutionalized surveillance area residents, >18 years of age.Conditional logistic regression identified the risk factors for invasive GAS infection: in adults 18 to 44 years of age, exposure to one or more children with sore throats (relative risk [RR]=4.93,p=0.02),HIV infection (RR =15.01, p=0.04), and history of injecting drug use (RR=14.71,p=0.003); in adults >45 years of age, number of persons in the home (RR=2.68,p=0.004), diabetes (RR= 2.27, p=0.03), cardiac disease (RR=3.24,p=0.006), cancer (RR= 3.54, p=0.006), and corticosteroid use (RR=5.18,p=0.03).Thus, host and environmental factors increased the risk for invasive GAS disease.I nvasive GAS infection can lead to dramatic, rapidly-pro- gressive syndromes such as necrotizing fasciitis and streptococcal toxic shock syndrome (STSS).An estimated 9,500 cases of invasive GAS disease occurred in the United States in 1999, resulting in approximately 1,100 deaths.The overall case-fatality rate of invasive GAS is estimated to be from 10% to 15%, and the case-fatality rate for STSS can exceed 60% (1).Most of these infections are community-acquired.Although case series and population-based surveillance have identified several possible host risk factors for the development of invasive GAS disease, including age, Native American ethnicity, HIV infection, diabetes mellitus, cardiovascular disease, alcoholism, and other chronic diseases (1-3), these studies have not been able to assess household risk factors.In addition, surveillance studies identified possible risk factors by comparing prevalence of host factors among GAS patients (by using medical record data) to prevalence of host factors among the general population using population-based estimates (1,2).These comparisons are limited by the completeness and availability of both kinds of data.Household-based studies conducted in the 1950s demonstrated that school-aged children were most often responsible for introducing a GAS strain into a household and that mothers were more likely to subsequently acquire the bacteria than fathers (4).These studies suggest that exposure to children and duration of exposure to a GASinfected person influence the transmission of GAS within households.However, community studies have not shown the relative importance of these factors compared to host factors.We conducted a case-control study to evaluate the importance of previously identified risk factors for invasive GAS infection: contact with other persons in the home, with children, with persons symptomatic with GAS disease in the home, with other persons at work, and with persons symptomatic with GAS disease at work. MethodsInvasive GAS disease was defined as the isolation of Streptococcus pyogenes from a normally sterile site (e.g., blood, cerebrospinal fluid, pleural fluid, peritoneal fluid, pericardial fluid, joint fluid, surgical specimens, bone, and scrotal fluid) in a noninstitutionalized resident, >18 years of age, in a surveillance area.Persons who had group A Streptococcus isolated from a sterile site more than 48 hours after hospital admission were presumed to have a nosocomial infection (5) and were excluded.Cases of invasive GAS disease were identified through active, laboratory-based surveillance in three areas: metropolitan Atlanta, Georgia, from July 1, 1997, through June 30, 1999; metropolitan Baltimore, Maryland, from July 1, 1997, through June 30, 1999, and the Toronto-Peel region, Ontario, Canada, from July 1, 1997, through December 31, 1997.The surveillance area population was estimated to include 9 million people (3,627,184 in metropolitan 970

Source: Emerging infectious diseases

DOI: 10.3201/eid0908.020745