7 | Holobiont: The Mycobiome and the Human Body

IN THE PAST TWO DECADES, DNA sequencing has let us look inside our human bodies in ways never before possible. With the Human Genome Project we gained a draft of all 3.2 billion nucleotide base pairs in our hereditary material.1 We don’t yet know the complete meaning of all the words that these letters spell, but the parts that we do understand illuminate some of the molecular mechanisms underlying human health and disease. It has shown us that one person’s genome sequence is 99.9 percent identical to any other individual’s. And sometimes a single nucleotide change in a single gene can cause disease. Another surprise is that about 25 percent of our DNA does not code for genes and that about 8 percent comes from viruses now permanently melded into our chromosomes.

More recently the Human Microbiome Project has surveyed the microbes on and in our bodies. Using the magnifying glasses of the polymerase chain reaction (PCR) and next-gen sequencing, scientists have detected thousands of times more symbiotic bacteria and hundreds of times more fungi than anyone had ever guessed. This constellation of micro-organisms, known as the human microbiome, varies considerably from one person to the next, from body part to body part, from hour to hour, and from infancy through old age. We’ve seen complex multiorganismal symbioses like this before, between trees, their ectomycorrhizal and endophyte symbionts, and rhizosphere fungi. Now we know that we are like that too. Almost every living thing big enough to see-wild and domesticated animals, reptiles, fish, and all our friends and relatives—is a collection of symbionts. Among animals, only some bats and insects, in particular some ants, seem to lack a prodigious bacterial microbiome. As we saw in chapter 3, this kind of mega-multipartnered symbiotic association is known as a holobiont. Even most fungi have bacterial symbionts living inside them or latching on to their outer walls. Russian matryoshka nesting dolls must have been inspired by microbiology. Humans are walking ecosystems.2

In mammal holobionts like us, microbial symbionts do seem to be heavily skewed towards bacteria. We have about 37.2 trillion of our own cells and something like 20,000 to 25,000 genes on our chromosomes. A slightly higher number of symbiotic bacterial cells are in our bodies (earlier estimates of ten times as many are now discounted), and they contribute an extra 50,000 genes to keep our digestion and other internal functions advancing and adapting.3 But the contributions from fungal genes tend to be downplayed. Only about 0.01 to 0.1 percent of genes in human fecal samples are from fungi. One reason for this low number may be a medical preoccupation with bacteria, and the use of detection methods that often overlook fungi. But it may also just reflect a reality that fungal symbionts are less frequent in mammals than they are in plants or trees because bacteria prefer liquids and fungi prefer solids. Bacteria do better than most fungi at our body temperature of 98 degrees Fahrenheit and readily adapt to the lower oxygen concentrations in our digestive systems.

The inside of the human body is warmer than the average temperature in any outdoor ecosystem on Earth. The so-called fungal infection-mammalian selection (FIMS) hypothesis suggests mammals rose to dominance because dinosaurs were killed off by fungal infections. After the Chicxulub asteroid hit the Earth and our planet began to cool, dinosaurs were unable to increase their body temperature enough to combat pathogenic moulds, whereas mammals had evolved a self-regulating thermal system. What we call fever—an increase in body temperature—protects us from disease. Even today, the closest relatives of dinosaurs, birds, suffer more fungal diseases than mammals do. Infectious bacteria therefore cause more human diseases than fungi do, and we know comparatively little about the fungal component of our microbiome—our mycobiome. Still, DNA surveys have identified about four hundred species in the human mycobiome, and that number keeps increasing.4

Microbes colonize our bodies from our diet and from surrounding environments. Until the Human Microbiome Project, we mostly considered them aggressive, infectious pathogens that swoop in from outside and attack. That idea underlies the germ theory of modern medicine, which aims to wipe out microbes with antibiotics and other treatments. But we are beginning to understand that only a tiny proportion of the millions of bacteria and fungi in our environment are harmful, and that a healthy microbiome naturally balances the competing interests of individual microbes. More and more we see microbes colonizing our bodies and holding each other in check to ensure an “everybody wins if we work together” outcome.

Microorganisms on and in our bodies stimulate or suppress our immune system. Our immune system includes several kinds of amoeba-like cells collectively known as white blood cells that engulf and kill unwelcome viruses and microbes. When the body detects an invader, white blood cells travel to the site of attack and slide through the walls of veins and arteries into the affected tissues of the body. Like bouncers in a nightclub, they expel the undesirables and let the beautiful microbes in, at least when everything is working properly.

A few fungi grow on us or in us and seem to be truly symbiotic partners. We’ve been aware of some of them for a while, in particular those on our skin, but their contributions to our health—positive or negative—are a puzzle. Who are these fungal teammates? Which ones should we fear, and which should we welcome as essential or neutral partners?

Skin: Dandruff and Other Fungal Discomforts

Our skin is the surface that interacts with the outer world. When we say that someone has beautiful skin, we are really admiring how gracefully their bacterial and fungal partners interact with their epidermis. We tend to disdain exuberant microbial growth and the associated odors on our scalps and in the humid folds of our crotches, armpits, or toes. But the list of fungi detected by next-gen surveys of our skin is quite extensive. It reads a lot like the lists of moulds we find living in house dust, which suggests that we pick up and drop off most of them in places in our homes. Among the most prevalent are dandruff yeasts, which make an almost continuous coating over our skin. Although we’ve known about them for more than a hundred years, nobody thought very much about these fungi until scientists started to study the microbiome. Then we found out that about seven billion people are colonized by only a few species of basidiomycetes in the genus Malassezia. Different species of dandruff yeasts occupy different regions of the body. Some are more common on other mammals and move back and forth when people handle pets or farm animals.

Up to ten million yeast cells are found on the average scalp, each of them living about a month. What are they doing there? The layer of yeasty paste seems to both protect our skin from drying out and discourage potentially infectious microbes. Dandruff yeasts lack the genes to make their own lipids, so they soak up fats from their hosts. If you want to culture them, you need to add olive oil or milk fats to the agar. The flakes that most of us associate with dandruff are simply the result of our epidermal cells ejecting to make sure yeast cells don’t smother our skin. A normal adult sheds about thirty to forty thousand dead skin cells per day, or up to 9 pounds per year.5 Normally this is enough to keep the dandruff mycobiome and associated bacteria of the skin under control. But the human-Malassezia symbiosis seems a bit unsteady, and there is a tipping point when dandruff yeasts become a pest and the skin cells last only a few days before being banished. Applying a glutinous shampoo laced with selenium sulfide, a chemical that represses the growth of dandruff yeasts, usually tames them again.

Doctors only worry about dandruff yeasts when they irritate skin in a serious way; for example, when they cause scratchy, dry, flaky patches of eczema. Severe dandruff can develop into conditions needing medical treatment, like seborrheic dermatitis, which causes itchiness and irritation on warm, oily areas of the body. In tropical climates, tourists sometimes suffer from discolored patches of skin called tinea versicolor (also known as pityriasis versicolor or sun fungus). And when Malassezia gets into the wrong tissues it can provoke a dramatic immune response. This is dangerous for premature babies receiving lipids through catheters or for immunocompromised adults being given intravenous nutrients.6 Dandruff yeasts are probably commensal or slightly mutualistic symbionts that drift towards parasitism if they have a chance.

How significant are fungi on skin to our health? Hyphae are seldom seen when the epidermis is examined under a microscope, so it is yeast cells and scatterings of spores that are normally present. Saccharomyces shows up a lot. So do moulds that make a lot of spores, like Aspergillus and Penicillium. Not only do the fungi from your home and outdoor environment leave their traces on you, but by molting all those dead skin cells colonized by dandruff yeast, you in turn shed a fungal fingerprint onto your surroundings.

Although dandruff is usually benign, other skin infections are more contagious, including athlete’s foot, ringworm (caused by a fungus, not a worm), and the uncomfortably named jock itch or crotch rot.7 Family doctors are very familiar with these common skin conditions. About 70 percent of people worldwide have fungal foot infections in their lifetime, and I am one of them. Although by most criteria I would not be considered sporty, every few years a warm itch breaks out between my pinky and “ring” toes, the typical starting point for athlete’s foot. It feels as if someone has wiped the web with heating lotion, then scratched at it with a scalpel. The irritated skin blushes red, and the outer layer softens into loose, grayish-green, rubbery flakes that rub off when scratched. The fungus suppresses the immune response of the skin long enough for hyphae to colonize the outer epidermis. The problem is that the hyphae then grow into the nail bed. And the toenail is so rugged and impenetrable that antifungal drug molecules can’t get through to the hyphae. The infection seems impossible to shake.

Over the years I’ve tried several different over-the-counter antibiotic creams, rubbing them between my toes twice a day for a few weeks. Clotrimazole seems to do the trick for me, but doctors can prescribe different classes of drugs or enroll your toes in drug trials, or you can buy exotic laser treatments or miracle cures off the internet. The success rate of all these interventions remains about the same, which is to say that the condition often lies dormant for a while before it flares up again. My symptoms recur every few years, usually in winter when my feet are wrapped in thick, warm socks in heavy, humid boots. Perhaps I should feel some professional pride for hosting a pet fungus on my feet, or at least a commensal that becomes a parasite now and then. It’s likely to stick with me for life, and to become more aggressive when I am older and my immune system is on the decline.

My feet are likely hosting an invasive species. Most athlete’s foot, jock itch, and ringworm infections are caused by one fungus, Trichophyton rubrum, which originated in Africa but probably hitched a ride to other continents in the nineteenth century when people started wearing closed shoes. Trichophyton rubrum doesn’t reproduce sexually; instead, it seems to be a clone. And once a few hyphae install themselves in the outer layer of skin, the tiny spores of the fungus easily get tangled into towels, socks, or other clothing, giving them a chance to jump to fresh, hairless skin in public changerooms. This species and the various others that cause skin infections are close relatives of moulds that live in soil and favor the pelts, hooves, and antlers from deceased animals lying about there. Perhaps these treats were abundant enough to favor moulds that could make protease enzymes to break down the keratin and collagen that make up hair, nails, and skin. Many have given up entirely on plants and their cellulose as a food source.

Dandruff yeasts and other skin fungi rely on us dropping or swapping epidermis cells so they can get around. Maybe some of our social customs, like shaking hands, hugging, kissing, and the rest of it, are subtle manipulations by the members of our mycobiome so they can find their way to new homes or find themselves new mates. But if a fungus wants to participate in the inner social network of the human holobiont, it needs to find a way in.

The Gastrointestinal Tract: Candida

Much of the diversity of the human microbiome is inside the body. Our skin has regular pores and gaps, but the most obvious entrance for a microbe is through our mouths. Our digestive system, which comprises the throat, stomach, small and large intestines, and other organs, is a lot like the fermenters used in biotechnology—or, if you prefer, fermenters are like our gut. Everything is temperature and pH controlled. Nutrients and liquids shuttle from one compartment to the next so that larger molecules can be broken down into smaller pieces and reassembled in more useful forms. With all its pockets, side branches, twists, and turns, the digestive system is a sophisticated symbiotic pipeline optimized to digest complex foods. Most of the symbiotic bacteria in our microbiome live in our gut. For some parts of the digestion and waste management process, bacteria completely take over. Our own genes and enzymes need not deal with those steps at all.

Insect guts are the traditional hangout of wild yeasts, and several species find their way into our innards too. One of the common fungi inside our digestive tract is our old buddy the brewer’s yeast. It floats around in the intestines of about half of adults, presumably picked up from handling dough or drinking unpasteurized beer—or perhaps by kissing trees. We’re uncertain whether it’s a true symbiont because its cells tend to pass through us in a few days. It is usually considered harmless, although some forms of inflammatory bowel or autoimmune disease correlate with elevated levels of antibodies against brewer’s yeast. A particular strain, sometimes given the name Saccharomyces boulardii, was discovered after French microbiologist Henri Boulard noticed native Asians chewing on lychee or mangosteen skins as a natural remedy for cholera. It is sold as a probiotic to ease stomach and gut problems like ulcers, and especially to remedy diarrhea in people with AIDS or discomfort associated with infections by the anaerobic fecal bacterium Clostridioides difficile (usually known as C. diff).8

But it is the yeast-like Candida species that are the most frequent and enigmatic fungal symbionts in the human digestive tract, and in the vicinity of its various entrances and exits. Candida species live with about half of us, especially in our mouths, stomachs, intestines, and vaginas. Two closely related species, Candida albicans and C. tropicalis, are common; there are several other rarer species. They are frequently called dimorphic, which means they grow in two forms: as yeasts in some conditions and as hyphae (or chains of swollen cells called pseudohyphae) in others. The yeasts are nicely streamlined vessels for sailing along in moist tissues. Their floppy hyphae tend to get tangled up and are unsuitable for navigating through wet entrails. In Candida, the growth forms change in response to different temperatures or oxygen concentrations.

The presence of Candida on and in our bodies is a mixed blessing. We can still only speculate about the precise contributions of these yeasts, but they are so common in healthy people that there must be some benefits. Some microbiome studies show that the bacteria and fungi in the gut keep each other under control by marking off territory with noxious metabolites, as if we have two internal police forces each keeping watch over the other. Further, at least in mice, Candida primes the immune system to be more reactive against infections by other fungi. It also seems to form antibiotic barriers around vulnerable portals into the body, such as the urethra and anus. This action may block other intestinal symbionts from dripping into areas where they are unwelcome.9 Candida, however, is known more for its pathogenic than its beneficial properties.

When humans are born, Candida spreads from the mother’s birth canal and colonizes the baby’s gastrointestinal tract by seeping in through the mouth. Within a few months, it settles into much of the infant’s gut. In the child’s first year, Candida is a major cause of diaper rash, but then the immune system learns to tame it. As we mature, Candida sometimes gets out of control, probably because of changes in the bacterial microbiome, and blossoms into the infections known as candidiasis. White pustules form on the mucous membranes of mouths or vaginas. From a distance, these resemble the patchy feather patterns of a particular bird, hence its common name, thrush. Candida often contaminates hospital equipment and is very difficult to clean up. Tainted catheters can result in deep tissue and blood infections in immunocompromised patients. Candidiasis then becomes one of the most lethal fungal infections, with a mortality rate higher than 40 percent.

The Air We Breathe (Part 2): Aspergillus and Other Fungi Growing in Lungs

Every time we breathe in, the rush of air sucks spores, dust particles, pollen, and pollution past the stiff hairs and moist membranes of our nostrils, through the trachea, and into smaller and smaller branches and branchlets of the respiratory system. Floppy little hairs swat at the intruders, trying to bat them out, but some evade the obstructions and crash, cushioned, into the alveoli of the lungs. These tiny round sacs, just the right size for fungal spores, are where oxygen and carbon dioxide pass between the air and our blood. The immune system of healthy lungs drenches intrusive spores with white blood cells. We expel the mucus left behind by coughing, sneezing, or snorting. But for spores that can hide in the smallest niches, or have tricks to outsmart the immune system, lungs are a great place to be. There is oxygen, a steady supply of food leaching through from the blood, and high humidity. As long as they can manage at our body temperature, the spores can germinate and explore.

Many of the truly life-threatening fungal diseases start out in our lungs. At first, many mimic viral or bacterial infections—coughs, chest pain, fevers, pneumonia—and are often misdiagnosed as a cold or the flu. On X-rays, the shadowy, shapeless blobs are sometimes confused with tuberculosis or cancer. And if the prescribed treatments target the wrong disease, the fungus continues to grow. If it remains untreated for long enough, it finds its way out of the lungs and spreads through the body.

The classic fungal respiratory diseases are caused by a trio of related ascomycetes. They are known as histoplasmosis (histo, or Caver’s disease, caused by Histoplasma capsulatum), blastomycosis (blasto, or Gilchrist’s disease, caused by Blastomyces dermatitidis), and coccidioidomycosis (coccidio, or valley fever, caused by Coccidioides immitis).10 All three are endemic to parts of North America, but histo in particular is an invasive pathogen on several continents, perhaps spread by migrating bats. Fortunately, the infections are not transferred between people. They begin when people inhale spores from soil or from masses of bird or bat droppings. Instead of making more hyphae, the spores of histo and blasto respond to the warm, liquid environment and start to bud into small round yeast cells. Histo yeasts are engulfed by the white blood cells but not killed; those of blasto are too big to be consumed. They flow through the blood but also accumulate in the lungs. The inhaled spores of coccidio don’t turn into yeasts but swell into sac-like cells called spherules. These burst and release hundreds of new spores, each repeating the cycle until the lungs clog up with fungal cells. Thanks to fungal drugs, these diseases are seldom fatal if accurately diagnosed. But people with AIDS, or those whose immune systems are repressed for other reasons, often suffer severe consequences from coccidio or histo infections.

Nearly all DNA surveys of human lungs report Aspergillus fumigatus, but no one would ever call it a symbiont. Its spores are almost everywhere, so it is no surprise that we breathe them in. In nature, this mould is a saprobe that breaks down plant debris. It amplifies dramatically in warm conditions, like self-heating compost piles, where its spores can be so abundant that they hover in a haze.11 It seems to get stirred up by excavations for building foundations or during renovations, and then its spores get drawn into buildings. Surveys in hospitals find low levels of A. fumigatus spores behind false ceilings, in ventilation systems, and in other nooks where moulds are prone to hide indoors. It also likes potted plants and is a contaminant in some marijuana-growing operations. Fortunately, it is easy to recognize when it grows on agar media because of the long columns of dry spores that jut up from its colonies like grayish-blue towers of cigarette ash. Individual spores of A. fumigatus are the perfect size to get lodged in the alveoli. For most people, however, inhaling a few spores provokes a response that is similar to ordinary hay fever, and for those with a robust immune system, the usual antihistamines will suffice. The spores get mopped up by the white blood cells, and the fungus causes no further problems.

Heavy exposure to the spores of A. fumigatus can lead to hypersensitivity, though, just as some people develop severe allergies with their second bee sting. People who overreact to these spores suffer the constricted airways, coughing, wheezing, and breathing difficulties that characterize serious asthma. Severe reactions may cascade into anaphylactic shock. Prolonged exposures to A. fumigatus lead to a condition called allergic bronchopulmonary aspergillosis (ABPA), in which the mould grows along the lining of the bronchial airways, resulting in inflammation and sometimes permanent lung damage.12

Here the line between allergy and infection gets fuzzy. A. fumigatus is a thermophile, quite happy growing at human body temperature, and if the spores settle into the alveoli for long enough they germinate and hyphae start to grow. They begin to release a mycotoxin called gliotoxin, which represses the immune system. The mycelium coils up like wads of cotton, growing into masses called aspergillomas that lodge in the lungs and sometimes penetrate other nearby tissues. The disease, a type of chronic pulmonary aspergillosis, is a major hospital-acquired infection and kills thousands of people every year. Patients with deep skin punctures called “major barrier breaks,” or those with a suppressed immune system, are particularly at risk. If the fungus spreads to the blood or central nervous system, the disease is about 95 percent fatal. A small percentage of people who survive serious flu or SARS-CoV-2 infections (COVID-19) later develop Aspergillus infections—which should encourage you to keep up with your vaccines.

AIDS and the Rise of Fungal Diseases

Until recently, humans had little fear of dying from a fungal infection. Human immunodeficiency virus (HIV) changed that. HIV causes acquired immunodeficiency syndrome (AIDs), a condition in which the body’s immune system is too weak to stop infections that an uninfected person would easily shake off. When the AIDS epidemic hit in the 1980s, doctors were caught off guard by the sudden increase in virulent fungal diseases. Previously rare or benign diseases became more common or deadly because the weakened immune system couldn’t repel them. The catalog of fungi that might turn up in hospital patients rose from about a hundred to more than five hundred. After antiretroviral treatments against HIV were introduced in the mid to late 1990s, the annual global number of deaths from AIDS fell from about 2 million to less than 1 million, with the developing world lagging behind. In sub-Saharan Africa alone, between 15 and 25 million people still live with AIDS. Between 45 and 50 percent of deaths among patients with AIDS are caused by fungal infections running amok because of reduced immune function.13

One of the most serious diseases to co-occur with AIDS was the previously rare Pneumocystis pneumonia (PCP), an infection that was often the first clinical symptom. The pathogen, a single-celled fungus with lemon-shaped cells, colonizes lung tissue. All mammals have Pneumocystis species in their lungs. They seem to be ancient symbionts that joined their evolutionary destiny to mammalian lungs long ago and are seen nowhere else. The species associated with humans is Pneumocystis jirovecii, although it was often called P. carinii; the latter species name is now used for a pathogen of dogs.14 Children often test positive for Pneumocystis, but only 20 percent of adults do. There are usually no symptoms and it is eventually cleared out by the immune system. It becomes an opportunistic pathogen only when the immune system is suppressed. Nevertheless, Pneumocystis cells can transmit from host to host through the air, and asymptomatic humans are considered the main source of infection in people with AIDS. Diagnosis and treatment have improved, and mortality rates have fallen from as high as 40 percent to 10 to 20 percent, but there are still about 10,000 cases per year in the United States. Where does Pneumocystis fall in the symbiotic continuum? Rather than an invasive pathogen, it often looks more like a commensal that becomes a parasite when the immune system fails to keep it in check.

Today the most serious fungal disease of people with AIDS is cryptococcosis, or crypto. Around the world every year, about 220,000 people are infected by yeast-likebasidiomycetes called Cryptococcus.15 About 180,000 die annually, some 165,000 of them in sub-Saharan Africa and most of them with HIV. Roughly the same number of people with HIV die every year from tuberculosis. In nature, crypto grows as a yeast in soil, in bird droppings, and on tree bark and produces hyphae only in anticipation of sex. Infections start when the resulting sexual spores are inhaled. The yeast form has a mesh of fibrous polysaccharides that swells out as a halo-like capsule. In the wild, this capsule protects the cells from being digested when they are swallowed by predatory amoebae; in the lungs, it protects them from similar attacks from white blood cells.

Patients who develop cryptococcosis progress from coughs, fatigue, headaches, and fever to weight loss, chest pain, vomiting, and stiff joints. Like most other fungal diseases that start in the lungs, it usually does not spread from one patient to another. Once inside a human host, the two species involved behave differently. The cells of C. neoformans cross into the central nervous system, forming cysts and lesions in the brain. This leads to a meningitis that is 100 percent fatal if untreated, and still 30 percent fatal after treatment with antifungal drugs. Until recently, the closely related C. gattii was considered a tropical curiosity growing on Eucalyptus trees, until it was noticed infecting porpoises and dogs in North America in the late 1990s. Then it was recognized as an overlooked cause of crypto in people with AIDS. Its infections tend to remain in the lungs, where it causes pneumonia. As with PCP, most people with intact immune systems who are exposed to crypto don’t become ill.

At the same time fungal diseases were rising because of reduced immune function in people with AIDS, they were becoming more common in patients whose immune systems were compromised for other reasons. The awareness of PCP in people with AIDS led doctors to recognize that the same disease often occurred after organ transplants or chemotherapy for cancer. Now 60 percent of PCP infections are diagnosed in people who don’t have AIDS.

The Mycobiome and Antifungal Drugs

Presently, at least a billion people are infected by pathogenic fungi of one kind or another. The annual death toll is between 1.2 and 2 million people per year, more than double that from malaria and in the same ballpark as the 1.4 million deaths from tuberculosis.16 When it comes to designing or discovering effective drugs to treat fungal infections, it is unfortunate that humans are so closely related to fungi. What is toxic to them is often also toxic to us. Antifungal drugs can be tough on humans, and if an infection is not life-threatening, the cure sometimes feels worse than the disease.

The first effective antifungal antibiotics were discovered during the bioprospecting boom of the 1950s to the 1970s. Amphotericin B (AmB) and nystatins were both isolated from two species of actinomycete bacteria in the genus Streptomyces.17 Both antibiotics are polyenes, long lipid-like chains that bind with ergosterol, a structural component of fungal cell membranes. This makes the cells fatally leaky. Because ergosterol is chemically similar to cholesterol in animal cell membranes, polyenes are somewhat toxic to humans and can cause intestinal problems, fever, fluctuations in blood pressure, and in the long term, kidney failure. Today, most fungal infections are treated with chemically synthesized antibiotics known as triazoles, which have bouncy names such as fluconazole, itraconazole, clotrimazole, or ketoconazole. These also interact with ergosterol but interfere with enzymes involved in its biosynthesis, meaning the fungal cell membranes cannot form. Again, some patients react badly to these drugs, and about 1 percent of patients using triazoles suffer gastric discomfort, muscle and joint pain, headaches, or ringing ears.

Our growing discomfort with the use of antibiotics is partly because they affect the stability of our microbiomes. Humans are already unstable holobionts, with a vacillating population of bacterial and fungal species. As with any ecosystem, microbial succession takes place in our bodies as we age. For example, a fungus like Candida behaves differently at different times of our lives, and it can be a dangerous pathogen in one part of our body and a commensal in another. These variations make treatment difficult. When we attack one pathogen with an antibiotic, we attack the whole microbiome. Opportunistic former friends take advantage of the changed conditions and transform into serious parasites. For example, in Crohn’s disease (a type of inflammatory bowel disease), the acid-tolerant yeast Debaryomyces hansenii, commonly found in fermented cheeses or meats, appears to colonize the gut lining after its symbiotic bacteria are disrupted by antibiotic therapy. The immune response to the yeast cells causes inflammation that interferes with the normal healing of wounds in the bowel. Many chronic disorders that are difficult to manage or cure seem to correlate with changes in our microbiomes. Conditions like obesity, heart problems, and autoimmune disorders (type 1 diabetes, lupus, rheumatoid arthritis), or the many diseases that lack satisfactory genetic explanations, may develop after our mutualist symbionts are knocked off-kilter, a situation called dysbiosis.18

Medicine is evolving to include the view that disease can be an ecological problem. Instead of believing that every microbe is a pathogen and eradicating them all, our strategy will shift to figuring out how to coax the wavering loyalties of opportunistic symbionts back into equilibrium where we need them. The same will be true for dealing with the problems we have with fungi in nature and in our homes. We need to embrace biological complexity if we are going to be wise stewards of our world. The health of our microbes is our physical and mental health; their genes are our genes. They are part of our inheritance from our parents, partners, children, houses, foods, and everywhere we’ve ever been. If we are going to make peace with fungi, we need to be aware of their biodiversity and embrace their talents for biodegradation, symbiosis, and biochemistry that make them such significant players in the environment. Only then will we be able to work with them effectively for our own prosperity and health, while they also collaborate with us.

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