Recurrent group G Steptococcus bacteremia, associated with lymphatic disorders and possibly emm stG 840.0, is described.

No abstract

We performed emm typing of M nontypeable invasive group A streptococcal (GAS) isolates collected in a prospective population-based study in Israel. One hundred twenty of 131 isolates (92%) had emm sequences compatible with GAS, consisting of 51 different emm types. Eleven isolates were found to be group G streptococcus. Of the 120 isolates, 55 (46%) belonged to 32 types for which there were no typing sera available in the Streptococcal Reference Laboratory in Israel. The other 65 (64%) isolates, consisting of 19 types, had sera available and therefore could have been serotyped. Forty-three isolates had T and emm types which were not correlated according to standard M-typing protocols and were therefore missed. The principal effect of emm typing was the addition of 32 types not previously identified in Israel and the discovery of new associations between emm and T types. emm typing did not significantly change the proportion of M types; the five most common types were 3, 28, 2, 62, and 41. Twenty different types comprised 80% of all isolates. No new emm sequences were discovered. emm typing emphasized the unusually low incidence of M1 strains causing severe disease in Israel. As serological typing of GAS becomes more problematic due to lack of sera and the appearance of new emm types, reference laboratories should replace M typing with emm sequence typing. Development of a GAS vaccine relies on the emm type distributions in different geographical locations. In our study, 7% of isolates (types 41 and 62) are not included in a 26-valent vaccine that is being studied.Group A streptococcus (GAS) causes a variety of human infections. These range from mild, self-limited diseases like pharyngitis and impetigo to severe, sometimes life-threatening illnesses such as bacteremia, necrotizing fasciitis, and toxic shock syndrome. Typing of GAS has long been the hallmark of both epidemiological studies and the understanding of diseases caused by different strains (2). M protein is a major virulence determinant of GAS that is associated with resistance to phagocytosis, adherence to cells, and virulence in a mouse model of necrotizing fasciitis (1, 24). Serological M typing was developed many years ago and was the only means for typing GAS. Initially, only 50 serotypes were described (12), but later several reference laboratories added some 30 more serotypes (12). This laborious method is becoming obsolete because it is time-consuming and expensive. Many centers have stopped producing specific antisera in rabbits. Sequence analysis of the hypervariable portion of the emm gene encoding M protein (emm typing) has simplified GAS typing and has recently expanded the number of known GAS types from ϳ80 to 124 (12).In various regions of the world, the percentage of M nontypeable strains varies from Ͼ90% (20) to Ͻ20% (15). The reasons for this variation include technical difficulties and a high prevalence of new emm types, for which serum is not available for M typing (15). In Israel, 67% of 21,517 GAS isolates (mostly from pharyngeal s...

Commensal symbionts may become pathogens upon escaping their habitat. In the gut, Bacteroides fragilis protects against colitis through induction of interleukin 10 (IL-10) by CD4(+) T cells. When intestinal integrity is disrupted, B. fragilis and colonic contents escape into the peritoneum, causing abscesses and bacteremia. Whether the virulence mechanisms employed by B. fragilis during infections differ from those employed for symbiosis during commensalism is unknown. We demonstrate T cell-independent IL-10 production in response to B. fragilis during its pathogenic interactions with the host, and demonstrate the ability of the whole organism to activate Toll-like receptor 2-mediated MyD88 signaling in macrophages. Upon challenge with B. fragilis, mortality rates and serum proinflammatory cytokine levels were higher among IL-10(-/-) mice than among wild-type mice. Deaths were due to exuberant proinflammatory responses, not increased bacterial burden. During infection or commensalism, induction of IL-10 by B. fragilis is critical to this microbe's interactions with the immune system.