The burden of extended-spectrum β-lactamase-producing Enterobacteriaceae in patients with cirrhosis.

Abstract

Patients with cirrhosis have high susceptibility to bacterial infections [1]; 24 % of patients admitted to the hospital for an acute decompensation of cirrhosis have bacterial infection [2]. The most common infection is spontaneous bacterial peritonitis (SBP) [1, 2]. It is well known that SBP is caused by Gram-negative bacteria such as Escherichia coli or Klebsiella pneumoniae originating from the intestinal lumen [3]. The translocation of intestinal bacteria is a crucial step in the process leading to SBP [1, 4]. Little is known about underlying mechanisms that explain bacterial translocation [4]. During the last 30 years the mortality of SBP has decreased from 70 to 30 % [3]. This was the result of large use of a strategy which includes high index of suspicion leading to diagnosis paracentesis, diagnosis of SBP based on neutrophil count C250/mL in the ascitic fluid and subsequent rapid initiation (before results of culture) of wide spectrum, non-nephrotoxic antibiotics (e.g., third generation cephalosporins) against Enterobacteriaceae (E. coli, K. pneumonia) which are the most common causes of SBP [3]. In the late 1990s mortality of SBP was further decreased to 10 % with the combined use of empiric antibiotics and the intravenous administration of human albumin [5]. This beneficial effect was related to a significant decrease in the development of kidney failure (known as hepatorenal syndrome, HRS) [5]. Today, SBP remains the most common trigger of infection-induced acute-onchronic liver failure (ACLF) [2]. ACLF whichever its trigger, is characterized by the failure(s) of organs (including kidney, cerebral, liver, coagulation, circulation and lungs) and high risk of death depending on the number of failing organs [2]. Due to the severity of SBP, efforts have been made to prevent this complication. In patients who survive an episode of SBP long-term prophylaxis with the fluoroquinolone norfloxacin significantly decreases the risk of recurrent SBP [3]. The impact on survival is unknown. In patients with low ascitic fluid protein levels (\1.5 g/dL) but without a prior episode of SBP the efficacy of primary prophylaxis using a fuoroquinolone is still unclear. One trial has shown that norfloxacin significantly decreased the risk for developing a first episode of SBP [6], a finding that was not confirmed in another trial with ciprofloxacin [7]. Recently, an increasing number of cases of SBP due to extended spectrum b-lactamase (ESBL)-producing E. coli, K. pneumonia have been reported in Asia [8–11] and Europe [12–16]. Some risk factors for SBP caused by ESBL-producing bacteria Enterobacteriaceae have been identified including the in-hospital acquisition of infection [10–15], long-term norfloxacin prophylaxis [13], use of blactams within the last 3 months [13], and infection by multiresistant bacteria in the last 6 months [13]. ESBLproducing strains are resistant not only to third-generation cephalosporins, amoxicillin-clavulanic acid but also to quinolones and trimethoprim-sulfamethoxazole [13]. R. Moreau (&) Inserm UMR_S 1149, Centre de Recherche sur l’Inflammation (CRI), Inserm et Universite Paris-Diderot, Paris 7 – Site Bichat, 16 Rue Henri Huchard, 75890 Paris Cedex 18, France e-mail: Richard.moreau@inserm.fr