Twenty-one consecutive patients with streptococcal toxic shock syndrome (TSS) between December 1994 and April 1995 were treated with a median dose of 2 g of intravenous immunoglobulin (IVIG)/kg (cases) and were compared with 32 patients with streptococcal TSS between 1992 and 1995 who did not receive IVIG therapy (controls). The outcome measure was 30-day survival. Patient plasma was tested for its ability to inhibit T cell activation induced by the infecting strain. The proportion of cases with 30-day survival was higher than that of the controls with 30-day survival (67% vs. 34%, respectively; P Å .02). Multivariate analysis revealed that IVIG administration and a lower Acute Physiology and Chronic Health Evaluation II score were associated with survival; the odds ratio for survival associated with IVIG therapy was 8.1 (95% confidence interval, 1.6 -45; P Å .009). IVIG therapy enhanced the ability of patient plasma to neutralize bacterial mitogenicity and reduced T cell production of interleukin-6 and tumor necrosis factor a. IVIG may be an effective adjunctive therapy for streptococcal TSS, possibly because of its ability to neutralize bacterial exotoxins.Streptococcal toxic shock syndrome (TSS) is the most severe tion and cytokine production [7]. Administration of intravenous immunoglobulin (IVIG) can block in vitro T cell activation by manifestation of invasive disease due to group A streptococcus (GAS); the case-fatality rate associated with streptococcal TSS staphylococcal and streptococcal superantigens [8 -10]. Several case reports have been published in which IVIG adminisis as high as 81% [1 -6]. The mechanism whereby gram-positive organisms cause shock is as yet not determined, but there tration in the setting of streptococcal TSS appeared to correlate with clinical improvement [11 -15], and there is evidence that is increasing evidence that it is the result of cytokine induction by exotoxins(s) belonging to the family of gram-positive bacte-IVIG contains superantigen-neutralizing antibodies [16]. The Ontario Streptococcal Study Group has conducted popurial superantigens. This family includes the enterotoxins and TSS toxin-1 produced by Staphylococcus aureus and the streplation-based surveillance for all invasive GAS disease in Ontario, Canada, since 1 January 1992 [6]. The case-fatality rate tococcal pyrogenic exotoxins of Streptococcus pyogenes [7,8].Superantigens bind to cells expressing major histocompatiassociated with streptococcal TSS has been ú65% and has remained stable over time [6,17]. In the winter of 1994, noting bility complex class II molecules and interact directly with the b chain of the T cell receptor to cause massive T cell proliferaan increase in rates of streptococcal TSS [17] and recognizing the potential for IVIG to decrease the high case-fatality rates associated with this disease, we initiated an observational study of the use of IVIG to treat patients with GAS TSS.

In 1996, a population-based surveillance program for invasive adult group B streptococcal (GBS) diseases in Canada was undertaken, to define the epidemiologic and microbiologic characteristics of the disease. Nine public health units across Canada, representing 9.6% of the population, participated in the program. In total, 106 culture-positive cases of invasive adult GBS disease were reported, which represented an incidence rate 4.6 per 100,000 adults (41/100, 000 for pregnant and 4.1/100,000 for nonpregnant adults). Sixty-two (58.5%) of the 106 cases occurred in females, and, of these, 15 (14. 2%) were associated with pregnancy. Serotype V was the most common, accounting for 31% of the 90 GBS isolates typed (26.7% of nonpregnant and 4.4% of pregnant cases). This was followed by serotypes III (19%), Ia (17%), Ib (10%), II (9%), and VII (1%). Thirteen percent were nontypeable. All isolates were susceptible to penicillin, ampicillin, and vancomycin. Resistance to erythromycin and clindamycin was 6.7% and 4.4%, respectively.

Background. Antibiotic administration to individuals with Shiga toxin-producing Escherichia coli (STEC) infection remains controversial. We assessed if antibiotic administration to individuals with STEC infection is associated with development of hemolytic uremic syndrome (HUS).Methods. The analysis included studies published up to 29 April 2015, that provided data from patients (1) with STEC infection, (2) who received antibiotics, (3) who developed HUS, and (4) for whom data reported timing of antibiotic administration in relation to HUS. Risk of bias was assessed; strength of evidence was adjudicated. HUS was the primary outcome. Secondary outcomes restricted the analysis to low-risk-of-bias studies employing commonly used HUS criteria. Pooled estimates of the odds ratio (OR) were obtained using random-effects models.Results. Seventeen reports and 1896 patients met eligibility; 8 (47%) studies were retrospective, 5 (29%) were prospective cohort, 3 (18%) were case-control, and 1 was a trial. The pooled OR, including all studies, associating antibiotic administration and development of HUS was 1.33 (95% confidence interval [CI], .89-1.99; I 2 = 42%). The repeat analysis including only studies with a low risk of bias and those employing an appropriate definition of HUS yielded an OR of 2.24 (95% CI, 1.45-3.46; I 2 = 0%).Conclusions. Overall, use of antibiotics was not associated with an increased risk of developing HUS; however, after excluding studies at high risk of bias and those that did not employ an acceptable definition of HUS, there was a significant association. Consequently, the use of antibiotics in individuals with STEC infections is not recommended.

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