Two statements hold true for ESBL producers: carbapenems are usable (indeed preferred) and the resistance is plasmid-borne. Extended-spectrum beta-lactamases are mutant enzymes (TEM, SHV and the dominant CTX-M families) that cleave penicillins, the oxyimino third-generation cephalosporins and monobactams; they are classically inhibited by clavulanate on a test plate. Genetically, the determinants ride on transferable plasmids, which is why ESBL organisms spread between patients and species and frequently carry linked fluoroquinolone and aminoglycoside resistance. Therapeutically, a carbapenem such as meropenem is the stable backbone for serious disease. The two false claims: third-generation cephalosporins are substrates of the enzyme and must be avoided regardless of an in-vitro 'susceptible' flag, and piperacillin-tazobactam is unreliable in severe infection owing to the inoculum effect. Hence the true pair is carbapenem use and plasmid transmission.\[\boxed{\text{Carbapenems usable + plasmid-transmitted}}\]