Dying, it turns out, is not like flipping a switch. Genes keep working for a while after a person dies, and scientists have used that activity in the lab to pinpoint time of death to within about nine minutes.

During the first 24 hours after death, genetic changes kick in across various human tissues, creating patterns of activity that can be used to roughly predict when someone died, researchers report February 13 in Nature Communications.
“This is really cool, just from a biological discovery standpoint,” says microbial ecologist Jennifer DeBruyn of the University of Tennessee in Knoxville who was not part of the study. “What do our cells do after we die, and what actually is death?”

What has become clear is that death isn’t the immediate end for genes. Some mouse and zebrafish genes remain active for up to four days after the animals die, scientists reported in 2017 in Open Biology.
In the new work, researchers examined changes in DNA’s chemical cousin, RNA. “There’s been a dogma that RNA is a weak, unstable molecule,” says Tom Gilbert, a geneticist at the Natural History Museum of Denmark in Copenhagen who has studied postmortem genetics. “So people always assumed that DNA might survive after death, but RNA would be gone.”
But recent research has found that RNA can be surprisingly stable, and some genes in our DNA even continue to be transcribed, or written, into RNA after we die, Gilbert says. “It’s not like you need a brain for gene expression,” he says. Molecular processes can continue until the necessary enzymes and chemical components run out.

“It’s no different than if you’re cooking a pasta and it’s boiling — if you turn the cooker off, it’s still going to bubble away, just at a slower and slower rate,” he says.

No one knows exactly how long a human’s molecular pot might keep bubbling, but geneticist and study leader Roderic Guigó of the Centre for Genomic Regulation in Barcelona says his team’s work may help toward figuring that out. “I think it’s an interesting question,” he says. “When does everything stop?”

Tissues from the dead are frequently used in genetic research, and Guigó and his colleagues had initially set out to learn how genetic activity, or gene expression, compares in dead and living tissues.

The researchers analyzed gene activity and degradation in 36 different kinds of human tissue, such as the brain, skin and lungs. Tissue samples were collected from more than 500 donors who had been dead for up to 29 hours. Postmortem gene activity varied in each tissue, the scientists found, and they used a computer to search for patterns in this activity. Just four tissues, taken together, could give a reliable time of death: subcutaneous fat, lung, thyroid and skin exposed to the sun.

Based on those results, the team developed an algorithm that a medical examiner might one day use to determine time of death. Using tissues in the lab, the algorithm could estimate the time of death to within about nine minutes, performing best during the first few hours after death, DeBruyn says.

For medical examiners, real-world conditions might not allow for such accuracy.

Traditionally, medical examiners use body temperature and physical signs such as rigor mortis to determine time of death. But scientists including DeBruyn are also starting to look at timing death using changes in the microbial community during decomposition (SN Online: 7/22/15).

These approaches — tracking microbial communities and gene activity — are “definitely complementary,” DeBruyn says. In the first 24 hours after death, bacteria, unlike genes, haven’t changed much, so a person’s genetic activity may be more useful for zeroing in on how long ago he or she died during that time frame. At longer time scales, microbes may work better.

“The biggest challenge is nailing down variability,” DeBruyn says. Everything from the temperature where a body is found to the deceased’s age could potentially affect how many and which genes are active after death. So scientists will have to do more experiments to account for these factors before the new method can be widely used.

Knocking back an enzyme swept mouse brains clean of protein globs that are a sign of Alzheimer’s disease. Reducing the enzyme is known to keep these nerve-damaging plaques from forming. But the disappearance of existing plaques was unexpected, researchers report online February 14 in the Journal of Experimental Medicine.

The brains of mice engineered to develop Alzheimer’s disease were riddled with these plaques, clumps of amyloid-beta protein fragments, by the time the animals were 10 months old. But the brains of 10-month-old Alzheimer’s mice that had a severely reduced amount of an enzyme called BACE1 were essentially clear of new and old plaques.
Studies rarely demonstrate the removal of existing plaques, says neuroscientist John Cirrito of Washington University in St. Louis who was not involved in the study. “It suggests there is something special about BACE1,” he says, but exactly what that might be remains unclear.

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One theory to how Alzheimer’s develops is called the amyloid cascade hypothesis. Accumulation of globs of A-beta protein bits, the idea goes, drives the nerve cell loss and dementia seen in the disease, which an estimated 5.5 million Americans had in 2017. If the theory is right, then targeting the BACE1 enzyme, which cuts up another protein to make A-beta, may help patients.
BACE1 was discovered about 20 years ago. Initial studies turned off the gene that makes BACE1 in mice for their entire lives, and those animals produced almost no A-beta. In humans, however, any drug that combats Alzheimer’s by going after the enzyme would be given to adults. So Riqiang Yan, one of the discoverers of BACE1 and a neuroscientist at the Cleveland Clinic, and colleagues set out to learn what happens when mice who start life with normal amounts of BACE1 lose much of the enzyme later on.

The researchers studied mice engineered to develop plaques in their brains when the animals are about 10 weeks old. Some of these mice were also engineered so that levels of the BACE1 enzyme, which is mostly found in the brain, gradually tapered off over time. When these mice were 4 months old, the animals had lost about 80 percent of the enzyme.
Alzheimer’s mice with normal BACE1 levels experienced a steady increase in plaques, clearly seen in samples of their brains. In Alzheimer’s mice without BACE1, however, the clumps followed a different trajectory. The number of plaques initially grew, but by the time the mice were around 6 months old, those plaques had mostly disappeared. And by 10 months, “we hardly see any,” Yan says.

Cirrito was surprised that getting rid of BACE1 later in life didn’t just stop plaques from forming, but removed them, too. “It is possible that perhaps a therapeutic agent targeting BACE1 in humans might have a similar effect,” he says.

Drugs that target BACE1 are already in development. But the enzyme has other jobs in the brain, such as potentially affecting the ability of nerve cells to communicate properly. It may be necessary for a drug to inhibit some, but not all, of the enzyme, enough to prevent plaque formation but also preserve normal signaling between nerve cells, Yan says.

Ultrasounds during pregnancy can be lots of fun, offering peeks at the baby-to-be. But ultrasounds aren’t just a way to get Facebook fodder. They are medical procedures that involve sound waves, technology that could, in theory, affect a growing fetus.

With that concern in mind, some researchers have wondered if the rising rates of autism diagnoses could have anything to do with the increasing number of ultrasound scans that women receive during pregnancy.

The answer is no, suggests a study published online February 12 in JAMA Pediatrics. On average, children with autism were exposed to fewer ultrasounds during pregnancy, scientists found. The results should be “very reassuring” to parents, says study coauthor Jodi Abbott, a maternal fetal medicine specialist at Boston Medical Center and Boston University School of Medicine.
To back up: Autism rates have risen sharply over the last several decades (though are possibly plateauing). Against this backdrop, researchers are searching for the causes of autism — and there are probably many. Autism is known to run in families, and scientists have found some of the particular genetic hot spots that may contribute. Other factors, such as older parents and maternal obesity, can also increase the risk of autism.

Scientists suspect that in many cases, autism is caused by many factors, all working together. Could prenatal ultrasounds, which have become more routine and more powerful, be one of those factors? These scans use sound waves that penetrate mothers’ bodies, and then collect the waves that bounce back, forming a picture of fetal tissues. During this process, the waves may be able to heat up the tissue they travel through.

Work on animals has suggested that ultrasounds can in fact interfere with fetal brain development, derailing the normal movements of cells that populate the brain. Mice exposed to 30 or more minutes of ultrasound in utero had abnormal brain development, for instance. But it’s not at all clear whether a similar thing might happen in humans, and if so, whether such effects might contribute to autism.
The new study compared ultrasound exposure among three groups: 107 children diagnosed with autism spectrum disorder, 104 children diagnosed with a developmental delay, and 209 typically developing children. On average, the children with autism were exposed to 5.9 ultrasound scans over the course of pregnancy. Children with developmental delays were exposed to 6.1 scans, and typically developing children were exposed to 6.3 scans, the researchers found. (For all groups, these numbers are way above the one to two scans per low-risk pregnancy recommended by the American College of Obstetricians and Gynecologists.)

For all three groups, the duration of the scans was similar. So was the thermal index, an indication of how much warming might have happened. “In almost every parameter we looked at, ultrasound seemed perfectly safe,” says study coauthor N. Paul Rosman, a pediatric neurologist at Boston Medical Center and Boston University School of Medicine.

One measure was different, the researchers found: During the first trimester, mothers who had children with autism had slightly deeper ultrasounds than women who had typically developing children and children with developmental delays. Ultrasound depth measures the distance from the transducer paddle that emits the waves to the spot that’s being imaged. The measure “has a lot to do with the size of the mother and the distance between her skin, where the ultrasound transducer is, and where the baby is,” Abbott says.

Lots of questions remain about whether — and how — ultrasound depth, or other aspects of the technology, might affect fetuses. “The study certainly wasn’t perfect,” Rosman says. It combed back through medical records of women instead of following women from the beginning. And it didn’t control for certain traits that may influence autism, such as smoking.

The results suggest that on their own, ultrasounds don’t cause autism spectrum disorder, says Sara Jane Webb of Seattle Children’s Research Institute and the University of Washington, who cowrote a JAMA Pediatrics companion piece. “At this time, there is no evidence that ultrasound is a primary contributor to poor developmental outcomes when delivered within medical guidelines,” she says.

While there’s more science to sort out here, the news is reassuring for women who might be worried about getting scanned. Women should follow their doctors’ guidance on ultrasounds, Rosman says. “We don’t think there’s anything in this study to recommend otherwise.”

What a spectacular Easter basket tardigrade eggs would make — at least for those celebrating in miniature.

A new species of the pudgy, eight-legged, water creatures lays pale, spherical microscopic eggs studded with domes crowned in long, trailing streamers.

Eggs of many land-based tardigrades have bumps, spines, filaments and such, presumably to help attach to a surface, says species codiscoverer Kazuharu Arakawa. The combination of a relatively plain surface on the egg itself (no pores, for instance) plus a filament crown helps distinguish this water bear as a new species, now named Macrobiotus shonaicus, he and colleagues report February 28 in PLOS ONE.
With about 20 new species added each year to the existing 1,200 or so known worldwide, tardigrades have become tiny icons of extreme survival (SN Online: 7/14/17).

“I was actually not looking for a new species,” Arakawa says. He happened on it when searching through moss he plucked from the concrete parking lot at his apartment. He routinely samples such stray spots to search for tardigrades, one of his main interests as a genome biologist at Keio University’s Institute for Advanced Biosciences in Tsuruoka City, Japan.
These particular moss-loving creatures managed to grow and reproduce in the lab —“very rare for a tardigrade,” he says. He didn’t realize it was an unknown species until he started deciphering the DNA that makes up some of its genes. The sequences he found didn’t match any in a worldwide database.

His two coauthors, at Jagiellonian University in Krakow, Poland, worked out that he had found a new member of a storied cluster of relatives of the tardigrade M. hufelandi. That species, described in 1834, kept turning up across continents around the world — or so biologists thought for more than a century. Realization eventually dawned that the single species that could live in such varied places was actually a complex of close cousins.

And now M. shonaicus adds yet another cousin to a group of about 30. Who knows where the next one will turn up. “I think there are lots more to be identified,” Arakawa says.

Adult mice and other rodents sprout new nerve cells in memory-related parts of their brains. People, not so much. That’s the surprising conclusion of a series of experiments on human brains of various ages first described at a meeting in November (SN: 12/9/17, p. 10). A more complete description of the finding, published online March 7 in Nature, gives heft to the controversial result, as well as ammo to researchers looking for reasons to be skeptical of the findings.

In contrast to earlier prominent studies, Shawn Sorrells of the University of California, San Francisco and his colleagues failed to find newborn nerve cells in the memory-related hippocampi of adult brains. The team looked for these cells in nonliving brain samples in two ways: molecular markers that tag dividing cells and young nerve cells, and telltale shapes of newborn cells. Using these metrics, the researchers saw signs of newborn nerve cells in fetal brains and brains from the first year of life, but they became rarer in older children. And the brains of adults had none.

There is no surefire way to spot new nerve cells, particularly in live brains; each way comes with caveats. “These findings are certain to stir up controversy,” neuroscientist Jason Snyder of the University of British Columbia writes in an accompanying commentary in the same issue of Nature.

“Pop” goes the knuckle — but why?

Scientists disagree over why cracking your knuckles makes noise. Now, a new mathematical explanation suggests the sound results from the partial collapse of tiny gas bubbles in the joints’ fluid.

Most explanations of knuckle noise involve bubbles, which form under the low pressures induced by finger manipulations that separate the joint. While some studies pinpoint a bubble’s implosion as the sound’s source, a paper in 2015 showed that the bubbles don’t fully implode. Instead, they persist in the joints up to 20 minutes after cracking, suggesting it’s not the bubble’s collapse that creates noise, but its formation (SN: 5/16/15, p. 16).
But it wasn’t clear how a bubble’s debut could make sounds that are audible across a room. So two engineers from Stanford University and École Polytechnique in Palaiseau, France, took another crack at solving the mystery.

The sound may come from bubbles that collapse only partway, the two researchers report March 29 in Scientific Reports. A mathematical simulation of a partial bubble collapse explained both the dominant frequency of the sound and its volume. That finding would also explain why bubbles have been observed sticking around in the fluid.

Shimmering, gelatinous comb jellies wouldn’t appear to have much to hide. But their mostly see-through bodies cloak a nervous system unlike that of any other known animal, researchers report in the April 21 Science.

In the nervous systems of everything from anemones to aardvarks, electrical impulses pass between nerve cells, allowing for signals to move from one cell to the next. But the ctenophores’ cobweb of neurons, called a nerve net, is missing these distinct connection spots, or synapses. Instead, the nerve net is fused together, with long, stringy neurons sharing a cell membrane, a new 3-D map of its structure shows.
While the nerve net has been described before, no one had generated a high-resolution, detailed picture of it.

It’s possible the bizarre tissue represents a second, independent evolutionary origin of a nervous system, say Pawel Burkhardt, a comparative neurobiologist at the University of Bergen in Norway, and colleagues.

Superficially similar to jellyfish, ctenophores are often called comb jellies because they swim using rows of beating, hairlike combs. The enigmatic phylum is considered one of the earliest to branch off the animal tree of life. So ctenophores’ possession of a simple nervous system has been of particular interest to scientists interested in how such systems evolved.

Previous genetics research had hinted at the strangeness of the ctenophore nervous system. For instance, a 2018 study couldn’t find a cell type in ctenophores with a genetic signature that corresponded to recognizable neurons, Burkhardt says.

Burkhardt, along with neurobiologist Maike Kittelmann of Oxford Brookes University in England and colleagues, examined young sea walnuts (Mnemiopsis leidyi) using electron microscopes, compiling many images to reconstruct the entire net structure. Their 3-D map of a 1-day-old sea walnut revealed the funky synapse-free fusion between the five sprawling neurons that made up the tiny ctenophore’s net.
The conventional view is that neurons and the rest of the nervous system evolved once in animal evolutionary history. But given this “unique architecture” and ctenophores’ ancient position in the animal kingdom, it raises the possibility that nerve cells actually evolved twice, Burkhardt says. “I think that’s exciting.”

But he adds that further work — especially on the development of these neurons — is needed to help verify their evolutionary origin.

The origins of the animal nervous system is a murky area of research. Sponges — the traditional competitors for the title of most ancient animal — don’t have a nervous system, or muscles or fundamental vision proteins called opsins, for that matter. But there’s been mounting evidence to suggest that ctenophores are actually the most ancient animal group, older even than sponges (SN: 12/12/13).

If ctenophores arose first, it “implies that either sponges have lost a massive number of features, or that the ctenophores effectively evolved them all independently,” says Graham Budd, a paleobiologist at Uppsala University in Sweden who was not involved in the research.

If sponges emerged first, it’s still possible that ctenophores evolved their nerve net independently rather than inheriting it from a neuron-bearing ancestor, Burkhardt says. Ctenophores have other neurons outside the nerve net, such as mesogleal neurons embedded in a ctenophore’s gelatinous body layer and sensory cells, the latter of which may communicate with the nerve net to adjust the beating of the combs. So, it’s possible they’re a mosaic of two nervous systems of differing evolutionary origins.

But Joseph Ryan, a bioinformatician at the University of Florida in Gainesville, doesn’t think the results necessarily point to the parallel evolution of a nervous system. Given how long ctenophores have been around — especially if they are older than sponges — the ancestral nervous system may have had plenty of time to evolve into something weird and highly-specialized, says Ryan, who was not part of the study. “We’re dealing with close to a billion years of evolution. We’re going to expect strange things to happen.”

The findings are “one more bit of the jigsaw puzzle,” Budd says. “There’s a whole bunch we don’t know about these rather common and rather well-known animals.”

For instance, it’s unclear how the nerve net works. Our neurons use rapid changes in voltage across their cell membranes to send signals, but the nerve net might work quite differently, Burkhardt says.

There are reports of potentially similar systems in other animals, such as by-the-wind-sailor jellies (Velella velella). Studying them in detail, along with nerve nets in other ctenophore species, could determine just how unusual this synapse-less nervous system is.

Northern elephant seals are the true masters of the power nap.

On long trips out to sea, the seals snooze less than 20 minutes at a time, researchers report in the April 21 Science. The animals average just two hours of shut-eye per day while swimming offshore for months — rivaling African elephants for the least sleep measured among mammals (SN: 3/1/17).

“It’s important to map these extremes of [sleep behavior] across the animal kingdom to get a better sense of the evolution and the function of sleep for all mammals, including humans,” says Jessica Kendall-Bar, an ecophysiologist at the University of California, San Diego. Knowing how seals catch their z’s could also guide conservation efforts to protect places where they sleep.
Northern elephant seals (Mirounga angustirostris) spend most of the year out in the Pacific Ocean. On these odysseys, the animals forage around the clock for fish, squid and other food to sustain their enormous bodies, which can be as hefty as a car (SN: 2/4/22). Because northern elephant seals are most vulnerable to sharks and killer whales at the surface, they come up for air only a couple minutes at a time between 10- to 30-minute deep dives (SN: 9/28/02).

“People had known that these seals dive almost all the time when they’re out in the ocean, but it wasn’t known if and how they sleep,” says Niels Rattenborg, a neurobiologist at the Max Planck Institute for Biological Intelligence in Seewiesen, Germany, who was not involved in the study.

To find out if the seals sleep while diving, Kendall-Bar and her colleagues developed a watertight EEG cap for the animals. Using the cap and other sensors, the team tracked the brain waves, heart rates and 3-D motion of 13 young female seals, including five at a lab and six hanging out at coastal Año Nuevo State Park north of Santa Cruz, Calif. EEG data recorded while seals were slumbering revealed what the animals’ naptime brain waves looked like.

Kendall-Bar’s team also took two sensor-strapped seals from Año Nuevo and released them at another beach about 60 kilometers south. To swim home, the seals had to cross the deep Monterey Canyon — a locale similar to the deep, predator-fraught waters frequented by seals on months-long foraging trips. Matching the seals’ EEG readings to their diving motions on this journey showed how northern elephant seals sleep on long voyages.

The animals first swim 60 to 100 meters below the surface, then relax into a glide, Kendall-Bar says. As they nod off into slow-wave sleep, the animals keep holding themselves upright for several minutes. But as REM sleep sets in, so does sleep paralysis. The animals flip upside-down and drift in gentle spirals toward the seafloor. Seals can descend hundreds of meters deep during these naps — far below where their predators normally prowl. When the seals wake after five to 10 minutes of sleep, they swim up to the surface. The whole routine takes about 20 minutes.

Looking for that distinct sleep dive motion, the researchers could pick out naps in the dive records of 334 adult seals that had been outfitted with tracking tags from 2004 to 2019. Those sleep patterns revealed that northern elephant seals conk out, on average, around two hours per day while on months-long foraging missions. But the seals sleep nearly 11 hours per day while on land to mate and molt, where they can indulge in long, beachside siestas without worrying about predators.
“What the seals are doing might be something like what we do when we sleep in on the weekend, but it’s on a much longer timescale,” Rattenborg says. He and his colleagues have found a similar feast-and-famine style of sleep in great frigate birds, which fly over the ocean (SN: 6/30/16). “Although they can sleep while they’re flying,” he says, “they sleep less than an hour a day for up to a week at a time, and once back on land, they sleep over 12 hours a day.”

Curiously, northern elephant seals’ sleep habits are quite different from how other marine mammals have been seen sleeping in labs. “Many of them … sleep in just half of their brain at a time,” Kendall-Bar says. That half-awake state allows dolphins, fur seals and sea lions to practice constant vigilance, literally sleeping with one eye open.

“I think it’s pretty cool that elephant seals are doing this without [one-sided] sleep,” Kendall-Bar says. “They’re shutting off both halves of their brain completely and leaving themselves vulnerable.” It seems the key to enjoying such deep sleep is sleeping deep in the sea.

MINNEAPOLIS — Bubbles of radiation billowing from the galactic center may have started as a stream of electrons and their antimatter counterparts, positrons, new observations suggest. An excess of positrons zipping past Earth suggests that the bubbles are the result of a burp from our galaxy’s supermassive black hole after a meal millions of years ago.

For over a decade, scientists have known about bubbles of gas, or Fermi bubbles, extending above and below the Milky Way’s center (SN: 11/9/10). Other observations have since spotted the bubbles in microwave radiation and X-rays (SN: 12/9/20). But astronomers still aren’t quite sure how they formed.
A jet of high-energy electrons and positrons, emitted by the supermassive black hole in one big burst, could explain the bubbles’ multi-wavelength light, physicist Ilias Cholis reported April 18 at the American Physical Society meeting.

In the initial burst, most of the particles would have been launched along jets aimed perpendicular to the galaxy’s disk. As the particles interacted with other galactic matter, they would lose energy and cause the emission of different wavelengths of light.

Those jets would have been aimed away from Earth, so those particles can never be detected. But some of the particles could have escaped along the galactic disk, perpendicular to the bubbles, and end up passing Earth. “It could be that just now, some of those positrons are hitting us,” says Cholis, of Oakland University in Rochester, Mich.

So Cholis and Iason Krommydas of Rice University in Houston analyzed positrons detected by the Alpha Magnetic Spectrometer on the International Space Station. The pair found an excess of positrons whose present-day energies could correspond to a burst of activity from the galactic center between 3 million and 10 million years ago, right around when the Fermi bubbles are thought to have formed, Cholis said at the meeting.

The result, Cholis said, supports the idea that the Fermi bubbles came from a time when the galaxy’s central black hole was busier than it is today.

Since early 2022, sea urchins have been mysteriously dying off across the Caribbean. Now scientists say they have identified the main culprit: a type of relatively large, single-celled marine microorganism called a scuticociliate.

The discovery is a little surprising given that “ciliates are not normally seen as agents of mass mortality,” says Ian Hewson, a marine microbial ecologist at Cornell University. But the evidence, described April 19 in Science Advances, all points to the organism, Philaster apodigitiformis, infecting the urchins, he says. “In all of my years of investigating marine diseases, this is the one which we are 100 percent confident about.”
Scuticociliates are found across the world’s oceans. Given their ubiquity, it’s unknown what conditions may have allowed P. apodigitiformis to become so detrimental to the urchins. It’s also unclear how it causes infection.

While there are no available treatments for the disease, knowing the pathogen’s identity allows for the development of possible options.
Long-spined sea urchins (Diadema antillarum) play a crucial role in Caribbean coral reefs, grazing algae that would otherwise smother corals (SN: 9/27/22). In the 1980s, the urchins nearly disappeared during a massive die-off, the cause of which remains unknown (SN: 6/16/84).

Decades of restoration efforts had made some progress when an alarmingly similar mortality event began to spread in January 2022, wiping out thousands of urchins. This time, scientists across the United States and the Caribbean sprang into action.

Three teams independently reached the same conclusion about P. apodigitiformis, using different approaches. Hewson’s team compared the entire set of active genes, or the transcriptome, of healthy and sick urchins from 23 sites across the Caribbean. The researchers noticed that some of the active genes in the sick urchins’ transcriptomes weren’t from the urchins but from the microorganism. Meanwhile, teams in Florida and Hawaii observed the scuticociliates in the tissues and fluids of sick urchins, reinforcing the genetic finding.

Upon a closer look, the scuticociliates tended to cluster in the sick urchins’ body walls and at the base of their spines. The microorganisms were absent from healthy urchins.
The next step was to isolate the pathogen and infect healthy urchins. Four days after infection, six of 10 infected urchins lost many spines — a common symptom of sick urchins. None of the uninfected urchins lost spines.

“It was really exciting to see,” says Michael Sweet, a marine disease ecologist at the University of Derby in England, who wasn’t involved in the study. “Scary, but also exciting to see the [ciliate’s] name mentioned in a different context because Philaster has never been related to urchin diseases before.” His research points to the involvement of the genus in several coral diseases.

While the scuticociliate clearly plays a pivotal role, Sweet says, there are almost certainly other factors at play, such as other microorganisms or environmental stressors, that could help explain what triggered the start of the recent die-off.

For now, it’s unknown if the same pathogen was involved in the 1980s die-off. Hewson’s team hopes to answer that question by looking at museum specimens from the period.