The polymer doesn't work in a way that resistance is likely or even possible. They spill the bacterias guts. Its like getting resistance to head-blowed-off - not going to happen.
To be fair... the mechanism of penicillin when described for the lay person is remarkably similar to the description that IBM provides.
"the polymer attaches to the bacteria's membrane and then facilitates destabilization of the membrane" vs "act by inhibiting the synthesis of the peptidoglycan layer of bacterial cell walls".
And the resistance isn't to getting your head blown off. That's thinking too much in the box. It's more like being resistant to having a bullet shot at your head, either by somehow becoming invisible to your assailant's vision, wearing a sufficiently good helmet, or having your vital organs located somewhere else.
While I agree that it seems much harder for bacteria to overcome this new approach, it really isn't safe to say that it's not possible. We have no idea about the microbial world. We barely know a fraction of the microbes that swarm around us, we have no idea what defenses, mechanisms and quirks they have that might provide a method of resistace.
And since this is a passive process (just some polymer floating around) that somehow does not damage human cells, you can bet that there's someway to spoof that.
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.
I would not be so sure of that until long term tests have been done to bacteria populations. All it would take is a random mutation which makes it harder for the polymer to attach to the bacteria.
Sure, given that, what does it matter? Don't kill the bacteria now because...what?
The old argument was, don't make our current antibiotics useless by breeding 'resistant' varieties. But now, IBM is making 'magic bullet' antibiotic polymers on their 3D polymer printer.
So what does it matter that new varieties mutate or whatever, if you can just print up a new polymer to handle it.
This is a game-changer. The old ways of thinking are probably obsolete.
