Before the introduction of antibiotics, serious infections caused by Streptococcus pyogenes (Group A streptococci) were common. Before World War II, this bacterium was responsible for as many as 50% of postpartum deaths and was the primary cause of death in patients with burns. Also common were the sequelae of post-streptococcal rheumatic fever and post-streptococcal glomerulonephritis.
With penicillin, however, Streptococcus pyogenes was believed to be virtually eliminated as a pathogen. The organism was consigned to the history books, but not for long. In the mid-1980s, focal resurgences of rheumatic fever began to be reported from different areas in the United States (US), such as Salt Lake City, Utah. In such communities, where increases in cases of rheumatic fever had been reported, the serotypes M-1, 3, 5, 6, and 18 were isolated, which, on culture, produced characteristic mucoid colonies. At the same time, reports of increases in invasive streptococcal disease began to surface in both the US and Europe.
Two syndromes were described:
- invasive streptococcal infection, occurring in previously healthy children and adults, commonly associated with septicemia resulting from a deep focus of infection (e.g., bone or lung), and
- streptococcal toxic shock syndrome, involving a cutaneous focus, accompanied by necrotizing or bullous soft tissue changes.
Septicemia is rare in streptococcal toxic shock syndrome, but the most characteristic feature is rapidly progressing multi-organ failure. A high proportion of the strains of Streptococcus pyogenes associated with this condition are serotype M-1, in which fatality rates approaching 50% have been reported.
