Kill it or just stop it?
A bactericidal drug actively kills bacteria; a bacteriostatic drug only stops them dividing and leaves the immune system to mop up. For most patients with a healthy immune system, the distinction barely matters — a paused infection is one your body can clear. But it becomes critical when the immune system can't help: in deep infections like endocarditis or meningitis, or in people who are immunocompromised, a truly killing drug is usually preferred.
MIC: putting a number on potency
The minimum inhibitory concentration (MIC) is the lowest drug concentration that stops a particular bacterial strain from growing in the lab. A low MIC means the drug is potent against that bug; a high MIC means you'd need a lot of drug — maybe more than you can safely give. The lab compares the MIC to the levels a normal dose can reach in blood and reports the organism as 'susceptible', 'intermediate', or 'resistant'. That single word steers the prescription.
Strain X, drug A: MIC = 0.5 mg/L --> susceptible (easy to treat) Strain X, drug B: MIC = 32 mg/L --> resistant (would need toxic doses) Is a dose 'enough'? Compare peak blood level (Cmax) to MIC: Cmax = 8 mg/L, MIC = 0.5 mg/L -> Cmax/MIC = 16 (plenty of headroom) Cmax = 8 mg/L, MIC = 32 mg/L -> Cmax/MIC = 0.25 (drug never reaches killing level)
Different classes also kill in different rhythms. Some (like aminoglycoides) are 'concentration-dependent' — a high peak (Cmax) relative to MIC does the killing, so you give a big dose once a day. Others (like beta-lactams) are 'time-dependent' — what matters is how long the level stays above MIC, so frequent dosing or infusions work better. Many also show a post-antibiotic effect, suppressing growth even after the drug level falls, which lets you stretch the dosing interval.
Spectrum: how wide a net?
A drug's spectrum of activity is the range of microbes it can treat. 'Broad-spectrum' sounds better, but wider is not always wiser: broad drugs also wipe out the harmless bacteria that protect your gut and skin, opening the door to overgrowth and to resistance. The skilled move is to start broad when the patient is sick and the cause is unknown, then de-escalate to the narrowest effective drug once the lab identifies the bug.