The climate crisis in the time of COVID-19 illustrates the difference between the important and the urgent.
There is, of course, no alternative to focusing on the current pandemic. But at the same time, the SARS-CoV-2 coronavirus has not changed the fact that the climate crisis is a coming wave whose health consequences will ultimately dwarf those of any single infectious agent.
Warming, which is the predominant effect of the climate crisis, is directly affecting health through extreme weather. 21st century heatwaves have already claimed tens of thousands of lives.
But while there are straightforward mitigation possibilities for those most direct effects, the indirect effects on the ecosystem are contributing to a changing landscape of infectious diseases.
Infectious disease is the only area of health that regularly has to grapple with new illnesses, and the only area of health where drugs naturally lose their effectiveness over time. Climate change both makes emerging outbreaks more likely and drugs less effective.
As far as emerging outbreaks are concerned, much attention has been paid to changes in vector geographic range.
There’s good reason for those worries, as mosquitoes in particular have been expanding their ranges. 2007 saw the first local European outbreak of chikungunya, also known as “break-bone fever.” Chikungunya is related to dengue and Zika – and transmitted by the same mosquitoes, Aedes albopictus and Aedes aegypti. Since 2007, both Italy and France have reported locally acquired cases of chikungunya.
Vector range changes are not the only way that increasing temperatures enable new infectious diseases to take hold, though. Temperature and climate, Erin Mordecai told BioWorld, affect myriad aspects of both mosquito and pathogen life cycle.
In temperate climates, warmer temperatures mean longer seasons and faster parasite maturation. On the other hand, pathogens have an optimal temperature for reproduction – around 23 degrees Celsius for West Nile virus, 25 degrees Celsius for the malaria parasite, and 29 degrees Celsius for Zika and dengue.
In some areas that are at the optimal temperature for the pathogen already, “if anything we might expect temperature changes to reduce the suitability for transmission,” said Mordecai, who is an assistant professor of biology at Stanford University.
“Temperature changes are going to have an effect,” she said. “But the effect will not always be linear and positive.”
Rising temperatures affect the possibilities of emerging pathogens in other ways as well.
While there are currently any number of microorganisms that cannot survive mammalian body temperatures, that may change as the bugs adapt to warmer temperatures.
“Most of us don’t really appreciate how much of a defense our warmth is,” Arturo Casadevall told BioWorld.
In an editorial published in the Journal of Clinical Investigation in February of 2020, Casadevall, who is a professor at the Johns Hopkins Bloomberg School of Public Health, wrote about the risks of such adaptation, particularly of fungi.
“We think that [adaptation] can happen with any organism,” he told BioWorld. “But it’s been very striking with the fungi.
“The fungal world, it has trouble with temperature – most fungi that live in the environment cannot live at 37 degrees,” Celsius, which is the regular human body temperature, he added.
How that restriction affects their infectious abilities is on view in an animal that, these days, is better known for seeding outbreaks rather than succumbing to them: bats.
North American bat colonies have been decimated by white nose syndrome, a disease caused by the fungus Pseudogymnoascus destructans. First observed in 2006, white nose syndrome has killed millions of bats in their sleep.
And only in their sleep.
“Bats are not susceptible in the summer, when they are at 37 degrees,” Casadevall said. “They are only susceptible in the winter when they are in hibernation” and their core body temperature drops.
“They can resolve the disease just by raising their metabolic rate,” he said.
What white nose syndrome is to bats, Candida auris is to humans.
Candida auris was first identified in 2009, though retrospective analyses have since identified strains as early as 1996.
C. auris was not even mentioned in the CDC’s 2013 reports on antimicrobial threats; by the 2019 report, it was one of five pathogens, and the only fungus, featured on the top-tier Urgent Threat List.
Drug resistant Candida has a separate spot on the serious threat list. According to the CDC website, C. auris, is concerning for several reasons, including frequent multidrug resistance and a propensity for causing outbreaks in health care settings.
Since 2011, there have been outbreaks of genetically unrelated C. auris strains in South America, Africa, South Asia and East Asia. All four have since made their way to the U.S.
According to the CDC’s antimicrobial threats report, “investigators still do not know why four different strains of C. auris emerged around the same time across the globe.”
Casadevall and his colleagues, though, have hypothesized that “this is the first fungus that has breached the thermal barrier.”
In a 2019 mBio paper, they investigated the heat tolerance of numerous Candida strains and found that C. auris was more heat-tolerant than its cousins.
The experiments could not determine whether heat tolerance was a recently acquired trait. But the authors noted in their paper that “the earliest description of C. auris came from a strain recovered from a human ear, which is much cooler than core body temperatures. Hence, this fungus may have gone through a short transient period during which it inhabited human surfaces before being associated with disease. Currently, C. auris preferentially colonizes the cooler skin rather than the hotter gut mycobiome, a preference that may be consistent with a recent acquisition of thermotolerance.”A collision course with increasing antimicrobial resistance
The adaptation of microorganisms to warmer temperature does not only make them better able to infect humans. It also increases their resistance to antibiotics, adding further fuel to what is already the Australian bushfire of coming antibiotic resistance.
In the most general sense, any antibiotic works by stressing bacteria, ideally to the point of death. And multiple classes of antibiotics induce stresses that are similar to either heat or cold shock.
Aminoglycosides like streptomycin and gentamycin in particular cause stress that is similar to increased temperature stress, and lead to the induction of heat-shock proteins as a bacterial defense mechanism. When the heat-shock response is already in operation, it increases the resistance of various bacteria, including Acinetobacter baumannii and Escherichia coli.
That increased resistance is not just visible in the laboratory. In 2018, researchers at Harvard University reported that in the U.S., locations with warmer average temperatures had more antibiotic-resistant bugs.
In their paper, the team showed that an increase in temperature of 10 degrees Celsius across regions was associated with increased antibiotic resistance for Escherichia coli, Klebsiella pneumoniae and Staphylococcus aureus, an association, they wrote, that was “consistent across most classes of antibiotics and pathogens and may be strengthening over time.”
Their conclusion? The O’Neill Report, which forecast the possibility of 10 million annual deaths due to antibiotic resistance by 2050, may be a significant underestimate.