Epidemiology of and risk factors for infection with extended-spectrum β-lactamase-producing carbapenem-resistant Enterobacteriaceae: results of a double case–control study

Abstract

PurposeCarbapenem-resistant Enterobacteriaceae (CRE) have been increasingly reported worldwide and pose a serious public threat, but the clinical significance of extended-spectrum β-lactamase (ESBL) production in CRE is not well established.Patients and methodsA retrospective case–case–control study was conducted to identify the clinical characteristics of patients with ESBL-CRE. The susceptibility of isolates obtained from these patients was assessed. The detection of ESBL and carbapenemase-related genes was performed by PCR methods. Predictors of 30-day mortality in patients with ESBL-CRE infection were also identified in our study.ResultsA total of 149 patients with CRE infection caused by Enterobacter cloacae (n=74), Escherichia coli (n=38), and Klebsiella pneumoniae (n=37) were identified in Chongqing, Southwestern China, between January 2011 and December 2014. Of the 35 isolates detected with carbapenemase-related genes, 16 isolates had New Delhi metallo-β-lactamase (NDM), nine isolates had K. pneumoniae carbapenemase (KPC), seven isolates had imipenemase (IMP), and four isolates had oxacillinase (OXA)-1. One strain of enterobacter cloacae carried both NDM-1 and IMP-8 genes. ESBL isolates included the genes CTX-M (72/149), SHV (64/149), and TEM (54/149). All ESBL-CRE isolates exhibited ertapenem resistance, and the rate of cephalosporin resistance was relatively high in general. Independent risk factors for infection with ESBL-CRE included previous exposure to β-lactam antibiotics, transfer from another hospital, and some underlying diseases. In addition, solid tumors, hypoalbuminemia, and central venous catheters were independent predictors of mortality in patients with ESBL-CRE infection.ConclusionPhysicians should understand the peculiar predictors for the identification of these organisms among high-risk patients.

Molecular Epidemiology and Risk Factors of Ventilator-Associated Pneumonia Infection Caused by Carbapenem-Resistant Enterobacteriaceae

“…mCIM was used to detect carbapenemase in Enterobacteriaceae and Pseudomonas aeruginosa , whereas eCIM was combined with mCIM to distinguish the Enterobacteriaceae bacteria of metallase- (Ambler B) and serine carbapenemase-producing (Ambler A). The phenotypic results of this study showed that metallase production and serine carbapenemase production are the main drug resistance mechanisms of CRE, which differs from the serine carbapenemase production reported by Tian and Zheng (Zheng et al, 2017; Tian et al, 2018).…”

Shifting trends and age distribution of ESKAPEEc resistance in bloodstream infection, Southwest China, 2012–2017

“…However, in pediatric patients, several studies have reported the predominance or outbreak of bla NDM-1 among CRKP in Beijing, Shanghai and Shandong [24–26]. Our previous studies also demonstrated a high prevalence of bla NDM-1 among CRKP in Chongqing [27, 28]. Therefore, more researches are ongoing to uncover the underlying molecular mechanisms of the high prevalence of CRKP in children BSIs and cautious adoption of carbapenems to fight against pediatric CRKP BSI is advocated.…”

<p>A Retrospective Analysis of Risk Factors and Patient Outcomes of Bloodstream Infection with Extended-Spectrum β-Lactamase-Producing <em>Escherichia coli</em> in a Chinese Tertiary Hospital</p>

“…We found that ESBL-EC was often more resistant to quinolones, aminoglycosides (except amikacin) and trimethoprim/sulfamethoxazole, which is consistent with other studies. [9][10][11] The reason may be that plasmids carrying genes encoding ESBL also often carry other drug-resistant genes encoding quinolones, aminoglycosides and trimethoprim/ sulfamethoxazole. 12 Our study found that BTI was an independent risk factor for ESBL-EC BSI.…”