Scanning electron micrograph image of cholera bacteria.
Scientists from the National Reference Center for Vibrios and Cholera at the Institut Pasteur, in collaboration with the Centre hospitalier de Mayotte, have revealed the spread of a highly drug-resistant cholera strain from Yemen down through Africa. The study was published in the New England Journal of Medicine.
Cholera is caused by the bacteria Vibrio cholerae and in its most severe forms, it is one of the most rapidly fatal infectious diseases: in the absence of treatment, patients can die within hours. Treatment primarily involves replacing lost water and electrolytes, but antibiotics are also used in addition to rehydration therapy. They are essential in reducing the duration of infection and breaking chains of transmission as quickly as possible.
A strain resistant to ten antibiotics – including azithromycin and ciprofloxacin, two of the three recommended for treating cholera – was identified for the first time in Yemen during the cholera outbreak in 2018-2019[1].
Scientists have now been able to trace the spread of this strain by studying the bacterial genomes. After Yemen, it was identified again in Lebanon in 2022[2], then in Kenya in 2023, and finally in Tanzania and the Comoros Islands – including Mayotte, a French département off the south-east coast of Africa – in 2024. Between March and July 2024, the island of Mayotte was affected by an outbreak of 221 cases caused by this highly drug-resistant strain.
“This study demonstrates the need to strengthen global surveillance of the cholera agent, and especially to determine how it reacts to antibiotics in real time. If the new strain that is currently circulating acquires additional resistance to tetracycline, this would compromise all possible oral antibiotic treatment,” concludes Professor François-Xavier Weill, Head of the Vibrios CNR at the Institut Pasteur and lead author of the study.
In a recent study published in the American Journal of Industrial Medicine, middle aged workers in the US who reported high job strain at the start of the study experienced significantly more sleep disturbances over an average follow-up of nine years.
The study analysed data from 1721 workers, with an average age of 51 years, who participated in the Midlife in the United States (MIDUS) study. Sleep disturbances were assessed with an established scale, based on four sleep-related symptoms: trouble falling asleep, waking up during the night and having difficulty going back to sleep, waking up too early in the morning and being unable to get back to sleep, and feeling unrested during the day no matter how many hours of sleep.
The team used six different formulations to quantify job strain based on Karasek’s Job‐Demand‐Control model, which defines job strain as a combination of high job demand and low job control. All formulations showed significant associations between higher job strain at baseline and increased sleep disturbances over time.
“Our findings also suggest that the continuous formulations of job strain demonstrate better model performance with consistent and robust results, offering empirical evidence for future psychosocial occupational health research in the United States,” said the first author Yijia Sun, an MS candidate at the University of California, Los Angeles.
Corresponding author Jian Li, MD, PhD, a professor of Work and Health at the University of California, Los Angeles, noted that there is an urgent need for workplace interventions to reduce stress. “Strategies such as redesigning workloads and promoting worker autonomy could play an important role in improving sleep health and workers’ well-being,” he said.
Neurons in the brain of an Alzheimer’s patient, with plaques caused by tau proteins. Credit: NIH
University of Pittsburgh researchers uncovered a surprising link between Alzheimer’s disease and herpes simplex virus-1 (HSV-1), suggesting that viral infections may play a role in the disease. The study results were published in Cell Reports.
The study also revealed how tau protein, often viewed as harmful in Alzheimer’s, might initially protect the brain from the virus but contribute to brain damage later. These findings could lead to new treatments targeting infections and the brain’s immune response.
“Our study challenges the conventional view of tau as solely harmful, showing that it may initially act as part of the brain’s immune defence,” said senior author Or Shemesh, assistant professor in the Department of Ophthalmology at Pitt. “These findings emphasise the complex interplay between infections, immune responses and neurodegeneration, offering a fresh perspective and potential new targets for therapeutic development.”
The scientists identified forms of HSV-1-related proteins in Alzheimer’s brain samples, with greater amounts of viral proteins co-localised with tangles of phosphorylated tau—one of the hallmarks of Alzheimer’s pathology—in brain regions especially vulnerable to Alzheimer’s across disease stages.
Further studies on miniature models of human brains in a Petri dish suggested that HSV-1 infection could modulate levels of brain tau protein and regulate its function, a protective mechanism that seemed to decrease post-infection death of human neurons.
While the precise mechanisms by which HSV-1 influences tau protein and contributes to Alzheimer’s disease are still unknown, Shemesh and his colleagues plan to explore those questions in future research. They aim to test potential therapeutic strategies that target viral proteins or fine-tune the brain’s immune response and investigate whether similar mechanisms are involved in other neurodegenerative diseases, such as Parkinson’s disease and amyotrophic lateral sclerosis.
Mycobacterium tuberculosis drug susceptibility test. Photo by CDC on Unsplash
Multidrug-resistant tuberculosis (MDR-TB) poses a particular threat to global health. A study led by the Swiss Tropical and Public Health Institute (Swiss TPH) shows that resistance to the new MDR-TB treatment regimen recently recommended by the World Health Organization is already spreading between patients. The findings, published in NEJM, highlight the urgent need for better surveillance and infection control to counteract the rise in antimicrobial resistance.
The traditional treatment regimen for MDR-TB is lengthy, expensive, and comes with severe adverse event. In 2022, the World Health Organization (WHO) endorsed a new 6-month regimen, the BPaL(M), based on evidence of its improved safety and efficacy from numerous clinical studies, including TB-PRACTECAL.
Monitoring the implementation of a new treatment regimen
“While this new regimen is a game changer for patients suffering from MDR-TB, we knew that it will be difficult to outsmart Mycobacterium tuberculosis, the bacteria causing TB,” said Sébastien Gagneux, Head of the Department Medical Parasitology and Infection Biology at Swiss TPH and senior author of the study. “It was therefore crucial to study how the TB bacteria would react to the global roll-out of this new regimen.”
This new study led by Swiss TPH in collaboration with the National Centre for Tuberculosis and Lung Diseases in Tbilisi, Georgia, now examined in detail whether resistance to the drugs in the new regimen has already emerged since its introduction, and whether this resistance is transmitting between patients.
Over a quarter of resistant strains result from transmission between patients
The researchers analysed the genomes of close to 90 000 M. tuberculosis strains from Georgia and many other countries around the world. They identified a total of 514 strains that were resistant to TB drugs, including both the old and the new treatment regimens. These highly drug-resistant strains were found in 27 countries across four continents.
Alarmingly, 28% of these strains were transmitted directly from one patient to another. “We already had anecdotal evidence of resistance emerging to the new regimen, but we did not know to what extent transmission was responsible for the spread of these highly drug-resistant strains,” said Galo A. Goig, postdoctoral collaborator at Swiss TPH and first author of the study.
“The good news is that the total number of these cases is still low. However, the fact that more than a quarter of these highly drug-resistant cases are due to patient-to-patient transmission, only two years after WHO endorsed the new regimen, is worrying,” added Goig.
Call for better surveillance and infection control
These findings have important implications for public health policy and interventions. “These new drugs have taken many years to develop, and to prevent drug resistance from emerging, it is essential to combine the deployment of these new regimens with robust diagnostics and surveillance systems,” said Chloé Loiseau, postdoctoral collaborator at Swiss TPH and co-author of the paper.
The authors emphasise the need for improved diagnostic tools, better infection control and robust surveillance systems to curb the spread of these highly drug-resistant strains, and to safeguard the efficacy of the new treatment regimen.
Tackling antimicrobial resistance
While there are already new TB drugs in the pipeline, experts worry that M. tuberculosis will continue to find ways to evade new drugs. “The example of these highly drug-resistant TB strains further illustrates that antimicrobial resistance is one of the most critical threats to global health today,” said Gagneux. “We must stay ahead in this constant race between drug development and bacterial resistance, and take proactive steps to prevent a ‘post-antibiotic era’ for TB and other diseases.”
Sex differences in brain structure are present from birth, research from the Autism Research Centre at the University of Cambridge has shown.
While male brains tended to be greater in volume than female brains, when adjusted for total brain volume, female infants on average had significantly more grey matter, while male infants on average had significantly more white matter in their brains.
Grey matter is made up of neuron cell bodies and dendrites and is responsible for processing and interpreting information, such as sensation, perception, learning, speech, and cognition. White matter is made up of axons, which are long nerve fibres that connect neurons together from different parts of the brain.
Yumnah Khan, a PhD student at the Autism Research Centre, who led the study, said: “Our study settles an age-old question of whether male and female brains differ at birth. We know there are differences in the brains of older children and adults, but our findings show that they are already present in the earliest days of life.
“Because these sex differences are evident so soon after birth, they might in part reflect biological sex differences during prenatal brain development, which then interact with environmental experiences over time to shape further sex differences in the brain.”
One problem that has plagued past research in this area is sample size. The Cambridge team tackled this by analysing data from the Developing Human Connectome Project, where infants receive an MRI brain scan soon after birth. Having over 500 newborn babies in the study means that, statistically, the sample is ideal for detecting sex differences if they are present.
A second problem is whether any observed sex differences could be due to other factors, such as differences in body size. The Cambridge team found that, on average, male infants had significantly larger brain volumes than did females, and this was true even after sex differences in birth weight were taken into account.
After taking this difference in total brain volume into account, at a regional level, females on average showed larger volumes in grey matter areas related to memory and emotional regulation, while males on average had larger volumes in grey matter areas involved in sensory processing and motor control.
The findings of the study, the largest to date to investigate this question, are published in the journal Biology of Sex Differences.
Dr Alex Tsompanidis who supervised the study, said: “This is the largest such study to date, and we took additional factors into account, such as birth weight, to ensure that these differences are specific to the brain and not due to general size differences between the sexes.
“To understand why males and females show differences in their relative grey and white matter volume, we are now studying the conditions of the prenatal environment, using population birth records, as well as in vitro cellular models of the developing brain. This will help us compare the progression of male and female pregnancies and determine if specific biological factors, such as hormones or the placenta, contribute to the differences we see in the brain.”
The researchers stress that the differences between males and females are average differences.
Dr Carrie Allison, Deputy Director of the Autism Research Centre, said: “The differences we see do not apply to all males or all females, but are only seen when you compare groups of males and females together. There is a lot a variation within, and a lot of overlap between, each group.”
Professor Simon Baron-Cohen, Director of the Autism Research Centre, added: “These differences do not imply the brains of males and females are better or worse. It’s just one example of neurodiversity. This research may be helpful in understanding other kinds of neurodiversity, such as the brain in children who are later diagnosed as autistic, since this is diagnosed more often in males.”
The research was funded by Cambridge University Development and Research, Trinity College, Cambridge, the Cambridge Trust, and the Simons Foundation Autism Research Initiative.
