Abstract
ObjectivesThe global spread and increasing incidence of carbapenem non-susceptible Klebsiella pneumoniae (CnSKP) has made its treatment difficult, increasing the mortality. To establish nationwide data on CnSKP spread and carbapenem-resistance mechanisms, we conducted a national surveillance study in Taiwanese hospitals.MethodsWe collected 100 and 247 CnSKP isolates in 2010 and 2012, respectively. The tests performed included antibiotic susceptibility tests; detection of carbapenemase, extended-spectrum β-lactamases (ESBL), and AmpC β-lactamases genes; outer membrane porin profiles; and genetic relationship with pulsed-field gel electrophoresis and multilocus sequence type.ResultsThe resistance rate of CnSKP isolates to cefazolin, cefotaxime, cefoxitin, ceftazidime, and ciprofloxacin was over 90%. Susceptibility rate to tigecycline and colistin in 2010 was 91.0% and 83.0%, respectively; in 2012, it was 91.9% and 87.9%, respectively. In 2010, carbapenemase genes were detected in only 6.0% of isolates (4 bla IMP-8 and 2 bla VIM-1). In 2012, carbapenemase genes were detected in 22.3% of isolates (41 bla KPC-2, 7 bla VIM-1, 6 bla IMP-8, and 1 bla NDM-1). More than 95% of isolates exhibited either OmpK35 or OmpK36 porin loss or both. Impermeability due to porin mutation coupled with AmpC β-lactamases or ESBLs were major carbapenem-resistance mechanisms. Among 41 KPC-2-producing K. pneumoniae isolates, all were ST11 with 1 major pulsotype.ConclusionsIn 2010 and 2012, the major mechanisms of CnSKP in Taiwan were the concomitance of AmpC with OmpK35/36 loss. KPC-2-KP dissemination with the same ST11 were observed in 2012. The emergence and rapid spread of KPC-2-KP is becoming an endemic problem in Taiwan. The identification of NDM-1 K. pneumoniae case is alarming.
Highlights
Klebsiella pneumoniae is an important pathogen causing various kinds of infection including bacteraemia, pneumonia, liver abscess, and urinary tract infections [1,2]
The susceptibility rates to cefepime, imipenem, and meropenem were less than 10%
The present report showed that the major mechanism underlying the carbapenem nonsusceptible Klebsiella pneumoniae (CnSKP) phenotype in Taiwan was the loss of outer membrane porins combined with blactamases such as AmpC enzyme or extendedspectrum beta-lactamase (ESBL)
Summary
Klebsiella pneumoniae is an important pathogen causing various kinds of infection including bacteraemia, pneumonia, liver abscess, and urinary tract infections [1,2]. The spread of carbapenem nonsusceptible Klebsiella pneumoniae (CnSKP) has made its treatment difficult and caused higher disease-related mortality [3,4]. Carbapenem resistance in K. pneumoniae can arise due to the presence of true carbapenemase, or via the combination of impermeability and production of extendedspectrum beta-lactamase (ESBL) or a strongly expressed AmpC enzyme [6,7]. Carbapenemase-producing K. pneumoniae (KPC-KP) strains were first reported in 2001 from strain isolated in 1996 in the USA [9]. Since they have been identified in many places around the world [8,10,11,12,13].
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