A lab accident in the Irkutsk region of Siberia led to the death of a 28-year-old woman from pneumonic plague last week, according to reports from . Nearly 200 people who might have come into contact with her are said to have been put under observation and several hospitals in the area have been quarantined.

There is no reason to think this is the start of a large outbreak. Plague cases are relatively common worldwide but they do not spread widely because the infection is now easily treated and prevented.

鈥淧lague is not a historical disease,鈥� at the University of Birmingham in the UK said in a statement. 鈥淗uman cases occur every year, including outbreaks of the pneumonic form.鈥�

The term 鈥減lague鈥� usually refers to ill health caused by a bacterium called Yersinia pestis, although there is no official confirmation the woman鈥檚 death was due to this pathogen. Y. pestis circulates in non-human animals in many parts of the world and .

The most common form of plague is bubonic plague, which is caused by flea bites and characterised by swollen lymph glands, or buboes. The bacterium can also infect blood, called septicaemic plague, or the lungs, known as pneumonic plague.

The woman in Irkutsk is said to have died of pneumonic plague two days after being hospitalised. This is the deadliest form of the condition and can spread via the air when infected people cough, for instance. However, measures such as wearing masks and avoiding close contact .

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鈥淭his can be controlled and stopped with appropriate surveillance and control measures,鈥� at the University of Reading in the UK said in a statement. Cases are also usually treatable with antibiotics.

The circumstances of the lab accident remain unclear. It is being reported that it was caused by a broken test tube, but if proper procedures for handling dangerous microbes were being followed, this should not have led to an infection. Workers should have been wearing protective equipment, for instance.

There has also been speculation that the woman鈥檚 death was caused by a modified form of the plague created for biowarfare, but there is no evidence this is the case. Pneumonic plague is nearly always fatal if not treated promptly, so there鈥檚 no reason to think this strain is especially dangerous. What鈥檚 more, Y. pestis frequently infects animals and people, so there are legitimate reasons for studying it in labs.

The former Soviet Union did have a large bioweapons programme, which included . Antibiotic-resistant strains have also evolved naturally, and were first .

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DNA evidence shows that plague bacteria devastated a community in Siberia more than 5000 years ago, challenging the idea that there were no major disease outbreaks before the advent of farming and large settlements

There is a long history of lab accidents leading to infections, deaths and even outbreaks. For instance, in 2007, an outbreak of foot and mouth disease in the UK was traced to labs. In 1979, , Russia, after what the US claimed was the accidental release of anthrax spore from a military facility. There is, however, no evidence the covid-19 pandemic was a result of a lab accident.

While lab-acquired infections with Y. pestis are rare, they are not impossible, Stamataki said. 鈥淭his incident warrants a full account of what happened. That account matters beyond Russia.鈥�

Russia has that Ukraine is developing bioweapons with the help of the US, but there is no evidence for this. In 2024, it was reported that in Russia called Sergiev Posad-6.

A blood test could determine whether a feverish baby has a bacterial or viral infection in 15 to 20 minutes. This would help doctors gauge whether the infection is serious or may pass without treatment, which could prevent unnecessary use of antibiotics.

When babies are brought into hospital with fever, they 鈥渁re considered high-risk until proven otherwise鈥�, says at the Giannina Gaslini Institute in Genoa, Italy.

A fever can be the result of several things, including infection by viruses or bacteria. These different types of pathogens require different medications. Furthermore, most common viruses are fairly benign, while bacterial infections are generally more dangerous, says Bellini.

Existing tests to gauge infection type take at least a few hours, so babies with fever are often given antibiotics against bacteria as a precautionary measure. But only about 15 per cent of them actually have a serious bacterial infection, says Bellini. This unnecessary use of antibiotics helps drive the spread of bacterial resistance.

To develop a test that determines infection type, Bellini and his colleagues followed 85 babies, all younger than 90 days old, who were brought into emergency rooms with fever after previously having no serious health concerns. The team took blood samples and tested for two proteins: CD64 and CD169.

Previous studies have shown that these proteins become more common in certain blood cells when the body responds to infections. CD64 is made at higher levels in response to bacteria and is found on the surface of white blood cells called neutrophils. and appears on the outer membranes of monocytes, another type of white blood cell.

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By in neutrophils and monocytes, the test correctly identified all 15 cases of bacterial infection, 44 incidences of viral infection and 26 cases of no infection. Bellini presented the results at the in Paris, France.

The results came through in 15 to 20 minutes in a lab, says Bellini, who is trying to develop a version that can be used as quickly in hospitals.

This builds on several years of research to develop a CD64/CD169 test. at Beckman Coulter Life Sciences in Marseille, France, has spent much of the past decade working on it. In 2021, his team found that among adults in an emergency room.

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Other groups have since , found ways to more , and demonstrated that . Performing the test on babies in a hospital setting is a significant advance, says Malergue. It was crucial to investigate the test in this age group because their immune systems are still developing, which meant 鈥渟ome people had doubts about the capacity of these [CD64 and CD169] markers to arise鈥�, he says.

Malergue says one of his collaborators used the test in Martinique during an outbreak of dengue fever, which is caused by a virus and is usually mild. The collaborator found that some people actually had a bacterial infection called leptospirosis, which is life-threatening without antibiotics.

Bellini now hopes to assess the test in a trial of 300 to 500 infants at multiple hospitals. Meanwhile, Malergue and his colleagues have developed that can quickly analyse finger-prick blood samples to determine whether an infection is viral or bacterial, which is approved for research use.

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.