To be clear (from an undergraduate microbiologist), my thought process behind the claim that IBM's polymer is less likely to promote resistance: Faster-acting agents that cause immediate destruction are much harder to develop resistance to because normal minor variation from mutations is much less likely to produce anything that will save a cell from death. So even if a cell produces a minor variation in its membrane protein it will likely still be killed and the "resistance" gets no chance to develop.

For something like penicillin, the bacteria gets quite some time to die (it inhibits synthesis!) and there are many different places in the peptidoglycan synthesis pathway for the cell to develop a resistance.

Does that make sense?