A fungus that recently evolved to infect humans is spreading rapidly in health care facilities in the United States and becoming harder to treat, a study from the U.S. Centers for Disease Control and Prevention finds.

Candida auris infections were first detected in the United States in 2013. Each year since, the number of people infected — though still small — has increased dramatically. In 2016, the fungus sickened 53 people. In 2021, the deadly fungus infected 1,471 people, nearly twice the 756 cases from the year before, researchers report March 21 in Annals of Internal Medicine. What’s more, the team found, the fungus is becoming resistant to antifungal drugs.
The rise of cases and antifungal resistance is “concerning,” says microbiologist and immunologist Arturo Casadevall, who studies fungal infections. “You worry because [the study] is telling you what could be a harbinger of things to come.” Casadevall, of Johns Hopkins Bloomberg School of Public Health, was not involved in the CDC study.

In tests of people at high risk of infection, researchers also found 4,041 individuals who carried the fungus in 2021 but were not sick at the time. A small percentage of carriers may later get sick from the fungus, says Meghan Lyman, a medical epidemiologist in the CDC’s Mycotic Diseases Branch in Atlanta, possibly developing bloodstream infections that carry a high risk of death.

Starting in 2012, C. auris infections popped up suddenly in hospitals on three continents, probably evolving to grow at human body temperature as a result of climate change (SN: 7/26/19). The fungus, typically detected through blood or urine tests, usually infects people in health care settings such as hospitals, rehabilitation facilities and long-term care homes. Because people who get infected are often already sick, it can be hard to tell whether symptoms such as fevers are from the existing illness or an infection.
Those most at risk of infection include people who are ill; those who have catheters, breathing or feeding tubes or other invasive medical devices; and those who have repeated or long stays in health care facilities. Healthy people are usually not infected but can spread the fungus to others by contact with contaminated surfaces, including gowns and gloves worn by health care workers, Lyman says.

Growing drug resistance
Infections can be treated with antifungal drugs. But Lyman and colleagues found that the fungus is becoming resistant to an important class of such medications called echinocandins. These drugs are used as both the first line and the last line of defense against C. auris, says Casadevall.

Before 2020, six people were known to have echinocandin-resistant infections and four other people had infections resistant to all three class of existing antifungal drugs. That resistance developed during treatment using echinocandin. None of those cases passed the resistant strain to others. But in 2021, 19 people were diagnosed with echinocandin-resistant infections and seven with infections resistant to multiple drugs.

More concerning, one outbreak in Washington, D.C., and another in Texas suggested people could transmit the drug-resistant infections to each other. “Patients who had never been on echinocandins were getting these resistant strains,” Lyman says.

Some health care facilities have been able to identify cases early and prevent outbreaks. “We’re obviously very concerned,” Lyman says, “but we are encouraged by these facilities that have had success at containing it.” Using those facilities’ infection control measures may help limit cases of C. auris, she says, as well as reducing spread other fungal, bacterial and viral pathogens.

The patient arrived at the hospital one hot night in Masi-Manimba, an agricultural town unfurled along the Democratic Republic of the Congo’s Lukula River.

He couldn’t speak, he couldn’t walk, he was conscious but “barely could make … gestures,” says Béatrice Kasita, a nurse who was there when he came in. She remembers his deformed posture, how his body curved into a fetal position.

He was also unusually drowsy — a telltale sign of his illness. The patient, a 27-year-old man, had been brought in by a medical team screening villagers for sleeping sickness, a deadly parasitic disease spread via the bite of a blood-feeding fly.
Since the first case report in the late 14th century, the illness has ebbed and flowed in sub-Saharan Africa. Across the continent, the predominant form of sleeping sickness shows up in about two dozen countries, most cases now occurring in the DRC. The disease is a nightmarish scourge that can maim the brain and ultimately kill. But today, cases hover near an all-time low. In 2021, the World Health Organization reported just 747 cases of the predominant form, down from more than 37,000 in 1998.

That precipitous plunge came out of decades of work, millions of screenings, spinal taps upon spinal taps, toxic treatments and the rapid rise of safer though often burdensome ones, countless IV infusions, long hospital days and nights, medicine lugged to remote villages, and communities on constant alert for sleeping sickness’s insidious symptoms.

Now, a promising drug has fanned hope for halting transmission of the disease. Called acoziborole, the drug is taken by mouth in just a single dose. Kasita’s patient, who arrived at the hospital in June 2017, was among the first to try it.

Her hospital is one of 10 clinical trial sites in the DRC and Guinea working to test the drug with the Drugs for Neglected Diseases initiative, or DNDi, a nonprofit organization based in Geneva. In a small trial reported last year, the drug appeared to be safe and effective. A larger trial is ongoing, with results expected by the end of this year.
If the findings hold up, the drug would be “a game changer,” says Emmanuel Bottieau, an infectious disease specialist at the Institute of Tropical Medicine in Antwerp, Belgium, who is not involved with the clinical trial. A single-dose medication is “really a dream for us, coming from such a long history of very difficult or toxic or cumbersome treatments.”

But he and others know that even a game-changing drug doesn’t guarantee a win. The dominant form of sleeping sickness is on a short list of neglected tropical diseases the WHO is targeting for elimination by 2030. That means bringing cases in certain areas down to zero knowing that some control efforts may still be required. Vastly harder to achieve is disease eradication, where cases worldwide stay parked at zero permanently. (To date, just a single human infectious disease — smallpox — has been eradicated.)
Even elimination is no easy task — and can get harder as you approach the finish line. “We are advancing very well,” says José Ramón Franco, a WHO medical officer based in Geneva, “but we [haven’t] reached the last mile.”

Still, tiptoeing along the edges of optimism, some, like Kasita, are finding moments to cheer. For the severely ill patient, her team initially wondered if acoziborole would work. “Are we really going to help him with this single-dose treatment?”

Two weeks later, he could stand, with some support, and had started speaking again, a radical recovery. Kasita smiles widely as she remembers it. Watching him heal “was a great pleasure,” she says.

The symptoms of sleeping sickness
About 400 kilometers to the west of Masi-Manimba, physician Wilfried Mutombo Kalonji is preparing to visit Kasita’s hospital. Afterward, he’ll hit up hospitals in Idiofa, Bagata and then Bandundu, three other acoziborole clinical trial sites in the DRC. To reach the sites, Mutombo will travel by boat, plane, car and motorbike. He’ll stay in both modern hotels and hotels without running water or electricity. Then, he’ll return home to Kinshasa, the DRC’s bustling capital. It’s a great and noisy city, he grins, with people playing music in the streets and “many, many, many traffic jams.”

In Kinshasa, Roi Baudouin hospital is one of the DNDi’s acoziborole trial sites. Mutombo has been organizing logistics and ensuring that each site has what it needs to treat and monitor patients. That includes generators for electricity, an internet connection, medical equipment and trained clinical trial staff.

Mutombo has worked with sleeping sickness patients since 2004. Two weeks after finishing his medical training in Kasaï province, he shipped out to Kasansa, becoming the only medical doctor in a village of about 11,000 people. In Kasansa, which lies in western DRC, north of the Angola border, sleeping sickness was then, and still remains, endemic.

The disease, also called human African trypanosomiasis, is caused by a single-celled, ruffle-edged parasite that worms its way into the brain. One subspecies, Trypanosoma brucei gambiense, causes the vast majority of cases and tends to plague western and central Africa. Another, T.b. rhodesiense occurs in the eastern and southern parts of the continent and causes a more rapid, acute illness with far fewer cases in people.
Both subspecies can ride in the guts and glands of tsetse flies, which often buzz near bodies of water; many of Mutombo’s patients in Kasansa were fishers or farmers. When the fly bites, the parasite enters the bloodstream. From there, it can get picked up again when other flies feed, shuttling from insects to humans in a disease-spreading cycle.

In the blood, T.b. gambiense sparks a slow-burning illness that can begin with a fever and, if left untreated, end with death. As the parasite multiplies, lymph nodes enlarge and the head, muscles and joints ache. Patients can also become intensely itchy, scratching hard enough to damage the skin, Kasita says.

When the parasite slips past the blood-brain barrier, patients enter the second stage of the disease. No one knows exactly where the parasite lodges in the brain, but neurological symptoms can vary. Doctors and nurses describe a range of distressing and bizarre behaviors. One common behavior gives the illness its name. Somehow, the parasite reverses people’s sleep/wake cycle. “They will sleep a lot during the day, and at night, they will be up, watching,” Kasita says.

Patients can also feel depressed and confused, neglect to care for themselves, hallucinate or experience logorrhea, words cascading from lips in nonsensical streams. In some infected people, personalities can swing like a wrecking ball. Jacques Pépin, an infectious disease specialist at the University of Sherbrooke in Canada, worked with sleeping sickness patients in the 1980s and remembers one who suddenly threw a large rock at his head.

Such outbursts can be scary for patients and families, says Antoine Tarral, a pharmacologist and infectious disease physician who works with Mutombo and led the DNDi’s sleeping sickness program for 10 years. Fear of the disease can prompt villages to reject infected individuals, he says.

Sleeping sickness carries a social stigma that makes people feel like outcasts, Mutombo agrees. “This disease is terrible.” When he first began treating patients, he says, “I was doing my best to make them feel like human beings.”

But for decades, available treatments were terrible, too.
Sleeping sickness has a history of terrible treatments
For most of treatment history, injected or intravenous drugs were the only option for sleeping sickness. They could cure patients, but only if doctors administered them in time. And when cases advanced to the second stage, medical staff had to switch tactics. For patients, that meant a spinal tap to confirm diagnosis followed by different drugs.

Until the late 2000s, the most-used treatment for advanced gambiense sleeping sickness was the highly toxic melarsoprol. The drug is derived from arsenic (and it’s still the leading treatment for advanced rhodesiense cases). Medical staff administered the drug for 10 days via daily intravenous infusions that burned entering patients’ veins, Mutombo says. The treatment could also be lethal, killing some 5 percent of patients.

Mutombo grows somber remembering two of his patients who died, young men he tried to cure in Kasansa. “That was a very bad experience,” he says. “When patients come to the hospital, they come to receive a treatment, not to die … [from] the drug we gave them.”

But doctors didn’t have a lot of options. Without melarsoprol, patients with serious cases faced near-certain death.

Not long after his patients died, Mutombo heard that the DNDi was launching a project on a new, less toxic treatment for advanced cases. He jumped at the chance, applied to be an investigator and joined the project in 2006. The new treatment, called NECT, combined eflornithine, an IV drug developed for cancer, with the oral drug nifurtimox. Eflornithine was already being used to treat sleeping sickness, but required dozens of infusions, and nifurtimox was a treatment for Chagas disease.

In 2009, after a clinical trial and the WHO’s endorsement, NECT took off, rocketing past melarsoprol or eflornithine alone as the first-line treatment for advanced sleeping sickness. But NECT had some logistical snafus, Mutombo says. It wasn’t easy to transport, for one. Treatment for four patients came in 40-kilogram packages that had to be trucked over bad roads into rural areas that lacked medical workers. “That was a problem with NECT,” Mutombo says. “It was effective, but it was heavy and needed trained staff.”

Less than a decade later, Mutombo, Tarral and their DNDi colleagues debuted an easier alternative. Fexinidazole, at long last, was a drug doctors could deliver exclusively via pills rather than an IV. It’s not perfect — it’s administered by a nurse, patients need to take it for 10 days and it’s not best for the most severe cases (for these, the WHO still recommends NECT). But easy-to-use oral drugs lower the burden on health systems, Mutombo says. Medical staff could more easily bring treatments to remote patients. And that brought scientists one step closer to sleeping sickness’s elimination.
A new drug could help bring cases to zero
Acoziborole, the drug now being tested in clinical trials, may be another big step in the right direction. Just one dose cured some 95 percent of patients with late-stage infections, Mutombo, Tarral and colleagues reported November 29 in the Lancet Infectious Diseases. That’s comparable to treatment with NECT. “Acoziborole is one solution to manage this disease,” Tarral says.

Not only does the drug seem to be effective, but “it’s given orally … and it needs to be given only once,” says the University of Sherbrooke’s Pépin, who was not involved with the trial but wrote an opinion piece that appeared alongside the new report.

Yet, as Pépin points out, the acoziborole study has some limitations. The scientists tested the drug in just 208 patients, so no one knows if serious adverse effects might occur in larger populations. And the study wasn’t performed like the classic gold-standard clinical trial, with patients randomly assigned into different groups receiving different interventions.

Tarral acknowledges these drawbacks, which he says were due to low participant numbers. The researchers included only people with video-confirmed parasitic infections, which required years of searching for patients across 10 hospitals in two different countries.

“It’s not the standard approach, but that was the only possible approach,” Pépin says. “They did what could be done with the number of cases that are occurring now.”

The study’s promising results spurred a new, larger trial that will include 1,200 participants. This time, the team is enrolling people with positive antibody blood tests even if the parasite’s presence hasn’t been confirmed. Many of these participants may not actually be sick, says Veerle Lejon, a scientist at the French National Research Institute for Sustainable Development in Montpellier who was not involved in developing the drug but is collaborating with the DNDi on evaluating sleeping sickness diagnostics.

What this trial will offer, she says, is a raft of new data that will help determine the drug’s safety.
The challenges of eliminating an infectious disease
Even if acoziborole gets the green light, stamping out sleeping sickness isn’t a sure bet.

Eliminating an infectious disease is a slippery task. Success can, paradoxically, churn out new challenges. When case numbers dip low enough, for instance, interest in the disease can wane. Donors move money to other public health priorities, and once-robust control programs wither.

That happened for sleeping sickness in the 1960s, the last time cases dropped. Over the next few decades, cases ratcheted up, and epidemics broke out in Angola, the DRC and South Sudan. “Control of the disease was neglected, and then slowly, the disease came back,” says WHO medical officer Franco.

A doubled-down effort to find cases and treat them with ever-improving drugs got sleeping sickness under control again, with case numbers cratering to their low point today. But that level of surveillance is not sustainable, Franco says.
Health care workers can also lose knowledge of how to recognize the disease as they encounter fewer and fewer infected individuals, says Jennifer Palmer, a medical anthropologist at the London School of Hygiene and Tropical Medicine. “The challenge is really in making sure that people are aware that sleeping sickness is still a problem,” she says. In a small study in South Sudan, reported in 2020, Palmer and colleagues found that lay people encouraging people in the community to get tested accounted for more than half of detected cases.

Still, getting patients tested and treated can depend on whether they’re able to safely travel to health facilities. With the threat of violence in South Sudan and armed conflict in eastern DRC, the fate of sleeping sickness may also be shaped by the whims of war.

Even if every infected person was promptly found and treated, the disease-causing parasite would likely linger in wild and domestic animals. Scientists have found T.b. gambiense, for instance, in dogs, pigs, goats and sheep. No one knows the role infected animals play in reigniting outbreaks in humans.

Though the road to elimination may still be rocky, the patients Kasita and others are treating in Masi-Manimba and beyond offer a lesson for those working on disease elimination: Don’t give up too soon. Maybe the world won’t reach zero sleeping sickness cases by 2030, Lejon says, “but I think we should really give it a try,” she says. “We have momentum at this moment to do it.”

Mutombo echoes her enthusiasm. In less than 20 years, new drugs have completely overhauled patient care, he says. “We’ve made a great change in less than one generation…. Now, we expect that elimination is within reach.”

Discoveries on the island of Borneo illustrate that cave art emerged in Southeast Asia as early as in Western Europe, and with comparable complexity, researchers say.

A limestone cave in eastern Borneo features a reddish-orange painting of a horned animal, possibly a type of wild cattle that may have been found on the island at the time. The painting dates to at least 40,000 years ago, concludes a team led by archaeologist Maxime Aubert of Griffith University in Southport, Australia. This creature represents the oldest known example of a painted figure anywhere in the world, the scientists report online November 7 in Nature.
The same cave walls contain two hand outlines framed in reddish orange pigment that were made at least 37,200 years ago and a similar hand stencil with a maximum age of 51,800 years.

Three nearby caves display instances of a second rock art style that appeared around 20,000 years ago, the investigators say. Examples include purple-hued, humanlike figures and hand stencils, some decorated with lines or dots. Painted lines link some hand stencils to others.

Age estimates rest on analyses of uranium in mineral deposits that had formed over and underneath parts of each cave painting. Scientists used known decay rates of radioactive uranium in these deposits to calculate maximum and minimum dates for the paintings.

Aubert’s group previously used this technique, called uranium-series dating, to calculate that people on the nearby Indonesian island of Sulawesi created hand stencils on cave walls nearly 40,000 years ago (SN: 11/15/14, p. 6).
“Cave art could have potentially been exported from Borneo to Sulawesi and all the way to Papua and Australia,” Aubert says. Australian cave paintings of humanlike figures resemble those found on Borneo, he says. But the ages of the Australian finds remain uncertain.

No Southeast Asian cave paintings have been found from when humans first arrived in the region, between 70,000 and 60,000 years ago. At that time and up to the end of the last Ice Age around 10,000 years ago, Borneo formed mainland Eurasia’s easternmost tip thanks to lowered sea levels.

Those first Southeast Asians may have created cave art that hasn’t been discovered, Aubert says. Or, small groups of early colonizers may not have painted on cave walls until their populations expanded, leading to more complex social and ritual behaviors. It’s also possible that another human migration from elsewhere in Asia brought rock art to Borneo roughly 50,000 years ago.
Whatever the case, “Western European and Southeast Asian cave art seem to first appear at about the same time and with remarkable similarities,” says archaeologist Sue O’Connor of Australian National University in Canberra, who did not participate in the new study.
Other investigators have used the uranium-series technique to date a painted red disk in a Spanish cave to at least 40,800 years ago (SN: 7/28/12, p. 15). Another report this year suggested that Neandertals painted abstract shapes and hand stencils on the walls of several Spanish caves at least 64,800 years ago (SN: 3/17/18, p. 6).

Aubert’s team has criticized that study, saying the researchers may have unintentionally dated mineral deposits that are much older than the artworks. If so, humans rather than Neandertals could have created the Spanish cave art.

Meanwhile, scientists who conducted the Neandertal cave art study express their own doubts about the reliability of dates for the Borneo paintings. Descriptions of sampled mineral deposits from the Borneo caves leave it unclear whether, for example, Aubert’s group dated the horned animal figure or adjacent paint remnants of some other, unidentified figure, says archaeologist João Zilhão of the University of Barcelona.

Zilhão and Neandertal paper coauthor Paul Pettitt of Durham University in England don’t doubt that cave painting emerged in Southeast Asia at least 40,000 years ago. But they and Aubert’s team disagree about how to collect mineral samples for dating rock art.

SAN DIEGO — Marijuana use during teenage years may change the brain in key decision-making areas, a study in rats suggests.

“Adolescence is a dangerous time to be insulting the brain, particularly with drugs of abuse,” study coauthor Eliza Jacobs-Brichford said November 7 at the annual meeting of the Society for Neuroscience.

Jacobs-Brichford and colleagues gave adolescent male and female rats a marijuana-like compound. Afterward, the researchers found changes in parts of the brain involved in making decisions.
Normally, many of the nerve cells there are surrounded by rigid structures called perineuronal nets, sturdy webs that help stabilize connections between nerve cells. But in male rats that had been exposed to the marijuana-like compound in adolescence, fewer of these nerve cells, which help put the brakes on other cells’ activity, were covered by nets. Drug exposure didn’t seem to affect the nets in female rats.

“Males look more susceptible to these drugs,” said Jacobs-Brichford, a behavioral neuroscientist at the University of Illinois at Chicago.

Losing one variety of gut bacteria may lead to type 2 diabetes as people age.

Old mice have less Akkermansia muciniphila bacteria than young mice do, researchers report November 14 in Science Translational Medicine. That loss triggers inflammation, which eventually leads cells to ignore signals from the hormone insulin. Such disregard for insulin’s message to take in glucose is known as insulin resistance and is a hallmark of type 2 diabetes.

Researchers have suspected that bacteria and other microbes in the gut are involved in aging, but how the microbes influence the process hasn’t been clear. Monica Bodogai of the U.S. National Institute on Aging in Baltimore and colleagues examined what happens to mice’s gut bacteria as the rodents age. The mice lose A. muciniphila, also called Akk, and other friendly microbes that help break down dietary fiber into short-chain fatty acids, such as butyrate and acetate. Those fatty acids signal bacteria and human cells to perform certain functions.
Losing Akk led to less butyrate production, Bodogai’s team found. In turn, loss of butyrate triggered a chain reaction of immune cell dysfunction that ended with mice’s cells ignoring the insulin.

Treating old mice and elderly rhesus macaques with an antibiotic called enrofloxacin increased the abundance of Akk in the animals’ guts and made cells respond to insulin again. Giving old animals butyrate had the same effect, suggesting that there may be multiple ways to head off insulin resistance in older people in the future.

DENVER — Three jugs placed as offerings in a roughly 3,600-year-old tomb in Israel have revealed a sweet surprise — evidence of the oldest known use of vanilla.

Until now, vanilla was thought to have originated in Mexico, perhaps 1,000 years ago or more. But jugs from the Bronze Age site of Megiddo contain remnants of two major chemical compounds in natural vanilla extract, vanillin and 4-hydroxybenzaldehyde, said archaeologist Vanessa Linares of Tel Aviv University in Israel. Chemical analyses also uncovered residues of plant oils, including a component of olive oil, in the three jugs.
“Bronze Age people at Megiddo may have used vanillin-infused oils as additives for foods and medicines, for ritual purposes or possibly even in the embalming of the dead,” Linares said. She described these findings at the annual meeting of American Schools of Oriental Research on November 16.

Vanillin comes from beans in vanilla orchids. About 110 species of these flowers are found in tropical areas around the world. The chemical profile of the vanillin in the Megiddo jugs best matches present-day orchid species in East Africa, India and Indonesia, Linares said.

Extensive Bronze Age trade routes likely brought vanillin to the Middle East from India and perhaps also from East Africa, she suggested.

“It’s really not surprising that vanillin reached Bronze Age Megiddo given all the trade that occurred between the [Middle East] and South Asia,” says archaeologist Eric Cline of George Washington University in Washington, D.C. But no evidence exists of trade at that time between Middle Eastern societies and East Africa, says Cline, who did not participate in the Megiddo research.
Vanilla orchids or their beans probably reached Megiddo via trade routes that first passed through Mesopotamian society in southwest Asia. However Bronze Age Middle Easterners ended up with those products, discoveries at Megiddo challenge the idea that vanilla use originated only in Mexico and then spread elsewhere, Cline says.

The vanillin-containing jugs at Megiddo came from a tomb of three “highly elite” individuals who were interred with six other people of lesser social rank, said archaeologist Melissa Cradic of the University of California, Berkeley, a member of the current Megiddo research team. Excavations uncovered the tomb in 2016, Cradic also reported at the ASOR meeting.

Primary burials in the tomb consist of an adult female, an adult male and an 8- to 12-year-old boy. Elaborate types of bronze, gold and silver jewelry were found on and around the three skeletons. Exact replicas of several pieces of jewelry appeared on each individual.

The tomb lies in an exclusive part of Megiddo near a palace and a monumental city gate.

“We can’t definitively say that these three people were royals,” Cradic said. “But they were elites in Megiddo and may have belonged to the same family.”

For the first time, humans have built a set of pushy, destructive genes that infiltrated small populations of mosquitoes and drove them to extinction.

But before dancing sleeveless in the streets, let’s be clear. This extermination occurred in a lab in mosquito populations with less of the crazy genetic diversity that an extinction scheme would face in the wild. The new gene drive, constructed to speed the spread of a damaging genetic tweak to virtually all offspring, is a long way from practical use. Yet this test and other news from 2018 feed one of humankind’s most persistent dreams: wiping mosquitoes off the face of the Earth.

For the lab-based annihilation, medical geneticist Andrea Crisanti and colleagues at Imperial College London focused on one of the main malaria-spreading mosquitoes, Anopheles gambiae. The mosquitoes thrive in much of sub-Saharan Africa, where more than 400,000 people a year die from malaria, about 90 percent of the global total of malaria deaths.

To crash the lab population, the researchers put together genes for a molecular copy-and-paste tool called a CRISPR/Cas9 gene drive. The gene drive, which in this case targeted a mosquito gene called doublesex, is a pushy cheat. It copies itself into any normal doublesex gene it encounters, so that all eggs and sperm will carry the gene drive into the next generations. Female progeny with two altered doublesex genes develop more like males and, to people’s delight, can’t bite or reproduce.

In the test, researchers set up two enclosures, each mixing 150 males carrying the saboteur genes into a group of 450 normal mosquitoes, males and females. Extinction occurred in eight generations in one of the enclosures and in 12 in the other (SN: 10/27/18, p. 6).

This is the first time that a gene drive has forced a mosquito population to breed itself down to zero, says Omar Akbari of the University of California, San Diego, who has worked on other gene drives. However, he warns, “I believe resistance will be an issue in larger, diverse populations.” More variety in mosquito genes means more chances of some genetic quirk arising that counters the attacking gene drive.

But what if a gene drive could monkey-wrench a wild population, or maybe a whole species, all the way to extinction? Should people release such a thing? To make sense of this question, we humans will have to stop talking about “mosquitoes” as if they’re all alike. The more than 3,000 species vary considerably in what they bite and what ecosystem chores they do.

The big, iridescent adults of Toxorhynchites rutilus, for instance, can’t even drink blood. And snowmelt mosquitoes (Ochlerotatus communis) are pollinators of the blunt-leaved orchid (Platanthera obtusata), ecologist Ryo Okubo of the University of Washington in Seattle said at the 2018 meeting of the Society for Integrative and Comparative Biology.
Estimating what difference it would make ecologically if a whole mosquito species disappeared has stirred up plenty of speculation but not much data. “I got pretty fed up with the hand-waving,” says insect ecologist Tilly Collins of Imperial College London. So she and colleagues dug through existing literature to see what eats An. gambiae and whether other mosquitoes would flourish should their competitor vanish.

So far, extermination of this particular mosquito doesn’t look like an ecological catastrophe, Collins says. Prey information is far from perfect, but diets suggest that other kinds of mosquitoes could compensate for the loss. The species doesn’t seem to be any great prize anyway. “As adults, they are small, not juicy, and hard to catch,” she says. The little larvae, built like aquatic caterpillars with bulging “shoulders” just behind their heads, live mostly in small, temporary spots of water.
The closest the researchers came to finding a predator that might depend heavily on this particular mosquito was the little East African jumping spider Evarcha culicivora. It catches An. gambiae for about a third of its diet and likes the females fattened with a human blood meal. Yet even this connoisseur “will readily consume” an alternative mosquito species, the researchers noted in July in Medical and Veterinary Entomology.

Collins also thinks about the alternatives to using genetically engineered pests as pest controls. Her personal hunch is that saddling mosquitoes with gene drives to take down their own species is “likely to have fewer ecological risks than broad-spectrum use of pesticides that also kill other species and the beneficial insects.”

Gene drives aren’t the only choice for weaponizing live mosquitoes against their own kind. To pick just one example, a test this year using drones to spread radiation-sterilized male mosquitoes in Brazil improved the chances that the old radiation approach will be turned against an Aedes mosquito that can spread Zika, yellow fever and chikungunya.

Old ideas, oddly enough, may turn out to be an advantage for antimosquito technologies in this era of white-hot genetic innovation. Coaxing the various kinds of gene drives to work is hard enough, but getting citizens to sign off on their use may be even harder.

For three years, a team of scientists kept a big secret: They had discovered a giant crater-shaped depression buried beneath about a kilometer of ice in northwestern Greenland. In November, the researchers revealed their find to the world.

They hadn’t set out to find a crater. But in 2015, glaciologists studying ice-penetrating radar images of Greenland’s ice sheet, part of an annual survey by NASA’s Operation IceBridge mission, noticed an oddly rounded shape right at the northern edge of Hiawatha Glacier. If the 31-kilometer-wide depression is confirmed to be the remnant of a meteorite impact — and the team has produced a wealth of evidence suggesting that it is (SN: 12/8/18, p. 6) — the discovery is exciting in and of itself. It’s rare to find a new crater, let alone one on land that has retained its perfect bowl shape.

“This is just a straight-up exciting discovery that starts with this wonderful element of serendipity,” says team member Joseph MacGregor, a glaciologist with Operation IceBridge.

But the crater — let’s call it that, for the sake of discussion — may have also reignited a debate over a controversial hypothesis about a mysterious cold snap known as the Younger Dryas. This cold period began abruptly about 12,800 years ago and ended just as abruptly about 11,700 years ago. For more than a decade, a small group of researchers, unconnected with the group behind the new discovery, has suggested that a cosmic impact triggered the cooling (SN: 7/7/18, p. 18).
Proponents of the Younger Dryas impact hypothesis say that the remnants of a comet exploded in Earth’s atmosphere and that the airbursts sparked wildfires across North America. Soot and other particles from the fires blocked out the sun, causing the cold snap, which has been blamed for everything from the extinction of the mammoths to the disappearance of a group of people known as the Clovis.

Most scientists reject that an impact was responsible, refuting the idea that there were vast wildfires at the time or that the Clovis people even disappeared. Another big objection: the lack of a smoking gun, a crater dating to the onset of the Younger Dryas.
The “mammoth in the room,” therefore, is whether the Greenland crater might be that smoking gun. But a large, recent impact would be extremely unlikely, given the rarity of such impacts on Earth, particularly on land, says planetary scientist Clark Chapman of the Southwest Research Institute in Boulder, Colo., who was not involved with the discovery.

Indeed, one sticking point is that there are no direct dates for the newly discovered crater, because it is still buried beneath all that ice. The radar data offer only tantalizing clues to the age, suggesting that the crater is between 2.6 million and 11,700 years old.

That’s a huge time range, but the proponents of the hypothesis are convinced that this crater is what they’ve been waiting for. “I think it’s transformational in terms of convincing a lot of skeptics,” says James Kennett, a geologist at the University of California, Santa Barbara.
There’s another big sticking point when it comes to linking this crater to the impact hypothesis: Instead of a fragment of a comet, the discoverers think the Hiawatha impactor was an iron meteorite. That determination is based on measurements of platinum and other elements in glacial outwash, sediments carried by meltwater from beneath the ice. An iron meteorite impact would probably not produce the kinds of explosive airbursts that could ignite continent-scale wildfires, says Michail Petaev, a geochemist at Harvard University.
Petaev and colleagues previously found a hint that an iron meteorite might have smacked into Greenland about 13,000 years ago. In 2013, his group examined Greenland ice cores and found a strange platinum anomaly dating to right before the Younger Dryas. The ratio of platinum to iridium measured in the ice cores points to an iron meteorite, the team reported.

Despite the platinum data, the impact hypothesis proponents hold firmly to the idea that the Hiawatha impactor was a comet. Because little is known about comet compositions, Kennett says, a comet might well have been the source for the platinum found in the glacial outwash and the ice cores. But Petaev maintains that the observed platinum ratios just wouldn’t occur in a comet, which is made of the primitive stuff of the universe. Instead, he says, those ratios require the cycles of melting and recrystallizing that form iron meteorites, the ancient cores of asteroids or planets.
Glaciologist Kurt Kjær of the University of Copenhagen, who led the team that identified the crater, and his colleagues don’t want to weigh in on the Younger Dryas debate. “We can’t prove it,” Kjær says. “But we can certainly not disprove it.”

Instead, the crater’s discoverers are planning to collect more sediments from the glacial outwash, and perhaps even drill directly into the crater to retrieve sediment cores that can be dated. And there may be other craters lurking beneath Greenland’s ice, or even Antarctica’s — perhaps more easily identifiable once you know what to look for, says MacGregor.

Asked whether the team has actually identified any other round shapes of interest, he pauses. Then MacGregor says, cryptically, “stay tuned.”

Quantum physics has earned a reputation as a realm of science beyond human comprehension. It describes a microworld of perplexing, paradoxical phenomena. Its equations imply a multiplicity of possible realities; an observation seems to select one of those possibilities for accessibility to human perception. The rest either disappear, remain hidden or weren’t really there to begin with. Which of those explanations pertains is debated by competing interpretations of the quantum math, pursued in a field of study known as quantum foundations.

Numerous quantum interpretations have been proposed — and an even greater number of books have been written about them. Two of the latest such books offer very different perspectives.
Philip Ball, in Beyond Weird, argues that much of the famous quantum weirdness lies in the popular descriptions of it, rather than in the math itself. Adam Becker’s What is Real? insists that the traditional “Copenhagen interpretation” is misguided; he extols the work of several physicists who reject it. Becker writes with exuberance and self-assuredness, often focusing on the personal stories of the scientists he discusses. Ball’s approach is less personal but more conversational, although he does not try to evade the sticky technicalities that illustrate and partially explain the quantum mysteries.
Ball contends that many of the analogies and illustrations used by popularizers (and physicists) to convey the weirdness of quantum theory (like a particle being in two places at once) are actually misleading. With less flamboyant phrasing, in Ball’s view, quantum physics can seem less perplexing, even almost understandable.

Without fully endorsing it, Ball gives a fairly sound presentation of the Copenhagen interpretation, based on the ideas of the Danish physicist Niels Bohr. Bohr held that quantum reality cannot be described apart from the experiments designed to probe it. A particle has many possible locations before you experimentally observe it; once observed, the location is established and the other possibilities vanish. And an electron will seem to behave as a particle or wave, depending on what sort of experimental apparatus you use to observe it.

Bohr expressed these truths by a principle he called complementarity — mutually exclusive concepts (such as wave or particle) are required to explain reality, but both concepts cannot be observed in any individual experiment. Bohr’s elaborations on this idea are famously convoluted and expressed rather obscurely. (When asked what is complementary to truth, Bohr replied, “clarity.”)

Bohr’s lack of clarity has led to many misinterpretations of what he meant, and it is those misinterpretations that Becker criticizes, rather than Bohr’s actual views. Becker’s main argument insists that the Copenhagen interpretation embraces the philosophy known as positivism (roughly, nothing unobservable is real, and sensory perceptions are the realities on which science should be based), and then demonstrates positivism’s fallacies. He does a fine job of demolishing positivism. Unfortunately, the Copenhagen interpretation is not positivistic, as its advocates have often pointed out. Bohr’s colleague Werner Heisenberg said so quite clearly: “The Copenhagen interpretation of quantum theory is in no way positivistic,” he wrote. And the philosopher Henry Folse’s 1985 book on Bohr’s philosophy thoroughly dispelled the mistaken belief that Bohr’s view was positivistic or opposed to the existence of an underlying reality.

Becker’s book commits many other more specific errors. He says Heisenberg found his famous uncertainty principle “buried in the mathematics of [Erwin] Schrödinger’s wave mechanics.” But Heisenberg despised wave mechanics and did his work on uncertainty wholly within his own matrix mechanics. Becker claims that physicists Murray Gell-Mann and James Hartle “had long been convinced that the Copenhagen interpretation had to be wrong.” But Gell-Mann and Hartle are on record stating that the Copenhagen view is not wrong, merely limited to special cases and not general enough to tell the whole quantum story.

Becker’s book does offer engaging discussions of the physicists who have questioned Bohr’s ideas and proposed alternate ways of interpreting quantum physics. But he allows the opponents to frame Bohr’s position rather than devoting any effort of his own to examining the subtlety and depth of Bohr’s philosophy and arguments. And Becker fails to address the important point that every quantum experiment’s results, no matter how bizarre, are precisely what Bohr would have expected them to be.

Becker does not engage deeply with the more recent body of work on quantum foundations, an area where Ball excels. Ball especially favors the perspective on quantum physics offered by the notion of quantum decoherence. Very roughly, the decoherence process dissipates various possible quantum realities into the environment, and only those versions of reality that are robustly recorded in the environment present themselves to observers. It’s of course much more complicated than that, and Ball admirably conveys those complications even at the occasional expense of clarity. Which puts his account closer to the truth.

The monarch butterfly isn’t the only insect flying up and down North America in a mind-boggling annual migration. Tests show a big, shimmering dragonfly takes at least three generations to make one year’s migratory loop.

Ecologist Michael Hallworth and his colleagues pieced together the migration of the common green darner, described December 19 in Biology Letters, using data on forms of hydrogen in the insects’ wings, plus records of first arrivals spotted by citizen scientists.
The study reveals that a first generation of insects emerges in the southern United States, Mexico and the Caribbean from about February to May and migrates north. Some of those Anax junius reach New England and the upper Midwest as early as March, says Hallworth, of the Smithsonian Migratory Bird Center headquartered in Washington, D.C.

Those spring migrant darners lay eggs in ponds and other quiet waters in the north and eventually die in the region. This new generation migrates south from about July until late October, though they have never seen where they’re heading. Some of these darners fly south in the same year their parents arrived and some the next year, after overwintering as nymphs.

A third generation emerges around November and lives entirely in the south during winter. It’s their offspring that start the cycle again by swarming northward as temperatures warm in the spring. With a wingspan as wide as a hand, they devote their whole lives to flying hundreds of kilometers to repeat a journey their great-grandparents made.
Scientists knew that these dragonflies migrated. Dragonfly enthusiasts have spotted swarms of the green darners in spring and in fall. But which generations were doing what has been tricky to demonstrate. “Going in, we didn’t know what to expect,” Hallworth says.
Tracking devices that let researchers record animals’ movements for more than a week or two haven’t been miniaturized enough to help. The smallest still weigh about 0.3 grams, which would just about double a darner’s weight, Hallworth says. So researchers turned to chemical clues in darner tissues. Conservation biologist and study coauthor Kent McFarland succeeded at the delicate diplomacy of persuading museums to break off a pinhead-sized wing tip fragment from specimens spanning 140 years.

Researchers checked 800 museum and live-caught specimens for the proportion of a rare heavy form of hydrogen that occurs naturally. Dragonfly wings pick up their particular mix of hydrogen forms from the water where the aquatic youngsters grow up. Scientists have noticed that a form called hydrogen-2 grows rarer along a gradient from south to north in North America. Looking at a particular wing in the analysis, “I can’t give you a zip code” for a darner, Hallworth says. But he can tell the native southerners from Yankees.

An adult darner, regardless of where it was born, is “a green piece of lightning,” says McFarland, of the Vermont Center for Ecostudies in White River Junction. Darners maneuver fast enough to snap insect prey out of the air around ponds across North America. The front of an adult’s large head is “all eye,” he says, and trying to catch samples for the study was “like hitting a knuckleball.”

Although the darners’ north-south migration story is similar to that of monarchs (Danaus plexippus), there are differences, says evolutionary biologist Hugh Dingle of the University of California, Davis, who has long studied these butterflies. Monarchs move northward in the spring in stepwise generations, instead of one generation sweeping all the way to the top of its range.

Also, Dingle says, pockets of monarchs can buck the overall scheme. Research suggests that some of the monarchs in the upper Midwest do a whole round trip migration in a single generation. As researchers discover more details about green darners, he predicts, the current basic migration scheme will turn out to have its quirky exceptions, too.