Amp C β-lactamase-producing Escherichia coli in neonatal meningitis: diagnostic and therapeutic challenge

Fakioglu, Esra; Queenan, Anne Marie; Bush, Karen; Jenkins, S G; Herold, Betsy C.

doi:10.1038/sj.jp.7211550

Cited by 13 publications

(7 citation statements)

References 16 publications

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“…Although this finding confirms older publications, a recent study failed to document relevant risk factors for the acquisition of ESBL-producing pathogens [49][50][51]. ESBLs are not the only broad-spectrum b-lactamase organisms recovered from the neonatal unit; E. coli harboring AmpC, which confers resistance to aminopenicillins and narrow-spectrum cephalosporins, was recently isolated from a neonate with meningitis [52].…”

Section: Pathogenssupporting

confidence: 64%

Healthcare-associated infections in neonates

Zingg

Posfay‐Barbe²,

Pittet³

2008

Current Opinion in Infectious Diseases

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Section: Pathogenssupporting

confidence: 64%

Healthcare-associated infections in neonates

Zingg

Posfay‐Barbe²,

Pittet³

2008

Current Opinion in Infectious Diseases

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“…Plasmid-mediated AmpC resistance has recently been reported in clinical isolates of the Enterobacteriaceae worldwide (6,7,9,22,23,(30)(31)(32). Few population-based studies have reported on the frequency or clinical impact of these isolates, and very little is known about the associated epidemiology in pediatrics.…”

Section: Discussionmentioning

confidence: 99%

“…The Enterobacteriaceae are also major pathogens in neonates, infants, and children, although little is known about the broad-spectrum ␤-lactamase-producing strains in this specific age group (7,9,19,(25)(26)28). The spread of ␤-lactam-resistant Enterobacteriaceae in children is of particular importance, since fluoroquinolones are not approved for use in this age group and are not considered firstline agents for use in this age group.…”

mentioning

confidence: 99%

Prevalence and Mechanisms of Broad-Spectrum β-Lactam Resistance in Enterobacteriaceae : a Children's Hospital Experience

Qin

Zerr

Weissman

et al. 2008

Antimicrob Agents Chemother

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The objective of this study was to investigate the trends and patterns of resistance in ␤-lactamase-producing members of the family Enterobacteriaceae in a children's hospital over a 9-year period (1999 to 2007). Clinically significant isolates of the Enterobacteriaceae were screened for patterns of broad-spectrum resistance to ␤-lactams. The strains likely to be resistant were subsequently confirmed by an inhibitor-based disc test. The plasmid-mediated resistance determinants in these isolates were identified by PCR and by in vitro transformation, which successfully reproduced the AmpC phenotype unrestricted by the species of the host organisms. Among 8,048 Enterobacteriaceae isolates belonging to the four chromosomal ampC-negative or -nonfunctional genera, 86 (1.07%) isolates (56 Escherichia coli isolates, 22 Klebsiella species isolates, 1 Proteus mirabilis isolate, and 7 Salmonella species isolates) exhibited broad-spectrum ␤-lactam resistance patterns. These organisms collectively produced three classes of ␤-lactamases, including class A extended-spectrum ␤-lactamases (n ‫؍‬ 47), class C or AmpC ␤-lactamases (n ‫؍‬ 36, including 4 isolates that produced both class A and class C enzymes), and class A or B carbapenem-hydrolyzing ␤-lactamases (n ‫؍‬ 3). The proportion increased from 0.46% during the first 3 years to 1.84% during the last 3 years (relative risk [RR], 4.04; 95% confidence interval [CI], 2.28 to 7.42; P < 0.001). The increase was mainly due to the emergence of a plasmid-mediated bla CMY-2 ␤-lactamase, the incidence of which increased from 0.11% during the first 3 years to 0.96% during the last 3 years (RR, 9.11; 95% CI, 2.76 to 30.1; P ‫؍‬ 0.001). Class A-type resistance increased slightly during the study period, from 0.35% during the first 3 years to 0.85% during the last 3 years (RR, 2.42; 95% CI, 1.15 to 5.07; P ‫؍‬ 0.02). A Proteus mirabilis strain was documented to possess a novel bla DHA determinant. Of special concern, three carbapenemase-producing isolates were identified between 2003 and 2006. The infections caused by resistant isolates of the Enterobacteriaceae mainly affected hospitalized patients with underlying conditions; however, 19 (22%) episodes were of community onset in otherwise well children. The rate of resistance to broad-spectrum ␤-lactams among isolates of the Enterobacteriaceae is increasing in children in both hospitaland community-acquired settings, and the resistance is driven largely by plasmid-mediated AmpC ␤-lactamases. These data have important implications for empirical antimicrobial strategies targeting serious pediatric infections. Further study of this problem is warranted.The ever increasing variety of ␤-lactamases produced by isolates of the family Enterobacteriaceae raises concerns about our dependence on ␤-lactam drugs and the emergence of panresistant species. Rapidly emerging ␤-lactamases include extended-spectrum ␤-lactamases (molecular class A ␤-lactamases and, to a lesser extent, class D ␤-lactamases in the Enterobacteriaceae), AmpC ␤-lactamases (clas...

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“…Sources of positive cultures included urine, blood, wounds, sputum, and stool. A CMY-2-producing E. coli isolate caused meningitis in a neonate (86). Often, the strain with a plasmid-mediated AmpC enzyme also produced other ␤-lactamases such as TEM-1 or an ESBL such as SHV-5, the presence of which may complicate detection of the AmpC phenotype.…”

Section: Plasmid-mediated Ampc Enzymesmentioning

confidence: 99%

AmpC β-Lactamases

2009

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SUMMARY AmpC β-lactamases are clinically important cephalosporinases encoded on the chromosomes of many of the Enterobacteriaceae and a few other organisms, where they mediate resistance to cephalothin, cefazolin, cefoxitin, most penicillins, and β-lactamase inhibitor-β-lactam combinations. In many bacteria, AmpC enzymes are inducible and can be expressed at high levels by mutation. Overexpression confers resistance to broad-spectrum cephalosporins including cefotaxime, ceftazidime, and ceftriaxone and is a problem especially in infections due to Enterobacter aerogenes and Enterobacter cloacae, where an isolate initially susceptible to these agents may become resistant upon therapy. Transmissible plasmids have acquired genes for AmpC enzymes, which consequently can now appear in bacteria lacking or poorly expressing a chromosomal blaAmpC gene, such as Escherichia coli, Klebsiella pneumoniae, and Proteus mirabilis. Resistance due to plasmid-mediated AmpC enzymes is less common than extended-spectrum β-lactamase production in most parts of the world but may be both harder to detect and broader in spectrum. AmpC enzymes encoded by both chromosomal and plasmid genes are also evolving to hydrolyze broad-spectrum cephalosporins more efficiently. Techniques to identify AmpC β-lactamase-producing isolates are available but are still evolving and are not yet optimized for the clinical laboratory, which probably now underestimates this resistance mechanism. Carbapenems can usually be used to treat infections due to AmpC-producing bacteria, but carbapenem resistance can arise in some organisms by mutations that reduce influx (outer membrane porin loss) or enhance efflux (efflux pump activation).

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Amp C β-lactamase-producing Escherichia coli in neonatal meningitis: diagnostic and therapeutic challenge

Cited by 13 publications

References 16 publications

Healthcare-associated infections in neonates

Healthcare-associated infections in neonates

Prevalence and Mechanisms of Broad-Spectrum β-Lactam Resistance in Enterobacteriaceae : a Children's Hospital Experience

AmpC β-Lactamases

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