Aspergillus fumigatus likes very warm temperatures; it grows happily in the steamy interior of a compost heap, which just happens to be the same temperature as the inside of our bodies. So once it settles in the lungs, the fungus reproduces wildly, spills into the bloodstream, and is conveyed to other organs, where it grows and overwhelms them in turn. That outcome is called invasive aspergillosis, and it is diagnosed as often as 500,000 times a year worldwide, in up to 10 percent of immunocompromised patients. It is deadly—or was, until a tiny group of drugs called triazoles came on the market in the 1990s and 2000s. The triazoles, which have names such as fluconazole and voriconazole, worked against many types of fungal infections—a rare feat, because fungi are more like us biologically than bacteria are, and it is harder to make an antifungal that will kill just them and not us than it is to make an antibiotic. Invasive aspergillosis had been a death sentence, but the triazoles dialed the death rate down from 100 percent to 40 percent. In other words, three out of every five patients who would have died began to survive their infections instead.
And then that trend reversed. At Radboud, the death rate began to creep up again, to 88 percent. Running a review of the samples his department had processed, Verweij spotted the reason: The patients’ infections were resistant to the triazoles, possessing cellular defenses that protected them from the drugs’ attack.
Source: When Tulips Kill – The Atlantic