کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5673594 | 1593678 | 2017 | 10 صفحه PDF | دانلود رایگان |

- High percentages of tetracycline resistant enterococci were recovered from the environmental isolates of Karachi city.
- High-level tetracycline resistance was evident by the presence of multiple Tet genes and transposable element.
- Major tetracycline resistance was observed in E. faecium followed by E. faecalis, E. hirae and E. casseliflavus.
- Tetracycline resistance gene tet(L) was more frequently found in E. faecium, while tet(M) in high prevalence in E. faecalis.
- Transposable element (Tn916) was detected in both clinical and soil isolates.
Resistance against antimicrobial agents in enterococci is a global concern that not only challenges infection therapy but also make them reservoir of antibiotic resistance in human and animal alike. This study was conducted to establish tetracycline resistance profiles, prevalence of tet genes and transposable element (Tn916) in enterococcal soil and clinical isolates. Enterococci (n = 1210) from different environmental niche were collected and subjected to molecular identification. In total, 361 isolates showed tetracycline resistance at the breakpoint of 32 μg mlâ1. MICs (32-512 μg mlâ1) were established by both agar and micro-broth dilution methods. Soil isolates (n = 76) were further investigated for Tet genes (tet-A, C, K, L, M, S, O) and Tn916. Major resistance was observed in E. faecium 67% followed by E. faecalis 22%, E. hirae 8% and E. casseliflavus 2.6%. Results revealed that tet(L) was more frequently found in E. faecium 74.5%, while tet(M) was in high prevalence in E. faecalis 82.3%. Tn916 was detected in both clinical and soil isolates (i.e. 43.3% and 19.7%, respectively). RAPD-PCR analysis showed high diversity among the investigated isolates. Cumulatively, our results revealed high-level tetracycline resistance and the presence of multiple Tet genes and transposable element Tn916 in enterococci.
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Journal: Microbial Pathogenesis - Volume 111, October 2017, Pages 252-261