Phylogenetic background of Escherichia coli resistant to quinolone and fluoroquinolone
Abstract number: P1232
Bas A., Moreno-Pujol E., Larrosa M.N., Andreu A., Prats G.
Objective: To assess how resistance to quinolone (Q) and fluoroquinolone (FQ), and production of extended-spectrum b-lactamases (ESBLs) relates to the phylogenetic background of clinical Escherichia coli isolates.
Methods: A total of 337 E. coli strains, isolated from clinical samples were selected. The first 222 strains were collected consecutively after the susceptibility test, which allow selecting 120 strains Q and FQ susceptible (SS), 36 Q resistant and FQ susceptible (RS) and 66 Q and FQ resistant (RR). Further strains RS and RR were selected consecutively, till completed a total of 105 and 112 respectively. Resistance to nalidixic acid and ciprofloxacin was tested by disc diffusion method according to CLSI and presence of ESBLs by synergy test between clavulanic acid and third generation cephalosporins. Phylogenetic group was performed by a triplex PCR.
Results: The prevalence of Q resistance was 45.9% (102/222), FQ 29.7% (66/222), and 4.6% (11/222) produced ESBLs. Among the total of 337 isolates, the most prevalent phylogenetic group was B2 with 177 strains, followed by group D with 68, group A with 49 and B1 with 43. E. coli SS and RS showed a similar distribution among phylogenetic groups (66.7% and 60.9% in group B2, 15% and 20% in D, 11.7% and 8.6% in A and 6.7% and 10.5% in B1). However RR strains exhibited a shift to non-B2 groups: 23.2% derived from group A, 21.4% from B1, 25.9% from D and 29.5% from B2, (RR vs. RS P < 0.01 in groups A, B1, B2; RR vs. SS P < 0.01 in groups B1, B2, D). Of the 337 E. coli studied, 20 produced ESBLs: 1 strain SS, 6 RS and 13 RR (P < 0.05 in SS vs. RS and SS vs. RR). ESBLs producers exhibited a similar distribution among phylogroups A, B1 and D (8.2, 11.6 and 10.2%); whereas were quite less prevalent in pathogenic group B2 (2.3%; P < 0.05).
Conclusion:E. coli resistant to Q mainly derived from phylogenetic group B2, whereas isolates resistant to both Q and FQ exhibited shifts towards groups A, B1 and/or D. This fact led us to suspect that these two subgroups represent distinct populations, RS isolates could have derived predominantly from susceptible E. coli group B2 (possibly within a human host), whereas RR isolates from susceptible E. coli group A isolates (possibly within an animal host), both in the context of drug exposure. The depletion for phylogenetic group B2 among ESBLs producers suggest a similar phenomenon.
|Session name:||18th European Congress of Clinical Microbiology and Infectious Diseases|
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