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The ability of a microorganism to grow under antibiotic exposure that inhibits a susceptible comparison, often reflected in an increased minimum inhibitory concentration. Survival alone does not establish resistance: antibiotic tolerance and bacterial persistence concern killing and survival without necessarily changing that growth threshold.

The bulky substituents of ceftazidime can hinder productive entry into the more restricted TEM-1 active site. A wider entrance in TEM-52 could accommodate this substrate and allow its beta-lactam ring to be hydrolyzed. The prediction is reduced susceptibility of TEM-52-expressing bacteria compared with matched TEM-1-expressing bacteria. This is a mechanistic prediction, not a quantitative conclusion from the penicillin G data: entry alone does not guarantee efficient catalytic chemistry for a different substrate. Test ceftazidime hydrolysis directly and measure its minimum inhibitory concentration in an otherwise matched bacterial background, controlling enzyme expression, growth, drug entry and other resistance mechanisms.