A severe outbreak of invasive meningococcal disease, which can cause meningitis and sepsis, in Kent in the UK earlier this year was driven by a bacterial strain that took genes from harmless microbes. This helped the resulting bacteria evade the immune system and obtain iron from blood, boosting their growth.

鈥淲hat was really unusual about the outbreak is quite how explosive it was,鈥� says at Queen Mary University of London, who wasn鈥檛 involved in the discovery. 鈥淸The bacterium] clearly gained a set of genetic changes that made it better at hiding from the immune system and better at harvesting nutrients. That made it a really super powerful bug.鈥�

In March, 21 people 鈥� mostly university or high school students 鈥� are known to have become infected with a strain of Neisseria meningitidis group B at a nightclub in Canterbury, Kent. N. meningitidis usually spreads via close and prolonged contact with saliva from an infected person via things like kissing and sharing drinks or vapes.

N. meningitidis lives harmlessly in the nose and throat of without causing any health problems, but genetic changes can allow it to become more invasive and enter the bloodstream, leading to invasive meningococcal disease (IMD). This can result in sepsis, a life-threatening immune reaction to bacteria, or meningitis, where bacteria infect the thin lining surrounding the brain and spinal cord, causing inflammation.

All the IMD infections in Kent occurred within about a week. Those infected were treated in hospital, with nine requiring intensive care. 鈥淭he incredibly rapid nature of the outbreak was unprecedented [for the UK],鈥� says Wall. 鈥淯sually these [outbreaks] roll over two or three weeks and there鈥檚 one or two cases that end up in hospital.鈥�

To understand this, at the University of Oxford and his colleagues sequenced the entire genome of live N. meningitidis in blood samples taken from six of those infected, including the two people who died.

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These bacterial genomes were almost identical, suggesting the outbreak started from one person. Next, the team compared one of these genomes with 48,000 others from Neisseria strains collected during prior outbreaks or from people without known health problems.

This revealed that the Kent strain had acquired several genes from a harmless strain of N. meningitidis and another bacterium called Neisseria cinerea that lives harmlessly in . Bacteria constantly exchange genetic material via a process called horizontal transfer, which can involve them forming tiny tunnels between each other, through which they transfer copies of genes.

Some of the genes acquired by the Kent strain enhanced its uptake of iron from blood, which it needs to survive and replicate. Others reduced the amount of sugar that was coating a tail-like structure, called the pilus, on the bacterium. This enabled bacteria to clump together and evade destruction by immune cells, such as neutrophils. 鈥淣eutrophils will try and come and eat an individual [bacterium], but they can鈥檛 eat a clump, it鈥檚 too big,鈥� says Wall.

鈥淭here was this catalogue of changes that made this organism really transmissible, but also really invasive,鈥� says Maiden. This meant that several people became very ill and were then less able to transmit the infection to the public. 鈥淚f you鈥檙e ill, you鈥檙e not going to be going around transmitting organisms, so the outbreak ended very quickly,鈥� says Maiden.

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It is unclear exactly when these genetic changes occurred in the person believed to have initiated the outbreak, but they probably happened gradually, until there was the right combination of genetics and social mixing, says Maiden.

Such insights could support the development of better vaccines against N. meningitidis if we can target the features that make the bacterium particularly invasive, says Wall. But they won鈥檛 help us predict the next highly invasive strain. 鈥淸These bacteria are] inherently highly unpredictable,鈥� says Maiden.

Following the Kent outbreak, the UK government launched a for young people starting university or further education in September or October this year. Symptoms of IMD include fever, headache, a stiff neck, joint and muscle pain, and a rash that doesn鈥檛 fade when pressed with a glass.

In the fight against common childhood illnesses, scientists have turned to an unusual source: the blood of paediatricians. It turns out this is a treasure trove of powerful antibodies that could be used as preventative treatments. These have even outperformed approved antibody therapies against respiratory syncytial virus (RSV) and a common cold virus.

Paediatricians are almost constantly exposed to respiratory viruses, making them a potentially underexplored resource in the hunt for highly potent antibodies against such pathogens. Although antibody therapies are available for preventing infections like RSV 鈥� which infects almost every child by the age of 2 and can trigger severe breathing difficulties 鈥� they only neutralise some strains. But a broader-acting treatment could now be on the cards.

A team including Hui Zhai at the Children鈥檚 Hospital of Chongqing Medical University screened the blood of 10 paediatricians who had been working at the hospital for over a decade. From this, the researchers discovered 56 potent antibodies against RSV from the paediatricians鈥� immune cells.

The researchers then generated artificial versions of these antibodies and tested them in the lab, finding that three were particularly active against a diverse range of RSV strains. One of the three also neutralised human metapneumovirus, which belongs to the same virus family as RSV and is a common cause of colds, but can also lead to severe illness in some children.

Subsequent tests in mice and rats showed that injections of these three paediatrician-derived antibodies, either on their own or in combination, stopped the animals from developing symptoms when they were infected with RSV or human metapneumovirus. In fact, the paediatrician antibodies were up to 25 times better at blocking RSV than existing antibodies called nirsevimab and clesrovimab, and they neutralised a wider range of strains.

This makes sense because it is common lore among paediatricians that they become increasingly resilient to respiratory viruses over the course of their careers, says at Port Macquarie Base Hospital in Australia. 鈥淚鈥檝e been working with paediatric patients for 10 years now and in my first few years, I would probably get two to three notable respiratory illnesses per year, and now I can go a year without getting any.鈥�

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Calcutt believes the paediatrician-derived antibodies appear promising enough to warrant further testing in human clinical trials. 鈥淭here are certainly stranger interventions out there, so I think this one is worth considering,鈥� he says.

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Currently, there are two ways to protect infants from RSV. One is to administer a vaccine during pregnancy, which protects babies once they are born. The other is to give them an injection of nirsevimab or clesrovimab, which neutralise the virus if a child catches it, thereby helping to prevent severe symptoms. But these only work against some RSV strains.

Nirsevimab and clesrovimab were similarly developed by screening the blood of adults who had previously been infected with RSV, but who didn鈥檛 work in healthcare. This identified antibodies that the individuals鈥� immune systems had naturally produced against the virus. There is no approved vaccine or antibody therapy for human metapneumovirus.

Traces of a bacterium related to syphilis have been found in a bone from a person who lived in the mountains of Colombia over 5000 years ago.

The discovery shows that this group of corkscrew-shaped bacteria was infecting humans thousands of years earlier than previously thought, before the rise of intensive agriculture, which many researchers consider a catalyst for the spread of pathogens.

Today, three subspecies of the bacterium Treponema pallidum cause the diseases syphilis, bejel and yaws. The deep history of these ailments is murky, and researchers have debated where diseases like syphilis arose and how they became widespread. Ancient bacterial DNA and markers of infection on skeletal remains lend us some clues, but these are rare and can be ambiguous.

So, when researchers studying the ancient DNA of 5500-year-old human remains in the Bogot谩 savannah detected the genome of Treponema pallidum in a human leg bone sample, it was a surprise.

鈥淭his finding was completely unexpected, because the individual studied had no skeletal evidence of a Treponema infection,鈥� says at the University of California, Santa Cruz.

It is widely thought that many common diseases started to affect humanity after the dawn of intensive agriculture, when people began living in denser communities. But this individual lived in a very different context, where small hunter-gatherer groups travelled frequently and were in close contact with wildlife.

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鈥淥ur results can tell us a lot about the long-term evolutionary history of [this bacterium] by revealing a long-standing association with human populations,鈥� says at the University of Lausanne in Switzerland.

When Broomandkhoshbacht, Bozzi and their colleagues compared the ancient genome to those of other T. pallidum bacteria, they found it was part of a completely different lineage from any known modern relatives. This indicates that, millennia ago, ancient relatives of syphilis had already diversified in the Americas and were infecting humans, and the team鈥檚 analysis suggests they had many of the same genetic features that make today鈥檚 strains harmful.

The findings point to an early presence of these pathogens in the Americas, but it is also possible that they have been infecting humans for even longer across the world.

at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, notes that the ancient strain might belong to an elusive, 鈥渕issing鈥� pathogen: Treponema carateum, which causes a skin disease called pinta. The bacterium is only known from physical descriptions, not genetics.

at the University of Zurich, Switzerland, wonders what additional ancient genomes can tell us. 鈥淲ere there perhaps many extinct lineages and perhaps different diseases caused by these pathogens in the past?鈥� she says.

For Bozzi, understanding how pathogens evolve to cause diseases like syphilis and yaws is a crucial step in finding the genetic quirks that allow pathogens to infect new hosts and make their associated illnesses more dangerous.

The Black Death, a bubonic plague outbreak that killed up to 60 per cent of the population of medieval Europe, may have been set in motion by volcanic activity around 1345.

The plague bacterium, Yersinia pestis, is spread by fleas feeding on rodents and then carried to humans bitten by infected fleas. It is unclear what led to the 14th-century outbreak in Europe, but historical sources suggest that the transport of grain from the Black Sea to Italy may have played a role.

鈥淭he Black Death is a central event of the Middle Ages and I wanted to understand why such an extraordinary amount of grain had to be brought to Italy specifically in 1347,鈥� says at the Leibniz Institute for the History and Culture of Eastern Europe in Germany.

To investigate, Bauch and his colleague at the University of Cambridge reviewed evidence about the climate from tree ring data, ice cores and written accounts.

Observers in Japan, China, Germany, France and Italy all independently reported reduced sunshine and increased cloudiness between 1345 and 1349. This was probably the result of a sulphur-rich volcanic eruption 鈥� or several eruptions 鈥� in an unknown tropical location, Bauch and B眉ntgen suggest.

Ice cores from Greenland and the Antarctic, along with thousands of tree ring timber samples collected across eight different European regions, also suggest a dramatic climate event may have happened.

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What鈥檚 more, the researchers found official records showing that, facing famine caused by the cold weather and failing crops, Italian authorities implemented an emergency plan to import grain from the Mongols of the Golden Horde around the Sea of Azov in 1347.

鈥淭hey acted in a highly professional, rational and efficient manner and achieved their goal to alleviate high prices and impending famine through grain imports before starvation deaths could occur,鈥� says Bauch. 鈥淧recisely because these societies practised excellent famine prevention, the plague bacterium arrived in Italy as a stowaway, carried in with the grain.鈥�

At the time, the cause of plague wasn鈥檛 known and the outbreak was blamed on things such as 鈥渁stral constellations and toxic vapours released into the atmosphere by earthquakes鈥�, he says.

While the plague may have reached Europe eventually anyway, perhaps the population losses would have been smaller if this emergency response hadn鈥檛 occurred, says Bauch. 鈥淢y argument is not against preparedness, but rather for an awareness that effective precautionary measures in one sphere can create problems in unexpected areas.鈥�

at the Australian National University in Canberra says it is likely that 鈥渁 perfect storm of factors鈥� led to the Black Death entering Europe. 鈥淩ising food prices, the widespread famine documented, together with the cold, wet weather, may have resulted in reduced immunity due to inadequate nutrition, and induced behaviour change such as spending more time indoors near others for extended periods,鈥� she says.

However, more work will be required to untangle causation from correlation, she says. 鈥淭he short-term perturbations caused by the eruptions appear to have had considerable impact on local weather patterns as documented, but whether they were the cause of the Black Death entering Europe, as stated, requires more evidence,鈥� says Lal.

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A form of leprosy affected people in the Americas long before the arrival of Europeans, contrary to popular belief.

鈥淭he narrative around leprosy has been always been that it鈥檚 this awful disease that Europeans brought to America,鈥� says at the Pasteur Institute in Paris. 鈥淲ell, our discovery changes that.鈥�

The vast majority of leprosy cases worldwide are caused by the bacterium Mycobacterium leprae. But in 2008, at the University of Texas MD Anderson Cancer Center and his colleagues , M. lepromatosis, in two people from Mexico who had leprosy. Since then, scientists have found more cases of this pathogen in the US, Canada, Brazil and Cuba 鈥� as well as in four people in Singapore and Myanmar.

Wanting to know more about this understudied pathogen, Rascovan teamed up with Han and other researchers, as well as Indigenous communities, to analyse ancient DNA from 389 people who lived in the Americas before European contact.

They found M. lepromatosis in the remains of one person near the Alaska-Canada border and two others along the south-eastern coast of Argentina, all carbon-dated to about 1000 years ago. The bacteria鈥檚 genomes varied slightly, hinting at distinct strains separated by around 12,000 kilometres. 鈥淚t spread so fast, on a continental level, in just a matter of centuries,鈥� says Rascovan.

DNA from dozens of modern cases 鈥� mostly from the US and Mexico 鈥� revealed that nearly all contemporary strains are essentially clones, showing only minor changes since ancient times. But the team also identified one rare and unusually ancient strain in a modern person that hadn鈥檛 turned up in archaeological remains, suggesting that at least two distinct lineages of M. lepromatosis are still infecting people in North America today 鈥� alongside the M. leprae strains introduced by Europeans.

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Combined, the analyses suggest that the bacteria have been branching out and evolving in the Americas for nearly 10,000 years. About 3000 years ago, one line of the pathogen mutated into a form that now 鈥� leading to problems like swollen skin and crusty lesions.

As for its origins, genetic data show that M. lepromatosis and M. leprae split from a common ancestor more than 700,000 years ago, although where in the world that divergence happened remains unknown.

Modern cases of M. lepromatosis seem to affect the blood vessels, especially in the legs and feet 鈥� unlike M. leprae, which mainly attacks the nerves, says Han. In some people carrying M. lepromatosis, the blood flow gets blocked, causing the skin to die and break down. That can lead to deadly complications, including severe secondary infections by bacteria like Staphylococcus aureus. This disease can also spread beyond the skin, turning up in organs like the liver and spleen. Consequently, some people die before their bones have time to show any signs of leprosy.

That could help explain why archaeologists hadn鈥檛 identified leprosy in ancient remains from the Americas, says Han. While skeletons in Europe and Asia often show classic signs of bone damage from leprosy, the ancient individual from Canada in this study had only vague jaw lesions that could be caused by many conditions 鈥� and the two skeletons from Argentina showed no signs of leprosy at all.

at Leiden University in The Netherlands says this 鈥渂eautiful study鈥� has forced a rethinking of the disease鈥檚 history. 鈥淢y teaching slides state that there was no leprosy in the Americas before Europeans colonised it,鈥� she says. 鈥淣ow I have to update my slides!鈥�

Beyond that historical significance, the research also sheds lights on a pressing public health issue. Leprosy is re-emerging in parts of the world, she says, and rising antimicrobial resistance could make it harder to treat. 鈥淪urveillance is very important,鈥� says Geluk. 鈥淲e need a global effort to map what strains are out there.鈥�