Pseudo-outbreak of methicillin-resistant Staphylococcus aureus.

OBJECTIVE: To determine whether a high rate of methicillin-resistant Staphylococcus aureus at our institution was due to laboratory misclassification and to evaluate the effect of this misclassification. MATERIAL AND METHODS: We evaluated all S. aureus isolates identified at our institution during a 60-day period in 1997. Automated susceptibility test results (using the Vitek system) from our clinical microbiology laboratory and an independent laboratory were compared with oxacillin agar screen plate results at both laboratories. Isolates with discordant results for susceptibility to oxacillin were tested by broth microdilution minimal inhibitory concentrations and for the presence of the mecA gene. RESULTS: Eighteen (72%) of the 25 organisms (obtained from 17 patients) found to be resistant to oxacillin by the Vitek system at our institution were susceptible by the oxacillin agar screen. Discordant isolates tested by broth microdilution minimal inhibitory concentrations and for the mecA gene were found to be oxacillin susceptible and mecA gene negative. Thus, at our hospital, almost three fourths of the organisms initially identified as methicillin-resistant S. aureus by the Vitek system were actually susceptible to oxacillin. This misclassification resulted in needless infection control measures and unnecessary vancomycin use. CONCLUSION: Hospitals that use only automated susceptibility testing for S. aureus should periodically validate their results with additional testing.

Development of quinolone-resistant Campylobacter fetus bacteremia in human immunodeficiency virus-infected patients.

Campylobacter fetus subspecies fetus has been recognized as a cause of systemic illness in immunocompromised hosts, including relapsing bacteremia in human immunodeficiency virus (HIV)-infected patients. Acquired resistance to quinolone therapy, while reported for a variety of bacteria, including Campylobacter jejuni, has not been previously documented for C. fetus. Two cases of quinolone-resistant C. fetus bacteremia were detected in HIV-infected patients. Cloning and nucleotide sequencing of the C. fetus gyrA gene in the 2 resistant isolates demonstrated a G-to-T change that led to an Asp-to-Tyr amino acid substitution at a critical residue frequently associated with quinolone resistance. In addition, comparison of the pre- and posttreatment isolates from 1 patient documented outer membrane protein changes temporally linked with the development of resistance. Relapsing C. fetus infections in quinolone-treated HIV-infected patients may be associated with the acquisition of resistance to these agents, and this resistance may be multifactorial.