Epidemiology and Clinical Features of Bloodstream Infections Caused by AmpC-Type-β-Lactamase-Producing Klebsiella pneumoniae

Abstract

Cases of bacteremia caused by AmpC-type-␤-lactamase-producing Klebsiella pneumoniae isolates were retrospectively studied to determine the epidemiologic features and clinical outcomes of bloodstream infections. Among 389 blood isolates recovered from 1998 to 2002, 65 isolates (16.7%) were found to be extended-spectrum ␤-lactamase (ESBL) or AmpC ␤-lactamase producers. The ␤-lactamases from 61 of the 65 isolates were characterized; 28 of 61 isolates produced AmpC-type enzymes (14 isolates each produced DHA-1 and CMY-1-like enzymes), 32 isolates produced TEM or SHV-related ESBLs, and 1 isolate produced a CTX-M-14-like enzyme. To compare the clinical features and outcomes of bloodstream infections caused by AmpC producers with those caused by TEM-or SHV-related ESBL producers, 27 patients infected with isolates producing AmpC-type enzymes (AmpC group) and 25 patients infected with isolates producing TEM-or SHV-related enzymes (ESBL group) were analyzed. There was no significant difference between the AmpC and the ESBL groups in terms of risk factors. When the initial response was assessed at 72 h after antimicrobial therapy, the treatment failure rate for the AmpC group was 51.9% (14 of 27 patients) and the 7-and 30-day mortality rates were 14.8 and 29.6%, respectively, which were similar to those for the ESBL group. When the mortality rate for the patients who received extended-spectrum cephalosporins as definitive treatment was assessed, all four patients in the DHA-1 group and one of three patients in the CMY-1-like group died. In summary, the prevalence of AmpC enzyme-producing K. pneumoniae was high at the Seoul National University Hospital, and the clinical features and outcomes for the patients infected with AmpC-producing organisms were similar to those for the patients infected with TEM-or SHV-related ESBL producers.

Emergence and risk factors of β-lactamase–mediated resistance to oxyimino-β-lactams in Enterobacteriaceae isolates

“…Two bla CMY-2 genes were identified in E. coli isolates in association with bla CTX-M-15 gene (Table 1). Indeed, as reported in Taiwan (Chen et al, 2007), the coexistence of ESBL and AmpC β-lactamases not only limits treatment options, but also complicates routine phenotypic detection of ESBLs, causing a growing problem for clinical microbiology laboratories (Hanson, 2003;Pai et al, 2004).…”

Laboratory Detection and Neutralizing Activity of Exocellular AmpC β-lactamases by Anti bla-CMY

“…Other parts suffer from annual increased incidence of bls-AmpC in E. coli and causing mainly urinary tract infections in older women [24]. Detection of plasmid-mediated AmpC-bls by threedimensional test, cefoxitin agar method, clover leaf test, and double-disk test have disadvantages of difficult results interpretation [25]. Currently, there are no recommendations available from the CLSI for detection of organisms producing plasmid-mediated…”

“…Anti-bla CMY used in bla-NT does not crossly react with other lactamases. Previously, no cross-reactivity of the anti-CMY-2 antibody was seen against TEM-1, SHV-1, K-1, or OXA-bla but polyclonal rabbit anti-bla CMY-2 could detect CMY-2, P99 and ACT-1 by ELISA [25]. Antibody based methods depended previously on extracted periplasmic bls from bacterial periplasm [18,26], and it was suggested that level β-lactamase expression due to either promoter mutations or gene copy number which may affect the ability of bla-SHV detection in Gram-negative bacilli using fluorescein-labeled anti-bodies [27].…”

AmpC β-lactamase Production in Pseudomonas aeruginosa: A Threat

“…This would help the physicians to optimize the current therapeutic treatment options. Although previous studies have indicated that 3 rd generation cephalosporins appears to be suboptimal choices for treating infections caused by pathogens producing AmpC β-lactamases, the role of Cefepime has been unsettled and many experts recommend resorting to Carbapenem therapy, which appear to have both excellent in vitro and vivo activity against these organism (25,26,27,28,29,30,31).…”

“…AmpC enzymes are also inhibited by 4 th generation cephalosporins (such as Cefepime) and the Carbapenems (IPM and MRP) and there production can either be caused by mutation or as a result of an inducing agent. Induction of resistance to 3 rd generation cephalosporins after exposure to these agents complicates treatment options and that infections caused by AmpC β-lactamase producing organisms can successfully be treated with Carbapenems (7,8). Cefepime a 4 th generation cephalosporins with broader spectrum activity compared to Ceftriaxone (9,10).…”