1887

Abstract

The emergence of resistance amongst commensal flora is a serious threat to the community. However, there is paucity of data regarding antibiotic resistance in commensals in the absence of antibiotic pressure.

Altogether, 100 vaginally delivered antibiotic naïve exclusively breastfed neonates were selected. Stool samples collected on day (D)1, D21 and D60 of birth were cultured. isolates were screened for nalidixic acid (NA) and ciprofloxacin susceptibility as per CLSI guidelines. In 28 randomly selected neonates, isolates (=92) resistant to NA and ciprofloxacin were characterized for the presence of plasmid-mediated quinolone resistance (PMQR) genes (, and , and ) and mutations in the quinolone resistance determining region (QRDR) of and genes by specific primers and confirmed by sequencing.

A total of 343 were isolated from 100 neonates. On D1, 58 % of neonates were colonized with at least one predominantly Overall resistance to NA was 60 % but ciprofloxacin resistance increased significantly from 15 % (14/96) on D1 to 38 % (50/132) on D60 (-value <0.001). The predominant mechanism of fluoroquinolone resistance was mutation in gyrA (=49) with or without PMQR. PMQR carrying isolates increased more than fivefold from D1 to D60.

A high level of fluoroquinolone resistance in gut flora of antibiotic naïve and exclusively breastfed neonates suggests a rampant rise of resistance in the community. The source of resistance genes on D1 is probably maternal flora acquired at birth. High load of PMQR genes in commensal flora are a potential source of spread to pathogenic organisms.

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2018-04-01
2021-10-20
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