Genetic drift always keeps life interesting.

H1N1, the disease that's kept supplies of vaccine low, doctors' offices and emergency rooms packed, and way too many people feeling like crap this season has thrown the medical community a curveball in recent weeks. Beginning early last spring Tamiflu-resistant strains of the virus started appearing around the country, most notably in Maryland, Virginia, and Washington state. The antiviral compound Tamiflu is one of those administered to the sickest of patients, and this means that physicians will have to figure out another drug or combination of drugs because their best treatment thus far is likely to become less effective as time goes on. It is thought that treating patients for extended periods of time with Tamiflu had something to do with resistant strains of H1N1 developing; it's also worth mentioning that the resistant strains were found in people who already had compromised immune systems, which may also play a part in the virus' mutation.

I find it interesting that the article seems to conflate a pathogen spontaneously mutating to be resistant to a particular drug with a human body developing a tolerance to a drug. The two are not the same; people develop tolerances to drugs because the body becomes adapted to metabolizing and excreting certain compounds to return to a state of homeostasis. Pathogens develop immunities to compounds (from their point of view, toxins) to remain functional and thus reproduce their genes more effectively. But now I'm splitting hairs because it's an easy mistake to make when an article's on a deadline.