Molecular and Clinical Characteristics of Invasive Group A Streptococcal Infection in Sweden

Abstract

Background. The incidence and severity of invasive group A streptococcal infection demonstrate great variability over time, which at least, in part, seems to be related to group A streptococcal type distribution among the human population.Methods. An enhanced surveillance study of invasive group A streptococcal infection (746 isolates) was performed in Sweden from April 2002 through December 2004. Noninvasive isolates from either the throat or skin (773 isolates) were collected in parallel for comparison. Clinical and epidemiological data were obtained from 88% of patients with invasive disease and were related to isolate characteristics, including T type, emm sequence type, and the presence of 9 superantigen genes, as well as pulsed-field gel electrophoresis pattern comparisons of selected isolates.Results. The annual incidence was 3.0 cases per 100,000 population. Among the patients with invasive disease, 11% developed streptococcal toxic shock syndrome, and 9.5% developed necrotizing fasciitis. The overall casefatality rate was 14.5%, and 39% of the patients with streptococcal toxic shock syndrome died ( ). The T3/ P ! .001 13/B3264 cluster accounted for 33% of invasive and 25% of noninvasive isolates. Among this most prevalent type cluster, emm types 89 and 81 dominated. Combined results from pulsed-field gel electrophoresis, emm typing, and superantigen gene profiling identified subgroups within specific emm types that are significantly more prone to cause invasive disease than were other isolates of the same type.Conclusions. This study revealed a changing epidemiology of invasive group A streptococcal infection in Sweden, with emergence of new emm types that were previously not described. The results also suggest that some clones may be particularly prone to cause invasive disease.

Streptococcus pyogenes Isolates Causing Severe Infections in Norway in 2006 to 2007: emm Types, Multilocus Sequence Types, and Superantigen Profiles

“…The average annual incidence of invasive GAS in Norway in 2006 to 2007 was 3.1 cases per 100,000 individuals, which was comparable to the average incidence rates reported from our neighboring countries and from the United States pre-2004 (13,25,26,30,43). Incidences in most of the age groups were comparable, as shown in Fig.…”

“…Temporal variation in the male-to-female ratio among patients with invasive GAS disease is unclear but may depend on the prevalence of the different circulating strains. The emm-28 type, associated with females of 20 to 49 years of age, is known for its association with puerperal sepsis (13,29,30), and the emm-82 strain which has been associated strongly with IDUs in the United Kingdom (27) caused 29% of the invasive cases in females aged 20 to 49 years.…”

“…These two emm types are predominant as a cause of invasive infections in children (0 to 17 years) in Europe (29) and are also known to be common in noninvasive infections in children (13,22).…”

Host–Pathogen Interactions in Streptococcal Immune Sequelae

“…Only a few S. pyogenes strains lack the streptococcal cysteine proteinase SpeB (Darenberg et al, 2007;Schmitz et al, 2003;Vlaminckx et al, 2003), which is another suspected nephritogenic factor. SpeB and its zymogen zSpeB interact with plasminogen.…”

Streptococcal toxic shock-like syndrome (TSLS)

“…Pirogeni egzotoksin (8) se ponaša kao superantigen (9) i za razliku od ostalih antigena ne prolazi proces obrade u antigen-prezentujućim ćelijama već se direktno vezuje za molekule glavnog histokompatibilnog kompleksa gena (GHK) klase II. Kompleks superantigen-MHC klase II reaguje sa Tćelijskimm receptorom i stimuliše veliki broj ćelija, do 20%, normalno 0,01-0,1%, što dovodi do disregulacije citokinskog odgovora i oslobađanja ogromne količine citokina: faktora α nekroze tumora (TNFα), interleuikina 1β (IL1β), interleukina 6 (IL6) (10). Masivno oslobađanje citokina je mehanizam nastanka dramatičnog šoka i oštećenja organa udruženih sa streptokoknim toksičnim šok sindromom.…”