The intestinal reservoir is central to the epidemiology of Pseudomonas aeruginosa, but the dynamics of intestinal colonization by different phenotypes have been poorly described. To determine the impact of antimicrobial exposure on intestinal colonization by multidrug-resistant (MDR) and extensively drug-resistant (XDR) P. aeruginosa, we screened intensive care unit (ICU) patients for rectal colonization on admission and at weekly intervals. During an 18-month study period, 414 ICU patients were enrolled, of whom 179 (43%) were colonized; 112 (63%) of these were identified at ICU admission and 67 (37%) during their ICU stay. At 10 days after ICU admission, the probabilities of carriage were 44%, 24%, and 24% for non-MDR, MDR-non-XDR, and XDR P. aeruginosa strains, respectively (log rank, 0.02). Pulsed-field gel electrophoresis showed 10 pairs of non-MDR P. aeruginosa and subsequent MDR-non-XDR strains isolated from the same patients to be clonally identical and another 13 pairs (8 MDR-non-XDR and 5 XDR) to be unrelated. There was one specific clone between the 8 MDR-non-XDR strains and an identical genotype in the 5 XDR isolates. The Cox regression analysis identified MDR P. aeruginosa acquisition as associated with the underlying disease severity (adjusted hazard ratio [aHR], 1.97; 95% confidence interval [CI], 1.22 to 3.18; P ؍ 0.006) and prior use of fluoroquinolones (aHR, 1.02; 95% CI, 1.00 to 1.04; P ؍ 0.039), group 2 carbapenems (aHR, 1.03; 95% CI, 1.00 to 1.07; P ؍ 0.041), and ertapenem (aHR, 1.08; 95% CI, 1.02 to 1.14; P ؍ 0.004). The epidemiology of MDR P. aeruginosa is complex, and different clusters may coexist. Interestingly, ertapenem was found to be associated with the emergence of MDR isolates.
Pseudomonas aeruginosa is one of the most common nosocomial pathogens worldwide, and continuously evolving resistance to multiple antimicrobial agents has become a significant health problem. The control of multidrug-resistant (MDR) P. aeruginosa in intensive care units (ICUs) is an important method for preserving the limited number of drugs available for treating P. aeruginosa infections. However, this control is difficult to achieve because the path of emergence and dissemination of MDR P. aeruginosa is not fully understood. As an endogenous source of endemic or epidemic infection with Gram-negative bacilli (GNB), the intestinal reservoir is central to the epidemiology of P. aeruginosa because prior rectal colonization is typically present in most patients developing GNB infections (1).Several studies have demonstrated that prior antimicrobial drug exposure is also a strong risk factor for colonization with a drug-resistant pathogen (2, 3). In fact, we have previously reported an association between carbapenem and fluoroquinolone consumption with the probability of colonization by carbapenem-resistant P. aeruginosa in ICU patients (4).In recent years, important changes have occurred in the epidemiology of MDR P. aeruginosa. First, in addition to the characteristic polyclonal pattern of endogenous ...