We report the presence of the cfr gene underlying the resistance mechanism involved in a clinical outbreak of linezolid-resistant S. aureus.

In hospital outbreaks of methicillin-resistant Staphylococcus aureus (MRSA) many patients are initially colonized without infection. The reasons why some progress to infection while others do not are not known. A cohort of 479 hospital patients, initially only colonized with MRSA, was followed prospectively for the development of MRSA infection. Risk factors for progression to infection were assessed using Cox proportional hazards survival analysis. Fifty-three patients (11 .l%) developed 68 MRSA infections. Intensive care setting, administration of three or more antibiotics, ulcers, surgical wounds, nasogastric or endotracheal tubes, drains, and urinary or intravenous catheterization were all associated with increased rates of MRSA infection. Multivariate analysis showed that intensive care patients, compared with medical natients. had a higher rate of develoning MRSA infection within the first' four days of admission, with a hazard ra;o of 26.9 (95% CI 5.7-126). Surgical wounds, pressure ulcers and intravenous catheterization were also independent risk factors, with hazard ratios (and 95% CI) of 2.9 (1.3-6.3), 3.0 (1.6-5.7) and 4.7 (l+15.6), respectively. These findings suggest that, during an MRSA outbreak, clinical infection would be reduced if surgical and intensive care patients received priority for the prevention of initial colonization with MRSA. Prevention of pressure ulcers, and strict aseptic care of intravenous catheters and surgical wounds would also reduce the development of MRSA infection. Since early treatment with vancomycin is known to reduce the mortality, patients colonized with MRSA who also have one or more of these risk factors may warrant empirical vancomycin therapy at the earliest suggestion of infection.

No abstract

Forty-six cases of nosocomial infection caused by Burkholderia pickettii were reported between June and November 1993 in three metropolitan hospitals in Madrid. A case-control study of the outbreak was conducted to identify its cause. Seventy-four percent of the patients were males; the mean age +/- SD of the patients was 54 +/- 20 years. Sixty-five percent of the patients presented with some gastrointestinal disorder, and 80% had a peripheral catheter; 98% were treated with intravenous fluids, and 96% were treated with intravenous ranitidine. On the basis of results of a descriptive study and knowledge of the epidemiologic features of B. pickettii, a provisional causal hypothesis was formulated: intravenous ranitidine was the source of the outbreak. As a control measure, it was advised to stop treatment with this drug. On the basis of results of logistic regression and the microbiological isolation of B. pickettii in an ampule of the drug, we concluded that intravenous ranitidine was the cause of the outbreak.

The incident registry was highly stable in terms of incidence rates over the observation period and served to highlight the large number of incidents recorded each year. The potential implications of the results are the need to explore reasons for increased exposures in certain areas, with the aim of focusing prevention efforts, and, similarly, to establish the factors associated with diminished incidence rates to model successful measures.