A Primer on AmpC β-Lactamases: Necessary Knowledge for an Increasingly Multidrug-resistant World.


Journal

Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
ISSN: 1537-6591
Titre abrégé: Clin Infect Dis
Pays: United States
ID NLM: 9203213

Informations de publication

Date de publication:
27 09 2019
Historique:
received: 15 01 2019
accepted: 26 02 2019
pmc-release: 06 03 2020
pubmed: 7 3 2019
medline: 15 9 2020
entrez: 7 3 2019
Statut: ppublish

Résumé

Understanding the nuances of AmpC β-lactamase-mediated resistance can be challenging, even for the infectious diseases specialist. AmpC resistance can be classified into 3 categories: (1) inducible chromosomal resistance that emerges in the setting of a β-lactam compound, (2) stable derepression due to mutations in ampC regulatory genes, or (3) the presence of plasmid-mediated ampC genes. This review will mainly focus on inducible AmpC resistance in Enterobacteriaceae. Although several observational studies have explored optimal treatment for AmpC producers, few provide reliable insights into effective management approaches. Heterogeneity within the data and inherent selection bias make inferences on effective β-lactam choices problematic. Most experts agree it is prudent to avoid expanded-spectrum (ie, third-generation) cephalosporins for the treatment of organisms posing the greatest risk of ampC induction, which has best been described in the context of Enterobacter cloacae infections. The role of other broad-spectrum β-lactams and the likelihood of ampC induction by other Enterobacteriaceae are less clear. We will review the mechanisms of resistance and triggers resulting in AmpC expression, the species-specific epidemiology of AmpC production, approaches to the detection of AmpC production, and treatment options for AmpC-producing infections.

Identifiants

pubmed: 30838380
pii: 5369903
doi: 10.1093/cid/ciz173
pmc: PMC6763639
doi:

Substances chimiques

Anti-Bacterial Agents 0
Bacterial Proteins 0
beta-Lactams 0
AmpC beta-lactamases EC 3.5.2.6
beta-Lactamases EC 3.5.2.6

Types de publication

Journal Article Research Support, N.I.H., Extramural Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

1446-1455

Subventions

Organisme : NIAID NIH HHS
ID : K23 AI127935
Pays : United States
Organisme : NIAID NIH HHS
ID : UM1 AI104681
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI104895
Pays : United States
Organisme : NIAID NIH HHS
ID : R21 AI123747
Pays : United States
Organisme : NIAID NIH HHS
ID : R21 AI135522
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI100560
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI063517
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI072219
Pays : United States
Organisme : NIAID NIH HHS
ID : R21 AI130608
Pays : United States

Investigateurs

P D Tamma (PD)
Y Doi (Y)
R A Bonomo (RA)

Commentaires et corrections

Type : CommentIn

Informations de copyright

© The Author(s) 2019. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.

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Auteurs

Pranita D Tamma (PD)

Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland.

Yohei Doi (Y)

Department of Medicine, University of Pittsburgh, School of Medicine, Pennsylvania.

Robert A Bonomo (RA)

Department of Medicine, The Louis Stokes Cleveland Department of Veterans Affairs Medical Center, Case Western Reserve University, Ohio.

J Kristie Johnson (JK)

Department of Pathology, University of Maryland School of Medicine, Baltimore.

Patricia J Simner (PJ)

Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland.

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Classifications MeSH