First of all I find quorum sensing to be generally facinating, so I'm happy to see the topic brought up here.
Dr. Bassler has many papers on the subject, but I think one of the most relevant ones to this question is here.
Regarding your question, you have the right idea, but you're missing the point of her comment. The Western shows a more dramatic difference in cqsA- bacteria because they are not inhibiting themseleves (as you suggested). Thus the lower concentrations have much higher levels of the toxin produced because the only CAI-1 being provided is the synthetic one. This makes the ramp up in administered CAI-1 seem more drastic because you start at a higher level.
I hope that makes since, if I can find an open writes version of the Western, I'll come back and give further analysis on it.
Regarding @AlanBoyd 's comments, V. cholerae is different because it seeks to create an acute infection, not a persistent one. Cholera toxin is what causes the majority of diarrhea and virulence from cholera. V. cholera produces the toxin until it's inhibited by ether auto-inducer (which should be after the pt already has massive diarrhea), then it switches to produce enzymes which detach it from the gut. The pt still has diarrhea at this point, cholera just doesn't need to make any more toxin for it to continue. To do so would probably waste energy, and not help the bacteria make it back to a water supply.