aeruginosa acquisition is complex. In the past, some molecular epidemiology studies have reported Volasertib a significant role of exogenous colonization [4-7,18], whereas others have predominantly identified the role of endogenous colonization [11,13]. Genotypic methods may detect an epidemic context where exogenous sources are the most important [23] and potentially overestimate its role. Hence, the same group has described two different levels of exogenous P. aeruginosa cross-transmission [9,11]. It is also likely that strains spread rapidly from patients to the environment and vice-versa, complicating environmental and patient screening because screening at distinct time intervals could misclassify some cases of exogenous acquisition [16]. Special attention should also be paid to so-called “endogenous” P.

aeruginosa acquisition. P. aeruginosa is not generally considered to be part of the normal human flora [16], and in most patients admitted to hospital for the first time, P. aeruginosa is not usually isolated from bacteriological specimens until the patient has been in the hospital for several days [22,24,25]. In these cases it is unclear if P. aeruginosa is really endogenous (that is, present on admission but undetected by screening and only revealed by antibiotic selective pressure) [17,18]. On the other hand, despite being absent from the flora on admission, P. aeruginosa could be acquired from the environment through repetitive daily healthcare procedures. Sequential cultures with P. aeruginosa isolation from oropharyngeal samples before the gastrointestinal tract support this hypothesis [26].

Moreover, Johnson et al. [22] recently observed that 50% of imipenem-resistant P. aeruginosa acquisition corresponded to neither the classical endogenous nor exogenous route. The question of an undiscovered environmental source was raised. This is the case in some endemic ICU contexts [27]. In our ICU the endemic context was suggested by the fact that one-third of the strains shared the same genotypic profile without an obvious exogenous source of acquisition or epidemic profile [3].Irrespective of the obvious, undiscovered exogenous or true endogenous source of P. aeruginosa [28], it is likely that acquisition of this microorganism by patients is related to a third factor, namely antibiotic treatment which could interact with the environment to facilitate P. aeruginosa acquisition. Our study confirms this hypothesis. It focused on individual patients with daily recorded antibiotic treatment rather than on a population with collective consumption data [29]. Daily antibiotic recording does not prevent misclassification Carfilzomib of antibiotic treatment as active, whereas it was eventually inactive due to poor PK/PD optimization.