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Every Clade, Everywhere, All at Once: The Strange Emergence of Candida auris

Writer: Heather McSharry, PhD
Heather McSharry, PhD
14 minutes ago
18 min read

Summary

In 2009, scientists described a strange new yeast isolated from a patient in Japan. Within a few years, Candida auris was appearing in healthcare facilities across the world—but genomic sequencing revealed that this wasn't simply one pathogen spreading from a single point of origin. Genetically distinct lineages appeared to have emerged independently in different regions at roughly the same time. In this episode, we explore the still-unsolved mystery of C. auris emergence, its newly revised name, Candidozyma auris, and the unusual combination of traits that has made it such a formidable healthcare-associated pathogen: persistent skin colonization, survival on surfaces, environmental transmission, and resistance to multiple antifungal drugs. Ahead of Fungal Disease Awareness Week, we also look at what C. auris can teach us about the larger and often overlooked threat of emerging fungal disease.

Listen here or scroll down to read full episode.



Full Episode

Something strange is happening

In 2009, researchers in Japan described a yeast that had been isolated a few years earlier from the external ear canal of a 70-year-old Japanese woman at the Tokyo Metropolitan Geriatric Hospital. It was something they hadn't seen before: a new species of Candida. They named it Candida auris. Auris means "ear." At the time, there wasn't much reason to think this obscure little yeast would become a global public-health problem.

But then it started turning up in other places. Different hospitals, different patients, different continents. And some of those patients were seriously ill. The obvious explanation was that Candida auris had emerged somewhere, found its way into healthcare systems, and started spreading around the world. But that's not what they found.

And beyond that strange provenance, Candida auris turned out to have an unusual collection of traits that make it especially well-suited to the modern healthcare system. It can colonize patients without making them sick. It can spread between people. It can contaminate rooms and medical equipment. It can survive on surfaces for long periods of time. Some disinfectants don't reliably kill it. And some strains are resistant to the antifungals we have. Once Candida auris gets established in a healthcare facility, getting rid of it is ridiculously difficult.

So this week, ahead of Fungal Disease Awareness Week, we're going to talk about this strange and not so...fungi....

This is Every Clade, Everywhere, All at Once: The Strange Emergence of Candida Auris

MEET CANDIDA AURIS

Before we get to the mystery of where Candida auris came from, we need to talk about what it actually is. And before we do that, there's one bit of fungal housekeeping we should take care of.

If you follow fungal taxonomy closely, you may know that Candida auris actually has a new name. In 2024, a major taxonomic revision moved the species out of the genus Candida and into a newly established genus, Candidozyma. So its current taxonomic name is Candidozyma auris. You'll still hear me call it Candida auris. That's the name under which the organism became known, it's still widely used in medicine and public health, and CDC continues to use Candida auris, or C. auris, while acknowledging the new classification. So: Candidozyma auris to the taxonomists, Candida auris to much of the healthcare world, and C. auris for the rest of this episode. unless I accidentally say its whole name. Could happen.

And despite that taxonomic reshuffling, understanding the organisms we've traditionally called Candida gives us a useful place to start.

These are yeasts—a group of single-celled fungi—and several species historically classified as Candida commonly live on or in the human body. Probably the best-known example is Candida albicans, which remains in the genus Candida. It can be found in places like the mouth, gastrointestinal tract, and reproductive tract, and most of the time its presence is fine. It can live with us without causing disease.

But under the right circumstances, Candida species can cause infections. Candida albicans can cause familiar conditions like oral thrush and vaginal yeast infections. But yeasts in this group can also cause something much more serious. If they enter the bloodstream or spread into internal organs, they can cause invasive disease.

And invasive fungal infections occur disproportionately in people who are already medically vulnerable. People who are critically ill, immunocompromised, recovering from major surgery, or who have devices like central venous catheters that can give microbes a route into parts of the body where they don't belong. So healthcare systems were dealing with invasive infections caused by Candida and related yeasts before anyone knew C. auris existed.

But the organism we came to know as C. auris didn't behave quite like the yeasts clinicians were used to. Even recognizing it was a problem.

When C. auris first began appearing in clinical laboratories, some of the standard biochemical systems used to identify yeasts didn't know what to do with it. Depending on the test being used, C. auris could be misidentified as another species.

Which means the first time you recognize something isn't necessarily the first time it was there.

The Japanese isolate described in 2009 gave Candida auris its familiar name. And once scientists knew what they were looking for, they could go back and look for it. And they found it.

In South Korea, researchers identified C. auris in stored clinical isolates collected years earlier, including one dating back to 1996. So 2009 wasn't really the beginning of the story. It was the moment we realized there was a story.

And that story was getting stranger, because this yeast had another characteristic that distinguished it from many of the yeasts clinicians were used to seeing. C. auris is very good at colonizing skin.

And that's not great. Because if a fungus primarily lives inside your GI tract, spreading it through a hospital requires a specific chain of events. But if it's living on your skin, there are a lot more opportunities for it to spread. A patient doesn't need to have an active C. auris infection to carry the organism on their skin. They can be colonized and feel perfectly fine.

And from there, it can enter the patient's environment anB hang out on surfaces. Like a bedrail, a bedside table, a piece of medical equipment, or any surface someone touches. Unlike many pathogens that quickly lose viability once they're outside the human body, C. auris can persist in the healthcare environment. This guy isn't just a fungal infection that happens to happen in hospitals. It can behave like a healthcare-associated pathogen. It can colonize patients, contaminate their surroundings, move through healthcare environments, reach other vulnerable patients, and remain there long enough to make infection control extremely difficult.

THE FUNGUS THAT APPEARED AROUND THE WORLD

By the middle of the 2010s, C. auris had been reported in healthcare facilities across several continents. In 2016, researchers used whole-genome sequencing to compare isolates from patients in Pakistan, India, South Africa, and Venezuela, along with the original Japanese isolate. The results revealed something weird. Within individual geographic regions, isolates were highly related. But between regions, the differences were enormous. The major populations were separated by tens of thousands of genetic variants.

In other words, this did not look like one recently emerged strain spreading from country to country. The organisms circulating in South Asia formed one genetically distinct group. Those from South Africa formed another. And it was the same in other regions. So, the genomic pattern was consistent with several genetically distinct populations becoming recognized as human pathogens independently in different regions. And they seemed to have done it within a surprisingly narrow period of time. And the strains in the different regions became known as the major C. auris clades, and additional clades have since been identified.

Now, within those clades, C. auris absolutely can spread. A strain can move between patients, between healthcare facilities, and eventually between countries and continents. International travel and patient movement are part of the modern C. auris story. But that doesn't explain the beginning of it.

There are important caveats here. We don't know exactly when each lineage began infecting humans, and as we've seen already, the dates when C. auris was first recognized are not necessarily the dates it first appeared. So we should be careful about saying that C. auris suddenly appeared everywhere at exactly the same moment.

But the broader pattern holds. Multiple genetically distinct lineages of the same species emerged as healthcare-associated human pathogens in geographically separated regions over a relatively short evolutionary timescale. Which brings us back to the question from the beginning of this episode: why? Well, we don't know.

There are several hypotheses, and they aren't necessarily mutually exclusive. One possibility involves antifungal selection pressure. Humans use antifungal compounds not only in medicine but extensively in agriculture, where azole fungicides are used to protect crops. Environmental exposure to antifungal compounds can create selection pressure favoring fungi that are better able to survive them. We've seen this with other medically important fungi like Aspergillus, so it's being investigated.

Another possibility under consideration is temperature. There are millions of fungal species in the environment, but relatively few are capable of causing serious disease in healthy mammals. One reason is that we're warm. Our body temperature creates what researchers sometimes describe as a thermal barrier. Many environmental fungi just don't grow well at mammalian temperatures.

C. auris, however, tolerates heat very well.

That observation led microbiologists to propose a provocative hypothesis. As the planet warms, environmental fungi are being exposed to higher temperatures. Over time, that could select for fungi capable of growing at temperatures that once restricted them. And if an environmental fungus gradually becomes more thermotolerant, the temperature barrier protecting mammals weakens.

So, could Candida auris be an early example of a fungus that adapted to a warming environment and, in the process, became better equipped to live at human body temperature?

Maybe.

But this is where we distinguish between an interesting hypothesis and an established explanation. We don't have evidence showing that climate change caused the emergence of Candida auris. We don't even know with certainty what ecological niche the ancestors of the major clinical lineages occupied before they became associated with humans. The climate hypothesis offers one possible explanation for a peculiar pattern, and researchers continue to investigate it, but at this point it isn't the answer to the mystery.

And the mystery has become even more interesting as scientists have found C. auris outside hospitals. In 2021, researchers reported C. auris from a natural environment on the Andaman Islands in the Indian Ocean, including isolates associated with a salt marsh and sandy beach. Since then, environmental investigations have added to the possibility that this organism—or close relatives of the populations now circulating in healthcare systems—may have had an environmental existence we just hadn't been looking for.

For now, we have several pieces of the puzzle: genetically distinct lineages, unusual tolerance for heat and salt, widespread antifungal resistance, an emerging environmental story, and multiple populations that somehow became very successful at colonizing humans. But we still don't know what brought all of those pieces together.

But once Candida auris entered healthcare environments, the next part of its story becomes much easier to understand. Because it had arrived in a place filled with exactly the kinds of hosts and opportunities it could exploit.

THE PERFECT ENVIRONMENT

Hospitals are designed to make sick people better. But from the perspective of a microorganism, they are also unusual ecosystems.

They bring large numbers of people together in one place, including people whose defenses against infection are already compromised. There are patients receiving chemotherapy or immunosuppressive medications, patients recovering from surgery, premature infants, people in intensive care, and people whose illnesses have kept them in healthcare facilities for weeks or months. There are central lines entering blood vessels, urinary catheters, feeding tubes, breathing tubes, surgical wounds, and countless other potential routes around the physical barriers that normally keep microorganisms out of vulnerable parts of the body.

There are also healthcare workers moving between patients, equipment moving between rooms, and patients moving between wards, hospitals, long-term acute-care hospitals, nursing facilities, and other parts of an interconnected healthcare system.

For most healthy people, Candida auris poses very little risk. It isn't a fungus you should be worried about encountering while you're walking through the grocery store or sitting next to someone at a restaurant. The people at greatest risk of developing invasive C. auris infections tend to already be medically vulnerable.

And C. auris's ability to colonize skin complicates things.

If C. auris is detected in someone's bloodstream, that's an infection and it requires treatment. But if a swab finds C. auris living on someone's skin and that person has no symptoms, antifungal treatment isn't generally recommended just to eliminate the colonization. We don't currently have an established treatment that reliably clears C. auris from the body, and people can remain colonized for long periods of time.

That means someone can recover from whatever originally brought them into the hospital and still carry C. auris. They might leave an intensive-care unit and move to another hospital ward. Or be discharged to a long-term-care facility. Later, they might be admitted to another hospital. Unless the receiving facility knows about the colonization and takes appropriate infection-control precautions, C. auris can move with them.

And this isn't only theoretical. Healthcare networks matter enormously in the epidemiology of C. auris. Public-health investigators don't just look at individual patients and individual hospitals. They look at the movement of patients between facilities, because an outbreak in one facility can become part of a much larger regional transmission network.

And one of the most frustrating infection-control problems healthcare facilities have encountered is that C auris can remain even after surfaces are cleaned. It can persist on surfaces for weeks and under some conditions much longer. It can contaminate reusable medical equipment. And some disinfectants commonly used against other pathogens don't work well against it.

That means that controlling an outbreak requires:

  • Finding the people who are colonized.

  • Understanding where they've been.

  • Considering where they're going.

  • And dealing with the environment they left behind.

And C. auris can also form communities called biofilms, which complicates things even more. A biofilm is basically a structured community of microorganisms attached to a surface and embedded in material the organisms themselves produce. If you've ever felt the slippery coating that develops on something left underwater, you've encountered the basic concept. Dental plaque is another familiar example.

Organisms living in a biofilm can behave differently from free-floating cells and the surrounding matrix makes them harder to reach. Their metabolism can change and the community can become more tolerant of antimicrobial treatment and environmental stress.

C. auris is capable of forming biofilms, although the strength and characteristics of those biofilms vary among isolates and experimental conditions. But combined with its ability to tolerate drying and persist on surfaces, biofilm formation adds another layer to the problem of eliminating it from healthcare environments.

Then there is the disinfectant problem.

Some disinfectants routinely used in healthcare settings—those relying solely on quaternary ammonium compounds—may not be sufficiently effective against C. auris. CDC therefore recommends products registered by the Environmental Protection Agency specifically for use against C. auris. When those aren't available, CDC recommends certain products effective against Clostridioides difficile spores.

That comparison tells us something about the level of environmental control we're talking about. This isn't just "wipe the counter and move

WHEN THE DRUGS DON'T WORK

Let's talk about antifungals. Compared with bacteria, our antifungal medicine cabinet is surprisingly small.

That's partly because fungi are actually much more like us than bacteria are.

Bacteria are prokaryotes. Their cells differ from ours in fundamental ways, which gives us a number of biological targets for antibiotics. We can interfere with bacterial cell walls, bacterial ribosomes, DNA replication, metabolic pathways, and other processes while trying to minimize damage to human cells.

Fungi are eukaryotes. So are we. Our cells share much of the same basic cellular machinery. That makes finding something you can target in a fungal cell without also damaging the patient a much more difficult pharmacological problem.

For serious invasive fungal infections, clinicians have to depend on a relatively limited number of antifungal drug classes. Three are particularly important to the Candida auris story: the azoles, the polyenes, and the echinocandins.

The azoles include drugs such as fluconazole. They interfere with the production of ergosterol, an important component of fungal cell membranes. Fluconazole has been used extensively against Candida infections because it's generally well tolerated and can be given orally or intravenously.

Then there are the polyenes, most famously amphotericin B. Amphotericin B also targets fungal membranes, but in a different way. It binds to ergosterol and disrupts membrane function. It's a really important antifungal drug, but it also has a reputation earned over decades of clinical use for potentially serious toxicity, especially to the kidneys. Modern formulations have improved its tolerability, but this is still not a drug clinicians use casually.

And then there are the echinocandins. Drugs like micafungin, caspofungin, and anidulafungin interfere with synthesis of an important component of the fungal cell wall. Human cells don't have that cell wall, which gives echinocandins a useful selective target.

For most adults with invasive Candida auris infection, an echinocandin is the recommended initial treatment. And that's why resistance to this class is worrying.

Antifungal resistance is one of the characteristics that first made C. auris stand out. And fluconazole resistance is very common among U.S. isolates. A substantial minority have also been resistant to amphotericin B. Echinocandin resistance has historically been less common, but it occurs and resistant isolates have become an increasingly important surveillance concern.

Some C. auris isolates are resistant to drugs from two antifungal classes. And isolates with resistance or markedly reduced susceptibility to all three major antifungal classes have been reported. And resistance can emerge during treatment.

Antifungal therapy itself creates selection pressure. Within a population of fungi, cells carrying mutations that help them survive a drug have an enormous advantage once that drug is introduced. The susceptible organisms die or stop growing. The resistant population survives.

With echinocandins, mutations in genes associated with the drug's target—particularly FKS1—can reduce susceptibility. So a patient may begin treatment with an isolate that appears susceptible and later harbor a resistant population.

This creates a difficult and simultaneous clinical and public-health problem. For the patient, resistance can mean fewer effective treatment options. For the hospital, that resistant organism may also be capable of colonizing skin, contaminating surfaces, and spreading to other vulnerable patients. And for public health, every successful resistant lineage creates another opportunity for resistance to become established in the healthcare network.

WHO ACTUALLY NEEDS TO WORRY ABOUT CANDIDA AURIS?

Healthy people generally aren't at risk of developing C. auris infections but when someone vulnerable does develope invasive C. auris infection, the consequences can be serious. But describing C. auris as having a mortality rate of 30 or 40 or even 60 percent needs context.

Many patients who develop invasive C. auris infections have severe underlying illnesses. Some would have had a substantial risk of death even without the fungal infection. That doesn't mean C. auris isn't dangerous—it absolutely can contribute to or cause fatal disease.

And C. auris isn't the only fungal pathogen we're worried about. And our defenses against fungi are much thinner than most people realize.

THE FUNGAL PROBLEM

Fungi often occupy a strange space in the public imagination somewhere between athlete's foot and mold growing behind the bathroom wall. But fungal diseases can be devastating. Cryptococcus can cause life-threatening meningitis, particularly in people with advanced HIV. Aspergillus can cause invasive disease in immunocompromised patients and has become a major focus of concern because of antifungal resistance.

Coccidioides—the fungus responsible for Valley fever—lives in soil in parts of the Americas and can cause disease when its spores become airborne and are inhaled. Histoplasma can cause severe disseminated infections. And Candida species remain important causes of healthcare-associated bloodstream infections.

Yet compared with our antibacterial arsenal, our options for treating serious fungal infections are seriously imited.

That is part of why the World Health Organization created its first fungal priority pathogens list in 2022. The list was intended to draw attention to fungi posing significant threats to human health and to encourage better surveillance, diagnostics, research, and drug development.

Candida auris was placed in the critical priority group. And it's easy to understand why. Once it becomes established in a healthcare network, eliminating transmission can be extraordinarily difficult. But there's another reason I think Candida auris matters. It reminds us how much we still don't know about where new fungal diseases come from.

For viruses, we're accustomed to talking about emergence. We talk about animal reservoirs and spillover. We sequence viral genomes. We reconstruct transmission chains. We ask when a virus crossed into humans and what ecological conditions made that possible. We don't always think about fungi that way. But fungi are everywhere.

They're in soil, water, plants, animals, buildings, dust, and air. They occupy ecosystems we understand well and ecosystems we've barely sampled. They are constantly responding to temperature, moisture, competition, agricultural chemicals, human land use, and every other environmental pressure acting on the microbial world.

Most of those fungi will never become human pathogens. Our immune systems, our body temperature, and the basic biology of the fungi themselves create formidable barriers. But barriers aren't necessarily permanent. Organisms evolve. Environments change. Human behavior changes. Healthcare systems change. And occasionally, something ends up on the other side of a boundary where we didn't expect to find it.

And underneath all of the very practical public-health problems of C. Auris is an unresolved story of emergence. Something changed. Or perhaps several things changed. And in different parts of the world, different populations of the same obscure fungus found their way into the same new ecological niche. Us.

CLOSING

And that is where we're going to leave Candida auris—with a fungus we didn't know existed until relatively recently, a global emergence we still can't completely explain, and a healthcare pathogen that has forced us to pay much closer attention to the fungal world.

The timing for this episode is intentional. Next week is Fungal Disease Awareness Week, an annual effort to bring more attention to fungal diseases, the people affected by them, and the need for better recognition, diagnosis, treatment, and prevention. Fungi don't always get the same attention as viruses and bacteria, but as Candida auris demonstrates, they are very much part of the emerging infectious-disease landscape.

And I think that's what makes this story so fascinating. C. auris is important because it shows us what emergence can look like when we aren't watching—when an organism is difficult to identify, when its environmental history is poorly understood, and when we only begin to recognize the pattern after it has already found a place where it can thrive.

It's worth remembering that the microbial world is much larger than the handful of pathogens that usually make the headlines. Sometimes the most important emerging threat is the one we haven't noticed yet.

If you know someone who would enjoy this episode, please send it their way. Following or subscribing to the show—and sharing an episode with someone else—is one of the easiest ways to help more people find Infectious Dose.

I'm Heather McSharry. Thanks for listening, and I'll see you next week.










Annotated Citations

Each citation is annotated to explain how the source connects to the episode and to help listeners who want to explore the science in greater depth.

Accessing the literature: Whenever possible, I've linked directly to free full-text articles and books that are legally available online. For subscription-only journal articles, many researchers are happy to share a personal copy of their work if you contact the corresponding author. For books, I've included links to free online lending copies or library catalogs when available. If a title isn't freely available online, I've linked WorldCat to locate it at a nearby library or you can ask your local library about interlibrary loans.

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