Noncarbapenems

Noncarbapenems is a term used to describe all beta-lactam antibiotics that are not carbapenems. This broad group includes penicillins, cephalosporins, monobactams, and related combinations with beta-lactamase inhibitors. Like other beta-lactams, they act by inhibiting bacterial cell wall synthesis through binding to penicillin-binding proteins and are typically bactericidal in effect, with activity depending on drug concentration and exposure.

Subclasses and representative agents vary in spectrum. Penicillins include natural penicillins (penicillin G, penicillin V), aminopenicillins (amoxicillin, ampicillin), anti-staphylococcal penicillins (oxacillin, nafcillin, flucloxacillin), and extended-spectrum penicillins (piperacillin, ticarcillin). Cephalosporins span generations and generally shift from Gram-positive preference toward broader Gram-negative coverage in later generations (examples include cephalexin, cefazolin; cefuroxime, ceftriaxone; cefepime). Monobactams, such as aztreonam, are active mainly against Gram-negative rods and have minimal activity against Gram-positive organisms or anaerobes. Cephamycins like cefoxitin and cefotetan have enhanced anaerobic activity and include some Gram-negative coverage. Beta-lactamase inhibitor combinations (amoxicillin-clavulanate, ampicillin-sulbactam, piperacillin-tazobactam) extend activity against beta-lactamase–producing organisms.

Resistance to noncarbapenems arises from beta-lactamase production, alterations of penicillin-binding proteins, reduced permeability, and efflux. Extended-spectrum beta-lactamases (ESBLs) and AmpC enzymes can limit many penicillins and cephalosporins, while aztreonam remains less affected by ESBLs but can be inactivated by other beta-lactamases and porin loss. Clinical use depends on infection type, local resistance patterns, and patient factors; adverse effects mirror those of other beta-lactams and include hypersensitivity, rash, and gastrointestinal symptoms.