Fungal Pathogens Are Adapting to Human Body Heat

For most of human history, our internal body temperature has served as a primary fortress against fungal infections. While bacteria and viruses have plagued humanity for eons, serious fungal infections have been relatively rare because most fungi cannot survive at 98.6 degrees Fahrenheit (37 degrees Celsius). However, new research suggests this biological firewall is cracking. As global temperatures rise due to climate change, fungi are evolving to tolerate higher heat, effectively training them to survive inside the human body.

The Cracking of the Thermal Barrier

The fundamental reason healthy people generally do not suffer from systemic fungal infections is a concept known as the “thermal exclusion zone.” Most of the estimated millions of fungal species on Earth thrive in temperatures between 54 degrees and 86 degrees Fahrenheit (12 to 30 degrees Celsius). Because the human body operates well above this range, we have historically been inhospitable hosts.

However, researchers are observing a concerning shift. As the environment warms, the gap between outside ambient temperatures and human body temperature is narrowing. Fungi that adapt to survive a hotter outside world are pre-adapting to survive inside us.

Dr. Arturo Casadevall, a microbiologist at the Johns Hopkins Bloomberg School of Public Health, has long hypothesized that mammalian body heat evolved partly to ward off fungi. He suggests that climate change is forcing fungi to adapt or die. Those that adapt are finding that the human body is no longer a forbidden zone but a viable new habitat.

Evidence from Duke University: The "Jumping Genes"

Recent studies have moved this theory from hypothesis to observable fact. A pivotal study led by Asiya Gusa at the Duke University School of Medicine provided concrete evidence of how heat stress alters fungal genetics.

The research focused on Cryptococcus deneoformans, a fungus that can cause severe infections in the brain and nervous system. The team grew the fungus at two different temperatures:

• 86°F (30°C): A standard environmental temperature.
• 98.6°F (37°C): Human body temperature.

The results, published in the Proceedings of the National Academy of Sciences (PNAS), showed that the higher temperature did more than just stress the fungus; it accelerated its genetic mutation. Specifically, the researchers observed high activity in “transposable elements,” often called jumping genes.

These are DNA sequences that change their position within the genome. At human body heat, these jumping genes moved five times more frequently than they did at the lower temperature. This rapid genetic shuffling allows the fungus to evolve much faster, potentially developing drug resistance and heat tolerance simultaneously.

The Case of Candida Auris

The most alarming real-world example of this phenomenon is Candida auris. This yeast, which can cause fatal bloodstream infections, was unknown to science prior to 2009. Then, it seemingly appeared out of nowhere.

What makes C. auris unique—and terrifying to epidemiologists—is how it emerged. It did not start in one location and spread via travel. Instead, distinct genetic families of the fungus appeared simultaneously on three different continents:

1. Asia (India/Pakistan)
2. Africa (South Africa)
3. South America (Venezuela)

Because these strains were genetically distinct but emerged at the same time, traditional transmission theories failed to explain the outbreak. The leading theory, supported by Casadevall and others, is that global warming raised the temperature of the environment enough to select for heat-tolerant strains in these disparate locations at the same time. These strains then made the jump to humans.

The CDC currently lists Candida auris as an “urgent threat” because it is often resistant to multiple antifungal drugs, spreads easily in healthcare settings, and can survive on surfaces for weeks.

Why Fungal Evolution is Harder to Fight

Bacterial infections are fought with antibiotics, and viral infections are managed with vaccines and antivirals. Fungal infections present a harder challenge for medical science.

Fungi are eukaryotes, meaning their cellular structure is remarkably similar to human cells. They share similar machinery for replicating DNA and building proteins. This biological similarity makes it difficult to create drugs that kill the fungus without harming the human patient.

Currently, there are only three major classes of antifungal drugs:

• Azoles: These stop the fungus from building cell membranes.
• Echinocandins: These target the fungal cell wall.
• Polyenes: These physically destroy the cell membrane (but can be toxic to human kidneys).

When heat stress causes fungi like Cryptococcus to activate their jumping genes, they can quickly mutate to evade these few available treatments. In the Duke study, researchers noted that the heat-induced mutations could lead to rapid resistance to antifungal treatments, sometimes within a single infection cycle.

Implications for the Immunocompromised

While this adaptation is concerning, it is important to understand who is most at risk. Currently, healthy individuals with robust immune systems are still capable of fighting off most fungal pathogens. The immediate danger lies with vulnerable populations.

As fungi become more heat-tolerant, the burden falls heavily on:

• Cancer patients undergoing chemotherapy.
• Organ transplant recipients taking immunosuppressants.
• People with HIV/AIDS.
• Patients with long-term viral infections (like severe COVID-19 or influenza).

For these groups, the “thermal barrier” was a critical line of defense. If that barrier is breached by heat-trained fungi, the reliance shifts entirely to antifungal drugs—drugs that are becoming less effective as the pathogens evolve.

The Future of Fungal Research

The recognition of heat as a driver for fungal evolution is changing how scientists approach the problem. Research is now pivoting toward understanding the specific genetic mechanisms of heat tolerance.

Scientists are looking for ways to stabilize the fungal genome to prevent the “jumping genes” from mutating. Additionally, there is a renewed push for fungal vaccines. Currently, there are no FDA-approved vaccines for fungal infections, a gap in medical science that researchers say must be closed as the planet warms.

Frequently Asked Questions

Is climate change creating new fungi? Climate change does not necessarily create “new” fungi from scratch. Instead, it acts as a filter or a training ground. It selects for existing fungi that can tolerate heat. This adaptation allows known environmental fungi to survive in places they previously could not, such as inside the human body.

What is the most dangerous fungal pathogen right now? Candida auris is widely considered one of the most dangerous emerging fungal pathogens. It is often multi-drug resistant, difficult to identify with standard lab equipment, and has caused outbreaks in healthcare facilities worldwide.

Can healthy people get these fungal infections? Most severe systemic fungal infections occur in people with weakened immune systems. However, some fungal infections (like Valley Fever caused by Coccidioides) can affect healthy people who inhale a large amount of spores. As fungi adapt to heat, the concern is that they may become more virulent, potentially posing a risk to a broader population.

How can I protect myself from fungal infections? For the general public, standard hygiene and avoiding areas with high spore counts (like construction sites or dusty excavations in specific regions) are the best defense. For those in hospitals, healthcare providers use strict isolation protocols to stop the spread of superbugs like C. auris.

Why are there so few antifungal drugs? Developing antifungals is difficult because fungal cells and human cells are biologically similar. It is hard to find a chemical target that attacks the fungus without causing toxic side effects in the human host. This makes the research and development process slower and more expensive than for antibiotics.