Now, here is how they work, the resistance: drug inactivation. I mentioned beta-lactamases already. target alteration. I mentioned that about ribosomes being altered by addition of methyl group to receptor sites so that antibiotics such as erythromycn can no longer bind to the ribosome. Altered gyrase enzyme can remain enzymatically active while being resistant to quinolone. Efflux pump, decrease permeability. This is common with tetracyclines. We didn't recognize it very early on but it's clear. What happens here is the drug gets into the cell but it's pumped out faster than it can get in. Therefore you never get a concentration high enough to inhibit the bacterium. Then metabolic bypass, that's the thing with inhibition of folic acid synthesis by sulfa drugs. A change in the organism that allows it to bypass the blockade produced by sulfa drugs along the metabolic pathway ultimately leading to folic acid would result in resistance of the organism to sulfa drugs. One way of countering this type of resistance is by use of agents that provide a double blockade. Since the organism would be required to adjust its metabolism a two points rather than one point along the pathway, you might have much better success with being able to prevent this type of resistance.

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