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Faecal transplants to be offered to hundreds with antibiotic-resistant superbug | UK News

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Hundreds of people with a hard-to-treat superbug are to be offered faecal transplants to tackle their infections.

A faecal microbiota transplant (FMT) involves taking healthy bacteria “in a mixture of prepared processed stool from a healthy donor” to the intestine of another person.

The National Institute for Health and Care Excellence (Nice) says the process should be considered for patients who have had two or more treatments for Clostridium difficile (C.diff) without success.

Treating these people with gut bacteria taken from a healthy person’s poo can help restore healthy gut bacteria, Nice said.

C.diff is a type of bacteria that can cause diarrhoea, and it often affects people who have been taking antibiotics.

The bug can usually be treated with a different type of antibiotic, but it is sometimes referred to as a “superbug” due to its resistance to treatment in some instances.

Nice said clinical trials have shown FMT treatment is significantly better than antibiotics alone at resolving a stubborn C.diff infection, and treatment using this method could save the NHS thousands of pounds.

Patients may need to take fewer antibiotics and have reported a better quality of life after treatment, it added.

‘Innovative’

The FMT section can be swallowed within a pill, or it can be delivered through a tube inserted directly into the stomach through the nose, or alternatively be deposited directly into the colon, also through a tube.

Mark Chapman, interim director of medical technology at Nice, said: “There is currently a need for an effective treatment of C.diff in people who have had two or more rounds of antibiotics.

“Our committee’s recommendation of this innovative treatment will provide another tool for health professionals to use in the fight against this infection, while at the same time balancing the need to offer the best care with value for money.

“Use of this treatment will also help reduce the reliance on antibiotics and in turn reduce the chances of antimicrobial resistance, which supports NICE’s guidance on good antimicrobial stewardship.”

Study

Nice said it made its decision to push ahead with FMT after reviewing evidence from five trials of 274 adults, which showed more C.diff infections were resolved with FMT, than antibiotic treatment, in four of the trials – and there was no difference in the other.

The data also showed the treatment can resolve up to 94% of infections.

FMT can be considerably cheaper than antibiotics if given as an oral capsule – saving more than £8,000; it can save hundreds of pounds if given as a colonoscopy, but it is more expensive when given as an enema.

Nice has estimated that 450 to 500 people in England could be treated using FMT for multiple recurrences of C.diff infections each year.

It said a strict donor screening programme should be in place and that treatments should be manufactured in accordance with human medicine regulations.

All donors will be been screened in advance to ensure the stool provided is healthy and tested for a wide array of viral, bacterial and parasitic infections, which also includes screening for COVID-19.

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Antibiotic-resistant superbug found in pigs and humans: study

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Scientists studying the C. difficile superbug say that its antibiotic-resistant genes have been found in pigs and humans, meaning that not only is transmission of the bacteria possible on a wider scale, but the genes that resist antibiotics themselves might be able to spread through an animal vector to humans.

Clostridioides difficile, or C. difficile, is a bacterium that causes gut infection, inducing symptoms such as diarrhea and inflammation of the colon, and is resistant to numerous antibiotics. Some strains have genes that allow them to cause extreme damage, and it can be life-threatening, particularly in elderly patients who are receiving antibiotics for other issues.

It is also considered one of the world’s most significant antibiotic resistance threats. In 2017, C. difficile caused more than 223,000 cases, 12,800 deaths and cost US$1 billion in health-care costs in the U.S., according to the U.S. Centers for Disease Control and Prevention. A Canadian study found that between 2009 and 2015, more than 20,600 adults reported C. difficile infection developed in a health-care setting.

“Our finding of multiple and shared resistance genes indicate that C. difficile is a reservoir of antimicrobial resistance genes that can be exchanged between animals and humans”, Dr. Semeh Bejaoui, a PhD student at the University of Copenhagen and one of the authors of the study, said in a press release. “This alarming discovery suggests that resistance to antibiotics can spread more widely than previously thought, and confirms links in the resistance chain leading from farm animals to humans.”

C. difficile actually lives in many people’s intestines as part of the regular balance of the digestive system, but its growth is normally kept in check by other bacteria.

The dangerous side of C. difficile can be unlocked by a regular tool of the health-care system: antibiotics.

When a person takes antibiotics to deal with an infection, the medication destroys some of the other bacteria in the gut as well as the infection that it was targeting — and since C. difficile is resistant to antibiotics, if the balance of the intestinal system is thrown off, C. difficile can grow out of control and attack the lining of the intestines. Having recently taken antibiotics is the biggest risk factor for developing an inflammation or infection caused by C. difficile.

Researchers wanted to identify if strains of C. difficile known to have antibiotic-resisting genes as well as toxin-producing ones were present in pigs as well as humans, something that could indicate that zoonotic transmission helps C. difficile evolve into more dangerous forms and spread faster.

In the study, which is being presented this week at the European Congress of Clinical Microbiology & Infectious Diseases conference in Portugal, researchers looked at samples of C. difficile across 14 pig farms in Denmark and compared those samples to those from Danish hospital patients.

They looked at stool samples from 514 pigs collected in 2020 and 2021, and found that 54 pigs had C. difficile. They then used genetic sequencing to isolate strains that had an increased amount of toxin-producing and drug-resistant genes. All of the samples from the 54 pigs had the toxin-producing genes.

Researchers compared the results from the pigs to 934 isolates from human patients who had been struck with a C.difficile infection in that time period.

Thirteen sequence types matched between the pigs and human patients, with an animal-associated strain, ST11, being the most common. In 16 cases, the ST11 strain was identical in the humans and animals.

Out of the 54 pig samples, 38 had at least one gene resistant to antibiotics, and in general, the resistance applied to a class of antibiotics that are commonly used to treat severe bacterial infections.

Researchers believe that this indicates that the use of antibiotics in farm animals is having the unintended side effect of producing more hypervirulent strains of C. difficile which could be capable of transmitting to humans through zoonotic transmission.

“The overuse of antibiotics in human medicine and as cheap production tools on farms is undoing our ability to cure bacterial infections,” Bejaoui said.

Experts have flagged the issue of antibiotics being overused in farm animals before — in August 2021, the UN put out a joint statement with the Global Leaders Group on Antimicrobial Resistance calling for a significant reduction of antimicrobials in food production and farm animals, warning that “the world is rapidly heading towards a tipping point where the antimicrobials relied on to treat infections in humans, animals and plants will no longer be effective.”

Bejaoui added that researchers were concerned to find some strains of C. difficile had many extra genes resistant against antibiotics which already did not affect the bacterium.

“Of particular concern is the large reservoir of genes conferring resistance to aminoglycosides, a class of antibiotics to which C. difficile is intrinsically resistant – they are not needed for resistance in this species. C. difficile thus plays a role in spreading these genes to other susceptible species,” she said.

“This study provides more evidence on the evolutionary pressure connected with the use of antimicrobials in animal husbandry, which selects for dangerously resistant human pathogens. This highlights the importance of adopting a more comprehensive approach, for the management of C. difficile infection, in order to consider all possible routes of dissemination.”

One of the big limitations of the study is that while scientists found similar strains of this bacterium in both pigs and humans, they were not able to determine a direction of potential transmission — i.e., whether this bacterium can jump from animals to humans, humans to animals, or both.

“The fact that some of the strains in both human and animal isolates were identical suggests that they could be shared between groups, but until we perform deeper phylogenetic analyses we cannot determine the direction of the transmission, which could also be bidirectional, with the bacteria being continuously exchanged and expanded in the community and farms,” Bejaoui said. 

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MRSA Superbug First Developed Antibiotic Resistance to Methicillin in Hedgehogs 200 Years Ago

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Antibiotics have been responsible for saving countless over the last century. But they’ve also put us into an evolutionary arms race with harmful bacteria. As more antibiotics are used to treat bacterial infections, the bacteria itself faces more pressure to mutate into strains that can resist these antibiotics. Humans go back to the drawing board and develop more powerful antibiotics, the bacteria evolve resistance against those antibiotics, and so forth.

At least, that’s been the conventional wisdom for how antibiotic resistance develops. But a new study published in Nature on Wednesday paints a more complicated picture, showing that methicillin-resistant Staphylococcus aureus (better known as the superbug MRSA) evolved naturally 200 years ago—long before methicillin was ever introduced as a clinical antibiotic.

And the culprit responsible for MRSA might surprise you: hedgehogs. Behind those adorable faces and underneath those spiny exteriors, hedgehogs are basically living factories for producing MRSA.

Methicillin was first discovered as an antibiotic in 1959. The first reports of MRSA emerged in 1961 in the U.K. It usually takes decades for bacteria to evolve resistance to a popular antibiotic, so scientists have always been baffled by why it took less than two years for MRSA to pop up after methicillin was first introduced to the general population.

Meanwhile, it’s been known for a while that hedgehog bodies are vulnerable to fungal disease. In the last decade, there’s been a string of new research (spearheaded by Danish researcher Sophie Rasmussen) that’s shown hedgehogs in northern Europe carry both Staphylococcus aureus and a fungus called Trichophyton erinacei on their bodies. The fungus produces its own antibiotics to kill the bacteria, but some of these S. aureus strains have been able to evolve a natural resistance to those fungal antibiotics.

“This completely changed my perspective of how to look at MRSA and antibiotic resistance,” Jesper Larsen, a researcher at The State’s Serum Institute in Copenhagen and the lead author of the new study, told The Daily Beast. “It meant there must have been some selective pressures in hedgehogs that caused them to carry MRSA.”

Through nasal and skin swabs of hundreds of hedgehogs originating from wildlife rescue centers, the new study found that hedgehogs across Europe and New Zealand carry high levels of an MRSA strain called mecC-MRSA. Larsen and his team specifically found that up to 60 percent of all wild hedgehogs in Denmark and Sweden carry mecC.

Furthermore, using gene sequencing techniques that could help date the MRSA-specific mutations, the team was able to determine that mecC first emerged on hedgehogs two centuries ago—well before methicillin was first used to treat humans and farm animals.

Ultimately, the authors believe that hedgehogs began as the first reservoir for MRSA, and this explains why MRSA was so quick to spread to livestock and humans later on even when methicillin had only just been introduced.

To be clear, the authors do not discount the role clinical antibiotics may have played in helping the growth of MRSA, which leads to more than 80,000 cases and 11,000 deaths in the U.S. every year. While the World Health Organization classifies MRSA as one of 12 “priority pathogens that threaten human health,” only about 1 in every 200 MRSA infections in humans are caused by the mecC strain. It must have further evolved in order to better adapt to humans, though hedgehog strains were a fertile starting point.

Larsen cautions there should not be a huge concern that hedgehogs—domestic or wild—are going to suddenly infect us all with MRSA. “Apparently, we have been living with this problem in hedgehogs for 200 years, even before we had antibiotics,” he said. “So no, it’s not a big problem.”

But what the study does do, said Larsen, is provide new insight into understanding the current antibiotic crisis. Random mutations can appear all the time, but they only stick around when there’s pressure to keep them. In this case, hedgehogs seem to be the origin point for MRSA genes, but these antibiotics in humans have helped maintain those genes in certain S. aureus strains.

Larsen and his team are keen to know whether other interactions between antibiotic-producing fungi and bacteria are happening in other host animals as well. There’s a bit of hope these studies could lead to a breakthrough into developing a silver-bullet solution for MRSA and other superbugs—one that ends the evolutionary arms race permanently.

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Hedgehogs to Blame for a MRSA Superbug, Not Modern Antibiotics, Study Suggests

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A woman handles a hedgehog on the first day of the Great Yorkshire Show near Harrogate in northern England on July 11, 2017.
Photo: Oli Scarff/AFP (Getty Images)

The origins of a notorious bacterial superbug can be traced back to hedgehogs that lived centuries ago, new research this week suggests. The study found evidence that one particular type of methicillin-resistant Staphylococcus aureus, also known as MRSA, first emerged on the skin of hedgehogs. The bacteria likely evolved resistance in response to fungus also living on hedgehogs that naturally produced antibiotic compounds to kill off their competitors—long before humans began using antibiotic drugs to treat these infections.

MRSA is one of the most well-known examples of antibiotic resistance. The term refers to any strains of S. aureus that are resistant to beta-lactam antibiotics—a class of antibiotics that include methicillin but also many other drugs, including penicillin. S. aureus strains, including MRSA, live naturally on our skin and elsewhere, typically without causing trouble. But when these bacteria do cause illness, often among people hospitalized or in poorer health, MRSA infections can be much harder to get rid of with conventional treatments and can turn deadly.

Scientists discovered the existence of MRSA almost immediately after methicillin became the standard drug of choice for staph infections in the 1960s. But it wasn’t until the 1990s that MRSA became widely known, as rates of hospital-related cases climbed and strains spreading between people outside of hospitals began to emerge. There has been some progress in stemming the tide of MRSA within hospitals since then, though this progress may have slowed down in recent years. The Centers for Disease Control and Prevention estimates that almost 120,000 Americans contracted serious bloodstream infections of MRSA in 2017, while nearly 20,000 died as a result.

The widespread use of antibiotics in medicine and agriculture since the 1940s has fostered the emergence of drug-resistant infections, including MRSA. But a few years ago, scientists made a curious discovery: Hedgehogs living in Sweden and other European countries seemed to widely carry a form of MRSA known as mecC-MRSA. mecC-MRSA is thought to cause only a sliver of MRSA infections in humans, and while other animals have been documented to carry it, rates of colonization were much higher in these hedgehogs (around two-thirds had it). This led scientists at the time to theorize that hedgehogs have been a natural host for mecC-MRSA for at least decades.

This new research, published in Nature on Wednesday, has found genetic evidence that this timeline goes back much further. An international group of researchers from the UK, Denmark, Sweden, and elsewhere, including some of the first to document mecC-MRSA in hedgehogs and other animals, collaborated for the study. They sequenced the genomes of hedgehog MRSA strains and compared them to other S. aureus strains in order to build a likely family tree.

Near as they can tell, the lineages that first gave rise to the hedgehog-related MRSA we see today began in the 19th century, about 200 years ago. The team also found that a common fungus living on hedgehog skin, known as Trichophyton erinacei, can produce two different types of beta-lactam antibiotics. And in the lab, hedgehog MRSA strains did appear better able to survive against these antibiotics than other strains.

All told, the findings paint a picture as old as time.

“Our study suggests that it wasn’t the use of penicillin that drove the initial emergence of MRSA, it was a natural biological process. We think MRSA evolved in a battle for survival on the skin of hedgehogs, and subsequently spread to livestock and humans through direct contact,” said senior study author Ewan Harrison, a researcher at the Wellcome Sanger Institute and the University of Cambridge and a senior author of the study, in a statement from Cambridge.

mecC-MRSA infections in humans are rare and are typically mild and easily treated with other antibiotics when they do happen. So even though these bacteria may have occasionally sickened us over the past 200 years, the findings shouldn’t make us fearful of hanging out with hedgehogs, the authors say.

But they do illustrate that the world is a smaller and more connected place than we might think. Because most antibiotics we use today are derived from natural sources, this may not be the only example of important antibiotic resistance that has existed prior to the antibiotic era of medicine. And we already know that antibiotic resistance found in other animals can have serious health consequences for humans. That said, while some animals may play host to their own native superbugs, our continued overuse of antibiotics in livestock also plays a major, if not leading, role in causing this resistance.

“These results underscore the importance of taking a broad One Health perspective on antibiotic resistance that recognizes the role of natural selection in wild animals and the connectivity of natural, agricultural and human ecosystems in the evolution and spread of antibiotic-resistant pathogens,” the researchers wrote.

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Oregon reports first 3 cases of drug-resistant ‘superbug’ fungus Candida auris

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All 3 patients at Salem Hospital, first with intl. health care exposures; cases are responding to existing treatments

PORTLAND, Ore. (KTVZ) — The Oregon Health Authority said late Tuesday it is investigating an outbreak of the state’s first three cases of Candida auris, a serious fungal infection that is often resistant to multiple antifungal medicines.

The Healthcare-Associated Infections Program at the OHA Public Health Division, working with a regional public health laboratory in Seattle and Salem Hospital, have identified Candida auris in three Salem Health patients.

The first case was detected at Salem Hospital Dec. 11 in a patient who had recent international health care exposures, and confirmed Dec. 17. Candida auris has only recently appeared in the United States.

Two of the cases did not have international health care exposures, but had epidemiologic links to first case, indicating health care-associated spread of Candida auris to the second and third patients – identified Dec. 23 and Dec. 27, respectively.

The Healthcare-Associated Infections Program is leading the investigation, working with local public health authorities, local health care partners, the Centers for Disease Control and Prevention, and the regional public health laboratory to identify cases and ensure appropriate infection control measures are in place.

“Candida auris is an emerging pathogen of concern because it can cause serious infections, particularly in those with serious medical problems, and can be resistant to the antifungal drugs we have to treat it,” said Rebecca Pierce, Ph.D., Healthcare-Associated Infections Program manager. “Fortunately, the organism we’re dealing with in this outbreak appears to respond to existing treatments. Nonetheless, it’s critical that we prevent the spread of the infection.”

Jasmin Chaudhary, medical director of infection prevention at Salem Health, said the health system is taking action on a number of fronts to prevent the spread of Candida auris at Salem Hospital.

“With the COVID-19 pandemic, we have seen a rise in multi-drug resistant organisms around the world and nationwide, and Salem is not immune,” Chaudhary said. “Salem Health is working with OHA and the CDC to execute a rigorous plan, implementing aggressive eradication measures that have been shown in other hospitals to be successful in eliminating Candida auris. These include proactive steps that will assist in preemptively identifying new cases to prevent spread.”

Among the measures in effect: working with the patients’ care teams to ensure frequent and effective disinfection of the health care environment; using transmission-based precautions for those infected or colonized with Candida auris; adhering to hand hygiene protocols; and conducting effective interfacility-transfer communication about a patient’s Candida auris status when being transferred to another health care facility.

In addition, OHA and Salem Health have been coordinating to notify health care facilities that previously received transferred patients from affected units at Salem Health, and to support safe discharge of patients from Salem Health during the anticipated COVID-19 surge.

Candida auris is a type of yeast that can cause severe illness, particularly those suffering from serious medical conditions in hospitals and nursing homes. According to the CDC, patients who have been hospitalized in a health care facility for long periods, have a central venous catheter or other lines or tubes entering their body, or have weakened immune systems are at highest risk of infection and serious complications. The risk of Candida auris infection to otherwise healthy people, including health care personnel, is extremely low.

The fungus can cause serious infections, including bloodstream infections and wound infections. It also has been isolated from respiratory and urine specimens and can colonize patients’ skin. A laboratory test is needed to determine whether a patient is colonized or infected with Candida auris, but laboratories should be aware that it can be misidentified as other types of fungi and should know when to suspect Candida auris, as misidentification could delay treatment and control measures. Health care facilities that suspect they have a patient with Candida auris should contact their local public health authority immediately.

Since 2013, more than 1,150 clinical cases of Candida auris have been identified in the United States. There have never been any cases of the fungus identified in Oregon until now.

Patients who test positive or had a high-risk exposure will be contacted by Salem Health.

Visit the CDC’s Candida auris website at https://www.cdc.gov/fungal/candida-auris for more information.

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Health officials warn of fungus ‘superbug’ outbreaks in Dallas, DC

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Health officials are warning of a fungus “superbug” outbreak in Dallas and Washington, D.C., that seem to be resistant to treatment.

The Centers for Disease Control and Prevention (CDC) said Thursday there were outbreaks of the Candida auris fungus in a nursing home in D.C. and two hospitals in Dallas, The Associated Press reported.

Three cases in D.C. and two cases in Dallas were resistant to all three major classes of medication.

Both the patients in Dallas who had cases resistant to medicine died, and one patient in D.C. died from a similar case.

“This is really the first time we’ve started seeing clustering of resistance” and patients getting infected from each other, CDC medical officer Meghan Lyman said, according to the AP.

The cases were seen from January to April, and investigators found the fungus was spread from person to person.

There have been more cases since April and the outbreak is still ongoing, according to the CDC, but the cases have not been reported yet.

The fungus has been known for years, but evidence that it can spread from person to person is new. 

The Hill has reached out to the CDC for comment.



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Outbreaks of a drug-resistant superbug fungus spread in two U.S. cities, CDC reports

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Outbreaks of a drug-resistant “superbug” fungus spread among patients in hospitals and long-term care facilities in Texas and Washington, D.C., the Centers for Disease Control and Prevention reported Thursday. The fungus, Candida auris, preys on people with weakened immune systems. The CDC said evidence suggests these cases involved person-to-person transmission, which would be a first for the U.S.

The clusters in the two cities appear to be unrelated to each other, the report said. The 30-day mortality in both outbreaks combined was 30%, although other health conditions may also have played a role.

Candida auris, which was first seen in the U.S. in 2013, is “resistant to multiple anti-fungal drugs that we have, and it’s also resistant to all the things that we use to eradicate bacteria and fungal strains in the hospital,” Dr. Neeta Ogden, an internal medicine specialist, told CBS News in 2019 after health officials issued a warning about the emerging threat. 

Of 101 cases of the fungus identified in Washington, D.C., from January to April 2021, three were isolated as being resistant to all three major classes of anti-fungal medications. Those cases occurred at a long-term care facility for severely ill patients. 

There were 22 cases identified in Texas during the same period, with two being resistant to all three anti-fungal medications, and five resistant to two of the medications. Those seven cases were found in patients at two acute care hospitals, one long-term and one short-term; two of the patients were treated at both hospitals. 

“This is really the first time we’ve started seeing clustering of resistance” in which patients seemed to be getting the infections from other patients, said the CDC’s Dr. Meghan Lyman, an author of the report.

Candida auris infections have been reported in hospitals and long-term care facilities around the world. People who have been hospitalized a long time or who have breathing tubes, feeding tubes or central venous catheters appear to be at highest risk. The fungus can cause wound infections or bloodstream infections, which can be fatal.

“Surveillance, public health reporting, and infection control measures are critical to containing further spread,” the report said, while noting that “data are lacking’ about how to treat cases that are resistant to all current drugs.

The Associated Press contributed reporting.

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Deadly hospital superbug found on a remote island beach

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A deadly hospital superbug has been discovered on a remote island beach, marking the first time researchers have seen this multidrug-resistant organism in the “wild.”

The findings, published Tuesday (March 16) in the journal mBio, may provide clues to the origins of this superbug, Candida auris, which mysteriously popped up in hospitals around the world about a decade ago.

“It’s a medical mystery, where did it come from,” said Dr. Arturo Casadevall, chair of the Department of Molecular Microbiology and Immunology at Johns Hopkins Bloomberg School of Public Health in Baltimore, who wrote an editorial accompanying the study. The new findings are “a very important part of the puzzle,” Casadevall told Live Science.

Related: Beachgoers beware? 5 pathogens that lurk in sand

C. auris is a fungus that was first discovered in 2009 in a patient in Japan. It seemed to quickly spread around the world, appearing on three different continents around the same time. The microbe can cause serious bloodstream infections, particularly in patients who require catheters, feeding tubes or breathing tubes, according to the Centers for Disease Control and Prevention (CDC). The infections can be difficult to treat because the microbe is often resistant to multiple antifungal drugs; and it can also linger on environmental surfaces. “When it gets into a hospital, it’s a nightmare” for infection control, Casadevall said. In 2019, the CDC declared C. auris an “urgent threat” to public health.

Although related species have been detected in plants and aquatic environments, C. auris hasn’t been found in natural environments. Casadevall and colleagues have previously hypothesized that increased temperatures due to climate change may have caused C. auris to adapt to higher temperatures in the wild, and thus allowed the fungus to make the jump to humans, whose normal body temperature is typically too hot for most fungi to survive.

Inspired by this hypothesis, study lead author Anuradha Chowdhary, a medical mycologist at the University of Delhi, India, and colleagues analyzed samples of soil and water collected from eight sites around the Andaman Islands, a remote, tropical archipelago between India and Myanmar.

The researchers isolated C. auris from two sites: a salt marsh wetland where virtually no people ever go, and a beach with more human activity.

The C. auris isolates from the beach were all multidrug resistant and were more closely related to strains seen in hospitals compared with the isolates found in the marsh, Chowdhary said in a statement.

One isolate found in the marsh was not drug-resistant and grew more slowly at high temperatures compared with the other isolates. This finding suggests that this isolate could be a “wilder” strain of C. auris, one that hadn’t yet adapted to the high body temperatures of humans and other mammals, Casadevall said.

The study provides some support for the global warming hypothesis because, first and foremost, it identified C. auris in a natural environment, which is a requirement for the hypothesis, the editorial said. In addition, the “wilder” isolate could be a missing link of sorts between wild C. auris and those that cause infections in hospitals.

Still, the study does not prove that C. auris naturally lives on the Andaman Islands, or that it originated there. It’s possible that the microbe could have been introduced by people, particularly at the beach site that had more human activity. In addition, some researchers have wondered whether the microbe may have been carried by ocean currents from areas where human waste was dumped into the water to the shores of the Andaman Islands, Casadevall  said.

The new findings will likely spur more researchers to look for C. auris in natural environments, and to compare wild strains with those from hospitals, Casadevall said. Studies could also examine whether wild C. auris isolates with less heat tolerance could “evolve” in a lab setting to grow at higher temperatures, thus providing more support for the global warming hypothesis, the editorial said.

If it is indeed shown that C. auris came from the wild, and that global warming was a factor in its jump to humans, researchers are concerned that more pathogens could make the same leap. Many fungal organisms are harmful to insects and amphibians,  but not to people because of our high body temperatures, Casadevall noted.

“If this idea gets validated … we need to start mapping out more of these pathogens that are out there so we don’t get surprised,” like we got surprised by the new coronavirus, Casadevall said.

Originally published on Live Science.  

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