What’s known about the fungus Candida auris confounds the scientists who study it, the doctors who struggle to treat the persistent infections it causes, and the infection control teams that endeavor to clear it from hospital rooms after infected patients leave.
But the list of what’s not known about this highly unusual fungus is longer still — and fascinating. Experts say there’s an urgent need for answers and for funding with which to generate them.
Candida auris was first spotted a decade ago in Japan, and more recently has been popping up in far-flung parts of the globe. The fungus doesn’t behave like a fungus. It causes outbreaks like a bacterium and is generally highly resistant to available antifungal drugs. It’s a growing problem, and a deeply concerning one.
Recently STAT asked a number of scientists to describe what they see as the most pressing research questions facing the field. Here are their thoughts:
Where does the darn thing come from?
Most fungi — and there are multitudes — are found in a variety of places. In soil, in insects, in plants. But the only place C. auris has been found to date is in people.
It has to be somewhere else in nature, said Tom Chiller, chief of mycotic ( i.e. fungal) diseases at the Centers for Disease Control and Prevention.
“They didn’t just ‘poof!’ appear,” Chiller insisted. “They’ve been here for a while. And I wonder where they were hiding.”
Tejas Bouklas, an assistant professor in the department of biomedical sciences at Long Island University, Post, campus, would like to know what other species C. auris can infect.
Knowing where the fungus lives in nature and how people are picking it up might help to answer another very pressing question.
Why and how did different clones of the fungus pop up across the world in a very short time span?
A few years after its 2009 discovery, a number of countries around the globe started reporting C. auris cases. Initially the thinking was that travelers or medical tourists were responsible for the movement. But when the genetic sequences were compared, it was clear that was not the case.
Samples of C. auris circulating in South Africa all looked a lot alike. So did the samples from Asia and from South America. But none of them looked like each other. And they don’t always act like each other.
Chiller noted that the C. auris cases reported in Japan seemed to be mainly ear infections — the original finding of the fungus was from an ear infection, hence the “auris” of the name. In Japan, the fungus doesn’t seem to cause invasive disease; it doesn’t get into the bloodstream. But in South Korea, the same clone (think strain) of C. auris does.
“Wouldn’t it be fascinating to know what changes in that organism that make it go from external ear infection to an invader?” Chiller mused. “Is there something that changes in the genome? … I wish people would just jump on that and study it.”
Knowing the how and the why are crucial, said Dr. Luis Ostrosky, professor of infectious diseases at McGovern Medical School at the University of Texas Health Science Center at Houston.
That’s “the only way we’re going to control it. Because if we don’t know the source, we’re kind of fighting the fire a little bit at a time,” said Ostrosky, who is director of his hospital’s laboratory of mycology research. “If you don’t know the source of an infection, you’re never going to control it completely. And it’s going to keep happening.”
The nearly simultaneous emergence on different continents of a highly drug resistant fungus that acts like a bacteria seems … well, kind of unsettling. What happened to allow this species of Candida to act in ways Candida fungi don’t normally act?
A related concern: If this fungal species learned this trick, can others? Is that what the future holds?
A just-published study in the journal mBio theorizes that climate change may have contributed in part to the emergence of C. auris. The authors say that historically the human body temperature has acted as protection against invasive fungal infections — in effect, we’re too hot for them to be able to grow well in us. But as the globe has warmed, they’ve adapted.
If the theory is correct, other fungi may follow C. auris’ path, posit Arturo Casadevall, of the Johns Hopkins Bloomberg School of Public Health, and his co-authors.
“Whether C. auris is the first example of new pathogenic fungi emerging from climate change … its emanation stokes worries that humanity may face new diseases from fungal adaptation to hotter climates,” they write.
Chiller said uncovering C. auris’ backstory is important. “These things are going to continue to emerge. And understanding how they emerge and where they emerge might lead us to prevention strategies or reactive strategies or preparation strategies for the next big thing.”
Could C. auris help other fungi adapt to be bigger threats to humans?
That’s a question Bouklas is wondering about. “The more ubiquitous it becomes, the more problematic. Because now it could potentially transmit DNA to other Candida species. And maybe even bacteria,” she said.
That idea is not far-fetched. Fungi can mate sexually, Chiller pointed out, allowing them to swap large amounts of DNA.
Where did it get its “Ironman suit”?
That’s the way Johanna Rhodes describes the drug-resistant superpowers of C. auris. Rhodes is an epidemiologist at Imperial College London who has worked on C. auris since a 2016 outbreak at London’s Royal Brompton Hospital.
Some of the patients in that outbreak developed resistance to an entire class of antifungal drugs within a month — “which is just unheard of,” she said.
Bouklas also has resistance questions. “Why does it have such a strong resistance to every known anti-fungal?” she asked. “All of them use a different mechanism of killing…. That’s the biggest question.”
Often pathogens that develop drug resistance pay for it in other ways — it’s called a “fitness cost.” Yes, Bacterium X can evade Drug Y, but in acquiring that skill it becomes less transmissible or weaker in some way.
Not C. auris.
“It seems that it’s got resistance at no fitness cost. It’s still able to form biofilms. It’s still able to persist [in an environment]. It’s still able to infect,” Rhodes said.
Biofilms are a layer of pathogens — in this case, fungi — that attach to a surface and effectively lay in wait there. Sometimes biofilms form in the drains or pipes leading from sinks in hospitals. Many like wet surfaces, but C. auris can form dry biofilms, lurking on surfaces like bed railings in a contaminated hospital room. These infectious residues can transmit C. auris from one patient to the next in a hospital room.
This fungus is really hard to get rid of. That’s something Dr. Anthony Fauci, director of the National Institute for Allergy and Infectious Diseases, thinks needs to be explored.
“Why is it so different from others that you could easily, by wiping it with whatever it is you wipe it with, it goes away? Whereas this just seems to stick there,” Fauci asked.
Ostrosky also wants to know why the fungus spreads so well in hospitals, which are not normally terribly hospitable to fungi.
What’s the best way to treat patients who develop C. auris infections?
That’s a question Ostrosky, who has treated patients with C. auris infections, would very much like answered.
Chiller has a related question: How often is C. auris causing death?
Between 30% and 60% of patients who develop C. auris infections die, the CDC estimates. But in the United States, anyway, C. auris infections occur in the sickest of patients: people whose immune systems have been compromised, who have spent prolonged periods on ventilators — machines that breathe for people whose lungs aren’t up to the task.
Are these people dying from their C. auris infections? Or are their other medical problems the cause of death? “Are they dying of C. auris or with C. auris? I still want to know that,” said Chiller, though he acknowledged that “those are really hard studies to do.”
Correction: An earlier version of this article misspelled Luis Ostrosky’s name.
My guess, it’s coming from dogs and cats. I’m a mycologist and study plant and animal fungal pathogens. My Mastiff gets a yeast ear infection about every two months. It’s resistant to treatments the vet gives him. It causes him terrible pain. It never completely goes away. Imagine that in dogs and cats around the world, imagine all the different antifungals it has been exposed to by vets. Now I’m magine people sleeping with and living in close association with their pets and it gets on our skin and doesn’t cause disease until it enters our bloodstream or ears or we are sick. My guess is if you look in dogs and cats you will find this fungus. Please share with CDC and whomever. This is the hypothesis I would test if given funding.
Check out this PubMed Article on a study by Dr. Klara Junker and her team. Mycoparasitic yeast Saccharomycopsis schoenii may provide some hope. According to Dr. Junker et al, “necrotrophic mycoparasitism describes the ability of a fungal species to kill other fungi”. Over a 6 hour period of co-culture, 34% of the Candida auris cells died due to predation by S. schoenii. In other words, they found S. schoenii can kill C. auris. Here is a layman’s version with pictures at nature.com:
So we learn in grade school that higher oxygen levels on the planet lead to insects getting bigger. So what if sterile environments in developed nations (mainly clinics) is the culprit. We already know that bacteria can go through generations far faster than multicellular creatures. So what if the yeast fungus was merely a yeast spore from a beer maker or baker who came in the emergency room. This person’s residue that wasn’t cleaned for some reason leaving this fungus in a sterile environment. That fungus went through different life cycles rather quickly which allowed the yeast to mutate into a whole new strand. With humans ability to travel around the world the new strain could have attached onto people and moved around the world. Using humans as hostes for survival. Like Venom…. I am no scientist but this is my reasoning skills being put to good use.
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