AmpCs

AmpCs are beta-lactamases belonging to the Ambler class C enzymes that confer resistance to a broad range of beta-lactam antibiotics. They can be encoded chromosomally in certain Enterobacterales or carried on plasmids, in which case they are referred to as plasmid-mediated AmpCs. Chromosomal ampC genes are common in species such as Enterobacter, Citrobacter, Serratia and Morganella, while plasmid-borne variants expand the resistance spectrum across Enterobacterales.

The enzyme action of AmpCs includes hydrolysis of penicillins and cephalosporins, with notable activity against cephamycins such as cefoxitin and cefotetan. AmpCs are typically poorly inhibited by many standard beta-lactamase inhibitors such as clavulanic acid and related compounds, which limits the usefulness of combinations like amoxicillin-clavulanate or piperacillin-tazobactam in infections caused by producers. Some plasmid-mediated AmpCs can be inhibited by newer inhibitors such as avibactam, restoring activity of certain cephalosporins (for example ceftazidime-avibactam). Aztreonam can be hydrolyzed by AmpC, but combinations with avibactam can mitigate this in some contexts.

Expression of AmpC can be inducible, and regulatory mutations (for example in ampD or ampR) can lead to derepression with constitutive high-level production, resulting in broader resistance during infection. Plasmid-mediated AmpCs facilitate rapid spread between species, contributing to the emergence of resistant infections in healthcare settings.

Clinically, AmpC producers pose diagnostic and therapeutic challenges, often reducing susceptibility to multiple beta-lactams and complicating empirical therapy. Carbapenems have traditionally been reliable for severe AmpC infections, while newer beta-lactamase inhibitors can offer alternatives in selected cases. Laboratory detection relies on phenotypic tests and molecular methods to identify AmpC genes.