Cadida auris, is a fugus that is “pretty much unbeatable and difficult to identify,” and which the CDC says causes nearly 50% of patients to die within 90 days. It has an overall mortality rate of 30%-60%. If you get this thing, it is very likely that you will die before they have even figured out what you have. And it’s so persistent that after you die, the hospital has to tear out the ceiling tiles to fully rid the hospital of the fungus:

Tests showed it was everywhere in his room, so invasive that the hospital needed special cleaning equipment and had to rip out some of the ceiling and floor tiles to eradicate it.

“Everything was positive — the walls, the bed, the doors, the curtains, the phones, the sink, the whiteboard, the poles, the pump,” said Dr. Scott Lorin, the hospital’s president. “The mattress, the bed rails, the canister holes, the window shades, the ceiling, everything in the room was positive.”


That last part about tearing out the ceiling tiles is what made me rewind the article as I listened to it back in April. Hospitals have had to shut down entire wings and even close entire hospitals because of C. auris. The reason you haven’t heard of it is because hospitals are reluctant to discuss C. auris and are fighting to keep infections secret because they are scared that no one will want to go to the hospital if this fungal invasion is present. The New York Times has a great series of articles on C. auris, and they go into the secrecy, and the reason you have likely not heard of it:

From this gem of an observation grew one of the most curious aspects of our series: The rise in resistant bugs is cloaked in widespread and chronic secrecy.

As our reporting continued, we discovered it was common for hospitals, doctors and public health agencies to clam up when it came to talking about their troubles with resistant bugs, though they widely acknowledged the existence of the problem and even encouraged our efforts.

We came to realize that the secrecy surrounding C. auris was a big part of the story. A doctor in Spain wrote me that the hospital didn’t want bad press by seeming to be a hotbed of the fungus. I got the same message from a doctor in England. One doctor in New York told me that patients, and their families, don’t like being associated with the illness, as if they had a scarlet letter — “A” for auris.

Even with the secrecy, I knew I would hear about C. auris again some time soon. Since its discovery in 2009 on a Japanese man’s ear (named Auris from the Latin for “ear”), it reemerged in humans again a few times between 2012 and 2015, and what was remarkable is that it happened pretty much simultaneously on three separate continents. The worst part was that all three of the strains were genetically different. So not only is this fungi resilient and spreading, but there are actually multiple strains with different evolutionary lineages that can infect humans (pathogenic). That tells us this is something systemic is going on, not just something locally, and that this is a global problem.

This also isn’t one of those cases of a pathogen emerging from thawing permafrost. Those are an entirely different nightmare of a problem, an example of which happened during a heatwave in Sibera in 2016, when a herd of reindeer that had died from anthrax decades earlier and frozen under the tundra, thawed out and transmitted the bacteria to humans. Ultimately, they had to kill 250,000 reindeer to halt the spread. While that is of great concern and also keeps me up at night, it is not even in the same league as the systemic problem of fungus being more able to survive inside humans.

The first hypothesis I heard, as proposed in the in NYT article on the secrecy at hospitals, stated that the cause might be from the increased use of fungicides to treat crops. A man in Netherlands died in 2005 from a fungus called Aspergillus that was resistant to anti-fungal drug itraconazole was unable to prevent the infection of a man who in the. That drug happens to be pretty much the exact same thing as a pesticide class called Azoles. The graphic below shows the mechanisms of action that fungi can use to become resistant to fungicides.

The theory had been that the excessive spraying of fungicides on plants, such as potatoes, beans, wheat, tomatoes, etc caused and increase in drug resistance. The theory, as the head of the fungal branch at the C.D.C, Dr. Chiller, stated to the NYT, went something like this:

C. auris may have benefited from the heavy use of fungicides… C. auris actually has existed for thousands of years, hidden in the world’s crevices, a not particularly aggressive bug. But as azoles began destroying more prevalent fungi, an opportunity arrived for C. auris to enter the breach, a germ that had the ability to readily resist fungicides now suitable for a world in which fungi less able to resist are under attack.

While this theory is in some ways plausible for other strains, other research points to a different, much more worrying process for the evolution of C. auris and other salt marsh fungi. The new study suggests that Climate Change may actually be to blame. By becoming more able to counteract the effects of a warmer ecosystem, fungi are now able to overcome one of the major defense system of our body, a high average body temperature and even warmer temperatures when we have a fever.

Check out the chart below of the thermal tolerance of 40,802 fungal strains from 144 genera. Most of them cannot grow at mammalian temperatures and therefore, automatically gives us resistance. The normal human body is 36.5-37.5 °C (97.7-99.5 °F), but during a fever goes up to 37.5-38.3 °C (99.5-100.9 °F) and higher. In the chart below, the “squares” show 49 mammal core temperatures. The higher position of the “square” on the chart equates to a greater percentage of mammals whose bodies are in that temperature range. You can see that towards the right of the graph, around 35 degrees °C, fungi can no longer easily survive. It has been posited that this is not a coincidence, and is known as the “thermal exclusionary zone” and, as will be discussed below, may have even been the adaption that allowed mammals to come to dominate the planet in the face of fungal infections.

While the theory on the increased resistant of fungi to pesticides holds some validity, in this case, it appears something much more sinister and foreboding is at play. The theory doesn’t make complete sense in this case because C. auris appears to have emerged independently on three continents simultaneously: the Indian subcontinent, Venezuela, and South Africa.Further, the emergence of azole-resistant Candida began long before the appearance of C. auris and there appears to be no correlation to the emergence of the azole-resistant Aspergillus that was mentioned above. In addition, simply acquiring drug resistance, while making the fungi harder to kill, does not necessarily make it evolve to become pathogenic. Normally, a fungi would be known as a pathogen, then treated, then it would evolve drug resistance, instead of acquiring drug resistance from agricultural fungicide use first, then somehow evolving to become a pathogen.

Something else had to be at play then and a new paper titled “On the Emergence of Candida auris: Climate Change, Azoles, Swamps, and Birds,” posits that Candida auris’ rise is the “first example of a new fungal disease emerging from climate change.Think about that chart above that shows fungi unable to survive at higher temperatures. As the Earth becomes warmer, the fungi are evolving to survive at these higher temperatures. Those higher temperatures of the planet are now getting closer to and in some places surpassing the temperature of the human body (37.5 °C), essential threatening our body’s fungal immunity and closing our “thermal restriction zone” that prevents us from being infected.

“[A]s the climate has gotten warmer, some of these organisms, including Candida auris, have adapted to the higher temperature, and as they adapt, they break through human’s protective temperatures”

Co-author of the new study, Dr. Arturo Casadevall, chairman of molecular microbiology and immunology at Johns Hopkins University, said the above, and in his paper. I personally was unaware how strongly the effects of our warmer bodies was on preventing fungal infections until doing the research for this article.

In fact, there is an entire body of evidence on how the “thermal exclusionary zone” allowed mammals to surpass dinosaurs as the dominant species on Earth! The theory is called the “Fungal Filter,” and states that as Earth transitioned from the Cretaceous to the Tertiary period, a time known as the K-T boundary, that mammals became the dominant earth land form due to our body’s ability to resist fungus. The theory proposes that after the catastrophic event at the end of the Cretaceous period, when a massive asteroid hit Earth, photosynthesis was inhibited for at least 6 months and nearly all plants died, turning Earth into a “massive compost” where fungi thrived. Dinosaurs are massive animals and as such require lots of food to keep up their body temperatures. As they began to starve, they became cooler and were immunologically impaired, leading to them being unable to fend off infections from the now abundant fungi. The death of the dinosaurs from fungi, while mammals were selected for due to high-body temperatures and the so called thermal exclusion zone, allowed our ancestors us to inherit the earth.

To follow up on this theory, researchers point to the existence of fungal infections in mammals that are opportunistic, in both humans with compromised immune systems and in bats that lower their body temperatures during hibernation. Humans with HIV have high incidences of fungal infections such as oral Candida alibcans (candidiasis). Bats are susceptible to White-Nose syndrome:

“The white-nose syndrome in bats occurs during their hibernation process, when their temperature drops. The thermal restriction zone that protects mammals is the difference between their high basal temperatures and the environmental temperatures. Human-induced climate change is anticipated to warm Earth by several degrees in the 21st century, which will reduce the magnitude of the gradient between ambient temperatures and mammalian basal temperatures. Consequently, there is concern that higher ambient temperatures will lead to the selection of fungal lineages to become more thermally tolerant,such that they can breach the mammalian thermal restriction zone.

The really bad news here is that even if we don’t have lower body temperatures or compromised immune systems, fungi have been shown in directed evolution studies to be able to fairly quickly adapt to higher temperatures through a process called thermal selection. As cities are hotter than the surrounding areas due to the “heat island effect,” by comparing the same species of fungi in both in rural and city locations, scientists were able to clearly demonstrate fungal thermal selection, with the urban strains being more resilient to higher temperatures:

So knowing that warmer climatic conditions can cause the evolutionary selection for fungi that can withstand warm temperatures, Casadevall and his group compared the “thermal susceptibility” of C. auris to some of its close relatives and found that the majority of them were not yet tolerant to mammalian temperatures.  That is good news, but as the study above shows, thermal selection of fungus can happen in a fairly short time period. In their reserach, they saw that Candida auris can survive up at up to 42 °C.

In the chart below, the color green represents temperatures that a fungus can stay alive at and red where it is cannot. I scaled the image from above so that you can see the temperature at which fungi can no longer survive compared against the body temperature of mammals. Any place there is the color green, to the right side of the black line at 37°C, is a type of fungus that could theoretically stay alive inside the human body. The bacteria all the way at the bottom, found in a forest mangrove can stay alive all the way up to 45°C (113°F), meaning even the highest fever you can have wouldn’t be able to kill it, and would probably kill you first.

That D. ranongensis strain all the way on the bottom that stays alive at 45°C tells us something about C. auris because it is theorized that it also comes from a marsh environment. In those areas, there are high temperature and high salinity, which can add it’s resilience. The paper gives some more details on C. auris:

C. aurisis an ascomycetous yeast and a close relative of the Candida haemulonii species complex, which includes species occasionally pathogenic in humans and animals and demonstrates a high level of baseline antifungal drug resistance. This phylogenetic connection may explain its low susceptibility to antifungal agents and the possession of virulence attributes that confer it with pathogenic potential.

They also note that because the first case of C. auris came from a human ear, that tells us that it may be in a transition period to being able to live inside our bodies and that its “thermotolerance” is newly acquired. The outside of our body is cooler than the inside and so, we may be on the cusp of this fungi’s thermal adaption to be able to fully survive inside of us, as other candida strains are able to.

So you can see it for yourself, here is where the reserachers make the formal proposal that “Candida auris is the first example of a pathogenic fungus emerging from human-induced global warming:”

With this background, we propose the hypothesis that Candida auris is the first example of a new pathogenic fungus emerging from human-induced global warming. We posit that prior to its recognition as a human pathogen, C. auris was an environmental fungus. The fact that C. auris fails to grow anaerobically, along with the fact that it is typically detected on cooler skin sites but not in the gut, supports the notion that C. auris was an environmental fungus, until recently…

Candida albicans is a different strain of Candida that is drug-resistant and pathogenic to humans and is typically found in the stomach. It is moves through the human body, some is being released by humans through our sewer systems which empty into wetlands and marshes. The marshes are serving as natural reservoirs of C. albicans. Fungi have a powerful evolutionary mechanism that gives them the ability to transfer DNA through plasmid transfer to help out nearby strains. A DNA analsysis for C. auris showed that it had the same virulence attributes of the human pathogenic strain C. albicans, even though it doesn’t share 99.5% of the rest of its genome. Again, C. auris is completely different from the C. alibcans with the “probability that these species belong to the same species or same subspecies [being] 0 as indicated by logistic regression of DNA-DNA hybridization.”

So the danger is that in the wild, various fungi can share the genetic material that provides fungicidal resistance. As the study on plasmid transfers between yeasts states in its conclusion, we aren’t even sure how they do this:

Although sexual activity between C. glabrata and S. cerevisiae cells has not been observed previously, we observed a relatively high frequency of transfer of genetic material between these yeast species. The mechanism(s) for this transfer is not clear… The transfer observed could allow the spread of virulence factors and resistance to medical drugs even between distantly related yeast species and could probably help in the “transformation” of harmless saprophytes into potential causative agents of human infections.

So basically, fungi have methods to transfer genetic material between themselves and so other types of fungi that are resistant to our drugs. When those fungi survive and make it through our sewer systems, they can then transfer those newly acquired abilities of resistance to the fungi that have been evolving thermal tolerance and structural resiliency to the salinity in marshes, basically becoming breeding pools of superfungi.

In the past, isolated fungi superpathogens adapted to warmth may never have made it to human populations, but due to our food processes, specifically the farming and the proximity to birds, we may have given C. auris a vector to transfer to us.

Here is an overview of a proposed process, followed by a graphic summarizing how the researchers suggest the spread of C. auris is connected to global warming and to our global food supply:

  1. As a first step, its emergence might have been linked to global warming (including climatic oscillations) effects on wetlands, and its enrichment in that ecological niche was the result of C. auris’s combined thermal tolerance and salinity tolerance.
  2. . Alternatively, the effect of higher UV radiation in combination with global warming might have contributed to mutagenic events that resulted in the suddenly increased fitness of a saprobe for survival in a host, via melanin- or non-melanin-dependent processes.
  3. C. auris’s jump from an environmental fungus to a fungus capable of transmission to, and pathogenic for, humans might have had an intermediate host, specifically an avian host, as fungi that can grow at 40 or 42°C can infect avian fauna. Of note, sea birds may serve as reservoirs for indirect transmission of drug-resistant Candida species, such as C. glabrata, to humans.
  4. The uncanny ability of C auris to adapt to specific niches, first in the environmentand then in an avian host, might have led as a third step to its ultimate establishmentas a human pathogen through genetic and epigenetic switches

The paper proposes an example of a possible pathway that C. auris followed to make it to humans:

The paper ends with a summary of the issue, that due to the thermal tolerance of fungi increasing as well as human expansion into more of the planet and global interactions, we may see the emergence of many more pathogenic fungi throughout the 21st cenutry:

If anything, the direct and indirect effects of climate changes induced by an exponentially growing human population as drivers of fungal evolution should be an area of intense research in the decades to come. Widening of the geographic range of innately thermotolerant pathogenic fungi and the acquisition of virulence traits in thermotolerant nonpathogenic environmental fungi may shape the 21st century as an era of expanding fungal disease for both the fauna and flora of the planet.

A previous paper from 2010 by the main author from above and Monica Garcia-Solache, titled “Global Warming Will Bring New Fungal Diseases for Mammals” lays out the issue more directly, pointing to the concept that each 1 degree of warming reduces our thermal gradient by 5%:

Global warming means narrowing of the thermal gradient between ambient and mammalian temperatures. The current gradient is approximately 22°C, and consequently, every degree increase in the global average temperature reduces the gradient by about 5%. We hypothesize that with current global warming, the prevalence of fungal diseases will increase by the mechanisms previously discussed. As thermotolerance is more commonly found within the basidiomycetes, this group may be the major contributor of new fungal pathogens.

The red line in the above graph shows our body temperature, 37°C, which does not easily change except during fevers. Yet the planet is getting warmer and warmer, eroding our ~22°C thermal gradient. As compared with the time period from 20,000-6,500 years before now, from 1941 to 2009, the planet is warming more than 17 times faster! As humans, we are not going to evolve higher basal temperatures anytime soon, so as the planet warms we are going to be at more and more risk of pathogenic fungi by that closing of the thermal gradient.

Who would have thought that increasing temperatures alone would make us more susceptible to fungal infection? Prior to reading the articles this post is based on, I had never even heard of this as a risk to humanity. But as we increase the temperature, we are seriously increasing our chances for all sorts of devastating risks we may not even be aware of yet. Regarding the fungi evolving pathogenic properties and thermotolerance, the even scarier part is that we do not have many antifungals drugs available. And we especially do not have many antifungals that can work against resistant strains like C. auris:

The risk from newly emerged fungal pathogens could be magnified by the fact that there are few antifungal drugs available and no licensed vaccines. An increased emphasis on developing vaccines with efficacy against broad fungal classes could help ameliorate new threats from the environment.

Basically, we have no real tools to fight these fungi once they evolve, so the best thing we can do right now is work to keep the temperature of the planet down to stop their further evolution. This is not my personal alarmism (although I am personally alarmed), the scientists themselves are saying it: “This information could…add urgency to ongoing efforts to slow global warming.” If every other reason wasn’t enough to slow global warming, you can now add drug-resistant pathogenic fungi to the list of top concerns.

The medical establishment does not currently have any solution to stopping Candida auris, and from everything I gleaned in reading every study linked in this article and reading between the lines of those, there are no solutions coming soon. Our abilities in this area are pretty pathetic. In fact, we have barely even developed the technology and techniques to identify C. auris in the first place, so I doubt we will have any real solutions to stop it once it spreads…

The threat from C. auris reminds us why EVERY DEGREE OF WARMING MATTERS! The next time someone tries to belittles the difference between a 3°C vs 1.5°C warmer planet, you now have a new statistic in your arsenal: We will lose 15% vs 7.5% of our protection against invasive and deadly fungal pathogens. With the increasing spread of C. auris, just as I knew when I saw the NYT series on it that that would not be the last I heard of C. auris, this will not be the last time you hear of it either.

What can you do?

  • Reach out to your elected representatives and let them know that we really are in a climate emergency and that these kinds of unknown unknowns can pose a danger to society from even slightly increased temperatures. Tell them how scared you are (or at least about how scared I am).
  • Don’t vote for politicians who don’t take a strong stance on stopping climate change AND reversing it with carbon dioxide removal (CDR) techniques. We are on target to shoot past of 1.5°C carbon budget, so CDR may be our only hope at this point to slow and potentially reverse the warming of the planet, thereby stopping the further evolution of thermally adapted funga pathogens.
  • Spread awareness of the lesser-known side-effects of climate change and why EVERY DEGREE OF WARMING MATTERS!

If you are in the medical field, please work on developing anti-fungal vaccines. If you are in the federal government or a funding agency, please provide funding for said antifungal vaccine development, as well as new anti-fungal drugs, because as of now we have no way to stop the spread of C. auris, and it is real.

As of July 12th, 2019, the CDC has identified  715 cases of C. auris infections in the United States.

Paper this blog post is based on linking C. auris to climate change: On the Emergence of Candida auris: Climate Change, Azoles, Swamps, and Birdshttps://mbio.asm.org/content/10/4/e01397-19

Worldwide emergence of resistance to antifungal drugs challenges human health and food security –https://science.sciencemag.org/content/360/6390/739

Culture of Secrecy Shields Hospitals With Outbreaks of Drug-Resistant Infections https://www.nytimes.com/2019/04/08/health/candida-auris-hospitals.html

Fungal Filter On Dinosaurs to Mammals https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1002808

DNA sequencing of Candida auris https://bmcgenomics.biomedcentral.com/track/pdf/10.1186/s12864-015-1863-z




Hospital Advisory on Auris https://www.advisory.com/daily-briefing/2019/05/10/resistant-fungus

Leave a Reply