There are no teensy cups. But a urine test for wild mosquitoes has for the first time proved it can give an early warning that local pests are spreading diseases.
Mosquito traps remodeled with a pee-collecting card picked up telltale genetic traces of West Nile and two other worrisome viruses circulating in the wild, researchers in Australia report April 4 in the Journal of Medical Entomology.
The tests were based on an innovative saliva monitoring system unveiled in 2010: traps that lure mosquitoes into tasting honey-coated cards. Among its advantages, this card-based medical testing doesn’t need the constant refrigeration that checking whole mosquitoes does. And it’s not as labor intensive as monitoring sentinel chickens or pigs for signs of infection. But testing traces of mosquito saliva left on these cards comes close to the limits of current molecular methods for detecting viruses. In part, it’s an issue of volume. A mosquito drools fewer than five nanoliters of saliva when it tastes a card. In comparison, mosquitoes excrete about 1.5 microliters of liquid per pee, offering a veritable flood of material. So Dagmar Meyer of James Cook University in Cairns, Australia and her colleagues created urine collectors using standard overnight light traps and longer-standing traps that exhale delicious carbon dioxide, a mosquito come-hither.
The team set out 29 urine traps in two insect-rich spots in Queensland along with traps equipped to catch mosquito saliva. When mosquitoes fell for the trick and entered a urine trap, their excretions dripped through a mesh floor onto a collecting card. Adding a moist wick of water kept trapped mosquitoes alive and peeing longer, thus improving the sample. Pee traps picked up three viruses — West Nile, Ross River and Murray Valley encephalitis — while the saliva ones detected two, the researchers report.
No one should have to sleep with the fishes, but new research on zebrafish suggests that we sleep like them.
Sleeping zebrafish have brain activity similar to both deep slow-wave sleep and rapid eye movement, or REM, sleep that’s found in mammals, researchers report July 10 in Nature. And the team may have tracked down the cells that kick off REM sleep.
The findings suggest that the basics of sleep evolved at least 450 million years ago in zebrafish ancestors, before the evolution of animals that give birth to live young instead of laying eggs. That’s 150 million years earlier than scientists thought when they discovered that lizards sleep like mammals and birds (SN: 5/28/16, p. 9).
What’s more, sleep may have evolved underwater, says Louis C. Leung, a neuroscientist at Stanford University School of Medicine. “These signatures [of sleep] really have important functions — even though we may not know what they are — that have survived hundreds of millions of years of evolution.” In mammals, birds and lizards, sleep has several stages characterized by specific electrical signals. During slow-wave sleep, the brain is mostly quiet except for synchronized waves of electrical activity. The heart rate decreases and muscles relax. During REM or paradoxical sleep, the brain lights up with activity almost like it’s awake. But the muscles are paralyzed (except for rapid twitching of the eyes) and the heart beats erratically.
For many years, scientists have known that fruit flies, nematodes, fish, octopuses and other creatures have rest periods reminiscent of sleep. But until now, no one could measure the electrical activity of those animals’ brains to see if that rest is the same as mammals’ snoozing.
Leung and colleagues developed a system to do just that in zebrafish by genetically engineering them to make a fluorescent molecule that lights up when it encounters calcium, which is released when nerve cells and muscles are active. By following the flashes of light using a light sheet microscope, the researchers tracked brain and muscle activity in the naturally transparent fish larvae.
The next task was to lull fish asleep under the microscope. In some experiments, the team added drugs that trigger either slow-wave or REM sleep in mammals to the fish’s water. In others, researchers deprived fish of sleep for a night or tuckered the fish out with lots of activity during the day. Results from all the snooze-inducing methods were the same.
Sleeping fish have two distinct types of brain activity while sleeping, the team found. One, similar to slow-wave sleep, was characterized by short bursts of activity in some nerve cells in the brain. The researchers call that state slow-bursting sleep. REM-like sleep, which the researchers dubbed “propagating-wave sleep,” was characterized by frenzied brain activity that spreads like a wave through the brain. The researchers aren’t calling the sleep phases REM or slow-wave sleep because there are some minor differences between the way fish and mammals sleep. A group of cells that line hollow spaces called ventricles deep in the brain seems to trigger that wave of REM-like brain activity. These ependymal cells dip fingerlike cilia into the cerebral spinal fluid that bathes the ventricles and the central nervous system. The cells appear to beat their cilia faster as amounts of a well-known, sleep-promoting hormone called melanin-concentrating hormone in the fluid increases, the researchers discovered. It’s unclear how the ependymal cells communicate with the rest of the brain to set off REM-like activity. Such cells are also present in mammals, but no one has yet been able to see that deeply into the brains of sleeping mammals to determine whether the cells play a role in sleep. But knowing about these cells may help researchers develop better sleep aids, Leung says.
Just as in mammals, zebrafish’s whole bodies are affected during sleep. Their muscles relax during sleep and their hearts slow from about 200 beats per minute when awake to about 110 to 120 beats per minute while asleep during the slow-wave–like sleep. During the REM-like sleep, the heart slows even more to about 90 beats per minute and loses its regular rhythm. And the fish’s muscles also go completely slack. The one characteristic that the fish lack is rapid eye movement. Instead, the eyes roll back into their sockets, says study coauthor Philippe Mourrain, a biologist at Stanford University School of Medicine.
Lack of eye movement could indicate that emotion-processing parts of the brain, such as the amygdala, aren’t as active in zebrafish as they are in mammals, says sleep researcher Allan Pack of the University of Pennsylvania Perelman School of Medicine. With their brain-activity monitoring, the researchers have taken sleep research “to the next level,” says Pack, and “they present pretty compelling evidence” of slow-wave and REM-like sleep in the fish.
The whole-body involvement that the researchers documented solidifies the argument that fish sleep is similar to mammals, says neuroscientist Paul Shaw of Washington University School of Medicine in St. Louis. In all organisms known to snooze, “sleep is manifest everywhere” in the body, he says.
Future experiments may show why poor sleep or a lack of Zs contributes to health problems in people, such as obesity, heart disease and diabetes.
Ice sheets expanded across much of northern Europe from around 25,000 to 19,000 years ago, making a huge expanse of land unlivable. That harsh event set in motion a previously unrecognized tale of two human populations that played out at opposite ends of the continent.
Western European hunter-gatherers outlasted the icy blast in the past. Easterners got replaced by migrations of newcomers.
That’s the implication of the largest study to date of ancient Europeans’ DNA, covering a period before, during and after what’s known as the Last Glacial Maximum, paleogeneticist Cosimo Posth and colleagues report March 1 in Nature. As researchers have long thought, southwestern Europe provided refuge from the last Ice Age’s big chill for hunter-gatherers based in and near that region, the scientists say. But it turns out that southeastern Europe, where Italy is now located, did not offer lasting respite from the cold for nearby groups, as previously assumed.
Instead, those people were replaced by genetically distinct hunter-gatherers who presumably had lived just to the east along the Balkan Peninsula. Those people, who carried ancestry from parts of southwestern Asia, began trekking into what’s now northern Italy by about 17,000 years ago, as the Ice Age began to wane.
“If local [Ice Age] populations in Italy did not survive and were replaced by groups from the Balkans, this completely changes our interpretation of the archaeological record,” says Posth, of the University of Tübingen in Germany.
Posth and colleagues’ conclusions rest on analyses of DNA from 356 ancient hunter-gatherers, including new molecular evidence for 116 individuals from 14 countries in Europe and Asia. Excavated human remains that yielded DNA dated to between about 45,000 and 5,000 years ago (SN: 4/7/21).
Comparisons of sets of gene variants inherited by these hunter-gatherers from common ancestors enabled the researchers to reconstruct population movements and replacements that shaped ancient Europeans’ genetic makeup. For the first time, ancient DNA evidence included individuals from what’s known as the Gravettian culture, which dates from about 33,000 to 26,000 years ago in central and southern Europe, and from southwestern Europe’s Solutrean culture, which dates to between about 24,000 and 19,000 years ago. Contrary to expectations, makers of Gravettian tools came from two genetically distinct groups that populated western and eastern Europe for roughly 10,000 years before the Ice Age reached its peak, Posth says. Researchers have traditionally regarded Gravettian implements as products of a biologically uniform population that occupied much of Europe.
“What we previously thought was one genetic ancestry in Europe turned out to be two,” says paleogeneticist Mateja Hajdinjak of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, who did not participate in the new study. And “it seems that western and southwestern Europe served as a [refuge from glaciation] more than southeastern Europe and Italy.”
Descendants of the western Gravettian population, who are associated with Solutrean artifacts and remnants of another ancient culture in western Europe that ran from about 19,000 to 14,000 years ago, outlasted the Ice Age before spreading northeastward across Europe, the researchers say.
Further support for southwestern Europe as an Ice Age refuge comes from DNA extracted from a pair of fossil teeth that belonged to an individual linked to the Solutrean culture in southern Spain. That roughly 23,000-year-old adult was genetically similar to western European hunter-gatherers who lived before and after the Last Glacial Maximum, Max Planck paleogeneticist Vanessa Villalba-Mouco and colleagues, including Posth, report March 1 in Nature Ecology & Evolution.
Meanwhile, the genetic evidence suggests that hunter-gatherers in what’s now Italy were replaced by people from farther east, probably based in the Balkan region. Those newcomers must have brought with them a distinctive brand of stone artifacts, previously excavated at Italian sites and elsewhere in eastern Europe, known as Epigravettian tools, Posth says. Many archaeologists have suspected that Epigravettian items were products of hunter-gatherers who clustered in Italy during the Ice Age’s peak freeze.
But, Hajdinjak says, analyses of DNA from fossils of Ice Age Balkan people are needed to clarify what groups moved through Italy, and when those migrations occurred.
Ultimately, descendants of Ice Age migrants into Italy reached southern Italy and then western Europe by around 14,000 years ago, Posth and colleagues say. Ancient DNA evidence indicates that, during those travels, they left a major genetic mark on hunter-gatherers across Europe.
Like so many others, I’ve been watching the HBO series The Last of Us. It’s a classic zombie apocalypse drama following Joel (played by Pedro Pascal) and Ellie (Bella Ramsey) as they make their way across the former United States (now run by a fascist government called Fedra).
I’m a big fan of zombie and other post-apocalyptic fiction. And my husband had told me how good the storyline is in the video game that inspired the series, so I was prepared for interesting storytelling. What I didn’t expect was to be so intrigued by the science behind the sci-fi. In the opening minutes of the series, two scientists on a fictional 1968 talk show discuss the microbes that give them pandemic nightmares. One says it’s fungi — not viruses or bacteria — that keep him awake. Especially worrisome, he says, are the fungi that control rather than kill their hosts. He gives the example of fungi that turns ants into living zombies, puppeteering the insects by flooding their brains with hallucinogens.
He goes on to warn that even though human body temperature keeps us fungus-free, that might not be true if the world got a little bit warmer. He predicts that as the thermostat climbs, a fungus that hijacks insects could mutate a gene allowing it to burrow into human brains and take control of our minds. Such a fungus could induce its human puppets to spread the fungus “by any means necessary,” he says. What’s worse, there are no preventatives, treatments or cures, nor any way to make them.
It’s a brief segment, but it had me hooked. It all sounded so chilling and … plausible. After all, fungi like ones that cause nail infections, yeast infections and ringworm already infect people.
So I consulted some experts on fungal infections to find out whether this could actually happen.
I’ve got good news and bad news.
First, the bad news.
Bad news: Climate change has already helped one fungus mutate to infect humans I wanted to know if warming has spurred any fungi to mutate and become infectious. So I called Arturo Casadevall. He has been thinking about fungi and heat for a long time. He’s proposed that the need to avoid fungal infections may have provided the evolutionary pressure that drove mammals and birds to evolve warm-bloodedness (SN: 12/3/10).
Most fungal species simply can’t reproduce at human body temperature (37° Celsius, or 98.6° Fahrenheit). But as the world warms, “these strains either have to die or adapt,” says Casadevall, a microbiologist who specializes in fungal infections at Johns Hopkins Bloomberg School of Public Health. That raises the possibility that fungi that now infect insects or reptiles could evolve to grow at temperatures closer to human body temperature.
At the same time, humans’ average body temperature has been falling since the 19th century, at least in high-income countries, researchers reported in eLife in 2020. One study from the United Kingdom pegs average body temperature at 36.6° C (97.9° F). And some of us are even cooler.
Fungi’s possible adaptation to higher heat and humans’ cooling body temperature are on a collision course, Casadevall says. He and colleagues presented evidence of one such crash. Climate change may have allowed a deadly fungus called Candida auris to acclimate to human body temperatures (SN: 7/26/19). A version of the fungus that could infect humans independently emerged on three continents from 2012 to 2015. “It’s not like someone took a plane a spread it. These things came out of nowhere simultaneously,” Casadevall says.
Some people argue that the planet hasn’t warmed enough to make fungi a problem, he says. “But you have to think about all the really hot days [that come with climate change]. Every really hot day is a selection event,” in which many fungi will die. But some of those fungi will have mutations that help them handle the heat. Those will survive. Their offspring may be able to survive future even hotter heat waves until human body temperature is no challenge.
Fungi that infect people are usually not picky about their hosts, Casadevall says. They will grow in soil or — if given an opportunity — in people, pets or in other animals. The reason fungi don’t infect people more often is that “the world is much colder than we are, and they have no need of us,” he says.
When people do get infected, the immune system usually keeps the fungi in check. But fungal infections can cause serious illness or be deadly, particularly to people with weakened immune systems (SN: 11/29/21; SN: 1/10/23).
The second episode of The Last of Us reveals that the zombie-creating fungi initially spread through people eating contaminated flour. Then, the infected people attack and bite others, spreading the fungus.
In real life, most human infections arise from breathing in spores. But Casadevall says it’s “not implausible” that people could get infected by eating spores or by being bitten.
Also bad: Fungal genes can adapt to higher heat I also wondered exactly how a fungus could evolve in response to heat. Asiya Gusa, a fungal researcher at Duke University School of Medicine, has published one possibility.
In 2020, she and colleagues reported in the Proceedings of the National Academy of Sciences on how one fungus mutated at elevated temperature to become harder to fight.
Cryptococcus deneoformans, which already infects humans (though it’s no zombie-maker), became resistant to some antifungal drugs when grown at human body temperature. The resistance was born when mobile bits of DNA called transposons (often called jumping genes) hopped into a few genes needed for the antifungals to work.
In a follow-up study, Gusa and colleagues grew C. deneoformans at either 30° C or 37° C for 800 generations, long enough to detect multiple changes in their DNA. Fungi had no problem growing at the balmy 30° C (86° F), the temperature at which researchers typically grow fungi in the lab. But their growth slowed at the higher temperature, a sign that the fungi were under stress from the heat.
In C. deneoformans, that heat stress really got things jumping. One type of transposon accumulated a median of 12 extra copies of itself in fungi grown at body temperature. By contrast, fungi grown at 30° C tended to pick up a median of only one extra copy of the transposon. The team reported those results January 20 in PNAS. The researchers don’t yet know the effect the transposon hops might have on the fungi’s ability to infect people, cause disease or resist fungus-fighting drugs.
So yeah, the bad news is not great. Fungi are mutating in the heat and at least one species has gained the ability to infect people thanks to climate change. Other fungi that infect people are more widespread than they were in the 1950s and 1960s, also thanks to a warming world (SN: 1/4/23).
But I promised good news. And here it is.
Good news: Human brains may resist zombification It may not be our body temperature, but our brain chemistry, that protects us from being hijacked by zombifying fungi.
I consulted Charissa de Bekker and Jui-Yu Chou, two researchers who study the Ophiocordyceps fungi that are the model for the TV show’s fungal menace. These fungi infect ants, flooding the insects with a cocktail of chemicals that steer the ants to climb plants. Once in position, the ants chomp down and the chemicals keep the jaw muscles locked in place (SN: 7/17/19).
Unlike most fictional zombies, the ants are alive during this process. “A lot of people get the misconception that we work on undead ants,” says de Bekker, a microbiologist at Utrecht University in the Netherlands. She’s glad to see the show “stick to the story of the host being very much alive while its behaviors change.” The fungi even help preserve the ant, keeping it alive even while feeding on it. But eventually the ant dies. Then a mushroom rises from the corpse, showering spores onto the ground where other ants may become infected.
Related species of Ophiocordyceps infect various species of ants and other insects. But each fungal species is very specific to the host it infects. That’s because the fungi had to individualize the chemicals they use to control the particular species they infect. The ability to manipulate behavior comes at the cost of not being able to infect multiple species. A fungus that specializes in infecting ants probably can’t get past humans’ immune systems, says Chou, a fungal researcher at the National Changhua University of Education in Taiwan. “Think of a key that fits into a specific lock. It is only this unique combination that will trigger the lock to open,” he says.
Even if the fungi evolved to withstand human body temperature and immune system attacks, they probably couldn’t take control of our minds, de Bekker says. “Manipulation is like a whole different ballgame. You need a ton of additional tools to get there.” It took millions of years of coevolution for the fungi to master piloting ants, after all.
While fungi do make mind-altering chemicals that can affect human behavior (LSD and psilocybin, for instance), Casadevall agrees that fungi that mind control insects probably won’t turn humans into zombies. “It’s not one of my worries,” he says.
Infected ants don’t turn into vicious, biting zombies either, de Bekker says. “If anything, we actually see the healthy ants being aggressive toward infected individuals, once they figure out that they’re infected, to basically get rid of them.” That “social immunity” helps protect the rest of the nest from infection.
Also good: Humans are innovative enough to develop treatments The fictional scientist’s assertion that we couldn’t prevent, treat or cure these fungal infections is also a stretch.
Antifungal drugs exist and they cure many fungal infections, though some infections may persist. Some that spread to the brain may be particularly difficult to clear.Some fungi are also evolving resistance to the drugs. And a few fungal vaccines are in the works, although they may not be ready for years.
The experts I talked to say they hope the show will bring attention to real fungal diseases.
Gusa was especially glad to see fungi in the limelight. And she shares my fondness for that retro series opening in which the scientist predicts climate change could spawn mind-controlling fungi bent on infecting every person on the planet.
“I was pretty much yelling at the TV when I watched the [show’s] intro,” in an excited kind of way, she says. “This is the foundation of a lot of my grant funding … the threat of thermal adaptation of fungi.… To see it played out on the screen was something kind of fun.”
Fledgling crustaceans have eyes like the sea, a peculiarity that could help them hide from predators.
Young shrimp, crab or lobster larvae already rock nearly translucent bodies to stay out of view. But dark eye pigments essential for vision pose the risk of exposing the animals anyway.
Some see-through ocean animals rely on mirrored irises or minuscule eyes to avoid detection. Young shrimp and prawns, on the other hand, camouflage their dark pigments behind light-reflecting glass made of tiny, crystalline spheres, researchers report in the Feb. 17 Science. Variations in the size and placement of the orbs allow the crustaceans’ eyes to shine light that precisely matches the color of the surrounding water, possibly rendering them invisible to predators on the hunt for a meal.
Technologies that mimic the nanospheres’ structure could one day inspire more efficient solar energy or bio-friendly paints, the scientists say.
“I’ve often wondered what’s going on with [these animals’] eyeshine,” says evolutionary biologist Heather Bracken-Grissom of Florida International University in Miami, who was not involved in the study. She and colleagues often collect crustaceans from the deep sea, giving them nicknames like “blue-eyed arthropod” or “green-eyed, weird-looking shrimp” because the creatures don’t resemble their adult forms. Now, she says, that eye color makes sense.
In the study, chemist Keshet Shavit and colleagues used an electron microscope to peer into the eyes of lab-raised and wild crustaceans. Inside shrimp and prawn eyes, the team found crystalline nanospheres made of isoxanthopterin, a molecule that reflects light.
The spheres are a bit like disco balls, with highly reflective surfaces pointing outward, says study coauthor Benjamin Palmer, a chemist at Ben-Gurion University of the Negev in Beer-Sheva, Israel. Each sphere is made of thin, isoxanthopterin plates that stick together to form balls that range in size from around 250 to 400 nanometers in diameter.
These balls are arranged in clusters at the base of protein-dense cones that focus light on the animal’s light-sensing nerves, and form a protective cover over the pigmented cells. But crustacean larvae can still see because there are small holes in the glass, Palmer says. “It’s basically allowing light to go down to the retina on some specific angles, but on other angles, it’s reflecting light back.” The size and order of the spheres seem to influence the color of the reflected light, the team’s observations and computer simulations show.
“The correlation between the particle size and the eyeshine color is beyond amazing,” says Shavit, also at Ben-Gurion University. Nanosphere size appears to help the animals’ eyes match the color of their native habitat, helping the critters blend into the background.
Blue-eyed shrimp that inhabit the Gulf of Aqaba’s clear blue waters off the coast of Israel, for instance, have spheres that are approximately 250 to 325 nanometers in diameter. The 400-nanometer-wide spheres of a freshwater prawn (Macrobrachium rosenbergii) glitter yellow-green, mimicking muddy waters found in the salty estuaries where they live. The prawn’s eyes also seem to be able to reflect different colors in different environments. Individuals exposed to sunlight for four hours in the lab had silvery yellow eyes, possibly a result of nanospheres arranged in a disorganized jumble. But individuals left in the dark overnight had green eyes. Their nanospheres are arranged in layers — though the orbs within each layer are still disorganized, Palmer says.
Such adaptable eyes could help larvae move undetected through different parts of the ocean as changing light levels alter the color of the water, Bracken-Grissom says. At night, young crustaceans migrate to shallow waters to feed and dive back down when the sun rises. “If they are in fact using it as a form of camouflage, it would be an ingenious way to camouflage themselves as they move through these different light environments.”
Following the most severe known mass extinction in Earth’s history, vibrant marine ecosystems may have recovered within just a million years, researchers report in the Feb. 10 Science. That’s millions of years faster than previously thought. The evidence, which lies in a diverse trove of pristine fossils discovered near the city of Guiyang in South China, may represent the early foundations of today’s ocean-dwelling ecosystems.
The conventional story was that the ocean was kind of dead for millions of years after this mass extinction, says paleontologist Peter Roopnarine of the California Academy of Sciences in San Francisco, who was not involved in the research. “Well, that’s not true. The ocean [was] very much alive.” The Great Dying, or Permian-Triassic mass extinction, occurred around 251.9 million years ago, at the end of the Permian Period, after a series of massive volcanic eruptions (SN: 12/6/18).
“The oceans warmed significantly, and there’s evidence for acidification, deoxygenation [causing widespread dead zones], as well as poisoning,” says Roopnarine. “There [were] a lot of toxic elements like sulfur entering into parts of the ocean.”
Life in the seas suffered. More than 80 percent of marine species went extinct. Some researchers have even proposed that entire trophic levels — castes in an ecosystem’s food web — may have vanished.
Figuring out how long life took to fully recover in the wake of all that loss has been challenging. In 2010, researchers studying fossils from the Luoping biota in China proposed that complex marine ecosystems fully rebounded within 10 million years. Later, other fossil finds, such as the Paris biota in the western United States and the Chaohu biota in China, led scientists to suggest that marine ecosystems reestablished themselves within just 3 million years.
Then in 2015, a serendipitous discovery narrowed the gap again. Paleontologist Xu Dai, then an undergraduate student at the China University of Geosciences in Wuhan, was studying rocks from the early Triassic during a field trip near the city of Guiyang, when he split open a piece of black shale. Within the rock, he discovered a surprisingly well-preserved fossil of what would later be identified as a primitive lobster.
The arthropod’s immaculate condition sparked a series of return trips. From 2015 to 2019, Dai, now at the University of Burgundy in Dijon, France, and his colleagues uncovered a bricolage of fossilized life: Predatory fish as long as baseball bats. Ammonoids in swirled shells. Eel-like conodonts. Early shrimps. Sponges. Bivalves. Fossilized poo. And the prizes kept coming. Both under and within the Guiyang biota, Dai and his colleagues discovered beds of volcanic ash. An analysis of the amounts of uranium and lead in the ash revealed that the Guiyang biota contained fossils from roughly 250.7 to 250.8 million years ago (SN: 5/2/22). The dating was further supported by the types of fossils found and by an analysis of the different forms of carbon in the rocks.
Finding a potpourri of life of this age suggests that marine ecosystems rebounded quickly after the Great Dying, within just 1 million years or so, Dai says.
Alternatively, it may indicate that the extinction event failed to wipe out entire trophic levels, says paleontologist William Foster from the University of Hamburg in Germany, who was not involved in the study. “You have this really environmentally stressful world, but some former marine ecosystems survive.”
Regardless, it seems clear that these ecosystems were hardy. Due to the motion of tectonic plates, the community preserved in the Guiyang biota was located in the tropics during the early Triassic. At that time, the temperature of the sea surface was nearly 35⁰ Celsius, and past research had suggested many organisms may have migrated away to escape the heat. But, the discovery of the Guiyang biota challenges that, Foster says. Sea creatures “are tolerating it somehow, they’re adapting.”
According to Dai, the fossils may be evidence that the roots of today’s marine ecosystems took hold shortly after the Great Dying. “These groups are related to modern fish, lobsters and shrimps, their ancestors,” he says. “The oldest time we can find similar seafood to today is [in the time of] the Guiyang biota.”
But Roopnarine is skeptical. It remains to be seen exactly how the Guiyang biota connects to today’s ecosystems, he says. The fossil assemblage could represent an ephemeral collective of life rather than a stable community, he adds, pointing out that ammonoids and conodonts went extinct.
Further work will help resolve the many questions unearthed with the Guiyang biota, Dai says. He and his colleagues plan to head back into the field this summer for the first time since 2019. When asked if he’ll be keeping his eyes peeled for another lobster, he responds: “Of course.”
Tanklike armored dinosaurs probably pummeled each other — not just predators — with huge, bony knobs attached to the ends of their tails. Thanks to new fossil findings, researchers are getting a clearer understanding of how these rugged plant eaters may have used their wicked weaponry.
Many dinosaurs known as ankylosaurids sported a heavy, potentially microwave-sized tail club. This natural sledgehammer has long been considered by both scientists and artists as a defensive weapon against predators, says Victoria Arbour, a paleontologist at the Royal British Columbia Museum in Victoria, Canada.
Fossil evidence for tail clubs’ targets was largely lacking, until Arbour and her colleagues chipped more rock away from the same skeleton they used to describe a new armored dinosaur, Zuul crurivastator, in 2017 (SN: 6/12/17).
The dinosaur had five broken spikes on its sides. The team’s statistical analyses showed the damaged spikes clustered in specific regions of the body. If a large carnivorous dinosaur made these injuries, says Arbour, they’d likely be more randomly distributed and include bite and scratch marks. Instead, the injuries are more consistent with clubbing, the researchers report December 7 in Biology Letters.
Armored dinosaurs’ tail clubs start out either absent or too tiny to mount a major defense, and they get proportionally larger with age. Similar growth patterns occur in some modern animal weaponry like antlers. It’s possible that tanklike dinosaurs sparred with each other for mates, food or territory much like male deer and giraffes do today.
And that tail could also be useful in a pinch. “Having a tail club you can swing around at the ankles of a two-legged predator is a pretty effective weapon,” says Arbour.
“Ankylosaurs are often portrayed as stupid, loner dinosaurs,” she adds. The findings “show that they probably had much more complex behaviors than we give them credit for.”
Books about the pandemic. Books about the ancient past. Books about outer space. These were a few of Science News staff’s favorite reads. If your favorite didn’t make this year’s cut, let us know what we missed at feedback@sciencenews.org.
Vagina Obscura Rachel E. Gross W.W. Norton & Co. $30
For centuries, scientists (mostly males) have ignored female biology, and women’s health has suffered. But researchers are finally paying attention, as Gross explains in this fascinating tour of what little is known about female anatomy (SN: 4/9/22, p. 29).
The Song of the Cell Siddhartha Mukherjee Scribner $32.50
Patient stories and conversations with scientific luminaries enliven this tale of cell biology’s past, present and future, and how advances in the field have reshaped medicine (SN: 11/5/22, p. 28).
Breathless David Quammen Simon & Schuster $29.99
In this portrait of the coronavirus and the scientists who study it, Quammen investigates some of the most pressing questions about the pandemic, including whether or not the coronavirus could have accidentally escaped from a lab (SN: 9/24/22, p. 28).
Virology Joseph Osmundson W.W. Norton & Co. $16.95
This wide-ranging collection of essays is a meditation on society’s complicated relationship with viruses. In pondering SARS-CoV-2, HIV and more, Osmundson calls for more equitable access to medical care (SN: 7/16/22 & 7/30/22, p. 36).
The Milky Way Moiya McTier Grand Central Publishing $27
This absorbing “autobiography,” written from the perspective of the Milky Way (a very sassy Milky Way), draws on mythology and astronomy to persuade readers that our home galaxy deserves respect and admiration (SN: 9/10/22, p. 28).
A Portrait of the Scientist as a Young Woman Lindy Elkins-Tanton William Morrow $29.99
In this moving memoir, Elkins-Tanton recounts her journey to becoming a planetary scientist and leader of a NASA asteroid mission. Her struggles with childhood trauma and sexism in her career lay bare the barriers that many women in science still face (SN: 8/13/22, p. 26).
An Immense World Ed Yong Random House $30
So much of the world is beyond the grasp of human perception, but this safari through animal senses helps readers imagine what we’re missing (SN: 7/16/22 & 7/30/22, p. 36).
How Far the Light Reaches Sabrina Imbler Little, Brown, & Co. $27
By drawing parallels between their own life and the stories of bobbit worms, octopuses, sperm whales and other deep-sea dwellers, Imbler muses on such weighty themes as adaptation, survival and sexuality.
The Last Days of the Dinosaurs Riley Black St. Martin’s Press $28.99
The basic story of the downfall of nonbird dinosaurs is familiar: They were killed off by an asteroid that slammed into Earth 66 million years ago. Using the most up-to-date science, Black fleshes out this tale, painting a vivid portrait of life before and after this apocalypse (SN: 4/23/22, p. 28).
The Rise and Reign of the Mammals Steve Brusatte Mariner Books $29.99
The perfect follow-up to Black’s book on how the Age of Dinosaurs ended is this sweeping history of how the Age of Mammals began. Brusatte traces the origins of the evolutionary innovations that have made mammals so successful (SN: 6/18/22, p. 28).
Origin Jennifer Raff Twelve $30
Exactly how and when humans first came to the Americas is still unsettled science. But Raff gathers archaeological and genetic evidence to piece together a convincing scenario. She also points out past mistreatment of Indigenous communities by geneticists and calls on researchers to do better and foster more collaborations (SN: 2/12/22, p. 29).
Pests Bethany Brookshire Ecco $28.99
So-called pests are a human invention, argues Brookshire, a former staff writer for Science News for Students (now Science News Explores). In coming face to face with rats, feral cats, pythons and even elephants, Brookshire teases out the various social factors that cause people to deem certain animals a nuisance (SN: 12/3/22, p. 26).
A parasite might be driving some wolves to lead or go solo.
Wolves in Yellowstone National Park infected with Toxoplasma gondii make more daring decisions than their uninfected counterparts, researchers report November 24 in Communications Biology. The wolves’ enhanced risk-taking means they are more likely to leave their pack, or become leaders of their own.
“Those are two decisions that can really benefit wolves, or could cause wolves to die,” says Connor Meyer, a field biologist at the University of Montana in Missoula. The findings reveal a parasite’s potent ability to influence a wolf’s social fate.
Disease is often considered important for wildlife, mostly in the context of killing its host, Meyer says. “We have evidence now that just being infected with a certain parasite — Toxoplasma — can have pretty major implications for wolf behavior.” Single-celled T. gondii has a track record of altering animal behavior. Its most important hosts are cats, which provide a breeding ground for the parasite in their small intestine. The parasite offspring hitch a ride on feline feces. Other animals then ingest the parasite, which then manipulates its new hosts’ behavior by tweaking certain hormones, making the hosts bolder or more aggressive. Infected mice, for example, can fatally lose their fear of cats, allowing the parasite to infect more hosts once the mice are consumed (SN: 1/14/20).
In Yellowstone National Park, many wolves are also infected with T. gondii, recent research has shown. So Meyer and colleagues wondered if gray wolves (Canis lupus) in the park showed any parasite mind-bending of their own. Wolves were reintroduced to Yellowstone in 1995. Ongoing study of the park’s packs meant that the researchers had access to about 26 years’ worth of blood samples, behavioral observations and movement data for 229 of the park’s wolves.
The team screened the wolf blood for antibodies against T. gondii parasites, which reveal an infection. The researchers also noted which wolves left their pack — usually a family unit consisting of a breeding pair and their offspring — or became a pack leader.
Both are high-stakes moves for a wolf, Meyer says.
Infected wolves were 11 times as likely as noninfected wolves to disperse from their pack, the team found, and about 46 times as likely to eventually become leaders. The findings fit in with T. gondii’s apparent ability to boost boldness across a wide range of warm-blooded life. The study fills a crucial gap in the Toxoplasma pool of knowledge, says Ajai Vyas, a neurobiologist at Nanyang Technological University in Singapore, who was not involved with the study.
“Most of the earlier work has been done in the lab,” Vyas says. But there are limitations to that approach, especially for re-creating how animals experience the effects of the parasite in their natural environment. Such research has “become almost like studying whale swimming behavior in backyard pools; [it] does not work very well.”
Wolves’ enhanced boldness may even form a feedback loop, the team proposes. The researchers found that not only do cougars (Puma concolor) in the park carry the parasite, but wolves’ infection rates were highest when the animals’ ranges overlapped with the park’s densest aggregations of cougars. Infected wolf leaders may be more likely to bring pack members into riskier situations, including approaching cougar territories, making additional infections more likely.
The feedback-loop idea is “very fascinating,” but more research is needed to confirm it, says Greg Milne, an epidemiologist at the Royal Veterinary College in London, who was not involved with the study. Such research may involve determining if infected wolves are more likely to migrate into an area with more cougars.
“I think people are just starting to really appreciate that personality differences in animals are a major consideration in behavior,” says study coauthor Kira Cassidy, a wildlife biologist at the Yellowstone Wolf Project in Bozeman, Mont. “Now we add a parasite-impacting behavior to the list.”
Next, the team is interested in examining the long-term consequences of a T. gondii infection, and whether infected wolves make better leaders or dispersers than uninfected wolves.
It’s also not known how infection impacts survival and reproduction rates, Cassidy says. “Infection may very well be detrimental in some ways and advantageous in others.”
As we head into our third pandemic winter, most people are all too familiar with the signs of COVID-19. The disease wears many different faces and can show up as chills, cough, difficulty breathing or other troublesome jumbles of symptoms. But sometimes, this illness can look positively peculiar.
On rare occasions, SARS-CoV-2 rears its head in body parts not typically touched by respiratory viruses. From head to COVID toe, doctors have seen a bevy of bizarre cases. Patchy tongues, puffy digits, hair loss — such issues can be worrisome for patients, says Peter Chin-Hong, an infectious diseases physician at the University of California, San Francisco.
But the outlook doesn’t have to be. That’s because such symptoms can end up going away on their own, says Chin-Hong, who has treated hundreds of people with COVID-19.
No one knows exactly how often COVID tongue, COVID toe, COVID eye or other rare conditions occur — and it’s not always clear that COVID-19 is the actual culprit. Still, the sheer scale of coronavirus infections means that SARS-CoV-2 has had many chances to show its stuff (SN: 9/8/22). The United States is now closing in on 98 million confirmed cases. Such a staggering case count means that “statistically speaking, you’re going to find people with more and more weird things,” Chin-Hong says. Doctors rely on medical case reports for leads on potential treatments and hints about how long symptoms may last. Even just knowing that someone else has had splotchy mouth sores or tender toes can be helpful, Chin-Hong says. That lets him tell his patients, “You’re not the only one,” he says. “That means a lot to a lot of people.”
Internal medicine doctor Saira Chaughtai published one such study in October in the Journal of Medical Case Reports after one of her primary care patients came in with a symptom Chaughtai had never seen. Ten days after testing positive for COVID-19, the patient’s tongue began to swell, eventually erupting in white-ringed lesions.
Certain spots looked “denuded,” says Chaughtai, of Hackensack Meridian Health in Neptune, N.J. It was as if some of the tongue’s surface bumps had been sandpapered away. The patient wasn’t someone doctors would typically consider vulnerable, either. She was 30 years old, fit and healthy.
“I was like, ‘Oh my god, COVID can do anything,’” Chaughtai remembers thinking. Oral sores can look different among patients. Chin-Hong has seen people with tongues coated white, as if they’d chewed a mouthful of tortilla chips. For Chaughtai’s patient, COVID tongue felt sensitive and irritated, with flare-ups that burned. Chaughtai wasn’t sure how to treat it.
She searched the scientific literature and prescribed an assortment of mouthwashes, which helped. But six months in, the patient’s tongue hadn’t fully healed. So Chaughtai got creative. She teamed up with a sports medicine doctor, who beamed low-level laser light at the patient’s tongue. He had previously used this photobiomodulation therapy to treat muscle injuries.
Laser light therapy makes blood vessels dilate, enhancing blood flow to treated areas, which could promote healing, Chaughtai says. It seemed to work for her patient. The tongue lesions began to heal and flare-ups subsided. The woman still occasionally feels some tongue sensitivity when stressed, but never as bad as her initial outbreak.
The effects of COVID toe About 1,300 kilometers west, a podiatrist in Crown Point, Ind., also dilated a patient’s blood vessels to treat a curious coronavirus condition: COVID toe. After infection with SARS-CoV-2, patients’ fingers and toes can plump up, sometimes painfully, and turn pink or reddish purple.
“We were seeing cases of these lesions that look like chilblains, which is something you get when you’re exposed to cold weather,” says Michael Nirenberg of Friendly Foot Care. But his patients hadn’t been in the cold — they’d been exposed to the coronavirus.
Nirenberg has seen as many as 40 people with the symptom, which he’s found tends to clear up in a month or two. But one of his patients, a 59-year-old man, just couldn’t kick COVID toe. It ultimately lingered for nearly 670 days — the longest documented case Nirenberg has seen. “The term we used was long COVID toe,” he says. Nirenberg and colleagues reported the case this spring in the Journal of Cutaneous Pathology. Nirenberg prescribed daily application of a nitroglycerin ointment to boost blood flow to the toes. That may have helped, Nirenberg says, “but I don’t know if time also did the trick.” After 22 months, the condition may have finally resolved on its own.
The number of COVID toes Nirenberg encounters these days has gone down, but he’s still seeing people come in with the condition. And though Chaughtai has not treated another case of COVID tongue, a man recently e-mailed her saying that he had suffered from a similar affliction for two years.
UCSF’s Chin-Hong says he thinks it’s important for people to know that COVID-19 can cause such a variety of symptoms (SN: 11/11/22). “We can’t really predict who’s going to get what,” he says. But in his experience, strange symptoms have tended to crop up more often in people who haven’t been vaccinated.
Such symptoms may not be as serious as COVID-affected hearts or lungs, but they can certainly look scary, Chin-Hong says. “If this is a reason why some people might get vaccinated,” he says, “I think that would be great.”
