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A female friend recently commented that women should never self diagnose yeast infections because if they don't actually have one and proceed with some kind of treatment, some kind of resistance will be built up which will reduce effective treatment in the event of a real future infection. I was a little surprised by this and went searching. Here's a similar sentiment on this Michagan State page (unofficial looking blogish thing):

Many wimmin (sic, women) assume that every vulvar or vaginal itch they have is due to a yeast infection, and run out to fill their crotches full of powerful antifungal creams. But sometimes it isn't really a yeast infection. The problem is that when you expose your naturally-occuring vaginal yeast to these drugs, some of the yeast may be resistant. Only the resistant ones thrive and multiply and then next time you get a yeast infection, you've got a crotch full of drug-resistant yeast, and you can't just run to the pharmacy and shell out $20 for a cure; you have to go to a doctor and get something much stronger. As much as 25-30% of yeast infections may now be resistant to over-the-counter treatments.

This variant of the claim seems to segregate "naturally-occurring" yeast and... only-during-infection-occurring yeast. I was skeptical that this differentiation should matter. Yeast are yeast. The article goes on to draw parallels with people not finishing penicillin prescriptions and thus creating resistance, however we're not talking about taking a partial treatment and then stopping -- that introduces another potential cause to this phenomenon. I want to know if a fully followed treatment during lack of an actual yeast infection would build some type of resistance to future treatment during a real infection.

I think the claim speaks for itself, but to reiterate:

  • Will using yeast infection treatment in the absence of an actual yeast infection lead to increased resistance of some sort in the event of a future yeast infection?
  • If so, approximately how many "false treatments" are needed to produce this effect? (My female friend seemed to think it was only once. I had a hard time imagining this.)
  • I think that the difference between normal yeast levels and yeast infection levels is that the yeast infection is beyond the bodies natural ability to combat and contain the yeast. It was explained to my wife when she went on antibiotics for a UTI that the bodies natural bacteria would be harmed allowing for the yeast to get out of control. – Chad Dec 12 '11 at 17:51
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Many microbial organisms communicate through a process called "quorum sensing". Individuals secrete a signalling molecule into their environment. When they encounter the signalling molecule it causes them to secrete more of it. This means that when there are few in the environment they won't be secreting much, but when there are a lot of them around it turns into a positive feedback loop, and each organism "knows" that it's got a lot of allies. When they are in strength, they are able to act collectively - such as forming a biofilm - or becoming pathological. Quorum sensing was first noted in bacteria, but also has been found in yeast such as Candida albicans.

There are a number of different species of yeast. Lactobacillus acidophilus, for example, keeps other species under control, while Candida albicans - that quorum sensing one from before - is the one which usually causes infections.

So you have L. acidophilus keeping the C. albicans numbers down, but if something perturbs that relationship then the C. albicans can proliferate, emitting their pheromone and sensing that they can now go pathological - that's a yeast infection [pdf, see page 2]. That's the distinction the article was talking about - naturally occurring (but controlled) C. albicans getting loose and going into their pathological state.

If you take treatment without an infection, you're creating the chance of breeding having those naturally-occurring C. albicans developing a resistance. There's even evidence to suggest that, much like bacteria, such species can share genes horizontally - horizontal transfer being a common mechanism by which bacterial resistance spreads. Then the next time they go pathological there'll be resistant yeast in the mix already, who will survive the treatment when it's actually needed.

As for the last point, resistance is a chance-based mechanism. Each time a treatment is misused, there's a chance resistance will develop. More misuse, more chances.

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