title: Bacterial infections in cirrhosis: epidemiological changes with invasive procedures and norfloxacin prophylaxis.
abstract: The extensive use of invasive procedures and of long-term norfloxacin prophylaxis in the management of cirrhotic patients may have influenced the epidemiology of bacterial infections in cirrhosis. We conducted a prospective evaluation of all bacterial infections diagnosed in patients with cirrhosis in a Liver Unit between April 1998 and April 2000. A total of 405 patients presented 572 bacterial infections in 507 admissions. Spontaneous bacterial peritonitis was the most frequent infection (138 cases). Gram-positive cocci were responsible for 53% of total bacterial infections in the study, being the main bacteria isolated in nosocomial infections (59%). Patients requiring treatment in an intensive care unit and those submitted to invasive procedures presented a higher rate of infections caused by gram-positive cocci (77% vs. 48%, P <.001 and 58% vs. 40%, P <.02, respectively). Fifty percent of culture-positive spontaneous bacterial peritonitis in patients on long-term norfloxacin administration (n = 93) and 16% in patients not receiving this therapy (n = 414) were caused by quinolone-resistant gram-negative bacilli, P =.01. The rate of culture-positive spontaneous bacterial peritonitis caused by trimethoprim-sulfamethoxazole-resistant gram-negative bacilli was also very high in patients on long-term norfloxacin administration (44% vs. 18%, P =.09). In conclusion, infections caused by gram-positive cocci have markedly increased in cirrhosis. This phenomenon may be related to the current high degree of instrumentation of cirrhotic patients. Quinolone-resistant spontaneous bacterial peritonitis constitutes an emergent problem in patients on long-term norfloxacin prophylaxis, with trimethoprim-sulfamethoxazole not being a valid alternative.
authors.affiliation: Liver Unit, IMD, and Department of Microbiology and IDIBAPS, Hospital Clinic, University of Barcelona, Barcelona, Spain.
authors.forename: Javier
authors.initials: J
authors.lastname: Fernández
authors.forename: Miquel
authors.initials: M
authors.lastname: Navasa
authors.forename: Juliá
authors.initials: J
authors.lastname: Gómez
authors.forename: Jordi
authors.initials: J
authors.lastname: Colmenero
authors.forename: Jordi
authors.initials: J
authors.lastname: Vila
authors.forename: Vicente
authors.initials: V
authors.lastname: Arroyo
authors.forename: Juan
authors.initials: J
authors.lastname: Rodés
mesh_terms: D000368:Aged; D000890:Anti-Infective Agents / Q000627:therapeutic use*; D001424:Bacterial Infections / Q000453:epidemiology* / Q000382:microbiology / Q000517:prevention & control*; D003422:Critical Care; D004352:Drug Resistance, Microbial; D004926:Escherichia coli / Q000302:isolation & purification; D005260:Female; D006090:Gram-Negative Bacteria; D006095:Gram-Positive Cocci; D006526:Hepatitis C; D006801:Humans; D007668:Kidney / Q000503:physiopathology; D008099:Liver / Q000503:physiopathology; D008103:Liver Cirrhosis / Q000382:microbiology* / Q000401:mortality / Q000821:virology; D008104:Liver Cirrhosis, Alcoholic / Q000382:microbiology; D008297:Male; D008875:Middle Aged; D009643:Norfloxacin / Q000627:therapeutic use*; D010538:Peritonitis / Q000382:microbiology; D011446:Prospective Studies; D013420:Sulfamethoxazole / Q000627:therapeutic use; D014295:Trimethoprim / Q000627:therapeutic use
chemical_list: D000890:Anti-Infective Agents; D014295:Trimethoprim; D013420:Sulfamethoxazole; D009643:Norfloxacin