
Extensively Drug-Resistant TB Outcomes Remain Poor in Europe
Only four out of 10 patients with extensively drug-resistant tuberculosis in Europe achieved successful treatment outcomes, a rate markedly lower than that for other forms of drug-resistant tuberculosis and comparable with cure rates from the pre-antibiotic era.
METHODOLOGY:
Researchers conducted a retrospective observational cohort study across 16 countries of the World Health Organization (WHO) European Region to evaluate treatment outcomes in 188 patients (median age, 42 years; 79.3% men) with extensively drug-resistant tuberculosis.
Data collected included patient characteristics, disease localisation, prior treatments, phenotypic and genotypic drug susceptibility testing results, and treatment regimens.
Treatment outcomes were categorised as successful, failure (microbiological or clinical reasons including regimen changes), lost to follow-up (treatment interrupted for 2 or more months), or not evaluated.
TAKEAWAY:
Among the 188 patients with extensively drug-resistant tuberculosis, 48.4%, 34.0%, and 17.6% of Mycobacterium tuberculosis strains were resistant to bedaquiline alone, linezolid alone, and both drugs, respectively.
Among 156 patients with available data for treatment outcomes, 40.2% (95% CI, 28.4%-53.2%) achieved successful outcomes in a pooled analysis accounting for between-country heterogeneity.
Patients with extensively drug-resistant tuberculosis had lower pooled success rates (P < .0001) and significantly higher pooled rates of treatment failure and death (P < .0001 and P = .008, respectively) than those with multidrug-/rifampicin-resistant or preextensively drug-resistant tuberculosis.
The likelihood of an unsuccessful outcome decreased with each additional effective drug in the regimen (P = .026) but increased among patients treated in upper-middle-income countries compared with that among those treated in high-income countries (P < .001).
IN PRACTICE:
"[The study] findings underscore the need for improved, rapid DST [drug susceptibility testing] tools and effective, shorter treatment regimens for extensively drug-resistant tuberculosis," the authors wrote.
SOURCE:
This study was led by Yousra Kherabi, Bichat-Claude Bernard Hospital, Assistance Publique-Hôpitaux de Paris, Université Paris Cité, Paris, France, and Ole Skouvig Pedersen, Aarhus University Hospital, Aarhus, Denmark. It was published online on July 15, 2025, in The Lancet Regional Health - Europe.
LIMITATIONS:
The coverage of the WHO European Region was limited. Most of the participating centres were specialist or referral centres, which may have introduced selection bias and limiting generalisability. Although the use of WHO-defined outcomes simplified data collection, it constrained a detailed understanding of treatment failures. Moreover, individual-level data were available only for patients with extensively drug-resistant tuberculosis, which may have introduced confounding from unmeasured patient-level factors.
DISCLOSURES:
This study did not receive any funding. One author reported serving as a co-principal investigator of clinical trials testing new regimens for multidrug-resistant tuberculosis, and some authors reported receiving honoraria for speaking engagements or serving on advisory boards of various pharmaceutical companies.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
Hashtags

Try Our AI Features
Explore what Daily8 AI can do for you:
Comments
No comments yet...
Related Articles


Bloomberg
an hour ago
- Bloomberg
Roche to Test Whether New Drug Can Prevent Alzheimer's Disease
Roche Holding AG plans to test whether an experimental medicine can prevent Alzheimer's disease symptoms in high-risk people, its latest investment in one of the most failure-prone areas of drugmaking. The new late-stage study will focus on people who are at risk of cognitive decline, Roche said in a statement late Sunday. The goal would be to slow down the emergence of symptoms, or prevent them entirely.
Yahoo
2 hours ago
- Yahoo
Millions of people are suffering from brain fog. A new study will find out why
Millions of people who recover from infections like COVID-19, influenza and glandular fever are affected by long-lasting symptoms. These include chronic fatigue, brain fog, exercise intolerance, dizziness, muscle or joint pain and gut problems. And many of these symptoms worsen after exercise, a phenomenon known as post-exertional malaise. Medically the symptoms are known as myalgic encephalomyelitis or chronic fatigue syndrome (ME/CFS). The World Health Organization classifies this as a post viral fatigue syndrome, and it is recognised by both the WHO and the United States Centers for Disease Control and Prevention as a brain disorder. Experiencing illness long after contracting an infection is not new, as patients have reported these symptoms for decades. But COVID-19 has amplified the problem worldwide. Nearly half of people with ongoing post-COVID symptoms – a condition known as long-COVID – now meet the criteria for ME/CFS. Since the start of the pandemic in 2020, it is estimated that more than 400 million people have developed long-COVID. To date, no widely accepted and testable mechanism has fully explained the biological processes underlying long-COVID and ME/CFS. Our work offers a new perspective that may help close this gap. Our research group studies blood and the cardiovascular system in inflammatory diseases, as well as post-viral conditions. We focus on coagulation, inflammation and endothelial cells. Endothelial cells make up the inner layer of blood vessels and serve many important functions, like regulating blood clotting, blood vessel dilation and constriction, and inflammation. Our latest review aims to explain how ME/CFS and long-COVID start and progress, and how symptoms show up in the body and its systems. By pinpointing and explaining the underlying disease mechanisms, we can pave the way for better clinical tools to diagnose and treat people living with ME/CFS and long-COVID. What is endothelial senescence? In our review, our international team proposes that certain viruses drive endothelial cells into a half-alive, 'zombie-like' state called cellular senescence. Senescent endothelial cells stop dividing, but continue to release molecules that awaken and confuse the immune system. This prompts the blood to form clots and, at the same time, prevent clot breakdown, which could lead to the constriction of blood vessels and limited blood flow. By placing 'zombie' blood-vessel cells at the centre of these post-viral diseases, our hypothesis weaves together microclots, oxygen debt (the extra oxygen your body needs after strenuous exercise to restore balance), brain-fog, dizziness, gut leakiness (a digestive condition where the intestinal lining allows toxins into the bloodstream) and immune dysfunction into a single, testable narrative. From acute viral infection to 'zombie' vessels Viruses like SARS-CoV-2, Epstein–Barr virus, HHV-6, influenza A, and enteroviruses (a group of viruses that cause a number of infectious illnesses which are usually mild) can all infect endothelial cells. They enable a direct attack on the cells that line the inside of blood vessels. Some of these viruses have been shown to trigger endothelial senescence. Multiple studies show that SARS-CoV-2 (the virus which causes COVID-19 disease) has the ability to induce senescence in a variety of cell types, including endothelial cells. Viral proteins from SARS-CoV-2, for example, sabotage DNA-repair pathways and push the host cell towards a senescent state, while senescent cells in turn become even more susceptible to viral entry. This reciprocity helps explain why different pathogens can result in the same chronic illness. Influenza A, too, has shown the ability to drive endothelial cells into a senescent, zombie-like state. What we think is happening We propose that when blood-vessel cells turn into 'zombies', they pump out substances that make blood thicker and prone to forming tiny clots. These clots slow down circulation, so less oxygen reaches muscles and organs. This is one reason people feel drained. During exercise, the problem worsens. Instead of the vessels relaxing to allow adequate bloodflow, they tighten further. This means that muscles are starved of oxygen and patients experience a crash the day after exercise. In the brain, the same faulty cells let blood flow drop and leak, bringing on brain fog and dizziness. In the gut, they weaken the lining, allowing bits of bacteria to slip into the bloodstream and trigger more inflammation. Because blood vessels reach every corner of the body, even scattered patches of these 'zombie' cells found in the blood vessels can create the mix of symptoms seen in long-COVID and ME/CFS. Immune exhaustion locks in the damage Some parts of the immune system kill senescent cells. They are natural-killer cells, macrophages and complement proteins, which are immune molecules capable of tagging and killing pathogens. But long-COVID and ME/CFS frequently have impaired natural-killer cell function, sluggish macrophages and complement dysfunction. Senescent endothelial cells may also send out a chemical signal to repel immune attack. So the 'zombie cells' actively evade the immune system. This creates a self-sustaining loop of vascular and immune dysfunction, where senescent endothelial cells persist. In a healthy person with an optimally functioning immune system, these senescent endothelial cells will normally be cleared. But there is significant immune dysfunction in ME/CFS and long-COVID, and this may enable the 'zombie cells' to survive and the disease to progress. Where the research goes next There is a registered clinical trial in the US that is investigating senescence in long-COVID. Our consortium is testing new ways to spot signs of ageing in the cells that line our blood vessels. First, we expose healthy endothelial cells in the lab to blood from patients to see whether it pushes the cells into a senescent, or 'zombie,' state. At the same time, we are trialling non‑invasive imaging and fluorescent probes that could one day reveal these ageing cells inside the body. In selected cases, tissue biopsies may later confirm what the scans show. Together, these approaches aim to pinpoint how substances circulating in the blood drive cellular ageing and how that, in turn, fuels disease. Our aim is simple: find these ageing endothelial cells in real patients. Pinpointing them will inform the next round of clinical trials and open the door to therapies that target senescent cells directly, offering a route to healthier blood vessels and, ultimately, lighter disease loads. Burtram C. Fielding is Dean Faculty of Sciences and Professor in the Department of Microbiology, Stellenbosch University This article is republished from The Conversation under a Creative Commons license. Read the original article.
Yahoo
3 hours ago
- Yahoo
Human Babies Aren't Supposed to Have 3 Parents—but Now They Can
"Hearst Magazines and Yahoo may earn commission or revenue on some items through these links." Here's what you'll learn when you read this story: The first babies with three biological parents were born out of a new technique to prevent mitochondrial disease. The nucleus of an egg fertilized in vitro was transferred into a donor egg without a nucleus, but with viable mitochondria. Eight healthy babies, including a set of twins, were born with low to undetectable levels of mitochondrial mutations. The only creatures known to conceive offspring from more than two parents are salamanders. Females from the genus Ambystoma (which are notoriously promiscuous) mate with up to three different males, and that DNA is then incorporated into what is known as a triploid genome in their offspring. Now a version of this has become possible in humans. It seems limb regeneration isn't the only way medical intervention can put humans on salamanders' level. Being born with three genomes is not a phenomenon that occurs naturally in Homo sapiens, but in an attempt to prevent certain genetic conditions caused by mutations in the mitochondria, scientists have found a way. Mitochondrial DNA or mtDNA is exclusively passed down from the maternal side. Dysfunction in the mitochondria can lead to metabolic diseases characterized by symptoms such as seizures, developmental delays, blindness, and loss of muscular function. Some can even be fatal. Mitochondrial diseases occur in about 1 in every 5,000 people. They were previously only preventable by using a donor egg or foregoing the conception of biological children altogether. This is why pediatric neurologist Bobby McFarland, of Newcastle University in the UK, led an experimental study that would reduce and potentially eliminate the risk of mitochondrial disease with a new method of in vitro fertilization. McFarland and his research team wanted see if removing the nucleus of an egg and placing it in a donor egg with viable mitochondria would result in healthy offspring. 'We found that pronuclear transfer, a form of mitochondrial donation, was effective in reducing the level of pathogenic mtDNA variant to substantially below the threshold for clinical disease in the offspring of women with homoplasmic (or high heteroplasmic) levels,' he said in a study recently published in the New England Journal of Medicine. When mitochondria are homoplasmic, all copies produced by cell division have mutations. Mutation levels vary in heteroplasmic mitochondria. Preimplantation genetic testing (PGT) can screen for these abonormalities, and women with homoplasmy or high levels of heteroplasmy can benefit from what is now known as pronuclear transfer. This involves eggs from both the mother and donor being fertilized with the father's sperm in vitro. Nuclei are then removed from both eggs after ten hours. Since the nucleus carries most genetic material and has no connection to mitochondrial disease, the mother's nucleus is implanted into the donor egg to take advantage of its mitochondria. While there is a chance that a few of the mother's mitochondria may end up in the embryo, it is unlikely to cause a debilitating disease. Levels of defective mitochondria in offspring conceived via pronuclear transfer were low enough to escape that fate. Eight pregnancies (including a set of twins) resulted from the experiment, and while there were a few minor health problems in the newborns, these were either treatable or corrected themselves. Not only were levels of heteroplasty low for the babies, but undetectable in five of them. Developmental progress also turned out to be normal. Though one baby had a form of infant epilepsy, and another had heart arrhythmia and hyperlipidemia, or high levels of fats and lipids in the blood, both of these conditions were treated and resolved. Whether the hyperlipidemia was even caused by mtDNA is uncertain, especially because the mother also had severe hyperlipidemia during her pregnancy. Though there was a chance that any of the mothers with pathogenic mtDNA had a higher risk of complications during pregnancy, which could possibly cause their children to have health issues, there is no proof for now. 'We are assessing, over the long term, the health and extent of heteroplasmy (if detectable) of the offspring,' McFarland and his team said. 'Indeed, the role of mitochondrial donation as a choice for women with a heritable pathogenic mtDNA variant will only be established with the availability of additional data.' You Might Also Like Can Apple Cider Vinegar Lead to Weight Loss? Bobbi Brown Shares Her Top Face-Transforming Makeup Tips for Women Over 50 Solve the daily Crossword