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.
If C. Auris is so fatal, then scientists better hop on the bandwagon and address this “neglected” rather powerful fungus. It thrives in hospitals, so it seems far more applicable to attribute its virulence to disinfecting techniques rather than adaptation to climate change (groan). Before any hint in that direction is made, it better be very thoroughly researched first. There is enough climate change hysteria already.
The clear ,and convincing evidence of the failure ,inept ,unprofessional and ineptitude groups of scientists and others within the faculties and institutions from which they preach their ?s holy grail as being perfectionist . than every one else .none more so than the alliances steeped within their icons about climate change or the made up other alternative global warming .yet still within so many other factors or areas of the health care system or industry .they are so obsolete and defunct to resolve or solve these deathly killers such as the number one Super Bugs .they in most cases ignore and avoid even making mention of the killer machine Super .Bugs . I thank you Trevor Merchant . Bronx . New York City . Tuesday . July , 23, 2019 at 4.16 p.m daylight savings time.
See for comparison: “A Concise Review of MicroRNA Exploring the Insights of MicroRNA Regulations in Bacterial, Viral and Metabolic Diseases” 9/9/17 and “Reduced expression of brain-enriched microRNAs in glioblastomas permits targeted regulation of a cell death gene” 9/14/11
See: “Why have microRNA biomarkers not been translated from bench to clinic?” 1/17/19 and more than 89,000 indexed publications from PubMed that mention microRNAs.
If people from other countries were as stupid as people in the countries of the Western World, President Trump would not need to change the focus of research to effects of nutrition or effects of nutrient stress and social stress on all pathology.
You may want to interview Dr. Jack Sobel at Wayne State Medical Center. He is in the department of Infectious Disease. He has studied Candida Albicans infections for his entire career and is an expert on vulvovginl candidiasis.
You may want to interview someone who has linked mating in yeasts to sexual orientation in humans via mate-choice for food energy-dependent pheromone-controlled genetic diversity in the Hutterites from the “Old” World to populations in North America and the mouse-to-human model of fixation of EDAR V370A alleles. See: “HLA and Mate Choice in Humans”
Use of fluorescent detection to determine protease activity would probably lead from the discovery of the bacteriophage that is linked to resistance, and then… to effective treatment via the anti-entropic virucidal effects of sunlight.
For example, the epigenetic effects of UV light on DNA repair via plant growth and the physiology of pheromone-controlled reproduction in yeasts have been reported in the context of the microRNA-mediated progression of cancers via the same molecular mechanisms.
Unfortunately, most researchers missed the facts from Schroedinger (1944) What is Life?
The likelihood that they will accept facts that link bacteriophages to all pathology across all kingdoms is negligible. Most are still focused on mutation-driven evolution instead of energy-dependent biophysically constrained ecological adaptations in the context of viral latency.
But see: “Virus-mediated archaeal hecatomb in the deep seafloor” and “Eukaryotic plankton diversity in the sunlit ocean” before Koonin and Krupovic formally announce their collaboration with scientific creationists from South Korea, who have linked Schrodinger’s claims to Ben Feringa’s claims via “Dynamic control of chirality and self-assembly of double-stranded helicates with light.”
This is a mindblower. I studied mycology for 3 years so understand what they’re talking about, but some new stuff here (mutations from mating fungi? wow). Oddest is that it’s never been seen anywhere except in people. I’m wondering how many people might carrying this without symptoms. Sounds like they’re just getting serious about tracking this down… could be there will be an accidental breakthrough (like with h.pylori) – standard lab practices can hinder discovery.
The problem with h.pylori is bacteriophage-induced pathology. Mutations in mating fungi are also typically biophysically constrained by the availability of food energy and the pheromone-controlled physiology of RNA-mediated sexual differentiation of all cell types in all living genera that sexually reproduce. See our section on molecular epigenetics in From Fertilization to Adult Sexual Behavior Published in: Hormones and Behaviour, 30, 333-353 (1996)
Look for a bacteriophage that can attach, kill or alter C. auris. Also, someone must be doing sequencing.
That’s what I thought would be best based on what is known about how the virus-driven degradation of messenger RNA leads to the creation of shiga toxins. If you tell others why they should do the sequencing (e.g., to link epigenetic effects of food and pheromones to viral latency) maybe someone will admit that they have done that, or that they have people who will do it before the bacteriophages kill us all.
That’s what I thought would be best based on what is known about how the virus-driven degradation of messenger RNA leads to the creation of shiga toxins.
When you tell others why they should do the sequencing (e.g., to link epigenetic effects of food and pheromones to viral latency via HERVs) maybe someone will admit that they have done that, or that they have people who will do it before the bacteriophages kill us all.
See for example: “Perspectives of Phage Therapy in Non-bacterial Infections”
Please email me updates
Come on. Let’s not blame every malady on climate change. Most likely the spread of this resistant “thing” is do to overpopulation, over medication, and lax sanitation routines. If our world population were to gradually decline to a more sustainable level, this “thing” and others which are sure to follow would likely disappear naturally.
It’s very difficult for me to not link global biogeochemical cycles of protein biosynthesis and degradation to all maladies via the virus-driven degradation of messenger RNA in all living genera. How do you do it post publication of: “Spindle-shaped viruses infect marine ammonia-oxidizing thaumarchaea” by scientific creationists in South Korea who have teamed up with Mart Krupovic and researchers from other countries?
If you’re suffering from drug resistant fungal infection, try getting into this company’s clinical trial, only treatment I’ve seen:
I have had something going on 7 years I have been to different Drs and they just won’t listen to me it started on my legs now it has took me down really bad no matter what I do it won’t leave it even has got into my gums it seems to feel like a moth or something I know that sounds crazy but really weird feeling I will think I have gotten rid of it but no it just comes back I need help about this it has took me from a normal woman to in a walker I have had a light stroke and other things .please help
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