A significant increase in the incidence of invasive disease due to GABS in children admitted to our hospital was noted beginning in the mid-late 1980s (J Pediatr 1991;118:341-6). Since that report, we have continued to prospectively monitor cases and herein review our experience during the subsequent 6 1/2 years (7/1/90-12/31/96). During this period, 35 pts had GABS isolated from normally sterile sites. Five (14%) had chronic underlying conditions. Eight(23%) had chicken pox. Among these 8 pts, 5 were bacteremic. Recent trauma excluding chicken pox was the source of infection in 8 (23%). Blood cultures were positive in 13 pts (37%). Sites of infection were: skin and subcutaneous tissues with or without bacteremia (n=12, 34%), lymph node (n=5), bone (5), joint (2), peritoneal fluid (2), pleural fluid (1), CSF (1), sinus (1), sinus and orbit (1), mastoid (1) and retropharyngeal abscess (1). One pt each had: endocarditis and cerebritis; necrotizing fasciitis (seen in 1995-no case had been seen in the 12 yrs prior); and toxic shock syndrome. One pt died (a one mo old with GABS sepsis and meningitis after RSV infection). Isolates from 24 pts seen through 1995 were studied. Serotypes were: M1 (n=4); M3 (4); M6 (2); M12 (3); M22 (3); M75 (1); and M-nontypable (7).

Thus, the clinical presentations and causative M-types of GABS invasive disease in children continue to vary. Further, review of the number of cases seen annually at our center from 1983 thru 1996 shows that the resurgence of invasive disease due to GABS in children noted during the mid-late 1980s continues thru the mid-1990s. In fact, the highest number of cases (10) seen at our center in a single year occurred in 1996. As about 1/4 of the cases seen from 1990 thru 1996 were associated with chicken pox, widespread use of the varicella vaccine may decrease the incidence of invasive disease due to GABS.