期刊
INFECTION AND IMMUNITY
卷 80, 期 2, 页码 668-678出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.06191-11
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资金
- International Graduate School of Life Sciences of the University of Wurzburg
- German Research Foundation [DO 789/4-1]
- Medical Faculty, University Munster [BD9817044]
- Swedish Medical Research Council
- Royal Physiographic Society
- Medical Faculty, Lund University
- Soderberg Foundation
- Osterlund Foundation
- Lundberg Foundation
- Maggie Stephens Foundation
- Persson Foundation
- Wallenberg Foundation
- ERA-NET PathoGenoMics II consortium UTI-Interference (Federal Ministry of Education and Research [BMBF] [0315436A]
Asymptomatic bacteriuria (ABU) is a condition where bacteria stably colonize the urinary tract, in a manner closely resembling commensalism at other mucosa! sites. The patients carry >10(5) CFU/ml for extended periods of time and rarely develop symptoms. Contrasting the properties of ABU strains to those of uropathogenic isolates causing symptomatic infection is therefore highly relevant to understand mechanisms of bacterial adaptation. The prototype ABU strain Escherichia coli 83972 has a smaller genome than uropathogenic E. coli (UPEC) strains with deletions or point mutations in several virulence genes, suggesting that ABU strains undergo a programmed reductive evolution within human hosts. This study addressed if these observations can be generalized. Strains causing ABU in outpatients or hospitalized patients after catheterization or other invasive procedures were compared to commensal E. coli isolates from the intestinal flora of healthy individuals. Notably, clonal complex 73 (CC73) was a prominent phylogenetic lineage dominated by ABU isolates. ABU isolates from outpatients and hospitalized patients had a similar overall virulence gene repertoire, which distinguished them from many commensals, but typical UPEC virulence genes were less frequently attenuated in hospital strains than in outpatient strains or commensals. The decreased virulence potential of outpatient ABU isolates relative to that of ABU strains from hospitalized patients supports the hypothesis that loss of expression or decay of virulence genes facilitates long-term carriage and adaptation to host environments.
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