Saksena Rushika, Gaind Rajni, Sinha Anju, Kothari Charu, Chellani Harish, Deb Manorama
Department of Microbiology, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India.
Department of Reproductive and Child Health, Indian council of Medical Research, New Delhi, India.
J Med Microbiol. 2018 Apr;67(4):481-488. doi: 10.1099/jmm.0.000686. Epub 2018 Feb 6.
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. Enterobacteriaceae isolates were screened for nalidixic acid (NA) and ciprofloxacin susceptibility as per CLSI guidelines. In 28 randomly selected neonates, isolates (n=92) resistant to NA and ciprofloxacin were characterized for the presence of plasmid-mediated quinolone resistance (PMQR) genes (qnrA, qnrB and qnrS, qepAand aac(6')-Ib-cr) and mutations in the quinolone resistance determining region (QRDR) of gyrA and parC genes by specific primers and confirmed by sequencing.
A total of 343 Enterobacteriaceae were isolated from 100 neonates. On D1, 58 % of neonates were colonized with at least one Enterobacteriaceae predominantly E. coli. Overall resistance to NA was 60 % but ciprofloxacin resistance increased significantly from 15 % (14/96) on D1 to 38 % (50/132) on D60 (P-value <0.001). The predominant mechanism of fluoroquinolone resistance was mutation in gyrA (n=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.
共生菌群中耐药性的出现对群体构成严重威胁。然而,在缺乏抗生素压力的情况下,关于共生菌抗生素耐药性的数据匮乏。
共选取100例经阴道分娩、未使用过抗生素且纯母乳喂养的新生儿。收集出生第1天(D1)、第21天和第60天的粪便样本进行培养。按照美国临床和实验室标准协会(CLSI)指南,对肠杆菌科分离株进行萘啶酸(NA)和环丙沙星敏感性检测。在28例随机选取的新生儿中,对92株对NA和环丙沙星耐药的分离株,通过特异性引物检测质粒介导喹诺酮耐药(PMQR)基因(qnrA、qnrB和qnrS、qepA以及aac(6')-Ib-cr)的存在情况,以及gyrA和parC基因喹诺酮耐药决定区(QRDR)的突变情况,并通过测序进行确认。
从100例新生儿中共分离出343株肠杆菌科细菌。在D1时,58%的新生儿至少被一种肠杆菌科细菌定植,主要为大肠杆菌。对NA的总体耐药率为60%,但环丙沙星耐药率从D1时的15%(14/96)显著增加至D60时的38%(50/132)(P值<0.001)。氟喹诺酮耐药的主要机制是gyrA基因突变(n = 49),伴有或不伴有PMQR。携带PMQR的分离株从D1到D60增加了五倍多。
未使用过抗生素且纯母乳喂养的新生儿肠道菌群中氟喹诺酮耐药水平较高,表明群体中耐药性正在急剧上升。D1时耐药基因的来源可能是出生时获得的母体菌群。共生菌群中高负荷的PMQR基因是向致病生物传播的潜在来源。