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In a prospective study, we screened specimens from 190 mechanically ventilated patients hospitalized in a surgical intensive care unit, and from the environment to assess risks and routes of colonization/infection. Specimens from various sites were collected on admission and once a week throughout each patient's stay. All P. aeruginosa isolates were typed by determination of DNA patterns. Data were collected from patients to identify risk factors. In vitro production of exoenzymes of different strains were compared. Forty-four patients were colonized with P. aeruginosa on the bronchopulmonary tract and 13 suffered from pneumonia. The 7-d and 14-d Kaplan-Meier rates of colonization were 2.21 and 7.03%. Twenty-one patterns of bronchopulmonary tract isolates were isolated from single patients and 10 from several patients. The lower airway was often the first site of colonization. The contribution of environment to patient colonization appeared to be small. The length of hospitalization, the previous use of third-generation cephalosporins less effective against P. aeruginosa, and chronic obstructive pulmonary disease were the most significant predictors of colonization/infection. The in vitro exoprotein production was not correlated with the presence of pneumonia. Our study may be useful in identifying which patients in the mechanically ventilated population are at greater risk of P. aeruginosa pneumonia.

During a 30-month survey, 55 patients were colonized or infected by a single clone of Pseudomonas aeruginosa in a surgical intensive care unit (ICU). This clone overexpressed an efflux pump system, and its antibiotic resistance pattern was extremely stable as it spread from patient to patient. Pulsed-field gel electrophoresis showed that isolates from different patients were genetically identical or very similar. We were unable to identify an environmental reservoir, but cultures of hand specimens from 2 health care workers were positive. It was not clear whether this carriage was the source of the epidemic or a consequence of it. However, the propagation of the epidemic clone was probably linked to its transmission by the staff from patient to patient. The outbreak was controlled, with difficulty, by strengthening isolation procedures, replacing the antiseptic soap being used by the staff, and changing the antibiotic prescription policy. This observation emphasizes the importance of compliance with hand washing and universal precautions.

A six month prospective study was carried out in a surgical intensive care unit (SICU) of a university hospital to assess the incidence and routes of exogenous colonization by Staphylococcus aureus. A total of 157 patients were included in the study. One thousand one hundred and eleven specimens (nasal, surgical wound swabs, tracheal secretions obtained on admission and once a week thereafter, and all clinical specimens) were collected over a four month period from patients without nasal decontamination (A). They were compared with 729 specimens collected over a two month period from patients treated with nasal mupirocin ointment (B). All S. aureus strains were typed by restriction fragment length polymorphism (RFLP) pulsed-field gel electrophoresis after SmaI macrorestriction. The nasal colonization rates on admission were 25.5 and 32.7% in groups A and B, respectively. Thirty-one untreated patients (31.3%) and three patients (5.1%) treated with nasal ointment, acquired the nasal S. aureuS in the SICU (P=O.O0027). Nasal carriers were more frequently colonized in the bronchopulmonary tract (Bp) and surgical wound (SW) (62%) than patients who were not nasal carriers (14%) (P

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