Abstract:Background
Although intestinal colonization precedes most extraintestinal Escherichia coli infections, colonization-promoting factors are incompletely understood. We compared within-household E. coli colonization patterns with host and bacterial traits.
Methods
Twenty-two veterans with a clinical E. coli isolate and their 46 human and animal household members underwent longitudinal fecal sampling. Distinct E. coli strains wer… Show more
“…Both global MDR groups of E. coli wield considerable cargoes of such genes [ 39 ]. It is established that ST1193 strains carry papG genes and K1 or K5 capsules more often than ST131 isolates [ 41 , 42 , 43 , 44 , 45 ]. We can assume that the virulence factor cargo of the MDR ST1193 clone may confer a superior capacity compared with the ST131 strains to colonize the human intestine.…”
Section: The Possible Role Of Virulence-associated Colonization Factorsmentioning
It is widely accepted that favorable fitness in commensal colonization is one of the prime facilitators of clonal dissemination in bacteria. The question arises as to what kind of fitness advantage may be wielded by uropathogenic strains of the two predominant fluoroquinolone- and multidrug-resistant clonal groups of E. coli—ST131-H30 and ST1193, which has permitted their unprecedented pandemic-like global expansion in the last few decades. The colonization-associated genes’ content, carriage of low-cost plasmids, and integrons with weak promoters could certainly contribute to the fitness of the pandemic groups, although those genetic factors are common among other clonal groups as well. Also, ST131-H30 and ST1193 strains harbor fluoroquinolone-resistance conferring mutations targeting serine residues in DNA gyrase (GyrA-S83) and topoisomerase IV (ParC-S80) that, in those clonal backgrounds, might result in a commensal fitness benefit, i.e., beyond the antibiotic resistance per se. This fitness gain might have contributed not only to the widespread dissemination of these major clones in the healthcare setting but also to their long-term colonization of healthy individuals and, thus, circulation in the community, even in a low or no fluoroquinolone use environment. This evolutionary shift affecting commensal E. coli, initiated by mutations co-favorable in both antibiotics-treated patients and healthy individuals warrants more in-depth studies to monitor further changes in the epidemiological situation and develop effective measures to reduce the antibiotic resistance spread.
“…Both global MDR groups of E. coli wield considerable cargoes of such genes [ 39 ]. It is established that ST1193 strains carry papG genes and K1 or K5 capsules more often than ST131 isolates [ 41 , 42 , 43 , 44 , 45 ]. We can assume that the virulence factor cargo of the MDR ST1193 clone may confer a superior capacity compared with the ST131 strains to colonize the human intestine.…”
Section: The Possible Role Of Virulence-associated Colonization Factorsmentioning
It is widely accepted that favorable fitness in commensal colonization is one of the prime facilitators of clonal dissemination in bacteria. The question arises as to what kind of fitness advantage may be wielded by uropathogenic strains of the two predominant fluoroquinolone- and multidrug-resistant clonal groups of E. coli—ST131-H30 and ST1193, which has permitted their unprecedented pandemic-like global expansion in the last few decades. The colonization-associated genes’ content, carriage of low-cost plasmids, and integrons with weak promoters could certainly contribute to the fitness of the pandemic groups, although those genetic factors are common among other clonal groups as well. Also, ST131-H30 and ST1193 strains harbor fluoroquinolone-resistance conferring mutations targeting serine residues in DNA gyrase (GyrA-S83) and topoisomerase IV (ParC-S80) that, in those clonal backgrounds, might result in a commensal fitness benefit, i.e., beyond the antibiotic resistance per se. This fitness gain might have contributed not only to the widespread dissemination of these major clones in the healthcare setting but also to their long-term colonization of healthy individuals and, thus, circulation in the community, even in a low or no fluoroquinolone use environment. This evolutionary shift affecting commensal E. coli, initiated by mutations co-favorable in both antibiotics-treated patients and healthy individuals warrants more in-depth studies to monitor further changes in the epidemiological situation and develop effective measures to reduce the antibiotic resistance spread.
Background
Superior gut colonization may underlie the pandemic emergence of the resistance-associated H30 subclone of Escherichia coli sequence type 131 (ST131-H30). Little is known about the associated host and bacterial characteristics, or the comparative persistence of non-ST131 intestinal E. coli.
Methods
Generic and fluoroquinolone-resistant E. coli isolates from volunteers' serial fecal samples underwent clonal analysis and extensive PCR-based characterization (phylogroup, selected sequence types, virulence genes). Kaplan-Meier survival analysis and Cox proportional hazards survival analysis using penalized regression (a machine-learning method) were used to identify correlates of strain persistence.
Results
Screening of 2,005 subjects at the Minneapolis VA Medical Center identified 222 subjects (117 veterans; 105 human and animal household members) for longitudinal fecal surveillance. Analysis of their 585 unique-by-subject fecal E. coli strains identified multiple epidemiological, ecological, and bacterial correlates of strain persistence. ST131-H30, a strong univariable correlates of persistence, was superseded in multivariable analysis by outpatient status, fluoroquinolone resistance, and diverse (predominantly iron uptake-related) "virulence genes".
Conclusions
ST131-H30 exhibits exceptional intestinal persistence, possibly due to a combination of fluoroquinolone resistance and "virulence factors", which may be primarily colonization factors. This identifies both likely contributors to the ST131-H30 pandemic and potential targets for interventions against it.
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