In the last days of the 1400s, a terrible epidemic swept through Europe. Men and women spiked sudden fevers. Their joints ached, and they broke out in rashes that ripened into bursting boils. Ulcers ate away at their faces, collapsing their noses and jaws, working down their throats and airways, making it impossible to eat or drink. Survivors were grossly disfigured. Unluckier victims died.

The infection sped across the borders of a politically fractured landscape, from France into Italy, on to Switzerland and Germany, and north to the British Isles, Scandinavia, and Russia. The Holy Roman Emperor declared it a punishment from God. “Nothing could be more serious than this curse, this barbarian poison,” an Italian historian wrote in 1495.

Out of the chaos, several things became clear. The infection seemed to start in the genitals. The pathogen seemed to travel along the paths of mercenary soldiers hired by warring rulers to attack their rivals, and with the informal households and sex workers that followed their campaigns. Though every nation associated the disorder with their enemies—the French called it the Neapolitan disease, the English called it the French disease, the Russians blamed the Poles, and the Turks blamed Christians—there came a growing sense that one nation might be responsible.

It seemed plausible that the great pox, later called syphilis, might have journeyed with Spanish mercenaries, who represented much of the army of Naples when France attacked that kingdom in 1495. And it might have arrived in Spain with the crews of Christopher Columbus, who returned there in 1493 from the first of his exploratory voyages.

For most of the centuries since, a significant historical narrative has blamed Columbus and his sailors for bringing syphilis to Europe. It arrived as a ravaging plague and then adapted to become a long-simmering disease that, before the discovery of penicillin, could cripple people and drive them mad. Investigating what’s called the “Columbian hypothesis” has proved challenging: The symptoms related in old accounts could describe several diseases, and the bacterium that causes it, Treponema pallidum, was not identified until 1905.

But for roughly two decades, paleopathologists examining European burial sites have suggested that medieval bones and teeth display signs of syphilis infection, disrupting the belief that the disease arrived there in the 15th century. Now, a team based in Marseille has used ancient-DNA analysis to reveal evidence of Treponema bacteria, and the body’s immunological reaction to it, in a skeleton that was buried in a chapel in Provence in the 7th or 8th century. It’s the best evidence yet that syphilis—or something related to it—was infecting Europeans centuries before Columbus sailed.

“To the best of my knowledge, this is the first, proven, strong piece of evidence that the Treponema of syphilis were circulating in the European population before Columbus,” says Michel Drancourt, a physician and professor of microbiology at Aix-Marseille University, who led the work published in the Journal of Infectious Diseases. “So far, this was a hypothesis in science and the medical literature, without any strong proof.”

Of course, as with anything in science, one finding doesn’t settle the question. It’s clear the historical record describes a catastrophic epidemic coincident with Columbus’s return. And there have always been other diseases caused by subspecies of Treponema bacteria—notably yaws, caused by T. pallidum pertenue, which passes skin-to-skin instead of through sexual contact, and mostly occurs in children. But, at least, the new identification adds narrative strands to the established story of syphilis’s global travel—without quite taking the responsibility off the famous colonizer’s back.

“It’s exciting that greater complexity is being introduced progressively by this work, and by some securely dated and accurately diagnosed ancient skeletons that have been published since 2016,” says Molly Zuckerman, a biological anthropologist and professor at Mississippi State University who collaborates on studies of ancient infections. “When we look at modern disease landscapes, we understand that a lot of the time we have co-circulating strains of diseases. If the origin of syphilis hadn’t been set up initially against the backdrop of the Columbian Exchange, we might have recognized that sooner.”

A Pfizer vaccine designed to protect newborns and infants from severe RSV illness won a recommendation from the Centers for Disease Control and Prevention Friday—but only for seasonal use.

The vaccine is Pfizer’s bivalent RSVpreF vaccine, called Abrysvo, and is administered to pregnant people late in gestation, between 32 and 36 weeks.

RSV, or respiratory syncytial (sin-SISH-uhl) virus, is the leading cause of hospitalization for infants in the US. Each year, 1.5 million children seek out-patient care for RSV, with 58,000 to 80,000 ending up in the hospital and 100 to 300 tragically dying from the infection.

The CDC’s Advisory Committee on Immunization Practices voted 11 to 1 on Friday in favor of the limited recommendation for the vaccine, which in a clinical trial appeared 91 percent effective at preventing severe RSV in the first three months of a baby’s life and 76.5 percent effective against severe disease in the first six months. It demonstrated 57 percent efficacy in preventing hospitalization in the first six months.

The vaccine did appear to increase the pre-term birth rate compared with placebo, but the increase was not statistically significant.

Ultimately, the committee only recommended the vaccine to be used seasonally—between September and January to protect babies born between October and March, when RSV transmission typically peaks. (There is an exception for pregnant people who live in an area of the US where RSV circulates year-round, such as Hawaii and Gaum.)

For pregnant people whose babies are due between February and August, the vaccine is not recommended. Instead, those babies will have the option of a monoclonal antibody immunization by Sanofi, called nirsevimab (Beyfortus), available to protect against RSV in the run-up to the seasonal transmission. The antibody has been shown to be about 80 percent effective at preventing severe RSV over five months.

The one dissenting vote on the CDC’s committee was Helen Keipp Talbot, a medical professor at Vanderbilt University, who questioned the complexity of the recommendation and the need for another option, given the availability of the antibody. But other members highlighted the benefits of having two options available.

Shortly after the advisory committee’s vote, CDC Director Mandy Cohen endorsed the recommendation.

“This is another new tool we can use this fall and winter to help protect lives,” Cohen said in a statement. “I encourage parents to talk to their doctors about how to protect their little ones against serious RSV illness, using either a vaccine given during pregnancy, or an RSV immunization given to your baby after birth.”

Both options come at steep prices. Pfizer plans to charge $295 for its shot, and Sanofi sells the monoclonal immunization for $495.

The dreaded rat lungworm—a parasite with a penchant for rats and slugs that occasionally finds itself rambling and writhing in human brains—has firmly established itself in the Southeast US and will likely continue its rapid invasion, a study published this week suggests.

The study involved small-scale surveillance of dead rats in the Atlanta zoo. Between 2019 and 2022, researchers continually turned up evidence of the worm. In all, the study identified seven out of 33 collected rats (21 percent) with evidence of a rat lungworm infection. The infected animals were spread throughout the study’s time frame, all in different months, with one in 2019, three in 2021, and three in 2022, indicating sustained transmission.

Although small, the study “suggests that the zoonotic parasite was introduced to and has become established in a new area of the southeastern United States,” the study’s authors, led by researchers at the University of Georgia College of Veterinary Medicine, concluded. The study was published Wednesday in the journal Emerging Infectious Diseases.

The finding is concerning given the calamitous infection the rat lungworm, aka Angiostrongylus cantonensis, can cause in humans. The parasitic nematodes are, as their name suggests, typically found in rats. But they have a complicated life cycle, which can be deadly when disrupted.

Sickening cycle

Normally, adult worms live in the arteries around a rat’s lungs—hence rat lungworm. There, they mate and lay eggs. The worm’s larvae then burst out of the lungs, get coughed up by the rat, and are swallowed and eventually pooped out. From there, the larvae are picked up by slugs or snails. This can happen if the gastropods eat the rat poop or if the ravenous larvae just bore into their soft bodies. The larvae then develop in the slugs and snails, which, ideally, are eventually eaten by rats. Back in a rat, the late-stage larvae penetrate the intestines, enter the bloodstream, and migrate to the rat’s central nervous system and brain. There they mature into sub-adults then migrate to the lungs, where they become full adults and mate, thus completing the cycle.

Humans become accidental hosts in various ways. They may eat undercooked snails or inadvertently eat an infected slug or snail hiding in their unwashed salad. Infected snails and slugs can also be eaten by other animals first, like frogs, prawns, shrimp, or freshwater crabs. If humans then eat those animals before fully cooking them, they can become infected.

When a rat lungworm finds itself in a human, it does what it usually does in rats—it heads to the central nervous system and brain. Sometimes the migration of the worms to the central nervous system is asymptomatic or only causes mild transient symptoms. But, sometimes, they cause severe neurological dysfunction. This can start with nonspecific symptoms like headache, light sensitivity, and insomnia and develop into neck stiffness and pain, tingling or burning of the skin, double vision, bowel or bladder difficulties, and seizures. In severe cases, it can cause nerve damage, paralysis, coma, and even death.