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Epidemic of Klebsiella pneumoniae ST11 Clone Coproducing KPC-2 and 16S rRNA Methylase RmtB in a Chinese University Hospital

BACKGROUND: Emergence of rmtB-positive Klebsiella pneumoniae carbapenemase (KPC)-producing K. pneumoniae (KPC-KP) poses a great threat to antimicrobial treatment options. METHODS: From January 2010 to December 2010, non-duplicate KPC-KP isolates from our hospital were screened for rmtB and multiple...

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Detalles Bibliográficos
Autores principales: Li, Jun-Jie, Sheng, Zi-Ke, Deng, Mei, Bi, Sheng, Hu, Fei-Shu, Miao, Hai-Feng, Ji, Zhong-Kang, Sheng, Ji-Fang, Li, Lan-Juan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3543704/
https://www.ncbi.nlm.nih.gov/pubmed/23259910
http://dx.doi.org/10.1186/1471-2334-12-373
Descripción
Sumario:BACKGROUND: Emergence of rmtB-positive Klebsiella pneumoniae carbapenemase (KPC)-producing K. pneumoniae (KPC-KP) poses a great threat to antimicrobial treatment options. METHODS: From January 2010 to December 2010, non-duplicate KPC-KP isolates from our hospital were screened for rmtB and multiple other resistance determinants with PCR. Subsequent studies included MIC determination, PFGE, and multilocus sequence typing. Records from patients with KPC-KP isolated were retrospectively reviewed. Comparisons of molecular and clinical characteristics between rmtB-positive and rmtB–negative isolates were systematically performed, as well as the environmental colonization study in ICU wards. RESULTS: A total of 84 KPC-KP strains were collected, including 48 rmtB-positive KPC-KP (RPKP) and 36 rmtB-negative KPC-KP (RNKP) isolates. All KPC-KP isolates were multidrug resistant, with colistin and tigecycline being the most active agents. Compared with RNKP, RPKP displayed a much severer resistance phenotype. Susceptibility rates for amikacin (0% for RPKP versus 88.9% for RNKP, p < 0.01), fosfomycin (8.5% for RPKP versus 88.9% for RNKP, p < 0.01), and minocycline (6.7% for RPKP versus 52.8% for RNKP, p < 0.01), were all significantly lower in RPKP strains. Isolates belonging to PFGE pulsetype A and sequence type 11 were predominant in both groups, including 39 (81.3%) RPKP and 22 (61.1%) RNKP isolates. Nevertheless, RNKP showed more complex genetic backgrounds compared with RPKP. Diverse clinical characteristics were found in both cohorts, however, no significant differences were observed between RPKP and RNKP patients. CONCLUSIONS: RPKP strains have spread widely and gradually replaced RNKP in our hospital. They seemed to show much severer resistance phenotypes compared with RNKP and had a bigger dissemination potential. Prudent use of available active agents combined with good control practices is therefore mandatory.