We provide epidemiological information on a large-scale sustained MRPA outbreak occurring at our hospital over a period of more than three years. An epidemic clone prevailing in the urology and ICU wards spread rapidly throughout many other wards despite an epidemiological surveillance program; no specific source of outbreak could be identified and the clone became endemic. This is a new epidemiological scenario with serious consequences.
Our observations contrast strongly with the classical view of the epidemiology of nosocomial P.aeruginosa infections. These nosocomial P.aeruginosa infections were considered to be polyclonal, endemic and opportunistic, affecting patients with underlying diseases undergoing multiple manipulations and receiving broad spectrum antibiotic therapy .
Several hospital outbreaks caused by multiresistant P.aeruginosa have been reported [9–15]. Although colonization by P.aeruginosa frequently precedes overt infection, the original source of the organism and the precise mode of transmission are often unclear.
In our large clonal endemic setting, we were unable to identify a particular reservoir responsible for the outbreak. We investigated all the wet areas that were likely to be sources of contamination. Environmental surveillance was performed in the urology and ICU wards, the wards with the highest incidence, but in neither case did the study provide a great deal of information. The level of detection improved when a moistened gauze was used (0% in ICU and 8% in non-ICU using swabs versus 6% in ICU and 18% in non-ICU with gauze), although no parallel analysis of the two techniques was performed. In addition, the sites that tested positive for the epidemic clone were near colonized patients, and the presence of this clone in the environment may have been a simple consequence of the outbreak rather than a source for transmission of the strain . Nevertheless, two specific interventions involving the reinforcement of cleaning procedures for extensive decontamination were applied in the urology wards and MRPA rates decreased significantly during the months following the interventions, a finding that supports the transitory efficacy of these epidemiological control measures
The results of our active surveillance program and environmental cultures in the ICU setting suggest that patients may indeed be a reservoir in the maintenance of the monoclonal MRPA outbreak. Our capacity of detection of MRPA intestinal carriers in ICUs was lower than the rates found in the screening programs of two other outbreaks at our hospital [33, 34]; however, in those two settings the capacity of the outbreak to spread was higher. These findings are borne out by the longer period of time recorded between ICU admission and digestive colonization: 22 days in the present study versus < 7 days in those outbreaks.
No doubt, cross-transmission plays a relevant epidemiological role in our MRPA ICU patients , but as no hand-print cultures of health care workers were performed in our study, we cannot provide direct evidence that strains were transmitted patient to patient by the health care workers.
Moreover, our data suggest that antibiotic pressure plays a decisive role, by altering the ecological niche in these patients and providing a selective growth advantage for MRPA organisms. Thus, given that the carbapenem consumption in our ICUs in 2006 was high, we assumed that carbapenem restriction might make a significant contribution to controlling the outbreak. The carbapenem restriction program carried out during 2007 was initially followed by a marked reduction; however, a moderate increase was recorded in the second semester and the levels rose again during 2008. Concomitantly, an increase in the level of piperacillin-tazobactam use was observed and a new cluster, particularly in the ICU, was found ; the dominant use of this antibiotic could have favored the emergence and spread of this different clone, and as a result, the carbapenem restriction was relaxed. Carbapenem restriction did not significantly reduce the number of MRPA cases, although this antibiotic program may not have been sufficiently rigorous or prolonged. Furthermore, we cannot rule the possibility that the use of fluoroquinolones may also have contributed to promoting these MRPA strains . Although fluoroquinolone consumption did not increase during the period analyzed (data not shown), overall fluoroquinolone use was considerably higher than that of other antipseudomonal antibiotics. Thus, the limitation of fluoroquinolone use should have been included in our antibiotic restriction program.
Finally, our epidemiological control program had several limitations. First, we did not perform decontamination in other hospital wards; second, it is possible that the evaluation of MRPA digestive tract carriers in certain non-ICU wards would have allowed earlier spatial segregation and would thus have prevented a substantial number of possible cross-transmissions; and third, an extensive antibiotic program restricted to non-ICU wards might have contributed to lower incidence rates.