I believed we would face an antibiotics apocalypse, until now

So, assuming I'm parsing you correctly, would you say that at this time, the benefit is that we can avoid the bacteria becoming resistant by creating a large range of things that it would have to become resistant to, and the down-side is that since these polypeptides are larger, they will not be as able to be administered where needed? Could this also mean that we end up treating an infection in a specific spot, but allowing it to continue to colonize a different part of the body? For instance, say, in the case of a UTI, where the infection could have moved further up the GI tract, and treatment with polypeptides would work for the urethra, but possibly not further up?

I agree the article is light on substance, but for a layperson reading it, much of that preamble is probably necessary.

Anyway, I don't think the idea is to generate completely random polypeptides. The analogy with the lego bricks sounds more like they're mixing and matching known protein domains. Proteins are made of subunits called domains, and these are relatively modular, in the sense that you can concatenate the sequences for multiple domains into a single polypeptide and reasonably often end up with a functional protein consisting of the desired domains tethered together. These are called fusion proteins. In this case, the lego analogy suggests that there is a range of domains that bind to different structures on the external surfaces of bacterial cells, and another range of domains that kill bacterial cells by different mechanisms.

So, if you want to kill species X, you first find a binding domain A that binds X cells, and then find an enzymatic domain B that can kill X cells, and create a fusion. This fusion protein AB will now attach to X cells and then kill them. If species X evolves to change its shape so that A no longer binds, you find a new binding domain C that does, and create a CB fusion, which can go on killing the evolved X cells via the same mechanism. If X evolves immunity to B's mode of action, then you find a new enzymatic domain D with another mode of action and create fusion AD. Repeat as necessary.

Obviously, the success of this method depends on how many binding and enzymatic domains are effective against a particular bacterial strain. I have no idea how many bactercins are known, but presumably there must be enough to give hope to the author of this article.

Maybe one could synthesize analogs that don't get hydrolyzed in the stomach.

There is indeed a kind of overlap between the approach in the article and phage therapy, which is to clone the lytic enzymes present in the phages and use the purified products directly on bacteria (I worked on characterizing these things during my PhD). Actually there are some bacteriocins that are homologous to their phage equivalents, and so at a molecular level these two efforts are basically the same.

Further reading for the interested: http://www.ncbi.nlm.nih.gov/pubmed/16125935

The problem with phage therapy is partly economic, partly regulatory, and partly practical.

Unlike antibiotics, phages are entirely natural, and so can't be patented; in a bacterial broth they multiply at an astonishing rate (about a thousandfold every hour IIRC); and they're obtained from stuff which we have so much of that a large part of our infrastructure has been built just to get rid of it (raw sewage). So there's no money to be made out of phage therapy, and it threatens whatever money pharmaceutical companies make out of selling antibiotics. So, it's no surprise they were a big success in communist countries and a failure in capitalist ones. After the fall of communism, they continue to be used in Georgia, but every attempt to make money out of them has failed.

Also, they're treated as a drug by regulatory bodies (which were established with pharmaceutical companies in mind), and so every phage strain, and every phage cocktail, would need extensive trials before approval is granted, despite their being completely safe and impossible to overdose on.

The practical reason for not using them is that antibiotics are trivial to administer compared to bacteriophage, you don't need to identify the exact strain, and antibiotics are less of a problem to store.

However, when bacteria develop resistance to a particular phage, the phage can and will evolve to kill the new strain of bacteria. Also, with phage therapy, dosage is not an issue as the phage multiplies on contact with its target bacteria. Phage doesn't mess with your gut flora. And finally, nobody is allergic to phage.

The NHS and other health services should follow Georgia's lead and develop stocks of phage (which are used at present to identify bacterial strains), as well as the expertise required to identify and administer them; fast-track them for use; and ignore any objections from pharmaceutical companies: the purpose is to cure people, not to make a profit.

I think the breakthrough was that a path of potential treatment was just paved...

It's a bit of an unclear sentence - bacteriocins are already present in humans, coming from bacteria living in our guts.

Maybe it's specifically about the group of bacteriocins he researches? He doesn't say which studies were presented in Beijing, so it's hard to check