Abstract
OBJECTIVE: To characterize the β-lactam, quinolone and macrolide resistance levels and mechanisms in 62 Escherichia coli isolates causing children bacteremia.
METHODS: Minimal inhibitory concentration of ciprofloxacin, nalidixic acid (NAL) and azithromycin was determined in presence and absence of Phe-Arg-β-Naphtylamyde. Additionally, the susceptibility levels to other 14 antimicrobial agents was established. Extended Spectrum β-lactamases (ESBLs) were identified, while mutations in gyrA and parC genes, presence of transferable mechanisms of quinolone-resistance (TMQR) and macrolide-resistance (TMMR) was also determined.
RESULTS: Forty-Nine (79.0%) isolates were multidrug resistant. High proportions of resistance to ampicillin (93.6%), NAL (66.1%) and cotrimoxazole (64.5%) was observed. No isolate showed resistance to carbapenems and only two were resistant to nitrofurantoin. Twenty-seven isolates carried ESBL-encoding genes: 2 blaSHV-12, 13 blaCTX-M-15, 4 blaCTX-M-2, 6 blaCTX-M-65 and 2 non-identified ESBLs. In addition 27 blaTEM-1 and 9 blaOXA-1-like genes were detected. All quinolone-resistant isolates showed target-mutations, while TMQR were present in 4 isolates; Efflux pumps played a role in the constitutive NAL-resistance levels. The association between quinolone-resistance and ESBL-production was significant (P=0.0011). The mph(A) gene was the most frequent TMMR (16 isolates), in addition msr(A) and erm(B) genes were detected. Only 1 TMMR carrying isolate (presenting the mph(A) and the erm(B) genes concomitantly) remained azithromycin-resistant when efflux pumps were inhibited.
CONCLUSIONS: A variety of ESBL encoding genes and widespread of blaCTX-M-15 in the area has been showed. The role of efflux pumps in azithromycin resistance needs to be further evaluated, as well as an effective control in the use of antimicrobial agents.
| Original language | English |
|---|---|
| Journal | Journal of Global Antimicrobial Resistance |
| Volume | 11 |
| Pages (from-to) | 28-33 |
| Number of pages | 6 |
| ISSN | 2213-7165 |
| DOIs | |
| Publication status | Published - 2017 |
Keywords
- Journal Article