ampCmediated

AmpC-mediated resistance refers to the activity of AmpC beta-lactamases, enzymes that hydrolyze many beta-lactam antibiotics and thereby confer resistance. AmpC enzymes can be produced by chromosomal genes present in several Enterobacterales species or carried on plasmids as acquired, disseminating determinants. Chromosomal ampC genes are often inducible or derepressed, leading to variable resistance patterns, while plasmid-mediated ampC genes can produce high-level resistance across species.

Genetic basis and expression patterns are important in AmpC-mediated resistance. In many Enterobacterales, ampC is chromosomal and regulated by cellular factors; exposure to certain beta-lactams can induce higher expression. Plasmid-mediated AmpC (pAmpC) genes, such as bla CMY and related families, can spread between species and produce stable, derepressed beta-lactamase activity, complicating treatment and infection control.

Phenotypic characteristics and laboratory detection are often variable. AmpC producers may show resistance to several penicillins and cephalosporins and to cephamycins like cefoxitin, with possible apparent susceptibility to some third-generation cephalosporins in routine testing due to inducible expression. Detection can require specific tests or inhibitor-based methods (e.g., boronic acid inhibitors) and molecular assays to identify the presence of ampC genes.

Clinical implications and treatment considerations are significant. Infections caused by AmpC producers are typically treated with agents stable to AmpC hydrolysis, such as carbapenems for serious infections. Some beta-lactam/beta-lactamase inhibitor combinations and newer agents like ceftazidime-avibactam can be effective against many AmpC producers, but resistance can vary by organism and gene variant. Susceptibility testing and local resistance patterns are essential for guiding therapy and infection control.