Role of host and bacterial virulence factors in Escherichia coli spontaneous bacterial peritonitis.
OBJECTIVE
Host factors and bacterial virulence determinants may play a role in Escherichia coli (E. coli) spontaneous bacterial peritonitis. We evaluated the importance of these factors in the emergence of fluoroquinolone-resistant strains and outcome in cirrhotic patients with E. coli spontaneous bacterial peritonitis.


METHODS
E. coli spontaneous bacterial peritonitis was detected in a 2-year period in three tertiary hospitals. Clinical and bacteriological data were obtained. Phylogenetic group and 15 virulence genes of E. coli strains were analyzed by polymerase gene reaction and compared with 50 isolates from pyelonephritis patients.


RESULTS
Forty-seven E. coli spontaneous bacterial peritonitis patients were identified, 18 (38%) were fluoroquinolone-resistant, a 12% increase compared with our earlier series from 1997 to 2002. Fluoroquinolone resistance was associated with norfloxacin prophylaxis, increased resistance to trimethoprim-sulfamethoxazole and cefotaxime, and less bacterial virulence, as demonstrated by a higher prevalence of 'nonpathogenic' phylogenetic groups A+B1 (56 vs. 28%; P=0.04) and lower virulence scores in fluoroquinolone-resistant E. coli compared with fluoroquinolone-susceptible E. coli. E. coli strains from cirrhotic patients belonged more frequently to 'nonpathogenic' phylogenetic groups A+B1, had fewer virulence factors and higher rates of fluoroquinolone resistance than isolates from pyelonephytis patients. Immunosuppression was independently associated with in-hospital and 3-month mortality. Bacterial virulence factors were unrelated to mortality.


CONCLUSIONS
Fluoroquinolone-resistant E. coli spontaneous bacterial peritonitis prevalence is increasing because of norfloxacin prophylaxis. Strains from peritonitis are less virulent than strains from pyelonephritis because of a higher prevalence of A+B1 phylogeny and quinolone resistance. Mortality is related to immunosuppression, but not to bacterial virulence factors.
Cereto
Ferran
F
Liver Unit, Department of Internal Medicine, Hospital General Universitari Vall d'Hebron, Barcelona, Spain.
Herranz
Xavier
X
Moreno
Eva
E
Andreu
Antònia
A
Vergara
Mertxe
M
Fontanals
Dionisia
D
Roget
Mercè
M
Simó
Maria
M
González
Antonio
A
Prats
Guillem
G
Genescà
Joan
J
D000328:Adult; D000368:Aged; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D019072:Antibiotic Prophylaxis / Q000009:adverse effects; D024881:Drug Resistance, Bacterial; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics / Q000472:pathogenicity*; D004927:Escherichia coli Infections / Q000276:immunology / Q000382:microbiology*; D005260:Female; D024841:Fluoroquinolones / Q000494:pharmacology; D054884:Host-Pathogen Interactions; D006801:Humans; D016867:Immunocompromised Host; D008103:Liver Cirrhosis / Q000150:complications; D008297:Male; D008875:Middle Aged; D010538:Peritonitis / Q000276:immunology / Q000382:microbiology*; D010802:Phylogeny; D011379:Prognosis; D011446:Prospective Studies; D011704:Pyelonephritis / Q000382:microbiology; D014774:Virulence / Q000235:genetics
D000900:Anti-Bacterial Agents; D024841:Fluoroquinolones