However, no significant interaction was found between tap water colonization and time period (before or after Week 11) (P = 0.69).Table 3Summarization of environmental screening data according to acquisition groupRisk factors for P. aeruginosa acquisitionBy univariate analysis, the presence of an invasive device (nasogastric tube), previous patient selleck inhibitor colonization pressure on the same ward and previous tap water colonization pressure from the ICU and shared rooms were significantly associated with P. aeruginosa acquisition (Table (Table4).4). Multivariate analysis revealed that the presence of a nasogastric device was independently associated with P. aeruginosa acquisition (OR = 7.72 (95% CI: 2.32 to 25.70); P = 0.001). In addition, the interaction between antibiotics inactive against P.

aeruginosa and the patient colonization pressure was also significant (P < 0.03). It means that, in patients receiving equal to or more than three days of antibiotics inactive against P. aeruginosa, the presence of at least one colonized patient on the same ward on the previous day increased the risk of P. aeruginosa acquisition on a given day (OR = 10.26 (95% CI: 1.83 to 57.43); P = 0.01) compared to patients without colonized patient in the same ward. This association was not observed in patients with less than three days of antibiotics inactive against P. aeruginosa.Table 4Risk factors for P. aeruginosa acquisition in the ICU (n = 126)DiscussionThis study suggests two main conclusions. First, P. aeruginosa acquisition should be related to the proximity of a patient colonized with P.

aeruginosa in the area (same room) with a chronological component (the previous day) along with selective antibiotic pressure. Antibiotic selective pressure alone did not influence P. aeruginosa acquisition. The hypothesis of a complex mechanism involving antibiotic selective pressure and patient colonization pressure should be relevant for P. aeruginosa acquisition in an ICU with endemic context. If the interaction of both pressures overriding each pressure taken separately is reviewed, there could be some practical implications. Developing strategies for either decreased antibiotic use for “endogenous-like” acquisition or hygiene improvement in response to environmental contamination in “exogenous-like” acquisition could be insufficient.

In an endemic ICU without obvious epidemic acquisition, it is arguable that a reduction in antibiotic selective pressure and improvement in hygiene standards should be combined. The second conclusion is that invasive devices remain an important determinant in P. aeruginosa Anacetrapib acquisition. Whether invasive devices are a surrogate of patient’s severity (an already known acquisition risk factor) or a step for bacteria in the chain linking the environment to the patients cannot be inferred from the results of this study.