Identification of the first imported KPC-3 Klebsiella pneumoniae from the USA to Taiwan

Tang, Hung‐Jen; Chen, Ying-Tsong; Chiang, Thomas M.; Fung, Chang-Phoné; Chuang, Yin-Ching; Siu, L. Kristopher

doi:10.1016/j.ijantimicag.2014.07.009

Cited by 10 publications

(6 citation statements)

References 19 publications

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“…In this study, we identified one novel bla KPC variant, namely, bla KPC-34 , and two that had not been reported in Taiwan before 2012. The first KPC-3 producer was isolated in 2013 and was geographically and genetically linked to those in the U.S. 42 , and the emergence of a KPC-17 producer in Taiwan was also previously observed 25 , 43 . Similar to the U.S. 10 and China 11 , KPC was the predominant carbapenemase in Taiwan; however, most of the Taiwanese KPC-producers were ST11, which is similar to China 44 , but different from the U.S., where the dominant clone is ST258 45 .…”

Section: Discussionmentioning

confidence: 79%

Carbapenem Nonsusceptible Klebsiella pneumoniae in Taiwan: Dissemination and Increasing Resistance of Carbapenemase Producers During 2012–2015

Chiu

Chan

et al. 2018

Sci Rep

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Before 2011, the prevalence rates of carbapenemase-producing Klebsiella pneumoniae (CPKP) among carbapenem nonsusceptible K. pneumoniae (CnSKP) isolates were below 10% in Taiwan. The study presents the dissemination and increased antimicrobial resistance of CPKP from January 2012 to August 2015, as shown by Taiwanese multicenter surveillance. Isolates with minimum inhibitory concentrations (MICs) of >1 μg/mL for imipenem or meropenem were collected, screened for various carbapenemase genes by PCR, and tested for antimicrobial susceptibility. Among 1,457 CnSKP isolates, 1,250 were collected from medical centers. The CnSKP prevalence in medical centers increased by 1.7-fold during the study. Among all CnSKP isolates, 457 were CPKP. The CPKP rate among CnSKP increased by 1.5-fold and reached 36.8% in 2015. The CPKP nonsusceptibility rate to aztreonam, fluoroquinolones, and aminoglycosides increased yearly. Six CPKP isolates carried dual carbapenemase genes. Three Ambler classes were identified in 451 isolates with a single carbapenemase: classes A (315 blaKPC-2, 2 blaKPC-3, 28 blaKPC-17, 2 blaKPC-34), B (26 blaIMP-8, 2 blaNDM-1, 36 blaVIM-1), and D (40 blaOXA-48). The blaOXA-48 rate among CPKP increased by 6-fold over three years. Most KPC and OXA-48 producers were ST11. CnSKP was increasingly prevalent, owing to CPKP dissemination. Additionally, CPKP became more resistant during the study period.

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Section: Discussionmentioning

confidence: 79%

Carbapenem Nonsusceptible Klebsiella pneumoniae in Taiwan: Dissemination and Increasing Resistance of Carbapenemase Producers During 2012–2015

Chiu

Chan

et al. 2018

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“…The widespread prevalence of bla KPC -carrying K. pneumoniae poses a serious threat to medical treatment. pKpQIL and its variants have played a significant role in the dissemination of KPC across bacterial sequence types and species ( 98 ). As bla KPC confers resistance to and hence survival in the presence of carbapenem and most other beta-lactam antibiotics, the use of these antibiotics is a factor driving global dissemination.…”

Section: Discussionmentioning

confidence: 99%

Clinically Relevant Plasmid-Host Interactions Indicate that Transcriptional and Not Genomic Modifications Ameliorate Fitness Costs of Klebsiella pneumoniae Carbapenemase-Carrying Plasmids

Buckner

Saw

Osagie

et al. 2018

mBio

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The rapid dissemination of antimicrobial resistance (AMR) around the globe is largely due to mobile genetic elements, such as plasmids. They confer resistance to critically important drugs, including extended-spectrum beta-lactams, carbapenems, and colistin. Large, complex resistance plasmids have evolved alongside their host bacteria. However, much of the research on plasmid-host evolution has focused on small, simple laboratory plasmids in laboratory-adapted bacterial hosts. These and other studies have documented mutations in both host and plasmid genes which occur after plasmid introduction to ameliorate fitness costs of plasmid carriage. We describe here the impact of two naturally occurring variants of a large AMR plasmid (pKpQIL) on a globally successful pathogen. In our study, after pKpQIL plasmid introduction, no changes in coding domain sequences were observed in their natural host, Klebsiella pneumoniae. However, significant changes in chromosomal and plasmid gene expression may have allowed the bacterium to adapt to the acquisition of the AMR plasmid. We hypothesize that this was sufficient to ameliorate the associated fitness costs of plasmid carriage, as pKpQIL plasmids were maintained without selection pressure. The dogma that removal of selection pressure (e.g., antimicrobial exposure) results in plasmid loss due to bacterial fitness costs is not true for all plasmid/host combinations. We also show that pKpQIL impacted the ability of K. pneumoniae to form a biofilm, an important aspect of virulence. This study used highly relevant models to study the interaction between AMR plasmids and pathogens and revealed striking differences from results of studies done on laboratory-adapted plasmids and strains.

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“…Polymerase chain reaction (PCR) was used for all isolates to detect carbapenemase genes (encoding Ambler class-A families NMC, IMI, SME, KPC and GES; Ambler class-B families IMP, VIM, GIM, SIM, SPM and NDM; and Ambler class-D family OXA-48-type), ESBL genes (encoding CTX-M, SHV and TEM) and plasmid-borne AmpC-like genes (encoding CMY and DHA) as described previously1819. Identification of outer-membrane porins (OMPK35 and OMPK36) was carried out as described previously18.…”

Section: Methodsmentioning

confidence: 99%

High minimum inhibitory concentration of imipenem as a predictor of fatal outcome in patients with carbapenem non-susceptible Klebsiella pneumoniae

Chuang

et al. 2016

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Carbapenem resistance in Klebsiella pneumoniae is important because of its increasing prevalence and limited therapeutic options. To investigate the clinical and microbiological characteristics of patients infected or colonized with carbapenem non-susceptible K. pneumoniae (CnsKP) in Taiwan, we conducted a retrospective study at Taipei Veterans General Hospital from January 2012 to November 2013. Carbapenem non-susceptibility was defined as a minimum inhibitory concentration (MIC) of ≥2 mg/L for imipenem or meropenem. A total of 105 cases with CnsKP were identified: 49 patients with infection and 56 patients with colonization. Thirty-one isolates had genes that encoded carbapenemases (29.5%), including K. pneumoniae carbapenemase (KPC)-2 (n = 27), KPC-3 (n = 1), VIM-1 (n = 1) and IMP-8 (n = 2). The in-hospital mortality among patients with CnsKP was 43.8%. A MIC for imipenem ≥16 μg/mL, nasogastric intubation and Acute Physiology and Chronic Health Evaluation II score were independent risk factors for in-hospital mortality for all patients with CnsKP. A MIC for imipenem ≥16 μg/mL was also an independent risk factor for 14-day mortality in patients with CnsKP. In conclusion, a positive culture for CnsKP was associated with high in-hospital mortality. A high imipenem MIC of CnsKP can predispose a patient to a poor prognosis.

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Identification of the first imported KPC-3 Klebsiella pneumoniae from the USA to Taiwan

Cited by 10 publications

References 19 publications

Carbapenem Nonsusceptible Klebsiella pneumoniae in Taiwan: Dissemination and Increasing Resistance of Carbapenemase Producers During 2012–2015

Carbapenem Nonsusceptible Klebsiella pneumoniae in Taiwan: Dissemination and Increasing Resistance of Carbapenemase Producers During 2012–2015

Clinically Relevant Plasmid-Host Interactions Indicate that Transcriptional and Not Genomic Modifications Ameliorate Fitness Costs of Klebsiella pneumoniae Carbapenemase-Carrying Plasmids

High minimum inhibitory concentration of imipenem as a predictor of fatal outcome in patients with carbapenem non-susceptible Klebsiella pneumoniae

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