infectious diseases
Carbapenems
Carbapenem resistance
Expanded use of carbapenems has resulted in some carbapenem resistance. This development is concerning because carbapenems are often the last resort for treating multidrug-resistant gram-negative organisms, particularly those that produce AmpC and extended-spectrum beta-lactamases, which destroy most beta-lactams except for carbapenems. The most common mechanism of carbapenem resistance is Carbapenemase production However, carbapenem resistance may also be mediated by the loss or alteration of porin channels, the expression of efflux pumps, or penicillin-binding protein (PBP) modification. Many carbapenemases are encoded on plasmids, facilitating the spread of resistance genes among organisms of the same species or even different bacterial species. If carbapenemase-producing pathogens are identified in a patient, infection control precautions and enhanced environmental cleaning should be instituted to prevent further transmission. The novel beta-lactamase inhibitors, avibactam, relebactam, and vaborbactam, can inhibit most carbapenemases but are ineffective against metallo-beta-lactamases (a type of carbapenemase that uses reactive zinc at the active site to destroy the carbapenem). The coformulation of avibactam withceftazidime, vaborbactam withmeropenem, or relebactam with imipenem increases activity against pathogens that produce serine carbapenemases. Examples of serine carbapenemases includeKlebsiella pneumoniaecarbapenemase (KPC) and OXA beta-lactamases. 