Since the mid-1980s, concern has grown that invasive group A streptococcal infections (IGASI) have been increasing in incidence and severity (1–3). In particular, the emergence of streptococcal toxic shock syndrome (STSS) during the 1980s is frequently cited as an example of increasing severity (4).
Person-to-person transmission of Streptococcus pyogenes (the causative agent for IGASI) primarily occurs through respiratory droplets, although it may also spread through body secretions from an infected patient (5,6). Additionally, M serotypes of S. pyogenes that cause severe disease in a patient are more likely to cause severe disease in subsequent patients (6). These serotypes include 3 (M1, M3, and M18) that are strongly associated with pathogenicity (7). Nonetheless, some evidence indicates that persons in whom IGASI from the same strain of S. pyogenes develops may have different clinical manifestations of this disease (8,9). Other risk factors for IGASI include patient’s age and underlying medical conditions (e.g., varicella). However, what factors may be associated with different clinical manifestations of IGASI is unclear (10–22).
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