The role of other broad-spectrum β-lactams and the likelihood of ampC induction by other Enterobacteriaceae are less clear. 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. Heterogeneity within the data and inherent selection bias make inferences on effective β-lactam choices problematic. Although several observational studies have explored optimal treatment for AmpC producers, few provide reliable insights into effective management approaches. This review will mainly focus on inducible AmpC resistance in Enterobacteriaceae. 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. Understanding the nuances of AmpC β-lactamase-mediated resistance can be challenging, even for the infectious diseases specialist.
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