Analysis of superantigenic toxin Vbeta T-cell signatures produced during cases of staphylococcal toxic shock syndrome and septic shock.

Most clinical isolates of Staphylococcus aureus harbour genes encoding superantigenic toxins that bind the Vbeta domain of T-cells, but little information is available concerning superantigenic toxin production during staphylococcal toxic shock syndrome (TSS) and septic shock. This prospective study investigated 14 patients with staphylococcal TSS or septic shock; the toxin gene profile of each isolate was determined and flow-cytometry was used to identify the discriminant Vbeta signature (DVbetaS) of each superantigenic toxin in vitro. Attempts were also made to identify in-vivo production of superantigenic toxin DVbetaS in patients' blood. The DVbetaS identified in vitro were: toxic shock syndrome toxin (TSST)-1, Vbeta 2; staphylococcal enterotoxin (SE), Vbeta 9, Vbeta 22; SEB, Vbeta 3, Vbeta 14, Vbeta 17; SED, Vbeta 1, Vbeta 8; egc, Vbeta 5.3, Vbeta 7.1, Vbeta 9, Vbeta 23; and SElK, Vbeta 5.1. The DVbetaS of TSST-1 and SEB were detected in patients with menstrual and non-menstrual TSS, respectively, whereas no Vbeta signature was detected during septic shock. All patients with septic shock (but only one patient with TSS) had lymphopenia and/or impaired cellular immunity. Detection of a superantigenic toxin DVbetaS may help to show which toxin is produced during staphylococcal TSS, thus confirming the diagnosis and hastening the administration of anti-toxin therapy. In contrast, this approach failed to demonstrate superantigenic toxin involvement in cases of septic shock. In this latter condition, a superantigenic toxin may not be produced by S. aureus, or its production may occur without expansion of targeted T-cells because of T-cell apoptosis and/or anergy.

One in five mortality in non-menstrual toxic shock syndrome versus no mortality in menstrual cases in a balanced French series of 55 cases.

Staphylococcus aureus superantigenic toxins are responsible for menstrual and non-menstrual toxic shock syndrome (TSS). We compared the clinical and biological characteristics of 21 cases of menstrual TSS (MTSS) with 34 cases of non-menstrual TSS (NMTSS) diagnosed in France from December 2003 to June 2006. All 55 S. aureus isolates had been spontaneously referred to the French National Staphylococcal Reference Center, where they were screened for superantigenic toxin gene sequences. Most of the patients had previously been in good health. The most striking differences between MTSS and NMTSS were the higher frequency in NMTSS of neurological disorders (p=0.028), of S. aureus isolation by blood culture (50% versus 0% in MTSS), and the higher mortality rate in NMTSS (22% versus 0% in MTSS). The tst and sea genes were less frequent in isolates causing NMTSS than in those causing MTSS (p<0.001 and 0.051, respectively). Higher mortality was significantly associated with the presence of the sed gene (p=0.041), but when considering NMTSS survivors and non-survivors, no clinical or bacteriological factors predictive of vital outcome were identified. Specific antitoxinic therapy was rarely prescribed, and never in fatal cases. Higher mortality was observed in NMTSS than in MTSS, and no definite factors could explain the higher severity of NMTSS. NMTSS would require more aggressive therapy, comprising systematic rapid wound debridement, antistaphylococcal agents, including an antitoxin antibiotics, and intravenous immunoglobulin.

Necrotizing gastritis due to Bacillus cereus in an immunocompromised patient.

Bacillus cereus is increasingly being acknowledged as a serious bacterial pathogen in immunocompromised patients. We present a case of acute necrotizing gastritis caused by B. cereus in a 37-year-old woman with acute myeloblastic leukemia, who recovered following total parenteral nutrition and treatment with imipenem and vancomycin. B. cereus was isolated from gastric mucosa and blood cultures. Up to now, no case of acute necrotizing gastritis due to this organism has been reported.

[Human herpesvirus 6 encephalitis in trimethoprim-sulfamethoxazole-induced hypersensitivity syndrome]. / Association d'une encéphalite à herpès virus 6 et d'un syndrome d'hypersensibilité médicamenteuse au triméthoprime-sulfaméthoxazole.

INTRODUCTION: Human herpesvirus 6 (HHV-6), the causative agent of the common exanthem subitum, is a known cause of central nervous system infection in immunocompromised patients. It has been suggested that HHV-6 participate in the development of drug-induced hypersensitivity syndrome. CASE REPORT: We reported a case of HHV-6 encephalitis associated with hypersensitivity syndrome induced by trimethoprim-sulfamethoxazole in a 72-year-old HIV-negative woman. DISCUSSION: Our case confirmed that reactivation of HHV-6 infection may contribute to the development of the hypersensitivity syndrome.

Loading dose of vancomycin in critically ill patients: 15 mg/kg is a better choice than 500 mg.

Delays in antimicrobial therapy in high-risk patients with infection may have deleterious effects on clinical outcomes. Therefore, appropriate treatment must be initiated promptly. The objective of this prospective study was to determine the better loading dose of vancomycin in critically ill patients with suspected Gram-positive infections. Two groups of patients were studied successively: Group A, loading dose of 500 mg; and Group B, loading dose of 15 mg/kg. The mean post-loading dose serum vancomycin concentration was significantly higher in Group B than in Group A (19.1 +/- 7.4 mg/L versus 10.4 +/- 2.7 mg/L; P < 0.001), without producing toxic peak levels. Clinical cure rates were significantly different for infected patients in Group B compared with Group A: 93% (14 of 15 patients) versus 56% (10 of 18 patients), respectively. However, the proportion of patients surviving to Intensive Care Unit discharge was similar. Because vancomycin is believed to achieve maximum killing at concentrations in serum of four to five times the minimum inhibitory concentration for the infecting organism, our results suggest that the 15 mg/kg loading dose should be preferred.

The relation between preprocedural C-reactive protein levels and early and late complications in patients with acute myocardial infarction undergoing interventional coronary angioplasty.

BACKGROUND: Inflammation is an important feature of arteriosclerotic disease, and the vulnerability of coronary plaques in acute myocardial infarction (AMI) may be related to the levels of serum C-reactive proteins (CRP). While some risk factors for early and late complications have been suggested, an accurate and definitive preprocedural risk stratification of patients undergoing percutaneous transluminal coronary angioplasty (PTCA) is still lacking. HYPOTHESIS: The study was undertaken to investigate whether early and late complications after PTCA could be predicted by evaluation of baseline serum CRP levels in patients with AMI. METHODS: Levels of serum CRP were measured in a total of 230 patients with AMI undergoing PTCA and provisional stent. They were divided into two groups: Group 1 (n = 48) with elevated CRP levels (> or = 5 mg/l) and Group 2 (n = 182) with normal CRP levels (< 5 mg/l). RESULTS: There were no significant differences in baseline clinical, angiographic, and procedural characteristics between the two groups. However, the incidence of in-hospital adverse coronary events (reinfarction, coronary reocclusion, target vessel revascularization, and death) and severe left ventricular dysfunction was significantly higher in Group 1 (18.3 vs. 6.1%, p < 0.05 and 20.9 vs. 6.1%, p < 0.05, respectively). In addition, bailout stenting was performed more frequently in Group 1 than in Group 2 (60.4 vs. 36.3%, p < 0.005). No significant late complications were noted. The serum levels of CRP were the only independent predictors of early adverse events. CONCLUSIONS: Preprocedural serum CRP level might be considered a powerful predictor of early but not late complications in patients undergoing PTCA/stent procedures.