TY - JOUR
T1 - Phylogenetic and pathotypic comparison of concurrent urine and rectal Escherichia coli isolates from men with febrile urinary tract infection
AU - Johnson, James R.
AU - Scheutz, Flemming
AU - Ulleryd, Peter
AU - Kuskowski, Michael A.
AU - O'Bryan, Timothy T.
AU - Sandberg, Torsten
PY - 2005/8
Y1 - 2005/8
N2 - Among men with febrile urinary tract infection (FUTI), whether the host's fecal flora is the source for the urine strain ("fecal-urethral" hypothesis), and whether pathogenesis is driven by prevalence versus special pathogenicity, are unknown. Accordingly, pretherapy urine isolates from 65 men with FUTI were compared with concurrent rectal isolates from the same hosts according to serotype, genomic profile, phylogenetic group, and virulence genotype. The host's multiple rectal colonies included only the urine clone in 25% of subjects, the urine clone plus additional clones in 22%, and only nonurine clones in 54%. Compared with the 67 unique rectal clones, the 65 urine isolates were significantly enriched for phylogenetic group B2, virulence-associated serotypes, and specific virulence genes and contained more virulence genes (median, 10 versus 6: P < 0.001). In multivariable models, phylogenetic group B2, hlyD (hemolysin), cnf1 (cytotoxic necrotizing factor), iroN (siderophore receptor), ompT (outer membrane protease), and malX (pathogenicity island marker) most strongly predicted urine source. These findings challenge the fecal-urethral and prevalence hypotheses for FUTI pathogenesis and instead strongly support the possibility of alternate infection routes in some men and the special pathogenicity hypothesis. They also identify specific bacterial traits as potential targets for anti-FUTI interventions.
AB - Among men with febrile urinary tract infection (FUTI), whether the host's fecal flora is the source for the urine strain ("fecal-urethral" hypothesis), and whether pathogenesis is driven by prevalence versus special pathogenicity, are unknown. Accordingly, pretherapy urine isolates from 65 men with FUTI were compared with concurrent rectal isolates from the same hosts according to serotype, genomic profile, phylogenetic group, and virulence genotype. The host's multiple rectal colonies included only the urine clone in 25% of subjects, the urine clone plus additional clones in 22%, and only nonurine clones in 54%. Compared with the 67 unique rectal clones, the 65 urine isolates were significantly enriched for phylogenetic group B2, virulence-associated serotypes, and specific virulence genes and contained more virulence genes (median, 10 versus 6: P < 0.001). In multivariable models, phylogenetic group B2, hlyD (hemolysin), cnf1 (cytotoxic necrotizing factor), iroN (siderophore receptor), ompT (outer membrane protease), and malX (pathogenicity island marker) most strongly predicted urine source. These findings challenge the fecal-urethral and prevalence hypotheses for FUTI pathogenesis and instead strongly support the possibility of alternate infection routes in some men and the special pathogenicity hypothesis. They also identify specific bacterial traits as potential targets for anti-FUTI interventions.
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U2 - 10.1128/JCM.43.8.3895-3900.2005
DO - 10.1128/JCM.43.8.3895-3900.2005
M3 - Article
C2 - 16081928
AN - SCOPUS:23744439445
SN - 0095-1137
VL - 43
SP - 3895
EP - 3900
JO - Journal of clinical microbiology
JF - Journal of clinical microbiology
IS - 8
ER -