Cholera strains behind worldwide outbreaks of the deadly disease over the last five decades are jet-setters rather than homebodies.

It had been proposed that these cholera epidemics were homegrown, driven by local strains of Vibrio cholerae living in aquatic ecosystems. But DNA fingerprints of the V. cholerae strains behind recent large outbreaks in Africa and Latin America were more closely related to South Asian strains than local ones, according to two papers published in the Nov. 10 Science.
This evidence that the guilty strains traveled from abroad could guide public health efforts, the researchers say. “If you don’t understand how the bug spreads, then it’s very difficult to try to stop the bug,” says François-Xavier Weill, a clinical microbiologist at the Institut Pasteur in Paris who coauthored both papers.

People are exposed to V. cholerae by consuming water or food contaminated by the bacteria. Poor sanitation and drinking water treatment can fuel an epidemic, as seen in Yemen (SN: 8/19/17, p. 4), where nearly a million people are suspected to have been infected and more than 2,000 have died in the world’s largest recorded cholera outbreak.

A cholera infection can produce mild or no symptoms. But about one in 10 people will rapidly develop severe diarrhea and dehydration that, without treatment, can kill within hours. Although underreported, cholera cases worldwide each year are estimated to range from 1.4 million to four million, and 21,000 to 143,000 people die from the disease, according to the World Health Organization’s Global Health Observatory.
There have been seven cholera pandemics, or global outbreaks, since the 19th century, when the bacteria spread from its original home on the Indian subcontinent. The seventh one, which began in Indonesia in 1961, reached Africa in 1970 and hit Latin America in 1991, is still ongoing. It’s attributed to strains that originated near the Bay of Bengal, where cholera is a seasonal occurrence.

But it was unclear whether the large outbreaks happening around the world were related to each other, or if they had each originated from local strains. Previous methods used to track V. cholerae were unable to distinguish strains with enough detail, Weill says. “It was impossible then, during the last 50 years, to understand the routes of propagation of cholera.”

Weill and an international research team analyzed the genetic information of about 1,700 strains of V. cholera, including those collected during and in between outbreaks over about 40 years from 45 countries in Africa and 14 countries throughout Latin America.

In both Africa and Latin America, the strains responsible for the large epidemics were most closely related to the South Asian strains, rather than strains existing in the local environment. These “epidemic” strains have been introduced 11 times in Africa since 1970 and have caused large outbreaks that lasted as long as 28 years, the researchers found.

In Latin America, there were three main introductions of the South Asian “epidemic” strains. One that came through Africa hit Peru in 1991. Another invaded Mexico around the same time, possibly arriving with coca smugglers using an airstrip near Mexico City. The third introduction, from Nepalese United Nations personnel, devastated Haiti in 2010 (SN: 2/25/12, p. 16).

“We now know what cholera is with much more precision,” says Nicholas Thomson, a genome scientist at the Wellcome Trust Sanger Institute in Cambridge, England, who also coauthored both papers. “You can find V. cholerae in the environment, no doubt about it, but the patterns of spread tell you that that’s not the primary route of transmission.” Rather, he says, it’s transmission between people that allows the bacteria to spread rapidly internationally.

“These studies affirm the primary role that people play in the spread of cholera,” says Yonatan Grad, an infectious diseases clinician at Harvard T.H. Chan School of Public Health in Boston who was not involved with the studies. “The emphasis on infected people as the vectors for spread underscores the importance of vaccination as a strategy to limit cholera.”

PHILADELPHIA — Protein-manufacturing factories within cells are picky about which widgets they construct, new research suggests. These ribosomes may not build all kinds of proteins, instead opting to craft only specialty products.

Some of that specialization may influence the course of embryo development, developmental biologist and geneticist Maria Barna of Stanford University School of Medicine and colleagues discovered. Barna reported the findings December 5 at the joint meeting of the American Society for Cell Biology and European Molecular Biology Organization.
Ribosomes, which are themselves made up of many proteins and RNAs, read genetic instructions copied from DNA into messenger RNAs. The ribosomes then translate those instructions into other proteins that build cells and carry out cellular functions. A typical mammalian cell may carry 10 million ribosomes. “The textbook view of ribosomes is that they are all the same,” Barna said. Even many cell biologists have paid little attention to the structures, viewing them as “backstage players in controlling the genetic code.”

But that view may soon change. Ribosomes actually come in many varieties, incorporating different proteins, Barna and colleagues found. Each variety of ribosome may be responsible for reading a subset of messenger RNAs, recent studies suggest. For instance, ribosomes containing the ribosomal protein RPS25 build all of the proteins involved in processing vitamin B12, Barna and colleagues reported July 6 in Molecular Cell. Vitamin B12 helps red blood cells and nerves work properly, among other functions. Perhaps other biological processes are also controlled, in part, by having specific types of ribosomes build particular proteins, Barna said.

In unpublished work presented at the meeting, Barna and colleagues also found that certain ribosome varieties may be important at different stages of embryonic development. The researchers coaxed embryonic stem cells growing in lab dishes to develop into many types of cells. The team then examined the ribosomal proteins found in each type of cell. Of the 80 ribosomal proteins examined, 31 changed protein levels in at least one cell type, Barna said. The finding may indicate that specialized ribosomes help set a cell’s identity.

Although Barna’s idea of diverse ribosomes goes against the classical textbook view, “the concept is not heretical at all,” says Vassie Ware, a molecular cell biologist at Lehigh University in Bethlehem, Pa., not involved in the work.
These findings may help explain why some people with mutations in certain ribosomal protein genes develop conditions such as Diamond-Blackfan anemia — a blood disorder in which the bone marrow doesn’t make enough red blood cells — but don’t have problems in other body tissues, Ware says.

That disease is caused by mutations in the RPL5 and RPL11 genes, which encode ribosomal building blocks. If all ribosomes were alike, people with mutations in ribosomal components should have malfunctions all over their bodies, or might not ever be born. RPL5 and RPL11 proteins may be part of specialized ribosomes that are important in the bone marrow but not elsewhere in the body.

Despite their name, pelican spiders aren’t massive, fish-eating monstrosities. In fact, the shy spiders in the family Archaeidae are as long as a grain of rice and are a threat only to other spiders.

Discovering a new species of these tiny Madagascar spiders is tough, but Hannah Wood has done just that — 18 times over.

Wood, an arachnologist at the Smithsonian National Museum of Natural History in Washington D.C., analyzed the genes and anatomy of live and museum pelican spider specimens to find these new species. She describes them in a paper published online January 11 in ZooKeys.
Like other pelican spiders, the new species have an elongated “neck” and beaklike pincers, or chelicerae. The way they use those long chelicerae to strike from a distance, earned them another name: assassin spiders. Once impaled, the helpless prey dangles from these meat hooks until the venom does its work (SN: 3/22/14, p. 4).

Probing the spiders’ tiny anatomy under a microscope, Wood looked for hints to distinguish one species from another. Arachnologists often look to spiders’ genitals: Males and females from the same species typically evolved specially shaped organs to mate. If the “lock” doesn’t fit the “key,” the spiders are likely of a different species.

Thanks to Wood, 18 more species of pelican spiders — some of which were previously misclassified — now have names. Eriauchenius rafohy honors an ancient Madagascar queen, and E. wunderlichi, an eminent arachanologist. Wood, one of the foremost experts on pelican spiders, says she expects there are still more species to find. Perhaps an E. woodi?

A teenage girl climbed into an underground cave around 13,000 years ago. Edging through the ink-dark chamber, she accidentally plunged to her death at the bottom of a deep pit.

Rising seas eventually inundated the cave, located on Central America’s Yucatán Peninsula. But that didn’t stop scuba divers from finding and retrieving much of the girl’s skeleton in 2007.

“First Face of America,” a new NOVA documentary airing February 7 on PBS, provides a closeup look at two dangerous underwater expeditions that resulted in the discovery and salvaging of bones from one of the earliest known New World residents, dubbed Naia.
The program describes how studies of Naia’s bones (SN: 6/14/14, p. 6) and of genes from an 11,500-year-old infant recently excavated in Alaska have generated fresh insights into how people populated the Americas. Viewers watch anthropologist and forensic consultant James Chatters, who directed scientific studies of Naia’s remains, as he reconstructs the ancient teen’s face and charts the lower-body injuries that testify to what must have been a rough life.
In one suspenseful scene, cameras record Chatters talking with scuba divers shortly before the divers descend into the submerged cave to collect Naia’s bones. The scientist describes how thousands of years of soaking in seawater have rendered the precious remains fragile. He uses a plaster cast of a human jaw to demonstrate for scuba diver Susan Bird how to handle Naia’s skull so that it stays intact while being placed in a padded box. Bird’s worried expression speaks volumes.

“On the day of the dive, there was so much tension, so many people on the verge of freaking out,” Bird recalls in the show. When the divers return from their successful mission, collective joy breaks out.
The scene then shifts to a lab where Chatters painstakingly re-creates what Naia looked like. Asian-looking facial features raise questions about how the ancient youth ended up in Central America. That’s where University of Alaska Fairbanks anthropologist Ben Potter enters the story. In 2013, Potter and colleagues excavated the remains of two infant girls at an Alaskan site dating nearly to Naia’s time. Analysis of DNA recovered from one of the infants , described in the Jan. 11 Nature , supports a scenario in which a single founding Native American population reached a land bridge that connected northeast Asia to North America around 35,000 years ago. As early as 20,000 years ago, those people had moved into their new continent, North America. Naia’s face reflects her ancestors’ Asian roots.
In tracing back how people ended up in the Americas, NOVA presents an outdated model of ancient humans moving out of Africa along a single path through the Middle East around 80,000 years ago. Evidence increasingly indicates that people started leaving Africa 100,000 years ago or more via multiple paths (SN: 12/24/16, p. 25). That’s a topic for another show, though. In this one, Naia reveals secrets about the peopling of the Americas with a lot of help from intrepid scuba divers and state-of-the-art analyses. It’s fitting that a slight smile creases her reconstructed face.

Bedbugs leave a lasting legacy.

Their poop contains a chemical called histamine, part of the suite of pheromones that the insects excrete to attract others of their kind. Human exposure to histamine can trigger allergy symptoms like itchiness and asthma. (Our bodies also naturally release histamine when confronted with an allergen.) Histamine stays behind long after the bedbugs disappear, scientists report February 12 in PLOS ONE.

Researchers from North Carolina State University in Raleigh collected dust from apartments in a building with a chronic bedbug infestation. After a pest control company treated the apartments by raising the temperature to a toasty 50° Celsius, the researchers sampled the dust again. They compared those two sample groups with a third, from area homes that hadn’t had bedbugs for at least three years.

Dust from the infested apartments had levels of histamine chemical that were 22 times as much as the low amount found in bedbug-free houses, the researchers found. And while the heat treatment got rid of the tiny bloodsuckers, it didn’t lower the histamine levels.

Future pest control treatments might need to account for bedbugs’ long-term effects.

AUSTIN, Texas — An analysis of the metals in dozens of Picasso’s bronze sculptures has traced the birthplace of a handful of the works of art to the outskirts of German-occupied Paris during World War II.

This is the first time that the raw materials of Picasso’s sculptures have been scrutinized in detail, conservation scientist Francesca Casadio of the Art Institute of Chicago said February 17 at the annual meeting of the American Association for the Advancement of Science. And the elemental “fingerprints” help solve a mystery surrounding the sculptures’ origins.
“In collaboration with curators, we can write a richer history of art that is enriched by scientific findings,” Casadio said.

Casadio and colleagues from the Art Institute of Chicago and Northwestern University in Evanston, Ill., studied 39 bronzes in the collection of the Picasso Museum in Paris. The team used a portable X-ray fluorescence spectrometer to record the amount of copper, tin, zinc and lead at several points on each sculpture.
Based on the percentage of tin versus zinc in the bronze, “we found that there are compositional groups that relate to a specific foundry,” Casadio said. Seventeen sculptures had a foundry mark on them, so the researchers could relate metal mixes to specific foundries.
But seven sculptures lack foundry marks. Based on their composition, researchers pegged five to a specific foundry — that of Émile Robecchi, a craftsman whose workshop sat in the southern outskirts of Paris. Original invoices from the foundry surfaced two years ago and revealed when some of the pieces were cast. For instance, the description, weight and size written on one invoice confirmed that the bronze of Tête de femme de profil (Marie­Thérèse) — a portrait of one of Picasso’s mistresses originally sculpted in plaster in 1931 — was cast at the foundry in February 1941.
At that time, the war had been under way for years and the Germans had just occupied Paris. Picasso worried that his fragile plaster sculptures could be easily destroyed and sought to have them cast in bronze.

The team’s analysis also found two distinct mixtures of bronze that came out of the Robbechi foundry. That difference makes sense in the context of 1940s occupied Paris, when the Germans instituted laws requiring that people turn in certain metals to go toward war efforts, Casadio said.

“A lot of [foundries’] archives are incomplete or nonexistent,” Casadio said. The new analysis “reinforces why it’s really important to collaborate and how science adds the missing piece of the puzzle.”

Chile’s Atacama Desert is so dry that some spots see rain only once a decade. Salt turns the sandy soil inhospitable, and ultraviolet radiation scorches the surface. So little can survive there that scientists have wondered whether snippets of DNA found in the soil are just part of the desiccated skeletons of long-dead microbes or traces of hunkered-down but still living colonies.

A rare deluge has solved that mystery. Storms that dumped a few centimeters of rain on the Atacama in March 2015 — a decade’s worth in one day — sparked a microbial superbloom, researchers report February 26 in Proceedings of the National Academy of Sciences.
That storm initially threw a wrench into plans for scientists to get a snapshot of microbial life under normal, hyperarid conditions in the Atacama. “But in the end, it came back as a lucky stroke,” says study coauthor Dirk Schulze-Makuch, an astrobiologist at the Technische Universität Berlin. He and his colleagues drove mining vehicles into the desert to collect soil samples just a few weeks after the storm, and then returned again in 2016 and 2017 to track changes as the moisture dissipated.

The team found microbes — a mix of extremophile archaea, bacteria and fungi — that were tolerant of desiccation, salinity and UV radiation. The kinds of species were fairly consistent across sampling sites, which suggests there’s something of a native microbial community that can survive in this salty sand by going dormant between periods of moisture, says Schulze-Makuch.

Schulze-Makuch and his colleagues also found evidence for enzymes that are by-products of cellular metabolism. And traces of ATP, the molecule that cells use for energy, lingered inside cells. Those markers of life were the most bountiful at the first sampling time, and then declined as the soil dried out again.

Collectively, it’s evidence that microbes aren’t just dying and leaving their DNA behind in the Atacama — they’re laying low to live another day. That’s encouraging to Schulze-Makuch: He’s interested in the Atacama as a proxy for conditions on Mars.
Armando Azua-Bustos, an astrobiologist at the Centro de Astrobiología in Madrid who was not part of this study, agrees. “If we’re finding that, on Earth, truly dry places are still inhabited,” he says. “That opens the door to finding life elsewhere in the universe.”