title: Role of immunosuppression in the development of quinolone-resistant Escherichia coli spontaneous bacterial peritonitis and in the mortality of E. coli spontaneous bacterial peritonitis.
abstract: BACKGROUND
  Norfloxacin decreases the incidence of spontaneous bacterial peritonitis in cirrhotics, but promotes the appearance of quinolone-resistant Escherichia coli.
  
  
  OBJECTIVE
  : To define the characteristics of quinolone-resistant E. coli spontaneous bacterial peritonitis.
  
  
  METHODS
  E. coli-positive ascitic fluid cultures were identified during a 6-year period. Data on quinolone-sensitive and quinolone-resistant E. coli spontaneous bacterial peritonitis were compared.
  
  
  RESULTS
  One hundred and two E. coli-positive ascitic fluid cultures were detected. Cirrhotics accounted for 67 cases. Spontaneous bacterial peritonitis was found in 47 of the 67 (70%) cases [35 (74%) caused by quinolone-sensitive and 12 (26%) caused by quinolone-resistant E. coli]. Norfloxacin prophylaxis was higher in the quinolone-resistant group (92% vs. 6%, P < 0.001). Compared with patients with quinolone-sensitive E. coli spontaneous bacterial peritonitis, those with quinolone-resistant E. coli spontaneous bacterial peritonitis showed a higher prevalence of associated immunosuppressive factors (immunosuppressive drugs, human immunodeficiency virus infection or cancer) (92% vs. 20%, P < 0.001). Steroid therapy was independently associated with quinolone-resistant E. coli spontaneous bacterial peritonitis (odds ratio, 49; 95% confidence interval, 3.4-699; P = 0.004). The Child-Pugh score (P = 0.03), immunosuppression (P = 0.02) and renal failure (P = 0.01) were independent predictors of E. coli spontaneous bacterial peritonitis-related mortality.
  
  
  CONCLUSIONS
  Associated immunosuppression is an important co-factor for the development of quinolone-resistant E. coli spontaneous bacterial peritonitis and for E. coli spontaneous bacterial peritonitis-related mortality.
authors.affiliation: Liver Unit, Department of Internal Medicine, Hospital Universitari Vall d'Hebron, Universitat Autónoma de Barcelona, Spain.
authors.forename: F
authors.initials: F
authors.lastname: Cereto
authors.forename: I
authors.initials: I
authors.lastname: Molina
authors.forename: A
authors.initials: A
authors.lastname: González
authors.forename: O
authors.initials: O
authors.lastname: Del Valle
authors.forename: R
authors.initials: R
authors.lastname: Esteban
authors.forename: J
authors.initials: J
authors.lastname: Guardia
authors.forename: J
authors.initials: J
authors.lastname: Genescà
mesh_terms: D000890:Anti-Infective Agents / Q000627:therapeutic use*; D001202:Ascitic Fluid / Q000382:microbiology; D024881:Drug Resistance, Bacterial / Q000276:immunology*; D004927:Escherichia coli Infections / Q000188:drug therapy / Q000276:immunology*; D006801:Humans; D007108:Immune Tolerance; D007165:Immunosuppression Therapy; D007166:Immunosuppressive Agents / Q000009:adverse effects; D008103:Liver Cirrhosis / Q000150:complications*; D009643:Norfloxacin / Q000627:therapeutic use*; D010538:Peritonitis / Q000188:drug therapy / Q000276:immunology* / Q000382:microbiology
chemical_list: D000890:Anti-Infective Agents; D007166:Immunosuppressive Agents; D009643:Norfloxacin