Aug 13, 2019 9:00 AM

The Desperate Race to Neutralize a Lethal Superbug Yeast

Candida auris spreads explosively in hospitals, but little is known about its origins. Figuring that out could help prevent a pandemic.

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Last September, an American traveling in Kenya suffered a serious stroke, and was hospitalized there for a month. The stay didn’t go well: The person suffered a bout of pneumonia, a urinary tract infection, and a brush with sepsis, a life-threatening immune reaction to infection.

Eventually the traveler’s condition stabilized enough to be brought home, to the intensive care unit of a hospital in Maryland. Because they had been in that foreign hospital for so long, the US institution decided to be extra careful. It put the patient (who hasn’t been named publicly, to respect medical privacy) into an isolation room and required that everyone on the treatment team wear a gown and gloves. After consulting the state health department, the hospital also decided to check the patient for any superbugs that might have been picked up overseas.

It was a smart decision. In addition to an array of very drug-resistant bacteria, the patient was carrying Candida auris, the potentially deadly “superbug yeast” that has alarmed health authorities around the world.

That prescient detective work prevented the Maryland hospital from enduring a fast-moving, fatal outbreak, as the Centers for Disease Control and Prevention detailed in a recent case report. That super-yeast has wreaked havoc in England and South Africa—as well as here in the US, where it has spread explosively in hospitals, infecting surgical wounds, brewing whole-body bloodstream infections, and clinging to every surface that investigators have thought to check.

The new report also confirms something that researchers have suspected for a while: Unlike other regions of the world, the United States doesn’t possess its own unique strain of C. auris. When outbreaks have burgeoned here, they came from somewhere else, carried unwittingly across the border by travelers.

What the Maryland case couldn’t illuminate is where C. auris originated. It’s a question epidemiologists urgently want to answer, because understanding this bug’s origin and evolution may hold the key to preventing it from disrupting health care even more.

The C. auris story is complex, but here are the basics. (We untangled its full early history here a year ago.) Over a period of about five years, physicians in Japan, Korea, India, South Africa, and the Middle East simultaneously diagnosed patients with infections caused by a strain of yeast that had not been recorded before 2009. This yeast was extraordinarily unlike any other: It caused grave wound and bloodstream infections, it spread easily from person to person, it survived without difficulty on cool inorganic surfaces—and because of those qualities, it sparked ferocious hospital outbreaks.

Worst of all, the super-yeast emerged already resistant to the limited drugs available to treat fungal infections. C. auris seemed like such a threat that, in 2016, the CDC broke its mandate of focusing on health problems within the United States and published a warning, even though no cases had occurred here. The agency was just in front of the curve: Within a few months, a dozen Americans were diagnosed with the super-yeast, and four died.

Three years later, there have been more than 700 cases in the US. C. auris has been diagnosed in patients in more than 30 countries on six continents, and when investigators talk about it, they use ominous phrases such as “pandemic potential.” (At an international conference last year, the head of fungal studies at the CDC described the super-yeast as “more infectious than Ebola.”)

“It’s difficult how rapidly this has spread across the globe,” says Johanna Rhodes, an infectious diseases research fellow at Imperial College London and coauthor of a new review of the yeast’s global spread. “We definitely weren’t ready for it.”

It’s common, when a superbug emerges, to be able to trace its unfolding history: either in real time, as patients carry an infection from one location to another, or retrospectively, when analysis of samples reveals adaptations over time. But C. auris has no such history. It was suddenly simply present, in multiple places at once.

Yet it must have come from somewhere, in some animal or plant or patch of soil where it sheltered unnoticed—and something must have happened to transform the super-yeast from a quiescent occupant of that niche to a raging threat.

So far there are no explanations. CDC scientists explored some of the leading hypotheses in a paper published last month. C. auris is unusually tolerant of salt; maybe its historic home was the border between land and sea. It can survive at higher temperatures than most other fungi; perhaps it adapted first to birds, whose body temperatures are even higher than humans. It flourishes in healthcare settings: Did medicine’s relatively recent success at saving the lives of the immunocompromised—AIDS patients, cancer patients, transplant recipients—offer the yeast a home it never had?

One plausible explanation focuses on a relatively new class of fungicides used around the world in huge amounts: agricultural compounds to preserve food and ornamental crops, and chemically similar antifungal drugs that protect patients with compromised immune systems. The vast use of those compounds, called azoles, has persuasively been linked to increases in a drug-resistant fungal infection known as aspergillosis—but they might simultaneously have cleared a path for yeast species to boom as well.

The most provocative hypothesis for the emergence of C. auris, however, is also the most discouraging, because it traces the yeast’s emergence to a problem that humans have been unwilling to control. In this telling, captured in another paper published last month, the super-yeast is a disease of the Anthropocene. It is flourishing because human-caused climate change has given it a boost.

That thinking goes like this: There are possibly millions of species of fungi in the world, yet relatively few of them succeed in attacking humans. What protects us from them is our warmth: At 37 degrees Celsius (or 98.6 degrees Fahrenheit), we are hotter than what most fungi can survive. But if something encouraged fungi to tolerate higher temperatures, more of them could become a threat to us—and the slow heating of the planet may be creating the perfect laboratory in which fungi can adapt.

“There is no better explanation for the simultaneous emergence of Candida auris than that, with the globe warming, some strains have adapted and are now able to survive in humans,” says Arturo Casadevall, one of the paper’s authors, who is a physician and the chair of molecular microbiology and immunology at the Johns Hopkins Bloomberg School of Public Health.

But as dire as that sounds, he argues, it also presents an opportunity. If C. auris could be tracked to its original niche, researchers might find that some strains of the fungus have not yet adapted to thriving at our bodies’ internal temperature. Bringing those strains into a lab and figuring out the evolutionary path C. auris took from heat-sensitive to heat-tolerant might also provide clues to the other ways in which it diverges dangerously from typical yeast behavior. Since those are the qualities that make it such a threat—passing from person to person and surviving on plastic and steel surfaces—understanding its evolution could provide clues to controlling its spread.

The urgency of keeping it from spreading further ought to be the spur for making fungal research a priority. (Right now, Rhodes says, “Funding is crazy hard to come by.”) C. auris is still only a hospital pathogen. But imagine if it adapted further to our environmental niche and became a pathogen that flourishes not just in hospitals but in homes and gyms and schools. Imagine every yeast problem that we consider unthinkably minor—skin rashes, vaginal problems, infections of the mouth and throat—being caused instead by a potentially lethal organism that no drug can touch.

Even more, what ought to persuade us to hunt for the origins of C. auris is the threat of what is coming next. “Every year, routinely, we find one or two emerging fungal species in patients, rare weird molds,” says Tom Chiller, a physician and chief of the CDC’s fungal diseases branch, who led last month’s exploration into C. auris’s origins. “They’re exceedingly rare, and they’re in highly vulnerable patients.”

Usually, he adds, those new threats fizzle out. C. auris might have been expected to, and didn’t. Its sudden success ought to show us where our defenses against new diseases are weak.

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