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The devil lurking in the dust

How extreme weather is driving a deadly fungus further into the American West

Millie von Platen for Vox

Part of the issue The 100-year-old-mistake that’s reshaping the American West from The Highlight, Vox’s home for ambitious stories that explain our world.

On a cloudless day in March, Marieke Ramsey crouches against the mossy wall of a shallow gulch just inside the Phoenix city limits. She brandishes a kitchen spoon — “Nothing really fancy with some of our tools,” she tells me — and motions toward a fist-sized crevice in a craggy section of the streambed.

It’s a rodent burrow, perhaps home to a kangaroo rat or a white-throated woodrat, although Ramsey isn’t sure. She stoops, awkwardly angling her wrist to scrape a few spoonfuls of loose dirt from just inside the burrow, then deposits it into a sterile plastic cup. “As minimal soil destruction as possible” helps preserve what is, after all, an animal’s home, she says: “Pack in, pack out.”

In a few weeks, Ramsey — a graduate student in mycologist Bridget Barker’s lab at Northern Arizona University — will analyze this and other soil samples from other Phoenix-area sites to look for signs that Coccidioides, the fungus that causes Valley fever, is claiming new territory within a state it has already besieged.

Valley fever — also called coccidioidomycosis, although both the disease and its cause are often shortened to “cocci” (rhymes with “foxy”) — can be serious and even fatal in humans and animals, and can cause disease ranging from flu-like illness to pneumonia to meningitis, a dangerous infection of the membranes surrounding the brain and spinal cord.

The infection spreads when fungal spores packed into dry soil get swirled into the air by dust storms that periodically roar through the desert, or when construction projects tear into the ground. Ramsey is hunting for Cocci in rodent dwellings to better understand the link between these small mammals and the fungus’s presence in soil. Although scientists have for decades understood that small rodents carry the infection in areas where the fungus is endemic, they’re still struggling to explain why exactly rodents and Cocci so often appear in the same places — and what that portends for the future.

Unlike respiratory diseases like the flu or Covid-19, where fresh air is often key to preventing infections, all a person needs to do to get Valley fever is breathe outdoor air in an endemic area. People have gotten infected while hiking, filming TV shows, and flying model airplanes, and those who work outdoors in some way that disrupts soil are at highest risk: construction workers, wildland firefighters, agricultural workers, archaeologists. And while most other fungal infections primarily impact immunocompromised people, Cocci is capable of causing disease in people with healthy immune systems.

Cocci isn’t new: It’s thrived in the Americas’ hot, arid climates for millennia. In the United States, the hotbed has largely included a relatively narrow strip of land spanning what’s now the Southwest’s Four Corners region and parts of California and Texas.

Estimated areas with coccidioidomycosis (Valley fever) in the United States. (Source: CDC.)

But now, that slim band is fast expanding. Researchers estimate that by 2095, the parts of the US where people will be most susceptible to Valley fever will more than double, the risk encroaching to envelop almost the entire Western half of the country.

Scientists and public health experts are still working to understand this fungus and its life cycle. But what they’ve learned so far suggests it will spread because of complex and interconnected issues fueled by climate change — change we can already see.

The Colorado River snakes through many of the states afflicted by Valley fever. This essential water source and the reservoirs it feeds are contracting at an alarming rate, making these regions dustier — and where there’s dust, there can be Valley fever.

Right now, on a national scale, infections are rare. But where they do occur, they are highly consequential. In the early 2000s, researchers found Cocci caused nearly a third of pneumonia cases in an outpatient clinic network in Tucson, Arizona. Experts recently projected that climate change will drive cases up threefold over the next 50 years.

Although states aren’t required to report fungal infections to federal agencies, in 2019, the Centers for Disease Control and Prevention heard of about 20,000 Valley fever cases annually, with about 200 of them fatal.

The fungus’s incursion northward, past state lines and into new territory, will probably happen undetected, at least for a while. That’s partly because outside research laboratories like the one where Ramsey works, no one is systematically charting its spread through desert soil.

But it’s also because the US undercounts Valley fever cases on a grand scale. Even in places where Cocci is literally underfoot, health care providers simply don’t think to test for the infection in people who show up sick. Some estimates place the true annual US incidence of Cocci upward of 350,000 cases — more than 17 times higher than what’s reported to the CDC — and suggest public health authorities are also broadly undercounting Cocci deaths.

For a pathogen with so much destructive potential, Cocci is shrouded in mystery. There’s no map to show, in real time, exactly where it’s lurking. We haven’t yet figured out how to vaccinate people against infection. And nobody’s certain how it spreads through the soil — which makes staying ahead of it a near-impossible task.

Still, we know the fungus’s territory is growing, driven by extreme dry-then-wet weather cycles and, perhaps, by their influence on small rodent life. The point of Ramsey’s work is to alert both the general public and their health care providers to the risk that poses: “You can’t just read a textbook” to pinpoint where Cocci is a threat, she said. She and others are working to build something approximating a real-time map of where the fungus is, although “it’s super early days,” said Barker, her boss.

A growing community of scientists is fervently seeking answers to Cocci’s biggest questions, and answers are within reach. But as climate-driven changes to the soil of the American West speed the fungus’s life cycle into overdrive — and bureaucracy and outdated medical practices sluggishly evolve — can we outrun a pathogen that seems engineered to evade us?

How is Cocci spreading?

Starting from its discovery in the late 1800s, Cocci has perplexed scientists. When they first observed it under a microscope — after being isolated from the facial sores of an Argentine soldier in 1892 — scientists first mistook it for a parasite called Coccidia. (The mistake in the spherule’s original identification led to the organism’s name, Coccidioides: literally, “like a Coccidia.”)

It turned out to be something from a completely different kingdom of life. In 1900, microbiologists realized the germ was actually a dimorphic fungus, so named because it takes one of two forms — small, round, thick-walled orbs called spherules or long, brittle chains of spores — depending on the moisture and temperature of its environment.

The organism’s shape-shifting trick makes it an especially prodigious chaos agent: Inside the lung, it transforms into its brawny spherule form, too strong to be taken down by the immune system’s front-line fighters. That form then births hundreds of mini-spherules, replicants equipped to make mischief anywhere and everywhere else in the body.

But before they get into our lungs, Cocci spores spend a lot of time living in the dirt.

Scientists first realized soil was the source of Cocci infection in 1932, when two bacteriologists from the University of California Berkeley isolated the fungus from soil gathered near the barracks of a Kern County, California, ranch where four workers had fallen ill.

This discovery only opened up more mysteries about the fungus. Cocci perplexed its observers by growing only sluggishly in soil. That raised a big question: How does an organism that can barely reproduce in the dirt get and stay there — and in quantities high enough to cause disease in people who are just passing by?

Over the following near-century, several hypotheses came and went. Early on, Chester Emmons, the granddaddy of American medical mycology, hypothesized rodents were the reservoir for the pathogen. That theory receded over the following years, until in 2009, graduate students working with John Taylor, a mycologist and fungal genomics specialist at UC Berkeley, had an epiphany: Cocci eats meat.

“Almost all fungi eat plants. A very few fungi can eat animals,” said Taylor. But Cocci DNA lacked the genes that would have encoded plant-metabolizing enzymes, and were chock full of the genetic markers of a carnivore. “When we saw that, we went, ‘Emmons was right.’” Taylor said.

The breakthrough helped explain two important things. First, how rodents get the fungus into the soil. And second, how climate change — and its drastic extremes of drought and wet weather — may be furthering Cocci’s spread.

The unifying theory was called the endozoan hypothesis, which Taylor and Barker, the Northern Arizona University mycologist, proposed in 2019.

It goes like this: A rodent inhales a Cocci spore, and for a long time, nothing happens. Although the rodent doesn’t get sick, the fungus lives inside it in a dormant state — in other words, as an endozoan. When the rodent dies, the fungus “wakes up” and goes to work, eating it from the inside out.

The strategy gives Cocci an enormous advantage over other microorganisms that eat dead animals. The fungus is first in the microbial chow line to devour this “wet bag of protein,” as Taylor put it — “a very good place to be if you’re patient.”

Climate change fits into this picture because temperature and precipitation have direct effects on the rodent life cycle.

Imagine, for example, what happens to a family of kangaroo rats during just one drought-flood cycle. The rats, named for their spring-loaded hind legs and feet, depend on desert vegetation to survive, and during a drought, there’s less for them to eat — which means more of them die. In the quarter or so of the rats whose lungs harbor dormant Cocci, the fungi, no longer constrained by the rodents’ immune systems, belly up to the all-you-can-eat carcass bar.

The fungi prefer to grow in moist environments, so the feast is over once the carcass dries out. In its wake, kangaroo rat-shaped clusters of bones, skin, and brittle fungal spores are left behind. The more drought, the more half-eaten rat bodies there are scattered underground.

But that’s not where it ends: Climate change could also increase the geographic region in which Cocci live — quite possibly, by driving migration of their rodent hosts.

Now, imagine that after several months of drought and death, big rains come. This pattern of drought followed by intense rains is sometimes called “weather whiplash” — and some climate scientists expect more of it in the decades to come.

During those rains, desiccated rat bodies rehydrate, and the Cocci consume what’s left of them, growing in number. Green shoots sprout where water has percolated into once-arid crevices, and the surviving kangaroo rats get fat amid the plenty: perfect conditions for making more of themselves. Rodent families multiply, perhaps to the point that their existing neighborhoods get crowded.

Some of these young kangaroo rats will get infected with Cocci, although how that happens isn’t entirely clear.

It’s plausible — although not officially part of the hypothesis — that the most adventurous of them, while migrating into heretofore unexplored territory, burrow past — whoops! — kangaroo rat-shaped clusters of spores and inhale a few of them. In this scenario, the newly infected (but still healthy-appearing) kangaroo rat now goes on to start the cycle all over again, only now in a new area.

If that’s indeed what’s happening, it could explain how heavy rains alternating with severe drought — all the result of a changing climate — drive Cocci’s expanding footprint.

Overall, the endozoan hypothesis is mostly still speculative, said Taylor. Proving rodents’ role in Cocci’s propagation could involve labeling rodents with tracking devices to figure out what’s going on underground, and perhaps sequencing Cocci genomes from different infected animals to see who infected whom. The field work would be quite a bit more complicated than Marieke Ramsey’s burrow floor sampling — although the lab work, like Ramsey’s, would need to be performed by trained personnel in high-level biosafety labs. None of this is impossible, but it is expensive.

Meanwhile, other scientists’ work suggests the climate parameters feeding into the trends are all but inevitable. By warming and drying the soil throughout the Western US, temperature and precipitation changes will likely more than double the area of cocci’s potential habitat by 2090, said Morgan Gorris, an earth system scientist at Los Alamos National Laboratory in New Mexico. Gorris has created models that forecast both the expansion of Cocci’s home region and its economic impact to come; she predicts costs associated with the infection will increase nearly 400 percent over the next 70 years.

Gorris’s findings were surprising even to her — “I was shocked that it was projected to reach the US-Canadian border by year 2100,” she said. “That was an ‘aha’ moment because it really showed the necessity of … reaching out to these public health departments that may not have been considering Valley fever as a risk for their communities.”

Even if scientists perfectly understood the Cocci life cycle and its interaction with weather, big knowledge gaps would remain. Existing maps of the fungus’s distribution are approximate at best, based as they are on people’s best guesses at where they got infected after being diagnosed with Valley fever, said Adrienne Carey, an infectious disease doctor who studies Cocci at the University of Utah School of Medicine.

“We, for the life of us, have a really hard time culturing the fungus in the soil,” Carey said. The organism is notoriously difficult to grow from soil samples using standard microbiological methods. Molecular methods — like Barker’s lab uses — are better, but prohibitively expensive, at least for now. “When you can’t culture it in the soil, you have a hard time knowing where it is,” said Carey.

The endozoan hypothesis is not the only one going: Scientists also suspect dust storms and other regional wind patterns play a role in Cocci’s spread. A recent cluster of cases in Washington state was linked to organisms isolated from soil in the arid eastern part of the state, hundreds of miles from its usual geographic range; strong winds might have played an important role in the pathogen’s migration.

Either way, mounting data suggests that, barring a dramatic reversal in the factors driving climate change and the weather changes it’s producing, Cocci’s march through the American West, overland and underground, is inevitable.

Who does Cocci hurt the most?

However many questions remain unanswered about how Cocci gets into and spreads through soil, we know what happens when it gets inside the lungs — for the most part.

Within the warm, wet, protein-rich embrace of a mammalian airway, a Cocci spore performs a feat that distinguishes it from other disease-causing fungi. Its cousins would, in this environment, round themselves into blobby single-cell organisms small enough to be fodder for the immune system’s macrophages (literally, “big eater” cells). But here, Cocci zags, hulking out into the massive spherules that earned it its name.

“Making a sphere is a good strategy for a lot of different problems” — at least from cocci’s perspective, said Barker. The fungus’s new shape and size render it inedible to macrophages. Plus, it’s ideal for germinating the hundreds of baby fungal cells, or endospores, that it readies to spread from the lung and raise hell elsewhere in the body. Spherulization is a tactic unique to Cocci: “There’s no other structure like that in this group,” Barker said, referring to the Onygenales order that includes a host of other fungal pathogens.

Unable to destroy the spherule by chewing it up, the immune system instead tries to smother the burgeoning threat with white blood cells. In about 60 percent of all human cases, the containment is successful, and happens so swiftly and quietly that the infection goes undetected and lies dormant — at least until the person dies.

In the other 40 percent, containment fails, and Cocci pushes past the body’s defenses. In this unlucky group, fungal spherules burst within a few weeks of inhaling the first spore, unleashing up to a thousand endospores into the blood and the neighboring lung tissue. Immunocompromised people are at particularly high risk for this scenario: Up to half of all cases in people with suppressed immune systems disseminate beyond the lungs.

As the immune system tries to contain the Valley fever infection, many people experience flu-like aches, fever, and fatigue. Symptoms of the fungus’s invasion of lung tissue, like cough and chest pain, are also common. Many patients report weird, often nodular rashes, and months to years later, a small minority develop even weirder rashes, most commonly in the laugh lines of the face. These oddities, like Cocci-related meningitis and infections of the bones, brain, and gastrointestinal tract, signal disseminated disease — that is, the spread of infection outside the lungs to other parts of the body.

People with symptomatic infection often feel sick for weeks or months, even if their immune system is strong. And while many recover without treatment, people with severe disease usually end up taking variably unpleasant antifungal medications, whose temporary side effects range from nausea to blurry vision to neurologic problems, like numbness or weakness.

Part of what makes Cocci infections last so long is that diagnosing them often takes a long time. Valley fever usually starts out looking like a respiratory infection, and often gets mistaken for more common bacterial and viral diseases.

Even in places where Cocci causes a significant proportion of pneumonias, the time between getting sick and getting diagnosed can be weeks or even months. Although blood tests can diagnose Valley fever in a few days, patients at one Tucson clinic network waited a median of three weeks for a correct diagnosis, according to a study in Emerging Infectious Diseases, and a related analysis showed more than half waited anywhere between one and six months.

It’s worse outside of the Southwest. At Ohio’s Cleveland Clinic — one of the nation’s top diagnostic centers — people with Cocci waited a median of three months for doctors to figure out what was causing their symptoms.

Scientists still don’t understand what distinguishes people who get sick from those who don’t, although Taylor thinks the quantity of spores the immune system has to contend with makes a difference. About three-quarters of people with symptomatic disease are men, and Filipino and Black people are more likely to have severe disease. That imbalance probably has something to do with exposure risk — people in these groups are more likely to do the outdoor work associated with infection — but there’s ongoing debate about whether genetics also play a role.

And it’s not just humans who are at risk: Cocci also causes a spectrum of disease in a variety of other vertebrates – most commonly dogs and cats, but also horses, llamas, alpacas, sea lions, dolphins, and other, less local species. “If you look at the records from the Phoenix Zoo — polar bears and kangaroos and wallabies and nonhuman primates — it’s kind of crazy how diverse the host range is,” said Barker.

Regardless of whether they have symptoms of their first infection, people who get infected with Cocci once don’t catch it again. “It’s a living vaccine,” said Taylor. But if the immune system of a person with a dormant Cocci infection gets distracted or disabled due to medications or disease, the fungus can wild out, bursting from its shell to wreak the havoc it failed to unleash on its first try.

That creates particular urgency for finding ways to prevent Cocci infections from settling in to begin with.

We know more Cocci is coming. How can we prepare?

The most obvious way to protect people from an infection they can’t help but encounter is with a vaccine. But despite ongoing efforts to develop a vaccine since the 1960s, there is still no prototype effective at reducing Cocci’s effects on humans.

Part of the challenge has to do with antibodies. Most vaccines are designed to get the body to generate neutralizing antibodies. But with Cocci, a different flank of the immune system, composed of T-cells, “is essential” for protecting people from repeat infection, said Chiung-Yu Hung, an immunologist at the University of Texas at San Antonio who’s working on a Cocci vaccine prototype.

The challenge: It’s hard to train up human T-cells without injecting a living but weakened version of the Cocci spherule, a so-called “live attenuated” vaccine. And that process comes with its own risks.

Live attenuated vaccines elicit a robust immune response — which includes T-cells. But many of them run the risk of replicating uncontrollably in people with compromised immune systems. That’s not what anyone wants — especially since immunocompromised people would benefit the most from a Valley fever vaccine.

So a live Cocci vaccine would only be a realistic option if the version of the spherule it contained had zero risk of replicating once injected into a person’s body.

That concept is no longer in the realm of science fiction, said John Galgiani, an infectious disease doctor who directs the Valley Fever Center for Excellence at the University of Arizona’s College of Medicine in Tucson. In 2016, a team led by his colleague Marc Orbach published a method for snipping out the gene that controls Cocci’s ability to multiply. A vaccine made from the resulting fungal mutant has been remarkably effective at reducing disease in dogs. The prototype is on track to be approved by the USDA for veterinary use in the first half of 2024.

Why isn’t the vaccine ready for human trials? “Well in my view, it is,” said Galgiani. But the manufacturing and licensing process for human vaccines is a completely different animal (sorry) than the one for veterinary vaccines — and the costs are much, much higher.

Shepherding the prototype through the Food and Drug Administration’s (FDA’s) hoops will probably take at least eight years, said Galgiani. And as with previous Cocci vaccine prototypes, there’s a chance that because relatively few people are currently at risk of infection — compared with, say, the global population-wide risk for polio or measles — the product’s modest profit potential would put off manufacturing partners. Without their investment, no prototype would get past the finish line.

Other vaccines are also under development but don’t yet exist as prototypes. For example, Hung’s team is working on an mRNA vaccine packaged in a faux-fungal capsule that enables it to induce a T-cell response.

This is where our lack of clarity on the true reach of Valley fever poses perhaps the clearest obstacle to doing something about it. If we’re massively undercounting cases, and if Cocci’s geographic intrusion into new regions is going undetected, we might be wildly underestimating the risk of the infection — and the benefit of a vaccine. Underinvesting in solutions now could leave us scrambling in an increasingly climate-weird future.

And weird it shall be. Climate change is altering our world in a million small ways that have big consequences. It changes the land, which changes how and whether animals live in it, which embeds further changes in the land, which impacts our health.

The desert, the rodents, the fungus, and the weather were all here before we were. We’ve dug too indiscriminately into the land and taken too much water from its rivers — and now, we face invisible threats in the desert’s imbalance. The consequences of a changing climate are not all as obvious as ice melting: Our world is changing in other ways whose fallout we might not notice until it literally hits our lungs.

The time to prepare for them is now.

John Taylor, the Berkeley mycologist, was once the expert witness in a court case involving a Cocci cluster among construction workers who built a culvert in California’s San Joaquin Valley — Valley fever’s namesake. Many became seriously ill; they hadn’t been informed of the Cocci risk, or told that respirator masks were necessary protective gear.

The trial cost California taxpayers millions of dollars. Still, when Taylor drives through the Valley to collect soil samples, he sees workers without protection. Vaccinating at-risk workers would be the best defense against the coming rise of Cocci, he said, perhaps because it accounts for our tendency as a species to ignore that which we cannot see. Because even if we can’t see the threat in a speck of dust, it’s there.

“It’s the little dangers that get you,” he said, “a mosquito, the Valley fever fungus. Not the wolf. Not the tiger.”

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