Risk factors and clinical features of infections caused by plasmid-mediated AmpC β-lactamase-producing Enterobacteriaceae
Introduction
The predominant mechanism for resistance to β-lactam antibiotics in Gram-negative bacteria is synthesis of a β-lactamase. Antibiotic-resistant strains that produce extended-spectrum β-lactamases (ESBLs), which provide resistance to oxyimino-cephalosporins (ceftazidime, cefotaxime, ceftriaxone, ceftizoxime and cefuroxime) and monobactams but not to 7-α-methoxy-cephalosporins (cefoxitin, cefotetan, cefmetazole and moxalactam), have emerged among members of Enterobacteriaceae family, predominantly in Escherichia coli and Klebsiella pneumoniae. In the past decade, a new problem has emerged in enteric bacteria, namely plasmid-mediated AmpC β-lactamases (plasmid AmpC). Resistance appeared in bacterial species such as K. pneumoniae, Salmonella spp. and Proteus mirabilis that lack an inducible AmpC enzyme as well as in E. coli that expresses the enzyme at a low level. Plasmid AmpC genes are derived from chromosomal AmpC genes of Gram-negative organisms such as Citrobacter freundii, Enterobacter cloacae and Aeromonas spp. and provide resistance both to oxyimino- and 7-α-methoxy-cephalosporins as well as monobactams [1].
By phenotypic susceptibility testing it is difficult to distinguish ESBL-producing organisms from plasmid AmpC-producing organisms because of their similar resistance profile [2]. Although increasing trends in the prevalence of plasmid AmpC in Enterobacteriaceae have repeatedly been reported [3], [4], [5], little is known about the risk factors and clinical features of infections caused by plasmid AmpC-producing Enterobacteriaceae. This study was therefore performed with the objective of analysing risk factors and clinical features of infections caused by plasmid AmpC-producing Enterobacteriaceae.
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Setting and study design
The study was conducted at two hospitals, Gachon University Gil Medical Center, a 1200-bed tertiary care facility located in Incheon, and Hanyang University Hospital, a 900-bed tertiary care facility located in Seoul, South Korea. To identify clinical characteristics and risk factors for the infections caused by plasmid AmpC-producing isolates, a case–control study was conducted in a prospective setting.
Microbiological identification of plasmid-mediated AmpC β-lactamase-producing isolates
The computerised microbiological database of each hospital was monitored daily from 1
Clinical analyses
During the study period, 10 and 20 inpatients were infected with plasmid AmpC-producing E. coli and K. pneumoniae, respectively, and were enrolled in the study.
To identify risk factors for the infection with plasmid AmpC-producing Enterobacteriaceae, the 30 case patients infected with plasmid AmpC-producing Enterobacteriaceae were compared with the matched 30 control patients infected with non-plasmid AmpC-producing Enterobacteriaceae (Table 1). Table 1 shows that length of hospital stay until
Discussion
There have been numerous studies assessing risk factors for colonisation and infection with ESBL-producing organisms. Although there has been a wide variety of reports of community-acquired infections with ESBL-producing organisms in recent years, in the hospital environment patients at high risk of developing colonisation or infection with ESBL-producing organisms are often seriously ill patients with prolonged hospital stay and in whom invasive medical devices are present (urinary catheters,
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2016, Journal of Global Antimicrobial ResistanceCitation Excerpt :Patients with pAmpC-Kp experienced more severe illness and their clinical outcomes at 72 h, 7 days and 30 days after treatment were less favourable. The median APACHE II score and 7-day mortality rate in this cohort were 25 and 47.8%, respectively, which were higher than those reported by Pai et al. [7] and Park et al. [8] in South Korea. We also confirmed the clear relationship between early appropriate empirical therapy for severe infection and mortality.
Molecular characterisation of acquired and overproduced chromosomal bla<inf>AmpC</inf> in Escherichia coli clinical isolates
2016, International Journal of Antimicrobial AgentsCitation Excerpt :Therefore, distinguishing between ac-AmpC and c-AmpC β-lactamases may be key to the prevention of their diffusion and the effective treatment of bacterial infection. Failures in β-lactam treatment of infections produced by c-AmpC-overproducing or ac-AmpC-producing strains have been reported [9,10]. Moreover, AmpC β-lactamase-producing E. coli isolates are frequently co-resistant to other families of antibiotics, such as fluoroquinolones and aminoglycosides, thus posing an even greater challenge for the clinician.