ORIGINAL ARTICLE Intestinal colonization with resistant bacteria: a prognostic marker of mortality in decompensated cirrhosis S. Pouriki 1 & G. Vrioni 2 & H. Sambatakou 1 & A. Alexopoulou 1 & L. Vasilieva 1 & I. Mani 1 & A. Tsakris 2 & S. P. Dourakis 1 Received: 16 August 2017 /Accepted: 17 September 2017 # Springer-Verlag GmbH Germany 2017 Abstract Infections due to drug-resistant (DR) bacteria are in- creasingly recognized as an emerging problem worldwide. Asymptomatically colonized patients may contribute to the res- ervoir in the hospital setting, causing both horizontal transmis- sion and endogenous infections. We aimed to evaluate the prev- alence of intestinal colonization with DR bacteria on subsequent clinical infection development and prognosis in patients with decompensated cirrhosis. One hundred seven patients without infection at baseline were screened and prospectively followed- up for 3 months. Among the patients screened, DR bacteria were isolated in 47 (43.9%), 14 colonized with multidrug- (MDR) and 33 with extensively drug (XDR)-resistant bacteria or a mixture of MDR/XDR bacteria. Severity of liver disease and demographic characteristics were similar among groups. The 20 (42.6%) with DR vs 14 (23.3%) without had hepatic encephalopathy and/or spontaneous bacterial peritonitis episodes over the past 6 months (p = 0.034). One third of both DR and non-DR groups developed infection during follow-up but in only 7 and 5, respectively, the infection was microbiologically documented. In a 3-month- follow-up period, mortality was higher in patients colonized with XDR compared to those without (log rank p = 0.027). In multi- variate analysis, colonization with XDR bacteria [HR = 1.074, (CI:1.024–1.126), p = 0.003] and MELD score [HR = 2.579 (1.109–5.996), p = 0.028] were independently associated with low survival. Asymptomatic GI colonization with DR bacteria is a risk factor for increased mortality in decompensated cirrhosis. Frequent hospitalizations for complications of the underlying disease and selective pressure induced by the use of antimicro- bials are probably the main determinants. Introduction Patients with cirrhosis have increased risk of developing bac- terial infections, with an incidence that is four- to five-fold higher than that observed in the general population [1, 2]. Despite progress in the pathogenesis, prevention and manage- ment, bacterial infections are still the main cause of hospital- ization, mortality [2] and admission to intensive care units (ICUs) of cirrhotic patients. There are many reports in the literature on the increasing rate of bacterial infections in cir- rhosis caused by drug resistant pathogens (DR) presenting either as multi-drug-resistant (MDR) or as extensively drug- resistant (XDR) [3–5]. Risk factors associated with resistance to antibiotics are nosocomial or health care-associated acqui- sition, long-term norfloxacin prophylaxis, recent use of β- lactams and recent infection with MDR [6, 7]. Spontaneous bacterial peritonitis (SBP) and spontaneous bacteremia are typical infections for patients with decompensated liver cir- rhosis and have enteric origin (endogenous infections) [8]. The pathogenetic mechanism explaining both the develop- ment of SBP and spontaneous bacteremia is the passage of viable bacteria from the intestinal lumen through the intestinal wall to the mesenteric lymph nodes or other sites. This phe- nomenon was first described in 1979 and was called bacterial translocation (BT) [9]. Increased intestinal permeability, bac- terial overgrowth and defect of gut-associated-lymphatic tis- sue promote impaired BT in cirrhotics. As the clinicians usu- ally approve the early antibiotic administration in cirrhotics, A. Tsakris and S. P. Dourakis contributed equally to this work. * A. Alexopoulou alexopou@ath.forthnet.gr 1 2nd Department of Internal Medicine and Research Laboratory, Medical School, National and Kapodistrian University of Athens, Hippokration Hospital, 114 Vas Sophias St, Athens, Greece 2 Department of Microbiology, Medical School, National and Kapodistrian University of Athens, Athens, Greece Eur J Clin Microbiol Infect Dis DOI 10.1007/s10096-017-3110-9