Last updated on October 28, 2020
Candida Auris is an emerging fungal disease that COVID 19 is threatening to force with additional infections because it is common in hospital settings. It is difficult to control the fungus as it primarily infects anything in hospitals, bedding, rails, and including patients' ears and open wounds. Patients that are on catheters and other tubes that enter the body are most at risk.
OVER CHRISTMAS BREAK in 2015, Johanna Rhodes received a panicked email from a doctor working at the Royal Brompton Hospital, the largest heart and lung center in the United Kingdom. A horrid yeast was invading the skin of patients, spreading through the intensive care unit even though the hospital maintained extensive protocols for infection control.“The doctor asked me to take a look … I thought, how bad can it be?” recalls Rhodes, an infectious disease expert at Imperial College London who studies antifungal resistance. Rhodes stepped in to help one of the world’s top cardiology hospitals identify the pathogen and clear it from the premises. The germ was Candida auris, little known at the time. What she saw stunned her: “You think COVID-19 is bad until you see Candida auris.”Candida auris is a superbug, a pathogen that can evade drugs made to kill it—and early signs suggest the COVID-19 pandemic may be propelling infections of the highly dangerous yeast. That’s because C. auris is particularly prominent in hospital settings, which have been flooded with people this year due to the coronavirus.The superbug sticks stubbornly to surfaces such as sheets, bed railings, doors, and medical devices—making it easier to colonize skin and pass from one person to another. Moreover patients who have tubes that go into their body, such as catheters or ones for breathing or feeding, are at the highest risk for C. auris infections, and these invasive procedures have become more common because of the respiratory failure associated with COVID-19.
Prior to its emergence in 2009, fungi in the genus Candida were best known for causing benign cases of thrush, a white overgrowth on the tongue or genitals. A few thousand C. auris infections have since spread to at least 40 countries where they’ve been tied to deaths in 30 to 60 percent of cases. By comparison, the coronavirus kills about one percent of the infected but has afflicted a larger number of people in a short timespan.
“Our worry right now is that we’re seeing published cases of patients with COVID-19 and other fungal infections, with people getting really sick and dying,” says Rhodes, as she and other clinicians in the U.K. face the coronavirus’s autumn surge. “We expect to see the same with C. auris.”
The most enigmatic aspect of the rise of Candida auris as a human pathogen is that it emerged simultaneously on three continents, with each clade being genetically distinct. Although new pathogenic fungal species are described regularly, these are mostly species associated with single cases in individuals who are immunosuppressed. In this study, we used phylogenetic analysis to compare the temperature susceptibility of C. auris with those of its close relatives and to use these results to argue that it may be the first example of a new fungal disease emerging from climate change, with the caveat that many other factors may have contributed.
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 (12). 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. In this regard, experiments with an entomopathogenic fungus have shown that these can be rapidly adapted to growth at higher temperatures by thermal selection (13), establishing a precedent for an animal-pathogenic fungus adapting to mammalian basal temperatures. Most worrisome, analysis of thermal tolerances for fungal isolates deposited in a culture collection showed a trend of basidiomycetes for an increased capacity to replicate at higher temperatures, an observation consistent with an early adaptation to higher ambient temperatures beginning in the late 20th century (14). Supporting the notion of adaptation in response to temperature, fungal species in cities have become more thermotolerant than their rural counterparts (15). An analysis of the correlation of temperature tolerance with latitude (for strains isolated in recent decades and described in reference 14) showed that the Pearson correlations between the maximum temperature growth of all fungi, ascomycetes (e.g., Candida spp., Aspergillus spp., Histoplasma spp., etc.), and basidiomycetes (e.g., Cryptococcus spp., etc.) were −0.14619, −0.054638414, and −0.304251976, respectively. The lack of a significant trend for the ascomycetes is consistent with the fact that this group can grow at higher ambient temperatures and can thus grow across the latitudes. For the basidiomycetes, the borderline significant trend suggests that these are adapting to the warmer conditions in higher absolute latitudes, possibly because of climate warming, consistent with our earlier analysis (14). Given the capacity of fungal species to adapt to higher temperatures and the fact that many fungal species that are currently nonpathogenic species are likely to have the necessary virulence attributes by virtue of their survival in soils, we previously hypothesized that climate change would bring new fungal diseases (12).
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. Several factors, not necessarily mutually exclusive, may have been operative as to why C. auris emerged in the last decade. For example, as C. auris constitutively overexpresses HSP 90, this may account for its multidrug resistance, virulence, thermal tolerance, and osmotic-stress tolerance (17). Thus, C. auris might have previously existed as a plant saprophyte in specialized ecosystems, such as wetlands. As a first step, its emergence might have been linked to global warming (including climatic oscillations) effects on wetlands (18), and its enrichment in that ecological niche was the result of C. auris’s combined thermal tolerance and salinity tolerance. Interestingly, areas where C. auris was first recognized overlap, at least in part, the impacted wetland ecosystems (18). Of interest, C. albicans can be a part of a wetland ecosystem (19), and although many of the virulence determinants in the C. auris genome have not been characterized, it is theoretically possible that human-pathogenic Candida spp. have passed some virulence traits to previously nonpathogenic C. auris strains through plasmid DNA transfer (20, 21), in the backdrop of changing ecological niches. Alternatively, the effect of higher UV radiation in combination with global warming (22) 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 (23). 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 (24). The uncanny ability of C auris to adapt to specific niches, first in the environment and then in an avian host, might have led as a third step to its ultimate establishment as a human pathogen through genetic and epigenetic switches (25).
This story is way over my paygrade. Please be kind.
I know that emerging pathogens will be enhanced as a direct result of our warming planet. Climate change, after all, is a threat multiplier.
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