Molecular prevalence of resistance determinants, virulence factors and capsular serotypes among colistin resistance carbapenemase producing Klebsiella pneumoniae: a multi-centric retrospective study
3 Biotech, ISSN: 2190-5738, Vol: 12, Issue: 1, Page: 30
2022
- 4Citations
- 32Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations4
- Citation Indexes4
- Captures32
- Readers32
- 32
Article Description
The emergence of colistin-carbapenem-resistant Klebsiella pneumoniae (CCR-Kp) in bloodstream infection results in high mortality, and virulence factor contributes further to the difficulty of treatment. A total of 158 carbapenem-resistant K. pneumoniae (CRKP) isolates causing bloodstream infection were collected from three Indian tertiary care hospitals during the 9-month study period, of which 27 isolates exhibited resistance to both colistin and carbapenem antibiotics. In this study, all the strains were characterized for antimicrobial resistance, virulence factors and capsular serotypes that facilitate the development of colistin and carbapenem-resistant K.pneumoniae (CCR-Kp) in bloodstream infection. Fourteen isolates displayed extremely drug resistance (XDR), susceptible only to tigecycline, and the remaining 13 isolates displayed multidrug resistance (MDR). The gene prevalence analysis for CCR-Kp isolates showed the predominance of bla (81.48%) followed by bla (62.96%), bla (37.03%) and bla (18.51%) genes. The distribution of virulence genes was found to be fimH (81.48%), wabG (59.25%), mrkD (55.56%), entB (48.15%), irp1 (33.33%), and rmpA (18.52%). The capsular serotypes K1, K2, K5 and K54 have been identified in 16 isolates. The absence of plasmid-mediated colistin resistance (mcr) genes implies the involvement of other mechanisms. The ERIC and (GTG) molecular typing methods detected 18 and 22 distinct clustering patterns among the CCR-Kp isolates, respectively. A strong correlation between ERIC and (GTG)5 genotyping method was established with antimicrobial resistance patterns and virulence determinants at P < 0.05, while no correlation was found with capsular serotyping. Similar virulence and resistance typing among the isolates suggest hospital-acquired infection in a health care setup. These outcomes will advance our awareness of CCR-Kp outbreaks associated with tertiary care hospitals and help forecast their occurrence in the near future.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85121872750&origin=inward; http://dx.doi.org/10.1007/s13205-021-03056-4; http://www.ncbi.nlm.nih.gov/pubmed/35070620; https://link.springer.com/10.1007/s13205-021-03056-4; https://dx.doi.org/10.1007/s13205-021-03056-4; https://link.springer.com/article/10.1007/s13205-021-03056-4
Springer Science and Business Media LLC
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