Life-threatening infections caused by Streptococcus pyogenes (group A streptococcus) include scarlet fever, bacteremia, pneumonia, necrotizing fasciitis, myonecrosis and Streptococcal Toxic Shock Syndrome (StrepTSS). This chapter focuses on the clinical and epidemiological features of these infections, as well as treatment options and bacterial pathogenesis. In brief, such invasive infections can simply be defined as any infection in which S. pyogenes is isolated from a normally sterile body site. Patients with invasive S. pyogenes infections have a relatively low mortality rate, unless they meet the established criteria for StrepTSS.
Patient mortality is also influenced by the site of infection and the patient’s presenting history. For example, in patients with S. pyogenes necrotizing fasciitis/myonecrosis that lacks a discernable portal of bacterial entry, classical cutaneous signs of a necrotizing process are not initially apparent. In the absence of such clinical clues, the correct diagnosis is often missed or delayed until the patient manifests systemic shock and organ failure. This delay results in high morbidity and mortality rates. Interestingly, patients in this “no portal” category frequently develop soft-tissue infection at a site of relatively minor antecedent soft tissue injury (strain, bruise) that did not break the skin. Pain at the time of presentation is often out of proportion to the injury itself, and is an important clinical clue. A molecular mechanism that links injury to secondary S. pyogenes infection has been recently proposed, and is discussed later in this chapter.
Development of severe invasive infections is associated with strains that produce streptococcal pyrogenic exotoxins (Spe)—a family of bacterial superantigens that includes the classical scarlatina toxins SpeA and SpeC, the cysteine proteinase SpeB, and a number of more recently described superantigens (such as mitogenic factor [MF, SpeF] and streptococcal superantigen [SSA]). Superantigens are potent immunostimulators that cause clonal proliferation of T cells and watershed production of pro-inflammatory cytokines that mediate shock and organ failure. This concept, as well as the molecular biology of streptococcal virulence, colonization, and tissue invasion, is discussed in more detail in the section on the pathogenesis of StrepTSS.
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