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Staphylococcus aureus clinical isolate 61/5896 exhibited methicillin resistance (MIC 64 mg/L), but lacked mecA, which encodes penicillin-binding protein 2'. The strain was isolated in England in 1961, and exhibited unstable heterogeneous methicillin resistance. When cultivated in drug-free medium, the methicillin resistance of 61/5896 increased after three daily passages, then decreased and was completely lost after 12 days' passage. Electron microscopy revealed that strain 61/5896 had a thicker and rougher cell wall than its methicillin-susceptible derivatives. It produced about three times more penicillin-binding protein 2 (PBP2) than methicillin-susceptible derivatives. The strain was characteristically a non-producer of autolytic enzyme, though the phenotype, which was lost easily, was not directly correlated with methicillin resistance.

Objective:To evaluate the possible presence of vancomycin-resistantStaphylococcus aureus(VRSA) in a Brazilian hospital.Design:Epidemiological and laboratory investigation of nosocomial VRSAMethods:140 methicillin-resistantS aureusstrains isolated between November 1998 and October 1999 were screened for susceptibility to vancomycin. The screening was carried out by using brain-heart infusion agar (BHIA) supplemented with 4, 6, and 8 μg/mL of vancomycin. The minimum inhibitory concentration (MIC) determination was carried out as standardized by the National Committee for Clinical Laboratory Standards using the broth macrodilution, agar-plate dilution, and E-test methods.Patients:Hospitalized patients exposed to vancomycin.Results:5 of the 140 isolates had a vancomycin MIC of 8 μg/mL by broth macrodilution, agar plate dilution, and E-test methods. Four VRSA strains were isolated from patients in a burn unit who had been treated with vancomycin for more than 30 days, and one from an orthopedic unit patient who had received vancomycin treatment for 7 days. Pulsed-field gel electrophoresis characterized four of the VRSA strains as belonging to the Brazilian endemic clone. All five strains were negative forvanA,vanB, andvanC genes by polymerase chain reaction. Transmission electron microscopy of the five strains revealed significantly thickened cell walls. One patient died due to infection caused by the VRSA strain.Conclusions:This is the first report of isolation of VRSA in Brazil and the first report of isolation of multiple VRSA strains from one facility over a relatively short period of time. This alerts us to the possibility that VRSA may be capable of nosocomial transfer if adequate hospital infection control measures are not taken.

Hidehito Matsui, Juri Kimura, Masato Higashide, Yoshio Takeuchi, Kuniyuki Okue, Longzhu Cui, Taiji Nakae, Keisuke Sunakawa, Hideaki Hanaki Research Center for Infections and Antimicrobials, Kitasato Institute for Life Sciences, Kitasato University, Shirokane, Minato-Ku, Tokyo, Japan; Graduate School of Infection Control Science, Kitasato University, Shirokane, Minato-Ku, Tokyo, Japan; Kotobiken Medical Laboratories, Inc., Kamiyokoba, Ibaraki, Japan; Kohjin Bio Co., Ltd., Chiyoda, Sakado, Saitama, Japan; Kitasato University Research Organization for Infection Control Science, Shirokane, Minato-Ku, Tokyo, Japan

Background The aim of this study was to determine whether clinical outcome of patients with methicillin-resistant Staphylococcus aureus (MRSA) bacteraemia was correlated with vancomycin susceptibility of the corresponding strains. Methods A retrospective study on MRSA bacteraemia was performed at a teaching hospital between January 1998 and October 2005 by linking vancomycin susceptibility profiles of patients' isolates with hospitalization data. Results A total of 20 out of 209 MRSA bacteraemia patients were treated with vancomycin for at least 5 days with adequate trough levels, and fulfilled the study's inclusion and exclusion criteria. Twenty-two S. aureus isolates from these patients' blood cultures were identified as MRSA, including two hetero-VISA from separate patients and two VISA with vancomycin MIC of 4 mg/L from one patient. Between patients who showed 'good' vancomycin response and patients who did not, there was a significant difference (p < 0.01) in their corresponding MRSAs' vancomycin susceptibility expressed by 'area under curve' (AUC) of population analysis. Significant correlations were found between AUC and initial vancomycin therapeutic response parameters of 'days till afebrile' (r = 0.828, p < 0.01) and 'days till CRP ≦ 30% of maximum' (r = 0.627, p < 0.01) Conclusion Our study results caution healthcare personnel that early consideration should be given to cases with a poor vancomycin treatment response that could signify the involvement of MRSA with reduced susceptibility to vancomycin.