Necrotizing soft tissue infections caused by Streptococcus pyogenes and Streptococcus dysgalactiae subsp. equisimilis of groups C and G in western Norway

Abstract

Streptococcus pyogenes (group A streptococcus, GAS) is a major cause of necrotizing soft tissue infection (NSTI). On rare occasions, other β-haemolytic streptococci may also cause NSTI, but the significance and nature of these infections has not been thoroughly investigated. In this study, clinical and molecular characteristics of NSTI caused by GAS and β-haemolytic Streptococcus dysgalactiae subsp. equisimilis of groups C and G (GCS/GGS) in western Norway during 2000-09 are presented. Clinical data were included retrospectively. The bacterial isolates were subsequently emm typed and screened for the presence of genes encoding streptococcal superantigens. Seventy cases were identified, corresponding to a mean annual incidence rate of 1.4 per 100 000. Sixty-one of the cases were associated with GAS, whereas GCS/GGS accounted for the remaining nine cases. The in-hospital case fatality rates of GAS and GCS/GGS disease were 11% and 33%, respectively. The GCS/GGS patients were older, had comorbidities more often and had anatomically more superficial disease than the GAS patients. High age and toxic shock syndrome were associated with mortality. The Laboratory Risk Indicator for Necrotizing Fasciitis laboratory score showed high values (≥6) in only 31 of 67 cases. Among the available 42 GAS isolates, the most predominant emm types were emm1, emm3 and emm4. The virulence gene profiles were strongly correlated to emm type. The number of superantigen genes was low in the four available GCS/GGS isolates. Our findings indicate a high frequency of streptococcal necrotizing fasciitis in our community. GCS/GGS infections contribute to the disease burden, but differ from GAS cases in frequency and predisposing factors.

Beta-haemolytic group A, C and G streptococcal infections in Western Norway: a 15-year retrospective survey

“…An increase in SDSE virulence, however, has also been recently proposed, partly based on observations of possible horizontal transfer of virulence factors from Streptococcus pyogenes [29]. Furthermore, there are several reports on GCGS infections with severe manifestations, such as NSTI and streptococcal toxic shock syndrome [8,12,19]. Taken together, these observations indicate that the increase in iGCGS is multifactorial.…”

“…They share multiple virulence factors with GAS, including the M protein (encoded by the emm gene) [7]. Furthermore, GCS and GGS display similar disease manifestations to GAS, including necrotizing fasciitis and toxic shock syndrome [8,9]. The incidence of invasive GCS and GGS-infections, however, is not systematically registered in Norway.…”

Laboratory risk indicator for necrotising fasciitis (LRINEC) score for the assessment of early necrotising fasciitis: a systematic review of the literature

“…After the application of inclusion and exclusion criteria at the first and second level of screening, 16 articles were included in the final analysis (Kappa 0.72; Fig 1). 9,[16][17][18][19][21][22][23][24][25][26][27][28][29][30][31] The mean MINORS score for comparative studies was 8.6 and 7.0 for non-comparative studies.…”

Disease Manifestations and Pathogenic Mechanisms of Group A Streptococcus

“…Early studies of STSS in which GAS serotypes M1 and M3 were associated significantly with infection suggested that there may be an association between the superantigen gene repertoire and invasive GAS disease (365)(366)(367); however, targeted mutagenesis of SpeA has a limited effect on the mitogenic activity of toxigenic GAS in vitro (368), and several recent studies indicate that there is no association between superantigen gene profile and disease outcome (369)(370)(371). Numerous allelic variants have been identified for SpeA, SpeC, SpeG, SSA, and SmeZ (355).…”