Uh, I'm checking notes from my Bacterial Pathogenesis lectures, and they say that YOU'RE wrong. The University of Southern Carolina med school site also has a page of notes on this matter that agrees with what I've learned; this isn't based soley on the TED talk, this is based on what I've learned from prior experience in bacterial pathology.

http://pathmicro.med.sc.edu/mayer/antibiot.htm

"Antibiotics are categorized as bactericidal if they kill the susceptible bacteria or bacteriostatic if they reversibly inhibit the growth of bacteria. In general the use of bactericidal antibiotics is preferred but many factors may dictate the use of a bacteriostatic antibiotic. When a bacteriostatic antibiotic is used the duration of therapy must be sufficient to allow cellular and humoral defense mechanisms to eradicate the bacteria."

Or am I misunderstanding something? Are you a biologist of some sort with experience in the field?

I doubt he invented the concept. In the afterward sections of his books, he often talks about how he draws from other sources. I'm pretty sure in one of his books he mentions how he consulted medical workers on plausible scenarios; Card could've simply picked up the idea of communicating via chemicals through such an experience. While the earliest scientific article I can find on quorum sensing, through PubMed and Web of Science, is from 1995, I'm sure the idea of microorganisms communicating through such a mechanism is much older and probably predates Xenocide.

The method of anti-bacterial action you say she presents is precisely how bacteriostatic antibiotics work, by inhibiting growth of bacterial populations; the point is to give your immune system a chance to catch up with the bugs, making them more manageable. In that sense, it's not a stretch that drugs that imitate quorum sensing signals could replace antibiotics. At the very least, more drug options would be provided. This would be important when the bugs become resistant to our existing drugs.

You are correct to say that IF we cannot provide hypotheses explaining how these proteins managed to aggregate and form the structure of a flagella we cannot prove evolution.

But, if one argues that our current state of knowledge provides no explanation for the evolution of the flagella, I would say they lack imagination.

Here's a hypothesis:

If the flagella began as a protein export mechanism, it could have evolved into the Type III secretion system and then into a flagella.

Further speculation:
The motor of this proposed protein export mechanism could have started out as a simple pore complex geared towards protein export. Mutations cause some of these exported proteins to adhere to extracellular portions of this export mechanism, forming the tube like structure of the Type III needle. Over time, mutations alter the structure slightly, without harming the function of this apparatus in protein export, causing it to resemble flagella more and more. Without selection pressure against these developments, these changes persist. In fact, genetic drift may cause these changes to become fixed in a population. Gradually, even more changes occur contributing to the drive motor, resulting in the flagella you see today.

Granted, all of the above is merely a story, but that's not to say that it isn't true. I don't think this scenario is that far fetched, and further study of the flagella may even validate it.

At this point I'd like to point out that it could be interesting to look at research into the specific events occurring during flagella assembly; if you think about it, the flagella IS assembled piece by piece. One would think that flagella intermediates would resemble intermediates in flagella evolution. By studying these "assembly line intermediates", function could possibly be derived (my old biology teacher's mantra: form gives function), further answering the question of flagella development.