LONDON — In the packed halls of the recent Alzheimer's Association International Conference in mid-July, over 10,000 experts in brain research discussed strategies to beat dementia. But in one room, attendees gathered to watch a video from a nonscientist named Isabel Beltre, whose life was transformed by a recent trial.

Beltre was one of 1,200 participants ages 60 to 77 who took part in the Latin American Initiative for Lifestyle Intervention to Prevent Cognitive Decline (LatAm-FINGERS), the first trial to test a culturally adapted lifestyle intervention to prevent cognitive decline in Latin America. Rather than attempting to treat dementia after it has developed, the trial tackled risk factors that raise the likelihood of the condition, like smoking and a sedentary lifestyle.

In her native Spanish, Beltre thanked both God and the project for its impact on her life. There was a celebratory air in the conference room as the trial's results were released. The lifestyle interventions, which included exercise programs and brain training, had statistically improved participants' thinking skills, compared with a control group who received only bare-bones support, like general health advice.

Trials like LatAm-FINGERS — including a related U.S.-based trial called the POINTER study — ultimately aim to cut rates of dementia around the world. The LatAm trial is the most successful of these trials to date, raising hopes that this approach could help to prevent dementia en masse.

Whether that promise pans out remains to be seen, though, experts told Live Science.

The lifestyle factors that increase dementia risk

When it comes to dementia prevention, few guidelines are as influential as those written by the Lancet Commission, an expert-led review of the available evidence on dementia. Three editions of this review have provided comprehensive overviews of risk factors; the most recent, published in 2024, identified 14 factors, including smoking, infrequent social contact, and a lack of physical activity.

The commission estimated that, together, the identified risk factors contribute to 45% of dementia cases at a population level.

Long before the 2024 report, Dr. Miia Kivipelto, a professor of clinical geriatrics at the Karolinska Institute in Sweden, wanted to tackle these risk factors at the individual and population level in her work as a medical doctor and epidemiologist.

"I felt that I wanted to move on to interventions to really show that if you do something, you can change the risk," Kivipelto told Live Science.

The many contributing factors that lead to cognitive decline, and ultimately dementia, couldn't be tackled in isolation, Kivipelto realized. She designed a trial in her native Finland, called the Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER) study, that would aim to tackle many risks simultaneously.

The two-year project recruited 1,260 participants ages 60 to 77 and divided them into two groups. The first group received general health advice, such as tips on healthy eating and exercise, at the start of the study and then again after six and 12 months.

The other group additionally received a multipart intervention consisting of meetings with nutritionists to discuss personalized meal plans, brain training, exercise programs, social activities, and metabolic and vascular tests. These programs lasted throughout the study period, with the brain training alone including 144 sessions over 12 months of the study.

At the end, the two groups' cognitive skills, such as thinking speed and memory, were tested; the trial did not track dementia rates, only overall cognition. In both groups, these skills improved by the end of the study. But the headline finding was that in the group given the comprehensive intervention, overall brain function was judged to be 25% stronger than in the control group.

What did that difference mean in concrete terms? It turns out, the improvement was relatively small.

It was calculated in terms of a statistical measure called a z-score, which represented the extent of the improvement in brain-function test scores in each group. In the end, the difference in z-scores between the two groups was just 0.04 points, which a 2021 review defined as "small."

However, Kivipelto maintained that the improvement is significant. "It's as big as anti-amyloid treatments," she said.

Several drugs approved by the U.S Food and Drug Administration for the treatment of Alzheimer's disease target amyloid, a protein that forms unruly tangles in the brain. These drugs have been reported to marginally slow the disease's progression, but statistically, their overall effect is small.

Targeting those most at risk of dementia

Despite criticism of the trial's moderate effects, Kivipelto's FINGER intervention has since been repeated all over the world, including by the U.S.-based POINTER study, and, most recently, LatAm-FINGERS.

Dr. Gill Livingston, a psychiatrist at University College London who led the 2024 Lancet Commission report, told Live Science that the data from these trials shows that dementia interventions need to be tailored to the risks the participants actually face.

In the POINTER study, 70% of the participants had a college degree, compared with roughly 43% of the wider U.S. population. "People who are usually in randomized controlled trials are usually highly educated people who are very interested in health," Livingston noted. "And that means they're at less risk of developing dementia, and therefore, less can be done to help them" through lifestyle interventions.

The difference between the test group and the control group in the POINTER study was even smaller than in the original FINGER trial — just 0.029 points.

LatAm-FINGERS tried to maximize flexibility in its approach by better tailoring its interventions to its study participants, said study first author Dr. Lucía Crivelli, a neuropsychologist at the neurology center FLENI in Argentina. Dietary advice reflected the produce available in each region. Exercise programs considered local environmental factors; for example, sessions were held outside, avoiding hot gyms during the sweltering summers in Ecuador and Mexico.

The trial recruited volunteers across Argentina, Brazil, Bolivia, Chile, Colombia, Costa Rica, Ecuador, Mexico, Peru, Puerto Rico, the Dominican Republic and Uruguay. The participants were less highly educated than the POINTER cohort had been; 37% had no education beyond a high school diploma, compared to just 5% in the POINTER study. That likely made the study participants more representative of people who might benefit from the trial's interventions.

When Crivelli announced the results of the trial at the conference, a large cheer filled the room. The intervention had achieved a difference of 0.11 points between the test and control groups' z-scores — more than twice the difference seen in the FINGER trial.

That difference corresponded to a relative 55% improvement in overall brain function in the test group compared to the control group at the end of the study.

What made the difference?

Crivelli, Kivipelto and Livingston all pointed to one key factor in explaining the project's relative success. "In Latin America, there are more modifiable risk factors," Kivipelto summarized.

The study participants had lower academic attainment and higher cardiometabolic risk factors, such as high BMI, than the participants in previous studies. The trial had reaped the rewards of delivering the intervention to people who needed it most, experts concluded.

But the approach wasn't perfect. said Dr. Claudia Suemoto, a neuroscientist at the University of São Paulo who presented a detailed breakdown of the trial's results. They found that the intervention didn't improve men's overall cognitive ability, compared with the control group. Only women benefited.

The difference may be that men simply didn't engage in the trial as much as women did, Suemoto's data suggested. Livingston pointed to the trials' exercise classes as an example of an activity that men may not be as likely to participate in, although that's an assumption rather than being based on the trial data.

Can we really prevent dementia?

The LatAm-FINGERS results show that addressing the dementia risk factors that people face is the most effective way to prevent dementia, Livingston said.

And Livingston is leaning into the idea. She's planning a dementia prevention trial in the U.K. that will ask participants about their risk factors and then give them tailored interventions based on the risks they can realistically avoid.

"We ask them to choose which ones they want," Livingston said. "If somebody doesn't want to stop drinking or smoking, then they're not going to."

While LatAm-FINGERS has been the most successful of the FINGER trials to date, it's still unclear whether such projects actually reduce dementia rates.

Only two previous prevention trials have attempted to measure dementia incidence, and neither saw a notable change in their test group. That said, neither trial included cognitive training interventions like FINGER did; they instead focused on cardiovascular risk factors, such as low exercise rates and high body weight.

Measuring changes in dementia rates requires trials much longer than two years, and they also need massive recruitment. Implementing an intensive study like LatAM-FINGERS in the wider community "is not practical," Crivelli said. Instead, she said the study's interventions would need to be distilled into their essential parts so that they could be implemented at scale.

Kivipelto is optimistic that advances in Alzheimer's screening, including new blood-based tests, could provide an early biological measure to show that FINGERS-style interventions can help stave off dementia. This would be an indirect measure but wouldn't require as long a trial as tracking dementia rates.

Some of the risk factors the Lancet Commission identified, like air pollution, can't be modified at an individual level, Livingston noted. A combination of personal and governmental change could address this, she said, as it has in the realm of infectious-disease prevention.

While the scientific field still has uncertainty about the scale of change that trials like FINGERS can bring about, Beltre has little doubt about the trial's impact.

While she previously relied on help from family members like her grandson to complete everyday activities, she said, "I do everything myself now."

This article is for informational purposes only and is not meant to offer medical advice.

See how much you know about the most complex organ in the human body with our brain quiz!

LONDON ‪—‬ New blood tests for Alzheimer's disease aim to catch the condition in its earliest stages. Scientists hope that, someday, by spotting very early signs of dementia and enabling earlier treatments, these tests could significantly improve patients' prognoses.

But how well do current blood tests work for that purpose?

At the Alzheimer's Association International Conference in London on July 12-15, Live Science spoke with researchers and clinicians who study and use blood tests for Alzheimer's disease. Here's their take on the current state of these tests and their practicality for real-world use

Scientists' big hopes for the tests

People diagnosed with Alzheimer's disease face an incurable condition, but their outlook is marginally more hopeful than it was 10 years ago. That's because the first "disease-modifying" drugs for Alzheimer's, which target the disease's causes rather than its symptoms, have been approved in recent years.

These drugs, which include the lab-made antibodies lecanemab and donanemab, only slow, rather than stop, the progression of the disease. However, researchers hope these medicines could be the precursors to more effective treatments.

Alzheimer's disease researchers hotly debate the exact causes of the condition, but they are united on the idea that early intervention is likely to produce the best possible outcome for patients. The aim is to remove disease-linked proteins before they can damage the brain.

That's why new blood tests for Alzheimer's disease, some of which have been approved in the past year, are exciting so many scientists. These tests, which measure chemical signals of the disease circulating through the bloodstream, are currently paired with other clinical exams to provide an accurate Alzheimer's diagnosis for patients with early symptoms, such as subtle changes to memory or personality.

The hope is that if these patients could be identified at this stage, they could access clinical trials and treatments when they might be the most helpful.

What do Alzheimer's blood tests measure?

The U.S. Food and Drug Administration (FDA) has approved two blood tests for Alzheimer's disease: Roche's Elecsys pTau181 assay and Fujirebio's Lumipulse G pTau217/ß-Amyloid 1-42 Plasma Ratio test.

An additional test from Roche (the Elecsys pTau217 test) has received a basic safety certification in the European Union and U.K., which allows it to be sold but is not equivalent to FDA approval. This test is not approved in the U.S. yet. A second test from Fujirebio (the Lumipulse G pTau 217 Plasma assay) is in the same boat.

Plus, there are a host of other tests made in specific clinical laboratories; these are not FDA-approved but they are available in certain specialist clinics.

All of these tests in varying stages of approval measure "a core part of the pathology of Alzheimer's disease in the brain," said Dr. Sebastian Palmqvist, a clinical neurologist at Lund University in Sweden. These include two proteins that build up in the brains of Alzheimer's patients: tau and amyloid.

The Elecsys tests and the FDA-approved Lumipulse test measure levels of tau in the blood, while the other Lumipulse test measures the ratio of tau to amyloid. Both measurements can be used to indirectly assess the presence of amyloid plaques, sticky deposits in the brain that are associated with the disease's progression.

It's important to note that the blood tests alone aren't diagnostics for Alzheimer's disease, said Dr. Jemma Hazan, an old-age psychiatrist at University College London. Instead, "the test is telling you whether you have certain abnormal proteins in your brain." This, she said, makes it important to use the test in a setting where patients can be properly directed to the next steps of diagnosis and treatment.

How are Alzheimer's disease blood tests used?

Currently in the U.S., Alzheimer's blood tests are approved for use only for adults ages 55 and older who have signs of cognitive impairment, like memory problems. Palmqvist said these tests are best used by specialists with knowledge of dementia, such as doctors in memory clinics. They aren't approved for use by primary care doctors in the U.S.

"The clinicians working there [at memory clinics] have many, many years of experience of interpreting these types of biomarkers," he explained.

Before the advent of these blood tests, memory clinics had to rely solely on expensive brain scanning technology or invasive lumbar punctures to identify physical signs of Alzheimer's disease. The new tests greatly simplify diagnosis, Palmqvist said, but they still need to be used in combination with other tests.

So currently, if a patient receives a positive blood test, they must undergo further cognitive testing, brain scans or invasive biomarker analyses to confirm the diagnosis.

While for now the blood tests are best used by specialists, data that Palmqvist presented at the conference suggested that access to a blood test result may improve a primary care physician’s diagnostic accuracy to levels closer to a memory clinic specialist's. That hints that the test may eventually be usable in primary care, without more invasive diagnostics.

How well do the approved Alzheimer's tests work?

In clinical trials, the approved Lumipulse test had a sensitivity of 97.6% and a specificity of 90.8%. Sensitivity refers to the percentage of people who do have amyloid in their brains that test positive — so it's the rate of true positives. Specificity refers to the percentage of healthy people who test negative, meaning true negatives.

However, the test was recalled in February because it returned an unusually high percentage of false-positive results when it was used in the real world, compared to clinical trials. Palmqvist said there's now a newer version of the same test that avoids this problem.

Analyses comparing pTau217 and pTau181, the two tau biomarkers that Roche uses in its tests, have concluded that pTau217 is a more accurate indicator of Alzheimer's disease. That means it more closely matches results from gold-standard amyloid brain scans.

Dr. Ashton Harper, global medical affairs lead for neurosciences at Roche Diagnostics, said the Roche pTau217 test correctly spotted Alzheimer's-linked proteins 96.1% of the time and accurately ruled out that pathology 94.7% of the time in trials. By comparison, pTau181 — the Roche test approved in the U.S. — correctly identified Alzheimer's pathology 83.6% of the time and ruled out pathology in healthy brains 72.2% of the time.

Patients who take this more-accurate test are given one of three possible results based on two cutoff points, Harper said. If their tau level comes back above the upper cutoff — giving a positive result — clinicians can be "highly certain" that the patient has disease-linked amyloid in their brain, he said.

Below the lower of the two cutoffs, clinicians can be confident that their patient doesn't have any disease-linked amyloid in their brain. If the reading comes back in between the two cutoffs, though, the result is uncertain.

Current guidelines set by the Alzheimer’s Association require that patients end up in that gray area no more than 20% of the time, and the pTau217 test meets that requirement, Harper said. As with patients who get a positive test result, patients who receive these uncertain results are also advised to undergo further testing, such as scans or cognitive tests.

There are other reasons a person without Alzheimer's disease might get a positive test result; rare cases of severe kidney disease, for example, can artificially inflate the test's readings.

Harper said early data suggests that Roche's pTau217 test is roughly as accurate at detecting Alzheimer's disease proteins in cognitively unimpaired people as it is in those with symptoms. This may someday open the door to prevent Alzheimer's in patients who have not yet developed symptoms, he suggested, clarifying that Roche's test is not intended for that use yet.

How do Alzheimer's tests actually affect patients' care?

In the U.S., these tests can help patients get a diagnosis more quickly, but treatment options for the condition remain limited.

The approved antibody drugs are available through both private and government insurers, but they still cost the patient thousands of dollars each month. And again, these drugs only slow, rather than stop, the progression of the disease.

Researchers hope that early treatment with the drugs will enhance their effectiveness, but as of yet, there's no published data to back this idea up.

In the U.K., disease-modifying drugs like the antibodies have not been approved by the U.K.'s National Health Service (NHS) yet. Because the drugs only modestly slow Alzheimer's progression, ultimately, the NHS determined that they were too costly to cover without clearer signs of efficacy. That means British patients cannot access the drug for free.

Still, Hazan said a positive test could be beneficial for patients.

"Diagnostic accuracy is important in its own right so that people feel more certain about the diagnosis and also there are management implications," Hazan said. While they can't access antibody drugs, patients do have access to drugs that help ease the condition's cognitive and behavioral symptoms, as well as non-pharmacological treatments like behavior management.

Diagnosed patients can also access one of the many clinical trials for the condition. It's estimated that 50,000 patients are needed to populate these ongoing trials worldwide.

Hazan and Palmqvist agreed that, despite the blood tests' accuracy, they should not be used to preventively screen for Alzheimer's in people with no symptoms. That's because testing in a wider population, where fewer people will have Alzheimer's disease, naturally increases the number of false-positive results, even while the assay itself retains the same level of accuracy. This could lead many healthy people to be incorrectly diagnosed with Alzheimer's disease, which would cause stress for patients and have significant financial implications for healthcare systems.

Newer tests that are still in development may help reduce the likelihood of false positives by measuring only a subset of tau protein that comes directly from the brain rather than from the rest of the body, Palmqvist said. But for now, mass screening remains a goal, rather than a reality, for these blood-based Alzheimer's diagnostics.

"I think that's the next frontier," Palmqvist said.

This article is for informational purposes only and is not meant to offer medical advice.

See how much you know about the most complex organ in the human body with our brain quiz!

Bats have long posed an immunological mystery: They can harbor viruses that cause severe diseases in other animals, including humans, yet they rarely show signs of illness. Now, scientists have discovered a big clue as to why that is.

Researchers uncovered an unusual feature of bat immunity that could help to explain how these mammals evade infections. Vesper bats, the world's largest family of bats, may possess two separate genetic systems for producing the building blocks of antibodies, the immune proteins that latch onto germs. This configuration has never been found before in mammals.

"It was really surprising," study co-author Hannah Frank, an associate professor of ecology and evolutionary biology at Tulane University, told Live Science. "The only other vertebrates we see something similar in are fish."

The findings, published Wednesday (July 29) in the journal Science Advances, could open new avenues for studying viral infections and the evolution of immunity.

"The study provides a novel view into the evolution and diversity of adaptive immunity in bats," said Daniel Becker, an associate professor of biology at the University of Oklahoma who was not involved in the study. "The duplication seen in vesper bats is really intriguing and suggests that we need more immunological study of this globally distributed family of bats," Becker told Live Science in an email.

'More diversity in their antibodies'

Antibodies are Y-shaped proteins that help the immune system recognize and neutralize foreign invaders, including viruses, as well as other threats, like toxins. Each antibody contains two "heavy chains" and two "light chains," structures that work together to recognize and bind to specific features of viruses, bacteria or other targets.

The tips of the Y shape are responsible for recognizing the targets, while other parts of the antibody help determine how the immune system responds — by blocking pathogens from infecting cells or flagging them for destruction by other immune cells, for instance.

In humans and most other mammals, the genes that build antibody heavy chains are organized into a single region of the genome, called a locus. Cells create a wide range of antibodies by mixing and matching the proteins encoded in different segments of that locus.

But when Frank and her team examined 26 bat species, they found two complete heavy-chain loci located on different chromosomes. The team then showed that both sets of genes were functional and actively used by immune cells to build antibodies. The finding was initially surprising enough that the researchers considered whether it could be an error in how they'd assembled the bats' genomes after sequencing them.

However, Frank's collaborator and former graduate student Dr. Taylor Pursell thought the finding might be genuine, rather than an experimental fluke.

"She said, 'No, Hannah; this is really weird ‪—‬ like, this doesn't happen,'" Frank recalled. "And I said, 'Oh my God; you're right. This is not just an experimental annoyance. This is actually super cool.'"

Using genetic analysis, the team found that one of the two loci contained a larger and more varied collection of gene segments that could be used to create a broad, ready-made repertoire of antibodies. The other had fewer of these building blocks but appeared to rely more heavily on a process called somatic hypermutation, in which antibody-producing cells make small genetic changes after encountering a pathogen.

Those changes can help antibodies become more "customizable" to whatever threatens the immune system, Frank said.

She compared this system to the different layers of defense seen in the 1998 Disney movie "Mulan." Upon seeing invaders at the Great Wall of China, guards raised an alarm to alert others without yet knowing the specific threat; this is like the innate immune system, the body's first, broad line of defense. The adaptive immune system is more like the heroine Mulan: highly targeted and capable of responding to a specific enemy, but slower to develop.

These two layers of immune defense are not unique to bats, but bats' two antibody systems may provide an additional layer of protection.

From each loci, bats can create a "cache of trainable, customizable cells," Frank said. This degree of customization could help the bats immune system ward off a wider range of threats than other mammals can.

"This extra set of genes gives the animals more diversity in their antibodies," said Michael Letko, a molecular virologist at Washington State University who was not involved in the study. "This study suggests bats have more diversity to start with, which may allow for faster and more effective responses from the start of an infection," Letko told Live Science in an email.

Letko added that the genetic analysis in the study was impressive and lends credibility to the results. "It is hard to dispute the validity of information solidly founded on the genetic organization of these bats," he said.

That interpretation remains a hypothesis, though; Frank and her team will need to study how these two systems behave when bats are exposed to viruses before they can determine exactly what advantages they provide.

"We think this discovery is an important piece of the puzzle," Frank said in a statement. "It doesn't fully explain why bats are such effective viral reservoirs, but it reveals a level of immune variety we didn't know existed and gives us an entirely new direction to explore."

Past studies of bat immunity have found that hotter body temperatures and a larger number of virus-filled packages in stem cells could also help bats' tolerate viruses better.

Understanding how bats tolerate viruses could help scientists predict which kinds of bats are most likely to affect human health and how we can mitigate those risks, Becker noted. Separately, bats have a notably low incidence of tumors and cancer, Letko said, and he wonders if their unique immune systems might hold clues as to why.

While bats are often viewed through the lens of the infectious diseases they carry, their story is far more complex, Frank said.

"Let's learn from the guys who've been evolving with them [viruses] for millions and millions of years," Frank said. "But let's try not to villainize them for surviving for millions and millions of years."

An outbreak of parasitic illness linked to iceberg lettuce is affecting nine U.S. states, federal health officials have announced. That's up from the five affected states that were identified in earlier stages of the officials' investigation.

This lettuce-related outbreak is one of several in the U.S. that are being caused by the parasite Cyclospora cayetanensis, which can enter the body when someone consumes food or water contaminated with the organism. The federal government has not officially identified a source of contamination in the other Cyclospora outbreaks yet, although some state officials have mentioned potential culprits. (North Carolina officials have pointed to cilantro and parsley, for example.)

The nine-state outbreak linked to iceberg lettuce includes cases in Illinois, Indiana, Kansas, Kentucky, Michigan, Ohio, Oklahoma, Pennsylvania and West Virginia, according to the Food and Drug Administration (FDA). To date, 1,947 people have been infected across these states and reported eating Taco Bell before they got sick. There have been 98 hospitalizations and no deaths.

Data collected by federal officials had previously pointed to shredded lettuce served at Taco Bell as a common source of exposure, and from there, they identified the supplier as Taylor Farms de Mexico. "Taco Bell has indicated they are no longer using lettuce from Taylor Farms de Mexico as of July 17, 2026," the FDA noted.

Specifically, the infections have been linked to lettuce sourced from central Mexico, prompting Taylor Farms to remove all of its iceberg lettuce from that region from the U.S. market. The company has also issued a recall. A complete list of recalled products can be found on the FDA's website.

The recall affects products that were distributed in the nine states listed above, as well as additional states, all of which are listed on the FDA's website. Consumers, restaurants and retailers that purchased or received recalled lettuce are advised to discard it immediately and not consume it.

"We also expect to continue to see the number of confirmed cases rise, despite the recall, due to the fact that it can take as long as six weeks for CDC [Centers for Disease Control and Prevention] and state officials to determine if a sick person is part of this outbreak," the FDA's latest update notes. "FDA will continue to work with federal and state partners to investigate this multistate outbreak and ensure products implicated in this outbreak have been removed from the market."

This article is for informational purposes only and is not meant to offer medical advice.

Editor's note: The supplier Taylor Fresh Foods has recalled its iceberg lettuce sourced from central Mexico in relation to the outbreak described below. The recall was conducted based on epidemiological evidence, and the investigation is ongoing.

U.S. health officials have identified shredded iceberg lettuce served at Taco Bell as one source of contamination behind an outbreak of parasitic infections affecting over 1,000 people.

The outbreak has been caused by the protozoan parasite Cyclospora cayetanensis, which can enter the body when someone consumes food or water contaminated with the parasite. Since May 1, there have been 1,644 confirmed cases across Indiana, Kentucky, Ohio, West Virginia and Michigan, which is currently the hardest-hit state.

(Health officials are also investigating additional cases of Cyclospora infection in the U.S. that have yet to be linked to this specific lettuce-related outbreak. Those other potential cases remain under investigation and total over 5,100, per the Centers of Disease Control and Prevention (CDC).)

In the five-state outbreak, there have been 94 hospitalizations and no deaths to date.

Through an investigation, health officials found that all 1,644 of the sickened people with confirmed cases of Cyclospora reported eating Taco Bell in Indiana, Kentucky, Michigan, Ohio or West Virginia before becoming ill. Interviews with the affected individuals suggested that shredded lettuce might be a common source of exposure.

The Food and Drug Administration (FDA) then investigated the source of the lettuce, identifying a single supplier of iceberg lettuce from Mexico that was used by Taco Bell locations where the people ate before becoming ill. News reports have named California-based Taylor Farms as the supplier.

"FDA is working directly with the identified supplier to determine if potentially contaminated shredded iceberg lettuce remains on the market," an FDA notice states. "As part of this investigation, FDA and state partners have initiated collection of product samples for testing and analysis."

The investigation is ongoing, and additional sources of contamination or affected restaurants could possibly be identified later, the FDA noted. In the meantime, Taco Bell has said it will stop using lettuce from the implicated supplier.

"Taco Bell is working to stop use of all lettuce implicated by this investigation. Not all Taco Bell locations in these states received implicated product," the FDA statement says.

Currently, the CDC is warning consumers not to eat shredded iceberg lettuce served at Taco Bell locations in Indiana, Kentucky, Michigan, Ohio or West Virginia.

Case counts reported by individual states may differ from the FDA's and CDC's counts, because states may include both probable and confirmed cases. The FDA and CDC will update their totals once they can confirm additional cases reported to them.

Symptoms of Cyclospora infection typically emerge two to 14 days after a person consumes the parasite. These symptoms include watery diarrhea, fatigue, cramping, bloating, gas and loss of appetite, and without treatment, they can last between a few days to a month or more. The infection is treated with an antibiotic, which blocks the parasite's ability to multiply.

This article is for informational purposes only and is not meant to offer medical advice.

The patient: An 83-year-old man in Belgium

The symptoms: The man sought medical attention at a hospital because the muscles on one side of his face had weakened suddenly, causing it to droop — a condition called unilateral peripheral facial-nerve palsy. He had also recently had a fever, which had since resolved.

Tests run by the neurology department found the man had anemia, fatty liver disease and an enlarged spleen. Combined with his recent fever, these findings led the team to assume he had a viral infection. However, he tested negative for a variety of germs, including Epstein-Barr virus, which causes mono; cytomegalovirus; human immunodeficiency virus (HIV); and hepatitis A, B, C, and E.

The man's liver abnormalities hadn't resolved by one week later, but his facial-nerve palsy cleared following a 10-day course of a strong corticosteroid. But then, over the next month, the man's knees and ankles became stiff and painful, and his legs and feet — and occasionally his face, arms and hands — began to swell. He reported feeling generally unwell, he had gained 11 pounds (5 kilograms), and his urine had darkened even though he had been drinking more water than usual. All of these signs pointed to problems with his kidney function.

Besides the conditions uncovered on his recent medical examinations, the patient had long-standing high blood pressure, high cholesterol, an enlarged prostate and chronic obstructive pulmonary disease (COPD), for which he was taking medications. He had also been diagnosed with rectal cancer 20 years beforehand and received various treatments over the years. He and his wife of 50 years had been sexually inactive since that cancer treatment, he told his doctors.

What happened next: After weeks spent in and out of the hospital, the man went to an emergency room after his skin suddenly became intensely itchy. He had a red, scaly rash on his calves. A neurological exam revealed "normal motor strength, sensation, reflexes, coordination, and gait," the doctors wrote in a report of the case.

At the ER, the patient was questioned further about his medical history, at which point he told doctors that, during his military service as a young man, he'd had unprotected sex with multiple casual partners. He reported being treated for various sexually transmitted infections (STIs) during that time but had forgotten the specific diagnoses.

Tests revealed that the patient was anemic and that his urine contained blood and an abnormal amount of protein. Additionally, a test for autoimmune diseases found abnormally high levels of antinuclear antibodies, which target the control centers of cells that house DNA. Because the patient had recently had facial-nerve palsy, the doctors analyzed his cerebral spinal fluid — the clear fluid that surrounds the brain and spinal cord. This revealed elevated levels of white blood cells, which hinted at an active infection.

The diagnosis: While tests for HIV and tuberculosis came back negative, an assay for Treponema pallidum, the bacterium that causes syphilis, was positive, confirming that the patient had an active syphilis infection.

Syphilis infections can progress through four stages, each with different symptoms. If an infected person doesn't get effective treatment during the primary and secondary stages, the bacteria can go latent, sometimes for decades. And in a minority of cases, latent syphilis can awaken and cause a late, or tertiary, infection.

Based on his positive T. pallidum test, rash, general unwell feeling, abnormal liver results, high urinary protein count, leg swelling, facial drooping and swollen lymph nodes, the man's doctors diagnosed him with secondary syphilis with early neurosyphilis, in which the bacteria attack the nervous system.

The treatment: The patient had been given a single injection of penicillin before the test results confirmed that his infection had neurological involvement. He was subsequently given a 14-day course of intravenous penicillin, which is the recommended treatment for neurosyphilis, according to the case report.

The severe itching was treated with antihistamines, and he was prescribed diuretics to reduce the swelling in his legs. The rash, itching and swelling had improved by his one-month follow-up appointment, and his liver tests and urinary output had normalized.

Public health authorities were informed of the patient's diagnosis, and his wife was referred for testing. The case report does not note whether his wife tested positive for syphilis.

What makes the case unique: Secondary syphilis normally occurs within the first year of an untreated infection and only rarely develops after four years have passed. Normally, smooth, hard sores appear on the mouth or genitals during primary syphilis, and once those sores disappear, secondary syphilis sets in within months, if left untreated.

"Although the patient's history of multiple sexually transmitted infections as a young man prompted testing for syphilis, an exposure from that period would not be expected to explain his current presentation," his doctors wrote.

There's a possibility that the man had a latent infection that recently reactivated, perhaps due to the immune-suppressing effect of his recent steroid treatment. But you'd expect the reactivation to cause only symptoms of tertiary syphilis — like nervous system problems — not symptoms associated with secondary syphilis, like fever, rash and weight loss.

Therefore, exactly when the man contracted the infection is uncertain. "A more recent, unreported exposure must be considered," the doctors wrote.

It is also rare for syphilis to affect the liver and kidneys, occurring in less than 10% of cases, according to the case report.

For more intriguing medical cases, check out our Diagnostic Dilemma archives.

This article is for informational purposes only and is not meant to offer medical advice.

This article was first published Feb. 18, 2026.

A years-long malaria control campaign in the Brazilian Amazon nearly eliminated the disease from a city — but then cases rebounded. Now, scientists think they've uncovered why.

The campaign took place in northern Brazil during the construction of the Belo Monte Dam in the Xingu River, one of the largest hydroelectric dams in the world. From 2013 to 2017, the initiative slashed annual malaria rates from more than 1,200 cases to fewer than 60. But the program ended, and within a few years, infections had rebounded to more than 700 cases a year. This time, they were concentrated in the rural communities surrounding the river in the city of Altamira.

In a study published Thursday (July 9) in the journal GeoHealth, scientists analyzed 15 years of malaria surveillance records alongside satellite images of forests around Altamira. Earlier studies have pointed to deforestation and dam construction as a driver of malaria because they can provide habitats for mosquito larvae, which inhabit the forest edge. In Altamira, large stretches of rainforest have been cleared for cattle ranching, logging and settlement along the Xingu River in the decades since the region was first opened up by road-building, leaving a patchwork of cleared land pressed up against the remaining forest.

However, the study found that the malaria resurgence wasn't simply a result of how much forest had been cut down. Instead, cases tracked most closely with the forest edge, the boundary where intact forest meets cleared or open land. There, mosquitoes get everything they need to thrive: shade from the tree line, sunlit pools of standing water for their larvae, and people living or working close by.

The findings highlight how the environment contributes to malaria risk, suggesting that maintaining surveillance in these high-risk landscapes could be just as important as driving cases down in the first place.

"What made Altamira compelling was that the timing gave us something rare, close to a natural experiment," study co-author Eloise Skinner, an epidemiologist and postdoctoral research fellow at the University of Queensland in Australia, told Live Science in an email. The results of that natural experiment could help Brazil in its efforts to eliminate malaria from the country in the next decade, she said.

A program tied to temporary funding

The researchers tracked malaria trends before, during and after the construction of the Belo Monte Dam. Before construction began, malaria was already a persistent problem in the region; Altamira city alone reported more than 1,200 cases a year.

As thousands of workers moved in, local health authorities and the dam's developers rolled out an intensive control program that involved spraying insecticides indoors, using mosquito nets, and deploying rapid diagnosis and treatment when cases did emerge. The goal was to head off outbreaks spread by Nyssorhynchus darlingi, the mosquito that carries the malaria-causing parasite in the Brazilian Amazon.

Mosquitoes pick up the parasite that causes malaria by feeding on the blood of infected people, and they can then spread that parasite to others they bite. Treating infected people quickly can help break that chain of transmission.

Cases plummeted despite the influx of workers, but once construction wrapped up and the program lost its funding, malaria came back.

To understand what drove the resurgence, the researchers combined three streams of data. Case records came from Brazil's national malaria surveillance system and covered 150 health centers in Altamira over 15 years. The team layered on temperature, forest cover and rainfall data, since both shape how favorable an area is for mosquito breeding and how efficiently the malaria parasite develops inside mosquitos. Plus, they added an estimate of travel time between each cluster of cases and the nearest town, as a proxy for how easily people and the diseases they carry might move around.

From the observations, the forest edge consistently emerged as the strongest predictor of increased malaria cases. For every 1% increase in the perimeter of the forest edge, malaria cases rose by roughly 0.7%; for every 1% increase in Altamira's population, who are located at the forest edge, cases rose by about 1.4%.

The rebound wasn't evenly distributed. Before the dam was built, most of Altamira's malaria cases came from clusters inside the city itself. Afterward, that pattern flipped: by 2020, the roughly 700 annual cases were concentrated almost entirely in remote, rural clusters near forest edges. Meanwhile, Altamira's urban center stayed comparatively protected, much as it had during construction.

"When the funded program wound down, malaria came back to the communities that are hardest for the health system to reach," Skinner said. "The city stayed protected, most likely because fast diagnosis and treatment are easier to deliver and keep going in a town."

That leaves the same communities exposed twice over, Skinner said. The places that are already the hardest to reach with health services also sit where the ecological risk is the highest.

But this pattern could point to solutions. The resurgence didn't scatter unpredictably. It came back to the same kind of place — rural communities at the forest edge — each time. That's the kind of risk that can be anticipated in the future.

Brazil aims to eliminate locally acquired malaria by 2035. Skinner said Altamira's near elimination of the disease, and its rebound within a few years of the control program ending, is a warning for that effort. When a community contains a strong environmental driver for malaria, like forest-edge ecosystems, stopping a control program short is sure to let the disease climb back.

"Because the resurgence wasn't diffuse, we can predict where malaria is likely to return first," Skinner said. "The message for a 2035 goal isn't only that elimination needs sustained investment. It is that where the environment drives risk, that risk is predictable, and planning for it from the start is what lets the money go where it matters most."

At least 20 people across 17 states have been hospitalized due to severe gastrointestinal illness as more than 1,000 cases of the parasitic infection cyclosporiasis have been reported across the country, the U.S. Centers for Disease Control and Prevention (CDC) reports.

The CDC and the Food and Drug Administration (FDA) are investigating several clusters of the illness in Illinois, New York, Pennsylvania and Texas, according to CNN. However, the worst-hit state so far is Michigan, with 1,251 cases reported as of July 9, the Michigan Department of Health and Human Services (MDHHS) reported. According to the Associated Press (AP), this marks the biggest cyclosporiasis outbreak in the state's history.

Cyclosporiasis is a gastrointestinal illness caused by the protozoan parasite Cyclospora cayetanensis, which can enter the body when someone consumes food or water contaminated with the parasite. It then infects the small intestines, invading epithelial cells that line the gut, causing inflammation and leading to watery and often "explosive" diarrhea, according to the CDC. Symptoms usually kick in around a week after infection and can last over a month without antibiotic treatment. While the illness can go away on its own, it is also common for symptoms to disappear for a bit and then return.

Cyclosporiasis is not usually life-threatening, but it can cause severe illness and dehydration, particularly in young children, older adults and people with compromised immune systems. In rare cases, the condition may lead to complications like biliary disease, in which the flow of bile gets blocked and impacts the liver and digestive health, according to the MDHHS.

As of July 1, there was no evidence of a single, multistate outbreak of cyclosporiasis, but the CDC is investigating several clusters. According to an email from the health agency, many of the clusters appear to be linked to Mexican-style restaurants, a chain of grocery stores and a catered event, CNN reported. The FDA is conducting trace-back investigations on white and green onions, cucumbers and cilantro, according to CNN.

Meanwhile, the MDHHS warned that, while the source of the current outbreak is still uncertain, previous Cyclospora outbreaks have been linked to contaminated fresh produce, including raspberries, basil and bagged salad.

Cyclosporiasis cases tend to rise during the spring and summer, with May 1 to Aug. 31 considered "cyclosporiasis season," according to the CDC. However, there have been more cases than usual this year: Whereas Michigan typically reports 50 cases over a whole year, the state has seen over 1,000 cases in just a few weeks, the AP reported.

Compared with outbreaks of E. coli and Salmonella, clusters of Cyclospora are much harder to trace back to their source. This is because the parasite can reproduce sexually, meaning its genetic material is mixed up with each generation, according to Charles River Laboratories. However, Dr. Natasha Bagdasarian, Michigan's chief medical executive, told the AP that "there is clearly a linked outbreak happening right now."

To minimize your risk of becoming infected with Cyclospora, wash all fruits and vegetables thoroughly before eating them; cut away any bruised or damaged areas; and refrigerate cut, peeled or cooked produce as soon as possible, the Michigan Department of Agriculture and Rural Development recommends. If you are experiencing sudden gastrointestinal issues, health officials suggest you visit your local health care provider.

This article is for informational purposes only and is not meant to offer medical advice.

The hantavirus outbreak that struck a cruise ship in April, killing three people and sparking fears of further spread, is over, the World Health Organization (WHO) has announced.

"Today, the final contact of a person exposed to hantavirus on the cruise ship MV Hondius completed their quarantine period, tested negative and returned home. No further cases have been reported since the 25th of May," Tedros Adhanom Ghebreyesus, the WHO's director-general, said in his opening remarks at a news conference Thursday (July 2). "We are therefore very pleased to say that WHO considers the outbreak of hantavirus over."

The total number of cases linked to the outbreak was 13. All those affected were either passengers or crew on the ship.

The outbreak began aboard the Dutch-flagged cruise ship MV Hondius after it departed southern Argentina on April 1. It involved the Andes virus, the only known hantavirus that can spread between people.

Hantaviruses are rodent-borne viruses that are found in the Americas, Europe and Asia and spread to humans relatively rarely, usually via contact with the urine, droppings or saliva of infected rodents. The Andes virus, however, has sparked short chains of human-to-human transmission in the past.

Before public health authorities were informed of the cases on MV Hondius, several dozen people disembarked the vessel on the island of St. Helena. To find them, authorities launched an international contact-tracing operation, tracking down more than 650 contacts in total who were then followed by health authorities in 33 countries and territories, according to the WHO.

Additionally, health authorities coordinated the monitoring, care and transport of the remaining passengers and crew aboard MV Hondius.

Of these contacts, those considered at the highest risk of infection were then quarantined and monitored for up to 42 days, because sometimes, hantavirus symptoms don't show up until weeks after exposure to the virus. Depending on their jurisdiction and degree of exposure, some contacts quarantined at home while others stayed in specialized facilities.

The initial unchecked travel of some contacts, alongside the virus's long incubation period, prompted concern from the public that the cluster of cases could explode into an enormous outbreak, or even a global pandemic. Many infectious-disease experts emphasized that the Andes virus does not spread easily between people and that the containment effort was going well, so the risk of a large outbreak was low. Still, some experts raised concerns that the international travel of contacts could trigger pockets of the deadly disease, and some argued that the Andes virus does have "pandemic potential."

Now, with the final contact having completed their quarantine period and no further cases reported, the WHO has declared the outbreak over. All of the contacts who were repatriated to the U.S. completed their quarantine period by June 21.

"WHO will continue working with governments and partners to advance our understanding of this outbreak and of hantavirus more generally," Tedros said. "We are also coordinating a study involving 21 countries to understand how the disease develops, which will support the development of diagnostics, therapeutics and vaccines for future outbreaks."

Besides rigorous contact tracing, the WHO credited the coordinated actions of national public health bodies as being vital to preventing the further spread of the disease. These measures included the response of the Spanish government, which created a safe zone on the island of Tenerife for the ship's remaining passengers to disembark before they were repatriated under quarantine.

As the hantavirus outbreak concludes, there's an ongoing Ebola outbreak in the Democratic Republic of the Congo and an outbreak of the Marburg virus in Uganda. These and future outbreaks will require similarly robust international cooperation, the WHO emphasized.

"The outbreaks of hantavirus, Ebola and Marburg all show why there is no alternative to international cooperation in the face of international threats," Tedros said. "No country alone can fight."

This article is for informational purposes only and is not meant to offer medical advice.

An 11-year-old boy in Ontario, Canada, has died after being bitten by a rabid bat that was resting on his face as he slept. The boy had no obvious bite or scratch marks and didn't show symptoms for the first 19 days after the incident, his doctors report.

While on vacation with his parents at a cottage in northern Ontario in 2024, the boy was woken up in the night by a bat on his nose and mouth, according to a report published in the Canadian Medical Association Journal on June 29. His father caught the bat in a cooking pot and released it outside, and because the child had no visible injuries and the bat did not seem to be particularly aggressive, his parents decided not to seek a medical assessment, the report noted.

A few weeks later, the child began to experience tingling, numbness and swelling on the right side of his face. When he was examined at his local hospital his vital signs appeared to be normal, aside from an elevated heart rate and white blood cell count.

The next day, the boy's symptoms worsened: he lost feeling in the right side of his face and his speech was beginning to slur. While waiting in hospital, he developed a fever, confusion, hallucinations and difficulty swallowing, followed by excessive production of saliva.

After four days in intensive care at McMaster Children's Hospital in Hamilton, Ontario, the child tested positive for rabies, and after five days his brain stem reflexes were absent, indicating a total loss of brain stem function. Seventeen days after admission, following a consultation between his family and medical experts, he was taken off life support and died.

Rabies is a viral disease that primarily affects the central nervous system, according to the CDC. It is mainly spread through bites and scratches from infected animals, with bats accounting for the majority of cases in North America, according to the boy's doctors.

"Bats pose a particular risk because bites or scratches may be small and are easily overlooked, and patients may not recollect or recognize a bat exposure," the medical team wrote in their report.

According to a report in the Journal of Virology in 2013, silver-haired bats (Lasionycteris noctivagans), are responsible for the majority of rabies cases in Canada. Skunks, foxes and raccoons also often carry the disease.

The rabies virus must travel to the brain before symptoms can occur, but once a patient develops symptoms the infection is almost 100% fatal, with most deaths occurring within one to two weeks of symptom development. However, prompt treatment after exposure — including wound cleaning, antibody administration and a series of vaccines — is nearly always effective at preventing the disease, according to the CDC.

Rabies in humans is very rare in North America, with fewer than 10 deaths reported in the U.S. every year, according to the CDC. In Canada, only 28 human fatalities have been reported since 1924, according to the Canadian Veterinary Medical Association. Even so, the boy's doctors have emphasized the importance of prompt medical attention following exposure to bats and other animals that could carry the disease.

"Early recognition of exposure and timely PEP [postexposure prophylaxis] remain the only effective means of rabies prevention," they wrote. "Any direct human contact with a bat, even in the absence of a visible bite or scratch, is an indication for PEP."

They added that rabid bats do not always display the classic symptoms commonly associated with rabies, such as aggressive behavior and frothing at the mouth. "Any direct human contact with [a] bat is considered high risk," they added.

This article is for informational purposes only and is not meant to offer medical advice.

Younger generations may be aging faster than their predecessors, and this may be linked to a rise in early-onset cancers, a new study suggests.

There have been recent increases in the rates of some cancers among adults under 50, including breast, colorectal, kidney and uterine cancers. One 2023 paper suggests that these early-onset cancer diagnoses rose by 25% globally between 1990 and 2019, and scientists are still investigating why.

"The trend of increased cancers at younger ages is very real, and it is not simply because of more efficient diagnosis, or diagnosis at earlier stages," said Dr. Jyoti Nangalia, a hematologist and cancer researcher at the Wellcome Sanger Institute in the U.K. who was not involved in the new study. "It is possible that we are being exposed to new cancer-causing risks or that [our] defences to them are somehow altered," she told Live Science in an email.

The new study, published June 22 in the journal Nature Medicine, suggests that younger generations may have a wider "gap" between their chronological ages and their biological ages — a measurement of how quickly the body's tissues and systems are aging — than older generations do. The greater gap among younger adults seems to be linked with a higher risk of developing cancer early in life.

The new study cannot prove that faster biological aging causes early-onset cancer, but it provides new clues for scientists trying to unpack what might be driving the worrying trend.

"This is really proof-of-concept," study co-author Yin Cao, a molecular and clinical epidemiologist at the Washington University School of Medicine and Siteman Cancer Center, told Live Science.

Concerning trends lurking in dense data

Chronological age is straightforward: It's the number of years that have passed since a person's birth. "Biological age," however, can vary wildly from one person to another. This catch-all term describes a range of metrics, including markers on DNA and in the bloodstream. These are often measured using "aging clocks," which aim to determine if the body is acting much older than its chronological age.

Scientists have increasingly used these summary measures in an attempt to understand why some people are more prone to age-related diseases than others. To check whether there could be a link between biological age and the rise in early cancers, the new study analyzed data from more than 150,000 adults in the UK Biobank, a long-running project that has been tracking the health of about half-a-million U.K. adults since the mid‑2000s.

The participants had provided blood samples, with many already measured for markers used to track biological aging. The study authors plugged these results into PhenoAge, a statistical model that estimates a person's "age gap" at a given chronological age. In essence, this model can compare snapshots of two 40-year-olds — one born in 1950 and the other in 1965 — and see if their blood markers suggest they're the same biological age.

"The traditional approach is really focusing on individual risk factors" for cancer, such as a history of obesity or a high intake of ultraprocessed foods, Cao said. "We are testing whether we can leverage these large biobanks and potentially find some biological imprint as a potential reflection of many exposures that can be linked with cancer risk," she said.

The analysis revealed a concerning pattern: UK Biobank participants born between 1965 and 1974 had a larger age gap than those born between 1950 and 1954 at the same chronological ages. Based on PhenoAge's metrics, the younger cohort had systemic aging levels about 0.23 standard deviations higher than the older cohort — a modest shift toward older-looking biology.

The researchers applied this same approach to about 10,000 participants in the U.S. National Institutes of Health's All of Us Research Program, another large biobank. There, they found a more pronounced pattern: People born between 1990 and 1999 had age gaps about 0.92 standard deviations higher than those born between 1965 and 1969.

Another blood-based aging clock, called the Klemera-Doubal method, showed broadly similar patterns to PhenoAge, albeit slightly weaker ones, the study found.

Real trend or data mirage?

In the UK Biobank cohort, the researchers found that participants with higher age gaps were more likely to develop early-onset solid cancers, meaning cancerous tumors that appear in tissues, rather than "liquid" cancers present in bodily fluids. This link was strongest for lung, gastrointestinal and uterine cancers. This finding was based on the patients' medical records.

When the participants were divided into three groups based on their biological ages, those in the highest group had a roughly 15% higher risk of early-onset solid cancer than those in the lowest group.

To probe deeper, the authors used a different model that estimates biological aging at the level of specific organs and systems, using patterns of proteins in the blood. In almost 20,000 UK Biobank participants, they found that markers suggesting an "older-than-expected" immune system were linked with a higher risk of early-onset lung cancer. Similarly, markers suggesting older-than-expected fat tissue were linked with a higher risk of early-onset colorectal cancer.

Does this mean younger generations are aging faster and that's causing the rise in cancers? Maybe, but maybe not — there are important caveats to the study's findings.

The patterns will need to be confirmed in other datasets and populations, Cao noted. Biological aging tests, including PhenoAge, are also relatively new, and their implications aren't fully understood. While they clearly capture something about health and risk at the population level, at the individual level, different biological age tests can give very different answers for the same person. That raises questions about what any single score really means for individual health.

It may be that the differences PhenoAge uncovered between younger and older people have to do with how the test was originally calibrated, Stephen Burgess, a professor of biostatistics at the University of Cambridge who was not involved in the study, told Live Science in an email. To know if that's the case, one would have to dig deeper into how PhenoAge scores are calculated and see if that might have skewed its assessment of the UK Biobank and All of Us cohorts, he said.

Cao added that, while PhenoAge scores have been tied to mortality risk across a range of adults, the test "requires further validations" when it comes to assessing cancer risk.

As with any observational study using large databases, it is hard to untangle cause and effect, Nangalia added.

"The main issue for this paper is one of correlation versus causality," she said. "Either way, it is useful — with the first, as a potential way of tracking population health and cancer risk, and with the second, as insights into cancer-causing mechanisms."

Cao hopes her team's approach will serve as another useful tool to figure out why more young people are getting cancer. " Hopefully this is just a starting point," Cao said.

The patient: A 28-year-old woman in New Hampshire

The symptoms: In March 2020, the woman developed a high fever, chest tightness, shortness of breath and diarrhea, and she lost her sense of smell and taste. She also experienced coughing fits so intense that they caused her to faint. Based on these symptoms, her primary care provider diagnosed her with COVID-19, although she was not formally tested for the illness due to the lack of diagnostic testing available at the time.

After her diagnosis, she did not seek further medical care due to concerns about out-of-pocket costs, according to a report of the case.

What happened next: Three weeks after her symptoms started, the patient felt well enough to work from home. However, four weeks after that, many of her symptoms returned. She also noticed new feelings of disorientation and felt that "something was off with faces." Her primary care doctor suggested she go to an emergency room, where a CT scan was taken of her brain. The scan didn't show any active bleeding, the report notes, and she was discharged.

In June 2020, the patient spent time with family for the first time since catching COVID-19 and found she could not recognize her father or visually distinguish him from her uncle. She still recognized people by their voices, though.

The patient worked part time as a portrait artist; she used to be able to check her reference photos every 15 to 30 minutes but found she now struggled to hold the details in her mind. She told doctors that "faces are like water in my head," according to the case report.

The patient also had trouble doing everyday tasks, such as navigating her local grocery store or finding her way back to her car in a parking lot. In November 2020, she also started having balance issues and frequent migraines.

The diagnosis: Based on her wide-ranging and relapsing symptoms and her suspected history of COVID-19, doctors diagnosed the patient with post-acute sequelae of COVID-19 (PASC), now known as long COVID. They diagnosed her difficulties with recognizing faces as "face blindness," or prosopagnosia.

Roughly 2.5% of the general population is thought to be born with some degree of face blindness, while others can acquire the condition later in life. The exact number of people with acquired prosopagnosia is unclear, but some estimates suggest roughly 1 in 30,000 people in the U.S. are affected.

Many people with acquired prosopagnosia also have issues navigating familiar spaces. That was also the case with this patient, likely due to the "proximity of brain regions critical for scene and face processing," the case report authors noted.

To assess the extent of the patient's prosopagnosia, doctors had her complete several tests of facial memory, which asked her either to memorize strangers' faces or recognize celebrities' faces. The patient performed markedly worse on these tests than 10 women of similar age who were used as a comparison group.

However, she performed as well as the comparison group on other types of cognitive tests, suggesting her deficits were fairly specific to faces. She also got normal scores on tests of facial perception — the ability to recognize that a face is a face — so her face blindness seemed tied more to memory deficits for faces, the report authors said.

The treatment: The case report does not detail a specific course of treatment, and in general, few treatments exist for face blindness. If there's a clear cause for the deficit — such as a tumor in a key part of the brain for facial processing — addressing that underlying issue can help reverse acquired face blindness.

If the condition ends up being permanent, there are various strategies that can help patients cope. For instance, "perceptual training" can improve patients' ability to identify and remember the features of a person's face. Additional strategies include training people to use other cues, like voices and social context, to identify people.

What makes the case unique: In this patient's case, the report authors suspect that her COVID-19 infection triggered her face blindness either acutely or in the aftermath of the infection.

Various infections have been tied to face blindness; both bacterial meningitis and Whipple disease (caused by the bacterium Tropheryma whipplei) have been flagged as culprits, although such cases are uncommon. In a second known case involving COVID-19, a different person developed face blindness after an infection but had also had a stroke in the right hemisphere of their brain, a known cause of prosopagnosia.

The 28-year-old woman, by contrast, wasn't thought to have suffered a stroke, and it's unclear exactly how COVID-19 led to her facial processing issues.

The case report authors surveyed more than 50 other people with long COVID, to see if they also had signs of face blindness. While many showed general declines in visual recognition and navigational abilities, the group didn't have a specific problem with faces. So while long COVID is known to cause a range of neurological issues, it appears that face blindness is a rare consequence.

For more intriguing medical cases, check out our Diagnostic Dilemma archives.

This article is for informational purposes only and is not meant to offer medical advice.

Can you guess the diagnosis in these strange medical cases? Find out with our diagnostic dilemma quiz!

The United States successfully eliminated measles decades ago by taking measures to ensure the virus stopped spreading consistently within the country — but now, it's likely that measles is back.

Toward the end of 2025, experts cautioned that the U.S. could lose its "measles elimination status" within months as various outbreaks raged across the country. If the U.S. does officially lose this status — meaning the country will have experienced sustained measles spread for over a year — it would join a list of countries, including the U.K. and Canada, that have also seen local resurgences of measles as their vaccination rates have declined.

An assessment of the United States' elimination status is scheduled for November. In the meantime, experts have issued a progress report for the nation. Live Science spoke with two authors of the report from Boston Children's Hospital — Dr. Anne Bischops, a pediatrician and postdoctoral research fellow, and Maimuna Majumder, a distinguished scholar in the Computational Health Informatics Program — to understand where America's elimination status stands and what to expect in coming months.

Nicoletta Lanese: We saw measles cases start to rise in the U.S. around January 2025. Were you concerned at that point about the country losing its elimination status?

Maimuna Majumder: I've personally been working on measles for over a decade, and given that, what I will say is that my concerns around elimination status far predate even January 2025.

When January 2025 picked up, I felt like this might be the point of no return. But it was not in any way the first red flag. I do want to just stress that measles elimination has always been a tenuous prospect, and it is, by design, tenuous. Maintaining elimination status is, by design, difficult.

When you start to see these clusters turn into outbreaks that threaten to spill over into neighboring states, when you see the rapidity with which small outbreaks become larger outbreaks — those tend to be the signals that [say] "I don't think that we're going to be able to get the cat back in the bag here."

Dr. Anne Bischops: The trend of the increase of vaccine-preventable diseases has been ongoing for several years already, and it's something that has spilled into the daily life working in the ER. We've seen increasing cases of measles. And especially after the COVID-19 pandemic, we have this increase of vaccine fatigue adding to that.

This has been, globally, an increasingly important topic. For the current outbreak in the U.S., our study team has been closely monitoring that from the beginning.

NL: What factors set our current situation apart from past measles outbreaks?

MM: My very first domestic measles response was during the Disneyland measles outbreak in [late 2014 and] 2015. It was a different time. It was a radically different political administration; it was a radically different time, culturally, for how the United States felt about vaccines. It was an optimal time to make strides in policies that would help ensure that we didn't lose our elimination status.

In response to the Disneyland outbreak, we ended up passing SB-277 in California and a number of other important vaccination bills across the United States that allowed us to get rid of personal belief exemptions, for example. That really led to fantastic strides in reclaiming our measles protection, as a whole.

Now, in the 10 years that have since passed, a lot of things have changed. We are now in the second Trump administration, and there has been a massive pandemic in between that eroded the public's trust in public health and vaccines. A lot of that is driven by the pervasiveness of misinformation that's run rampant.

When the Disneyland outbreak happened, we largely had a feeling of hope that, "We can use this opportunity to pass bills that are going to protect the American people." What happened when the [2025] Texas outbreak started was the opposite of that. That's when the likelihood that you're going to lose your status becomes imminent, because the levers that you would typically use to rescue elimination status are no longer viable.

NL: In your report, you describe seven indicators that should be met for a country to achieve elimination status, noting that the U.S. has now missed — or essentially, failed — four out of seven. Why is it useful to define these indicators?

AB: The Pan American Health Organization [PAHO] has these recertification meetings [such as the one planned for November] where very detailed, granular data for every single transmission chain are presented, and this is very time-intensive.

We saw that the meeting had been moved from April to November, so our goal with the seven indicators was to provide an early warning framework ahead of that decision, using readily available data that we can use now. We have looked on the broad national level, using only national estimates. We really see it as a rapid assessment before then, in November, when a very detailed analysis will be done on the transmission-chain level, where every single transmission chain will be followed.

NL: For the indicators that haven't been "missed" yet, do we suspect they've been missed but just don't yet have the data to show that?

AB: Exactly. For example, for the genotyping criteria, we have some samples where we can already see that they all share the same genotype, but we are lacking the detailed genotyping data for every single transmission chain. So we can assume that this has been missed, but we need to confirm with the detailed analysis.

For vaccine coverage, we only have the kindergartners' estimates [regarding the percentage of kindergarteners who are up to date on measles vaccination], and we don't have immunity data. But based on the data available, we could think that has already been missed.

NL: Experts have said we're likely undercounting our current measles cases. Is that a fair assessment?

MM: I personally agree that it is very likely an undercount. One reason is that measles in general does not have to be super severe in pathology. So sometimes, kids will get sick and their parents may not take them in to get looked at. When we think about the way that infectious disease surveillance is done in the U.S., in order for mandatory reportable diseases like measles to be reported, there needs to be an encounter with the healthcare system. If you have a disease where that may not always happen, then certainly, by default, you're going to be undercounting the disease.

Our best indicator is wastewater surveillance [where germs are screened for in wastewater], and right now, we don't do a ton of wastewater surveillance for measles. The next question would be, how do we track this better? That is perhaps one of the better solutions.

NL: Do you think wastewater surveillance is something that could be feasibly expanded? I know our current coverage differs state to state.

MM: The technology is there, so this is possible. What is challenging — and this is true for all wastewater surveillance, not just measles — is that our interpretability of wastewater signals is, mind my language, still very much in the shitter.

We see numbers go up in the wastewater, so we know that numbers are going up in the community. To what degree that scaling factor is true is dependent on so many things that it's really difficult to have kind of a 1:1 [translation] based off of what the wastewater signal says — just how many cases there are in a given community at the time.

One of the big factors, of course, is that wastewater is very, very vulnerable to rainwater fall [in that rainfall dilutes wastewater and must be taken into account to interpret the results]. So there are a lot of physical engineering components to this that we have not fully figured out yet. It's harder to say, "Oh, there are exactly this number of cases because there's this much wastewater indication of this disease in this location." We can't do that yet, not in a meaningful way.

What we can do is use wastewater to predict when hospitalizations for respiratory disease will increase, when we might expect upticks and people seeking PCP [primary care provider] care for a given disease — this is something that the wastewater is very, very useful for. That is where I do believe that there is room for improvement, and this is something that can be done.

Massachusetts is one of the leaders in wastewater surveillance, and we have our own dedicated wastewater surveillance teams. So if I were to think of states that would probably be leaders in this, states like Massachusetts would probably be the most likely to pilot a measles wastewater program.

NL: Your report indicates we're on the brink of losing elimination status, and getting vaccination rates up is a key solution. Will that effort mostly be at the state and local levels, given the federal government's stance?

MM: All of our states operate as their own little entities that manage their own state's health, so we don't have a ton of programs that are universal, national. Even if Trump were not in office, we would expect most vaccination campaigns to happen at a more localized level. That has always been the case.

However, now you have a federal government that is pretty staunchly anti-vaccine, even when RFK Jr. is reneging and saying, "Actually, vaccines are alright." There's quite a bit of waffling even at the federal government level that we should acknowledge. I would not call it vaccine hesitancy at the federal government level; I would call it skepticism. What that does is that it seeds doubt. That has a trickle-down effect to the individual who is living in a given state.

The public discourse around vaccines is very, very heavily influenced by federal discourse.

While federal discourse does not affect states' rights to pass bills that are going to protect their public by encouraging more vaccination, what it does do is affect the way that individuals in those states perceive vaccines. The vast majority of people in this country are more aware about federal politics than they are about state politics; that is the reality of the situation that we live in.

You end up with a situation where, even though the federal government does not really have much control over what the state will mandate is required for a child to enter public schools, there is a control that is exerted through the communication strategy that is used by the federal government to reach individuals across the United States.

AB: From the pediatrician perspective, we can see day to day, there can be 10 positive vaccine-promoting campaigns, but it only takes one short online comment to spread doubts everywhere. So, for me as a pediatrician, it's very important to be very careful with health communication about that — I think we need efforts on all levels.

NL: Is there anything else you hope people take away from your progress report?

MM: Because we see this global resurgence of measles and we have a bunch of other countries that have also lost their status or who are also on the brink, we think that this [framework] might also be applicable to other countries who could use it as an early warning.

It's not just the U.S. that is dealing with this problem; it's not something that's happening in a vacuum.

The politics across most high-income countries are exhibiting similarities across the board that are absolutely influencing the pervasiveness of this issue, and the fact that many high-income countries have lost their measles elimination status in the last year is a very, very good indicator of that. But I'd like to stress that it's not entirely politics, either. Part of it is system memory.

What I mean by that is, the people that are having kids right now are people who have never known a person who has been gravely affected by measles. They have no clue that in previous generations, people died from this disease or were left with terrible post-acute conditions that have plagued them for the rest of their lives. That lack of exposure makes it seem like it's not that serious.

When public health works, nobody knows that it's working — that's a statement that we often make in this discipline. The reason nobody died from measles when I was a kid is because everybody was vaccinated. This particular thing is very difficult; it's very human to start questioning the severity of something when you haven't seen that severity yourself.

NL: To date, all signals seem to point to the U.S. losing its status in November. Would you agree?

MM: I would be very surprised to see it turn out otherwise. I would be delighted if we can turn it around, but it is unlikely.

Why that might happen is if we as a society decide that the strict criteria that we have been using to date are no longer the criteria we want to use. We could say we still have elimination status because we're changing what the criteria are; we're moving the benchmark. If that happens, I will be extremely unhappy.

Either we lose the status because we kept the criteria the same and nothing changed, which seems like the most likely circumstance, or we don't lose status because we changed the criteria, because we don't want to be seen as failures. The least likely but the most positive option is somehow we manage to get it together in the next six months and we don't change the criteria.

AB: There's no standardized criteria or cutoff points for deciding elimination status. In the end, it's completely up to the expert panel in November, so we don't know what exact cutoffs they will use. But based on the data we saw, for now, I think it's highly likely that we will, sadly, lose status.

NL: Could the expert panel move the benchmarks, like you said?

AB: So, the CDC [Centers for Disease Control and Prevention] has determined an expert panel that runs the analysis and will then present to the Pan American Health Organization meeting in November.

MM: That's why I'm saying that that second option is a possibility. There are people [on the panel] that can decide that the criteria are different.

NL: But if the PAHO doesn't think the presented data is valid, could they say that?

MM: They can do it — will they do it is a different question. The World Health Organization [WHO] and its ancillary branches [like the PAHO] are not typically shy about making statements when they believe that certain governments are not being truthful. This tends to happen in highly politicized situations where you are expecting that the data coming out of the country are not fully viable.

So the WHO has absolutely made statements in the past to this effect. The U.S. is a different type of entity though, right? I think that we're now getting into the question of "Does it harm the WHO and PAHO too much to take a stand against the CDC?" It's a very interesting question that I don't think that there is a very clear answer to yet.

To answer that question, can they do that? They can. There is precedent for other countries. But the U.S. is not just any country, and we need to acknowledge that.

As a region, we've already lost that status [given that Canada lost its elimination status already]. My hope is that that would make everybody more honest. I do feel that the situation would be significantly more tense if the U.S. was going to be the "make or break" for whether or not the Americas lost their elimination status.

Editor's note: This interview has been lightly edited for length and clarity. Live Science spoke with Bischops and Majumder in May, so the text may not reflect more recent developments.

This article is for informational purposes only and is not meant to offer medical advice.

Emerging diagnostic tests for cancer aim to detect the disease in its earliest stages, to improve patients' chances of survival by enabling earlier treatment. Some of these diagnostics — called multi-cancer early detection (MCED) tests — screen for many cancers at once, which sounds great on paper.

However, in February, a flagship trial testing one such cancer test, called Galleri, failed to meet its primary endpoint: it didn't reduce the number of late-stage cancer cases identified. In May, at the American Society of Clinical Oncology (ASCO) meeting in Chicago, attendees got a closer look at some of the data behind the trial.

The trial was the biggest of its kind in the field to date and its high-profile failure drew a lot of attention. But experts told Live Science that it doesn't mean we should count out MCED technology.

Why Galleri was put to the test

The majority of cancer diagnoses and deaths are from cancers that have no well-established screening program, such as pancreatic cancer. Without these early-detection methods, like regular colonoscopies for colorectal cancer, many cancers are caught late.

The perfect MCED test could, in theory, make finding cancer a breeze. Such a test could use a single blood sample to screen for many cancers, detecting disease-linked changes in DNA and other cellular markers of disease floating in the bloodstream.

But designing a trial that proves that MCEDs can improve patient outcomes is difficult. Earlier diagnosis can be life-saving in some types of cancer, said Jessica Lloyd, a strategic evidence manager at the nonprofit Cancer Research U.K. Five-year survival rates drastically improve when lung or colorectal cancer are detected at an earlier stage. But for other cancers, such as melanoma, earlier diagnosis makes little difference to overall survival rates.

The ideal trial would follow a group of patients over many years; one half would receive MCED testing while the other would not. At the end of the trial, data would reveal whether overall cancer deaths were reduced in the group that received testing.

But there's already a lot of hype around MCED tests, and there's little appetite in the field to wait years for clear results that the tests improve outcomes, or to pay the high price tag that such long studies would incur.

Instead, the recent trial of Galleri, run in collaboration with the U.K.'s National Health Service (NHS), lasted only three years. It measured whether the test could identify cancers at an earlier stage, considering the early detection a proxy for mortality data. In other words, early detection was assumed to lead to lower death rates.

The trial recruited 142,000 healthy people ages 50 to 77. Participants had their blood drawn roughly once a year for three years. Each time, for a subset of participants, the Galleri test looked for markers linked to 12 different types of cancer. If a patient tested positive, they received further treatment. This tested group was compared to another that didn't have their blood tested.

The aim of the trial was to assess whether significantly fewer cases of late-stage cancers — meaning stages III and IV — would be detected in the test group; at that stage, disease has started spreading beyond the cancer's origin point to other tissue. The rationale was that the test would instead pick up these cancer cases in stages I and II, before the disease had spread. But Galleri failed to meet this endpoint.

Samantha Harrison, Lloyd's colleague and head of strategic evidence at Cancer Research U.K., said that the test's failure to reach its main target is "disappointing." However, she added that the trial's huge dataset hasn't been detailed in a peer-reviewed publication yet, which would shed more light on the trial's full value.

What went wrong for Galleri?

Galleri's problems were related to both the diagnostic test itself and the trial design, said Ruth Etzioni, a biostatistician at Fred Hutchinson Cancer Center in Seattle. Galleri caught an unexpected number of advanced cancer cases among the trial volunteers the first time they were tested.

These cases came as a surprise, because the volunteers recruited to the trial had not been diagnosed or treated for cancer over the previous three years. Etzioni said that if the trial were begun anew, these initial cases would likely be excluded from the analysis, which would have helped improve Galleri's performance.

But even with that adjustment, she added, it's unlikely the trial results would have significantly changed. That's because the test was unexpectedly bad at picking up early-stage cancer, she told Live Science.

"That's critical," she said. "You have to have an increase in stage I to II, and then that then coincides with the decrease in stage III to IV," she said.

The MCED test doesn't look for a lone marker that determines whether a patient has cancer or not. Instead, the various disease markers that the test looks for are weighed and a threshold is applied, above which the test yields a positive result. Etzioni said the test appeared to be conservative in how it registered these positive results; it applied a high threshold to deem a case "positive." That may explain why the harder-to-detect, early-stage cancer cases were not picked up.

But she added that some of the more dismissive commentary around Galleri's performance is "short-sighted."

"I don't think that this trial was a flop," she said. "I think it was hugely informative."

Galleri hopes that results from its upcoming Real-world Evidence to Advance Multi-Cancer Early Detection Health Equity (REACH) study, which has enrolled 50,000 patients in the U.S., will be more positive. The REACH trial has a slightly different endpoint in that it's measuring the test's ability to reduce stage IV diagnoses. The data from the NHS trial suggested Galleri did reduce these diagnoses, which was a secondary endpoint of the trial.

What does this mean for other MCED tests?

Galleri is just one of many MCEDs under development. What could the negative results from Galleri's initial trial mean for the future of cancer detection?

MCED tests are proliferating rapidly, and improvements to the panels used to detect cancer markers should enhance the performance of newer tests, said Etzioni. That said, she noted that, as these tests are closely guarded by manufacturers, it's hard to know exactly which markers would advance performance. Dozens of presentations at ASCO 2026 focused on other MCEDs in the field.

Galleri's results might mean a slightly longer wait before the tests are used widely, Etzioni said. She felt that some of the hype from GRAIL's earlier studies of the test has now dissipated. "They've maybe [previously] led the community to believe that the technology is more ready for prime time than it actually is," she suggested.

Harrison pointed to a position statement from the U.K. National Screening Committee (UK NSC), which provides advice to government ministers on implementing new disease screening programs. The statement, released in May, directly addressed so-called surrogate endpoints, such as the cancer stage-related endpoints used in the initial Galleri trial.

One concern, it pointed out, is that MCED tests may more easily detect aggressive cancers than slow-growing ones. So even if future trials show the tests find these cancers at earlier stages, patients may still die at similar rates because the types of cancer found at these early stages are harder to treat. So improvements in detection can't be assumed to translate to improvements in survival.

The UK NSC stated that further evaluation would likely be required before a MCED test would be adopted in widespread clinical practice, such as within the NHS. (For what it's worth, though, some MCEDs are available for direct-to-consumer purchase despite not proving their worth in gold-standard trials yet.)

The Galleri trial focused on the test's ability to identify cancer in a (presumably) healthy population, but this is just one potential use of the technology behind the tests. It could also be deployed to test people with non-specific symptoms that may hint at cancer or in populations who are known to be at high risk of the disease. Another NHS Galleri trial, called SYMPLIFY, suggested the test was accurate when used in symptomatic patient groups, Lloyd noted.

Galleri's results are not a reason to discount the value of MCED tests more widely, Etzioni said. She believes the tests will someday be used routinely for early cancer detection.

"This is just the beginning," she said.

This article is for informational purposes only and is not meant to offer medical advice.

A deadly Ebola disease epidemic is rapidly unfolding in the Democratic Republic of the Congo (DRC) and Uganda. In May, the World Health Organization (WHO) declared the epidemic a public health emergency of international concern, citing a high risk of further international spread.

As of June 6, there have been 515 confirmed cases and 91 confirmed deaths in the DRC, according to the WHO, and 19 confirmed cases including two confirmed deaths in Uganda.

The outbreak is being caused by the Bundibugyo virus, one of three ebolaviruses known to cause large outbreaks. Unlike the Zaire ebolavirus, which caused the largest Ebola epidemic to date, the Bundibugyo virus does not have a licensed vaccine or medicines.

To get a better understanding of the outbreak and its global implications, Live Science spoke with Dr. Ali S. Khan, professor of epidemiology at the College of Public Health, University of Nebraska and former assistant surgeon general of the U.S. Public Health Service.

Khan has been involved in 25 international and domestic disease outbreak responses, including muliple Ebola outbreaks, during which he worked in the DRC and Uganda. He was director of the Office of Public Health Preparedness and Response at the Centers for Disease Control and Prevention from 2010 to 2014 and currently serves on the WHO Steering Committee for Global Outbreak Alert and Response Network.

Here's what he had to say about the Ebola epidemic and the future of public health threats.

Sophie Berdugo: This year's outbreak currently stands as the third-largest Ebola outbreak ever recorded, spreading faster in its early stages than the largest outbreak in 2014. What factors have made it so big?

Ali S. Khan: This outbreak is occurring in the midst of a political and humanitarian emergency that's going on in the Democratic Republic of the Congo, in an area with significant ongoing political violence, and fighting that is ongoing. That makes it very difficult. It's a remote area, it's an impoverished area. There's little to anything in the way of government services for health care or public health. So, it's not surprising that we see an outbreak there. This is the 17th outbreak in the Democratic Republic of the Congo.

But given the nature of where it is, it was identified late and so there have been multiple chains of transmission that have occurred before it was identified. It was late enough that now we're seeing what many would characterize as "community transmission." So that's why it's big.

Whether it's spreading faster is up for debate because they're still trying to understand where it is. It may just be spreading faster because they're identifying where all the cases are. So it may have already spread. Not that it's not going to spread further, but the early stages of the outbreak is just trying to get a handle on how many cases, who's infected, and where they're infected.

Fever, headache, muscle aches as an initial set of symptoms is not unusual in a country with a whole lot of malaria. So it can look like almost anything. Sick healthcare workers, dead healthcare workers act as a signal for a disease like Ebola.

And in this specific case, there was one final factor which is when they suspected the outbreak: the initial set of diagnostic testing they did, the tool they used, does not test for Bundibugyo. It only tests for Ebola Zaire. So the initial diagnostic testing to them suggested that this is just some other severe tropical febrile disease, and it's not Ebola.

Then when the right set of samples eventually went to the Ministry of Health where they had more sophisticated testing they could go "Wait, it is Ebola; it's just a different strain of Ebola."

SB: Will we need to control this Bundibugyo outbreak differently from previous Ebola epidemics?

AK: A response to an Ebola outbreak is the same as a response to any Ebola outbreak. It's all about excellent monitoring to identify cases, get them into a health care facility so they can no longer infect people within their community, and make sure they have great care. And then make sure there's good infection control so that you don't infect other healthcare workers. So that's step one.

The second step is [an] excellent follow-up of the contacts of infected people [to] find them and then make sure that they're quarantined in a humane way. And the third piece is safe burials. You want to ensure that if people die in the community that you have safe, dignified burial practices.

So those are the three critical components. Every [response to an] Ebola outbreak will do that.

This outbreak is challenging for two reasons. One is with Zaire, we now have drugs that can help a patient. We do not have similar drugs [for Bundibugyo]. So that makes it more difficult within the health care setting to save people's lives.

The other thing from the prevention standpoint is that we don't have vaccines. So for Zaire, you can vaccinate people. For example, you can vaccinate healthcare workers, we can vaccinate people who are contacts to decrease the likelihood of them getting infected.

So you really are completely relying on good old-fashioned, boots-on-the-ground public health. And that's difficult in a humanitarian crisis. And it's exacerbated by the lack of trust that there is for the government, which isn't there anyway, [and an] additional lack of trust for international partners.

Let's remember these people are dying every day of preventable diseases like malaria and nobody shows up, and the moment they have an "exotic disease" for the West, hundreds of millions of dollars and thousands of [medical] responders are showing up. It's very easy to see why there may be mistrust in this situation.

At the end of the day, the biggest factor in every outbreak is risk communications and community engagement. You can get an outbreak under control very fast if the community really is engaged and you communicate it well with them and they want to help make this happen.

SB: Do you have any concerns about the current approach the U.S. is taking to this outbreak? How may have cuts to the U.S. Agency for International Development (USAID) exacerbated it?

AK: I think it's fair to say that USAID has always been a critical partner in these outbreaks for logistics, for provision of personal protective equipment, PPE. So there's no doubt that we have lost that connection on the ground that the U.S. government used to have with these outbreaks.

That said, we do know that the U.S. is supporting the response from a financial standpoint. CDC and other partners have been engaged with WHO to help coordinate their actions and understand what's going on and how they can potentially help.

It's easier to say in the abstract than in the concrete because there's hundreds of partners during an outbreak. To say "this is not happening because this partner is missing" is difficult, but there's no doubt that the lack of USAID is going to impact any outbreak where in the past USAID has been such a critical partner on the ground.

People have asked in the past, "If USAID was there, would we not have heard about this outbreak earlier?" In the abstract, yes, but there's no concrete evidence of that. I mean, the truth is this outbreak occurred in the midst of a humanitarian crisis and the initial diagnostic testing didn't trigger an appropriate response. And there's always outbreaks in DRC of unexplained severe febrile illness.

I'm not sure if we can say the USAID and other cuts led to this outbreak. These outbreaks are going to happen: It's in the right part of the world for them to happen. For the animals being infected then infecting humans. [Humans can become infected when exposed to the bodily fluids of infected animals, such as fruit bats and chimpanzees.] There is little to no infection control in the healthcare setting, so the outbreaks are going to spread regardless.

SB: On that point, you said in a 2020 interview that a "disease anywhere is a disease everywhere," emphasizing the need for a global effort given diseases can be spread anywhere.

AK: Absolutely. We worry about these transboundary diseases for lots of reasons. One is the local impact in communities. We worry about large national and regional spread as we saw in Ebola in 2014. And then as with SARS-CoV-2 [the virus behind COVID-19] or the next influenza virus, we worry about global spread.

The best approach for all of us as global citizens is to rapidly identify a disease where it is and address it there so that it doesn't spread. And that takes multiple partners in communities, in partnerships with governments, to make that happen. And that remains more critical today than ever because of the speed at which diseases can travel.

So yes, a disease anywhere is a disease everywhere, but a disease anywhere can be a disease everywhere tomorrow morning.

Nowadays, I could get infected in Bunia [the capital city of Ituri Province in the DRC] today, and tomorrow evening, I could be sitting in New York City. I've got the virus inside of me but I'm not going to be sick for another week or so, but there's no way to know about that hidden infection because of the incubation period. Our speed of travel has become faster than this incubation period, and that has proven to be a downfall in terms of our ability to protect ourselves.

The old strategies of "lock down borders, keep ships from coming to your ports" — that doesn't work because it's probably already there by the time you decide that's what you need to do.

SB: This Ebola outbreak was reported within weeks of a cluster of hantavirus cases aboard a cruise ship. Are we heading into a world where the threats of epidemics, and possible pandemics, become more likely?

AK: Yes, without a doubt. They're becoming more likely for lots of reasons. One is, as humans move out into the environment, there's an increased opportunity for this human-animal intersection and then spillover into humans. So that risk remains and is probably increasing.

Climate change is also having its own impact as vectors — mosquitoes, ticks and rodents, etc. — move into new areas where they weren't previously. That puts people at risk. So that also helps exacerbate what's going on. Travel exacerbates what's going on because you could be infected and get somewhere faster than you ever could before.

And it's not just the U.S. that is cutting global funding. International development aid has been falling from Germany and other European countries also. So it's not just the U.S. But when you do that then it makes it more difficult for low- and middle-income countries to develop the systems they need to quickly identify these diseases and alert [local people and organizations about] these diseases so that either they take care of it themselves or they get international assistance to help take care of it.

SB: It doesn't look like any vaccines will arrive for nine months, according to the WHO. Is there any way to speed that up, now or in the future?

AK: Yes: Embrace mRNA technology and stop demonizing mRNA technology. Nothing's faster in getting a vaccine than mRNA technology. Nothing comes close. Think about how fast we got this COVID vaccine through FDA [Food and Drug Administration] approval in the United States: less than nine months. And a licensed vaccine with hundreds of millions of doses right off the bat.

We need to embrace new technology to make vaccines so that the moment you have a new pathogen you can spin up the vaccine production and have these vaccines available for people. In the United States, unfortunately we have been demonizing mRNA technology, which is unfortunate because that truly will be the technology that will help us get to a rapid vaccine for the next pandemic.

And I believe CEPI [Coalition for Epidemic Preparedness Innovations] in Europe has made a $10 million investment in mRNA technology for this new Bundibugyo strain. And then the two other vaccines that are being worked on are more classical methods. Those are established technologies that are being modified.

SB: What does the U.S.'s response to this outbreak tell us about its preparedness to face others?

AK: Globally, the fact that we left WHO — even though we are still talking to WHO — puts the U.S. government outside of the typical information loop and coordination loop of what's going on with pandemics. It's not as if we're not talking to WHO, I know that from all my CDC friends that we're talking to WHO.

The U.S. has been a leader over decades — we actually helped establish WHO — for pandemic preparedness, and that lack of global leadership will have an impact on our ability to rapidly recognize and respond to these diseases, which puts not just us but other countries at greater risk of transboundary diseases.

And that message is not just to the U.S., I think that [is a] message to every country in the world which has all of a sudden been up in arms about a dozen hantavirus cases which we knew, those of us in the field knew, posed no threat of a global pandemic.

Communities are understandably fearful when they hear about these sort of "exotic diseases" that are spread from person to person. It makes sense then for governments to help protect them by recognizing that global health security is also domestic health security.

They [disease outbreaks] don't always have to start in Africa and Asia; they could start potentially right here in the United States. And there's no doubt that we've eroded public health authorities since the COVID pandemic here in the United States. Eroding those public health authorities and the continued disinformation that we see weakens our ability to respond to the next pandemic.

Editor's note: This interview has been edited and condensed for clarity.

Flu drugs may help ward off the low-grade inflammation and related cognitive decline that can come with HIV infection, an early study suggests.

Upwards of 24% of people with HIV experience some degree of cognitive impairment that interferes with functions like attention, concentration and multitasking. These declines are often mild but can worsen quality of life, and they can happen even when a person consistently takes HIV medications that suppress the virus.

Understanding why this impairment emerges and how to prevent it is especially relevant as the population of people with HIV grows older.

"This is very important," said study co-author Mohamed Abdel-Mohsen, an associate professor of medicine in the division of infectious diseases at Northwestern University Feinberg School of Medicine. "Despite the fact that people living with HIV live longer, so the lifespan is preserved, the 'health span' is not as preserved."

The new study, published Friday (June 5) in the journal Med, pinpoints a potential driver of this decline along with a strategy to reverse it. The scientists used mouse experiments and blood samples from HIV patients, so the work is at an early stage, but it could open the door to future treatments.

"Not only do they describe a mechanism, but they then report in animal models that this mechanism is something that potentially could be targeted by an intervention," said Dr. Alan Winston, a professor of HIV and genitourinary medicine at Imperial College and a consultant physician at St. Mary's Hospital in London. "That's really what's novel," said Winston, who was not involved in the study.

Anti-inflammatory sugars

HIV treatments are now so effective that people with the chronic viral infection can live nearly as long as people without HIV, provided they consistently take the medicines. In 2022 in the U.S., more than half of people living with HIV were over 50 years old, and that figure is expected to grow.

HIV treatment, called antiretroviral therapy (ART), suppresses the virus so that it can't multiply. This prevents the disease from progressing to AIDS while also driving down transmission rates, making the virus unable to spread via sex. But while ART wards off many symptoms of HIV/AIDS and extends an infected person's lifespan, it does not make the chronic infection completely benign. People with HIV still show various signs of accelerated aging, including earlier cognitive decline, in some cases.

"Before we had antiretroviral therapy, we saw profound effects of HIV in the brain," Winston noted. HIV-associated dementia is now rare, because its rates declined as the use of ART increased.

But some percentage of people still develop milder cognitive impairments, and "it can actually have quite a big impact on concentrating at work, for instance, and undertaking daily activities," he said. People have a higher risk of impairment when they've had a big gap between contracting HIV and starting ART, and interruptions in treatment can also raise the risk. However, the underlying cause of the impairments isn't fully understood, Winston said.

To unpack that mechanism, Abdel-Mohsen and colleagues investigated a clue that's recently emerged in the medical literature: sugar molecules called glycans.

These sugars are found throughout the body, including in the bloodstream, where they bind to proteins and fats. In circulation, they tag certain immune molecules to keep inflammation in check. But with age, the concentration of these inflammation-controlling glycans declines: This decline is fairly steady for males, while it has a sudden dip around menopause for females, Abdel-Mohsen said.

Scientists have previously explored how this decline might contribute to age-related diseases, including cancer, while Abdel-Mohsen and colleagues have investigated its relationship to HIV. In a 2024 study comparing people with and without HIV, they found that those with the infection show age-related shifts in their glycans at younger ages than usual. These shifts come with an increase in enzymes known to degrade the sugars, as well as increases in inflammation.

"While it's low-grade [inflammation], it's still damaging because it's continuous," Abdel-Mohsen said. "It's chronic; it doesn't get resolved."

Potential treatment?

In their latest study, the researchers wanted to see if they could connect the dots between the glycan loss, inflammation and cognitive decline.

They analyzed blood samples from more than 100 people with HIV who contributed data to the AIDS Clinical Trials Group, a global research network. All the individuals were taking ART and either had signs of cognitive impairment or did not, according to various assessments. The group with impairments showed greater losses in two glycans that help control inflammation: sialic acid and galactose. In particular, these losses were most pronounced in women, and they correlated with the degree of cognitive decline seen in a given person.

It's not clear why this pattern was more pronounced in women, and that remains a question for future study, Abdel-Mohsen noted. That said, it's known that glycans dip around menopause and that key immune cells bear estrogen receptors, so it's possible that estrogen levels play a role, he suggested. Winston wondered if the timing of diagnosis might also be relevant, since women tend to get diagnosed later than men and may therefore start ART later.

After studying the blood samples, the team used two models of HIV infection in lab mice. One enabled them to study the glycan changes and inflammation triggered by HIV, while the second let them examine signs of cognitive decline. They again found that infection was tied to a loss of glycans and increase in inflammation, as well as worse performance on cognitive tests.

Next, they set out to see if they could reverse those effects.

A class of drugs called sialidase inhibitors work by blocking the effects of enzymes that split sialic acid, one of the key inflammation-quenching glycans. These drugs include Tamiflu, because flu viruses rely on sialic acid to infect cells and spread through the body. The team found that, at least in mice, these flu drugs helped preserve sialic acid, prevent inflammation and improve cognition.

We saw that "this class of inhibitor could reduce inflammation caused by viral infection … and even more importantly, preserve cognition and and prevent memory deficits," Abdel-Mohsen said.

Abdel-Mohsen considers this work "proof-of-concept" that glycans may play a role in HIV-related cognitive decline, pointing to potential treatments. The end goal isn't necessarily to use flu drugs to treat cognitive impairment in HIV, but rather to identify compounds that could "either prevent the glycans from being degraded or just replace them," he said.

One limitation of the current study is that its definition of cognitive impairment was limited, Winston noted. It relied on cognitive test scores — how well participants solved various puzzles — and a standard "scoring" system that's used to assess a handful of cognitive functions. Including details of patients' symptoms and challenges they experience in daily life would have made the meaning of those scores more tangible, Winston said, and he would hope to see that in future work.

In the long run, Winston could see this research leading to a "precision medicine" approach in which patients' glycan levels are checked, and if they're low, they could get a treatment to address that. It's likely that different factors drive cognitive impairment in different people with HIV, so matching patients with the right treatment is imperative, he said.

And in theory, it may be that the loss of glycans also drives other issues seen in aging adults with HIV, such as increased rates of cardiovascular disease. If that's the case, the same treatments may serve multiple functions. "It will be definitely fantastic to study and see how targeting this mechanism could impact the multiple comorbidities," Abdel-Mohsen said.

This article is for informational purposes only and is not meant to offer medical advice.

A fly that deposits its parasitic, flesh-eating offspring inside cows has been detected in Texas for the first time in decades, the U.S. Department of Agriculture (USDA) reported Wednesday (June 3).

A second case in a cow in the same county was announced June 5, and two more cases — in a cow and dog — in other Texas counties were flagged on June 8. Another cow case was announced June 9, bringing the total to five.

Here's what to know about the New World screwworm (Cochliomyia hominivorax), a pest that was eradicated from the U.S. in the 1960s.

What is the New World screwworm?

New World screwworms are parasites that feed exclusively on the living flesh of warm-blooded animals, according to the American Society for Microbiology (ASM). The screwworms are the larvae, or maggots, of adult C. hominivorax flies.

The flies lay their eggs in animals' open wounds or body openings, such as the eyes, ears, nose, mouth or genitals. Once hatched, the maggots burrow into their host's flesh, using a screw-like motion that lends the species its name. The maggots have sharp mouth hooks that can cause extensive damage, deepening the wound and raising the chances of secondary infections. The infestation can be painful, cause swelling and bleeding, and can produce a foul smell.

After about a week of feeding, the maggots enter their next stage of development and exit the animal, burrowing into soil in order to "pupate" and mature into a fly.

Broadly, maggot infestations are known as myiasis, and myiasis caused by New World screwworms is a big problem for livestock agriculture. Across places where the fly species is endemic, or widespread, annual economic losses caused by the fly can amount to billions of dollars each year. The flies mostly infect large-hooved livestock, such as cows, sheep and horses. Less commonly, they can infect domestic dogs and wild mammals, such as deer, rabbits, opossums and birds.

Can the screwworm infect humans?

Yes, New World screwworms can sometimes infect humans, although it's fairly uncommon. The flies can potentially infect any warm-blooded animal, but livestock are most commonly affected.

People in endemic areas who work with livestock, have weakened immune systems, sleep outdoors, or have open wounds — however small — are most at risk for developing C. hominivorax infestations. As in animals, infestations in humans can be deadly, but they are treatable via physical removal of the maggots from the body.

Symptoms of infestation include feeling or seeing maggots move within a skin wound or sore, or in the ears, nose, eyes, or mouth; developing painful skin wounds or sores that worsen within a few days; bleeding from sores; and a foul-smelling odor at the site of the infestation.

The screwworms do not spread from infected animals to people or from person to person. Infestations start when a female fly lays eggs in a wound or bodily opening, like the eyes.

In 2025, the U.S. reported its first New World screwworm infection in a person in decades. That individual, in Maryland, had just returned to the U.S. after traveling to El Salvador, where the fly is endemic. That person recovered with treatment.

Can infected livestock be treated?

Yes, infected livestock with New World screwworms can be treated with antiparasitic medications. Treatment also involves physical removal of maggots from the flesh and disinfection of the wound sites. Treatment must be timely, as an infestation can kill livestock in 10 days, ASM notes.

Rather than culling whole herds — similar to what's done for commercial flocks infected with bird flu — affected farms are examined for additional cases and not allowed to move animals from the premises during that time, according to USDA. Infected animals are treated and quarantined until their wounds heal and they go a few weeks without any signs of reinfestation. Euthanasia for individual animals can sometimes be necessary if the infestation is too extensive.

If they meet all regulatory requirements, animals that have recovered from screwworm myiasis can enter the food supply, USDA says. Notably, screwworms do not infest dead meat, only healthy, living flesh. The screwworms thus pose a threat to food production but not to food safety.

Is it a big deal that it's been spotted in Texas?

Screwworm outbreaks can be incredibly costly if not snuffed out quickly — there's a reason the U.S. has poured so much effort into eradicating the pest. Experts estimate that, if a large outbreak took hold of the state today, the Texas economy could lose $1.8 billion due to disruptions to the livestock industry. Food prices would be expected to rise, in turn.

New World screwworms were declared eradicated from the continental U.S. in 1966, following an extensive effort that involved releasing sterilized male flies into the wild and breaking the species' reproductive cycle. Despite this local eradication, America still saw some major screwworm outbreaks due to flies and infected animals entering the country from Mexico. A 1972 outbreak was the worst recorded post-eradication, affecting multiple states and causing tens of thousands of cases in Texas alone.

A joint effort between the U.S. and Mexico was then established to prevent a similar outbreak from happening in the future, and the parasite had largely been eradicated in Mexico in the 1980s. But in recent years, there have been signs of a comeback. Cases have been moving northward from Central American countries, like Panama and Costa Rica, since 2023. In response, the U.S. has deployed a strategy, led by USDA, to drive cases back down.

"All models showed New World Screwworm entering the country in 2025," but these efforts likely bought the nation some time, USDA's June 3 statement notes.

So, the detection of C. hominivorax in a 3-week-old calf in Zavala County, Texas, was not necessarily surprising but it does require quick action. The case occurred in Southwest Texas about 50 miles (80 kilometers) from the U.S.-Mexico border. The maggots were seen around the calf's umbilical area. With treatment, the calf should recover, Agriculture Secretary Brooke Rollins told The Associated Press (AP).

"USDA urges residents to contact your veterinarian right away if you see any suspicious wounds, maggots, or infestations in your animals or herd," the agency said on X. "If you see signs of maggot infestations in live or very recently dead wild animals, especially in areas near the U.S./Mexico border, please call 866-4USDA-WS (866-487-3297) to report it to your local USDA Wildlife Services office."

The agency is now following strategies and actions outlined in the NWS Response Playbook to snuff out any potential danger in Texas. That includes establishing a quarantine zone around where the case was detected and limiting the movement of animals in that zone.

According to the AP, Rollins said the USDA is confident enough in its preparations that it believes "there is no threat of mass infestation." She added, "There is no reason to believe this incursion will result in establishment of the pest in our country."

Following the initial detection, USDA then detected a second screwworm case in Zavala County. The case was "within the established movement control zone and enhanced sterile insect dispersal area" that had been set up for the first case, Dudley Hoskins, Under Secretary for USDA's Marketing and Regulatory Programs, said in the June 5 statement.

On June 8, officials announced cases in a calf in La Salle County (just to the southeast of Zavala) and a dog in Andrews County (hundreds of miles northwest of Zavala), bringing the current total to four. Early reports indicate that the dog was recently in Mexico, hinting it may have caught screwworm there, but investigations are ongoing.

A case in another calf in La Salle County was reported June 9. Surveillance and response measures have been expanded in the area.

"While we address these instances that require immediate attention, and continue to sample suspected cases, we are simultaneously working to eradicate the pest entirely," Hoskins said in the June 8 statement. "We need the partnership of animal owners across the region — please stay vigilant, check your animals closely, and report anything that looks suspicious."

Editor's note: This story was updated June 9 with information about a fifth case. The article was first published June 4.

This article is for informational purposes only and is not meant to offer medical advice.

Google wants to release 64 million bacteria-riddled mosquitoes in California and Florida — but scientists aren't concerned.

The Environmental Protection Agency (EPA) is reviewing an application made by the tech giant for an experimental mosquito release permit, which, counterintuitively, could reduce mosquito populations that carry diseases.

The release is part of Google's Debug initiative, which aims to deploy millions of non-biting male mosquitoes infected with a bacterium called Wolbachia pipientis — commonly known as Wolbachia — into the environment. This bacterium doesn't harm infected males, but it does prevent any uninfected females they mate with from having offspring, thereby slashing mosquito populations over time.

In this case, Google is targeting southern house mosquitoes (Culex quinquefasciatus), an invasive species native to tropical and subtropical regions that can spread diseases like West Nile virus and St. Louis encephalitis in humans.

The proposal has scientists mostly buzzing with enthusiasm. Karthikeyan Chandrasegaran, an assistant professor at the University of California, Riverside, studies the ecology and behavior of mosquitoes in the context of public health, and told Live Science that using Wolbachia is a "reasonable" mosquito control approach, particularly when compared to the use of broad insecticides.

"Wolbachia-based strategies are generally species-specific and do not introduce novel toxins into the environment," Chandrasegaran said. "Importantly, Wolbachia is already widespread in many insect species and is a naturally occurring bacterial symbiont rather than a genetically engineered organism. From that perspective, they are among the more environmentally conservative mosquito control tools currently available."

The EPA has deemed Google's request to be of potential regional and national significance, and it will make a final decision whether to grant the permit following a public comment period ending on June 5. After this, the agency may give Google the greenlight to release up to 32 million mosquitoes in California and another 32 million in Florida over two years.

However, despite the scale of the proposed releases, Google's approach isn't new and has already been shown to work in another mosquito species.

"It is a technique that's been used actively to control mosquito populations since around 2011," Eric Caragata, an assistant professor at the University of Florida who studies Wolbachia for mosquito control, told Live Science.

Fighting mosquitoes with mosquitoes

Mosquitoes are the deadliest animal on the planet, according to the Centers for Disease Control and Prevention (CDC), killing between 500,000 to more than a million people a year by spreading harmful diseases. Given the blood-suckers are so small, widespread and numerous, reducing them at scale is tricky. Using insecticides can harm the environment and kill other pollinators, and increasingly, mosquitoes are building up a resistance to them.

"We have an ongoing battle with both mosquito-borne disease and insecticide resistance," Caragata said.

Wolbachia offers a potentially natural solution to these mosquito woes. The bacterium is common in insects but doesn't infect other animals, like humans. Through a process called cytoplasmic incompatibility, the bacterium creates a unique interaction between infected males and uninfected females.

In males, Wolbachia modifies the sperm genome in a way that kills embryos produced with that sperm. However, if a female also has Wolbachia and it's in the embryo, then the sperm genome impairment doesn't do any harm. This interaction means that if you release millions of infected males into a population, then the uninfected females will mate with them en masse and be unable to produce viable young.

"If a [female] mosquito has Wolbachia, that mosquito can mate and reproduce successfully with both infected and uninfected males," Caragata said. "All of her progeny will then have Wolbachia. However, if you have an uninfected female mosquito and she mates with a Wolbachia-infected male, none of her progeny will hatch."

Google is building machines to autonomously rear millions of infected mosquitoes, and then using artificial intelligence (AI) algorithms, sensors and other engineering to separate the males from the females.

Researchers have been using sterilized male mosquitoes to reduce populations for decades. Female mosquitoes bite humans because they need the protein and other nutrients found in blood to produce their eggs, but males get all their nutrition from flower nectar and fruit and not humans. So, releasing male mosquitoes theoretically poses no threat to people.

Most of the previous bacteria-based attempts have focused on Aedes aegypti mosquitoes, which carry diseases like Zika and dengue. In Singapore, where Google is also working, researchers have been using Wolbachia-infected males to fight dengue. Trials have found that the approach reduces the disease-carrying mosquito population by up to 90% and the subsequent risk of a person contracting dengue by 70%. However, Google's large-scale targeting of southern house mosquitoes is new.

More upsides than downsides

While there are some unknowns, neither Caragata nor Chandrasegaran expect any major ecosystem disruptions. Lots of animals feed on mosquitoes, but a sudden drop in southern house mosquitoes shouldn't result in lots of animals starving.

"Most predators that consume mosquitoes are generalists and feed on a broad range of aquatic and terrestrial insects," Chandrasegaran said. "Consequently, there is little evidence to suggest that local suppression of Culex quinquefasciatus would trigger substantial ecological cascades."

Chandrasegaran noted that ecosystems are complex, and so any large-scale intervention should be monitored. One potential consequence could be that reducing one mosquito species creates space for another, but Chandrasegaran thinks there will likely be more upsides than downsides.

"From a public health perspective, reducing Culex quinquefasciatus populations could yield meaningful benefits, as this species is an important vector of West Nile virus and several other pathogens," Chandrasegaran said. "If suppression can be achieved safely and sustainably, the public health benefits are likely to outweigh the ecological risks based on our current understanding."

In the U.S., West Nile virus is the leading cause of mosquito-borne disease. Around 2,000 people are diagnosed with the virus each year, with likely more infected but undiagnosed, according to the CDC. Most people don't develop symptoms and some experience mild flu-like symptoms; however, in some cases, it can result in severe illness and death. In California, there have been more than 8,000 human cases of the virus and more than 400 deaths since 2003 — none so far this year.

Internationally, C. quinquefasciatus and other Culex mosquitoes also play a major role in spreading Japanese encephalitis virus, which is a problem in Asia. There are an estimated 100,000 annual cases of Japanese encephalitis, for which the fatality rate can be as high as 30%, according to the World Health Organization (WHO).

Live Science reached out to Google for comment and was directed to a public statement about the Debug project.

An Ebola epidemic in Central Africa has been declared a "public health emergency of international concern" by the World Health Organization (WHO).

As of May 22, over 800 Ebola cases have been reported in the Democratic Republic of the Congo, including more than 180 deaths; these counts include both suspected and laboratory-confirmed cases of the disease. There are also two confirmed cases and one death in Uganda, specifically among people who had recently traveled to the DRC.

A number of factors are making this outbreak very challenging to contain, experts told Live Science — here's what to know.

Current Ebola outbreak

WHO officials suspect the Ebola outbreak centered in the DRC may have begun about two months ago. The earliest suspected death occurred April 20, and it was likely followed by a superspreader event at a funeral or healthcare facility, officials say. Reuters also reported that medical personnel failed to escalate the first patient's samples for further tests after they came back negative one type of ebolavirus.

That virus — known as Ebola virus, or Zaire ebolavirus — is the most common culprit behind Ebola disease outbreaks and deaths. There are two other viruses known to cause outbreaks of Ebola disease: Sudan virus and Bundibugyo virus. The latter is driving the current outbreak.

With only a handful of travel-related cases in Uganda, as well as one American receiving care in Germany after being infected in Congo, the outbreak remains concentrated in the DRC. The WHO anticipates a high risk of international spread, though, which prompted the agency's leader to make an emergency declaration without first convening a committee to discuss the decision.

"In our view, the scale and speed of the epidemic demanded urgent action," WHO Director-General Tedros Adhanom Ghebreyesus said May 19.

A virus with no vaccine

Part of the challenge with containment is that there is no effective vaccine against Bundibugyo virus, the germ driving this outbreak.

There are approved Ebola vaccines. "However, these vaccines have been designed specifically to address the Zaire ebolavirus," which has historically caused more outbreaks than Bundibugyo virus has, said Dr. Madeline DiLorenzo, clinical coordinator of infectious diseases operations and an associate hospital epidemiologist at New York University (NYU) Langone's Tisch Hospital. The largest Ebola outbreak to date, which happened from 2014 to 2016, involved the Zaire ebolavirus.

Zaire ebolavirus and Bundibugyo virus are genetically distinct, sharing only about 60% to 70% of their genetic material. The protein targeted by the existing Ebola vaccines is encoded by a specific gene, and that gene's sequence differs between the two viruses, DiLorenzo explained.

Studies suggest that immune responses against filoviruses — the family of viruses that includes Zaire ebolavirus and Bundibugyo virus — show limited cross-reactivity, meaning the immune response is narrowly focused on just one type of virus. So the Zaire-targeting vaccines likely wouldn't help in this outbreak.

WHO officials have said there is a promising experimental vaccine against Bundibugyo virus, but there are no doses available for a clinical trial. It could take six to nine months to manufacture those doses, the WHO estimates. Another vaccine in development could take two to three months to produce, but its efficacy is unknown because scientists are still waiting on results from lab-animal tests.

In Ebola disease outbreaks, vaccines are used for ring vaccination, in which people exposed to a suspected or confirmed case are inoculated against the disease. They can also be used for "targeted geographic vaccination," in which everyone in a given area is vaccinated because the outbreak is relatively concentrated there or contact tracing is too difficult to conduct. Without a Bundibugyo vaccine, both of those strategies are currently off the table.

Lack of diagnostics and treatments

Ebola disease can be difficult to spot in its early stages, in part because the first symptoms are fairly generic: fever, fatigue, malaise, muscle pain, headache and sore throat. These symptoms appear within two to 21 days of exposure to an ebolavirus.

There are tests for Bundibugyo virus that look for the virus's genetic material in bodily fluids; this approach is known as PCR testing. "However, it is not widely available for the Bundibugyo virus, making it difficult to diagnose and, as a result, contain the virus," Dr. Jill Weatherhead, an associate professor of infectious disease and tropical medicine at Baylor College of Medicine, told Live Science in an email.

Even when such tests are available, it can take several days after a patient develops symptoms for the virus to be detectable in blood, DiLorenzo noted, so repeat testing can be necessary. The recommended samples for Ebola tests are whole blood or plasma for living patients and an oral swab for deceased individuals, the WHO says.

There are additional tests that can detect Bundibugyo virus, including some that determine whether a sample contains a filovirus that infects humans in general, without specifying which one is present. These rapid tests look for specific viral proteins. However, these tests are less sensitive and "may not pick up specific proteins associated with Bundibugyo," DiLorenzo said. "This may have contributed to delayed detection of the current outbreak in the DRC."

On top of these diagnostic challenges, there are no specific antiviral treatments for Bundibugyo virus. There are lab-made antibodies approved for Zaire ebolavirus, and they improve survival by binding to the virus's surface and blocking it from infecting cells. Similar treatments for Bundibugyo virus haven't progressed beyond lab research or early-stage human safety studies, Weatherhead said.

Conflict, declining foreign aid hinder containment

In the absence of vaccines and treatments, other strategies, such as quarantining close contacts of infected people, become key to containing the outbreak, Weatherhead said. Clinicians treating patients with suspected or known cases should also follow strict infection-prevention-and-control protocols to prevent further spread, she added.

Ebola spreads via contact with infected blood and other bodily fluids, as well as contaminated surfaces or materials, such as clothing and bedding. This means using personal protective equipment to block splashes or other contact with infected materials, among other protocols.

The strategies available to contain this outbreak — finding and isolating cases and employing tight infection-control protocols — require public health infrastructure to execute. But in the DRC, that infrastructure is severely compromised. The outbreak's epicenter is the Ituri province in the northeastern DRC, which has "experienced armed conflict for decades, making it challenging for health systems to function optimally there," DiLorenzo said.

Joshua Walker, director of programs of the Congo Research Group at NYU's Center on International Cooperation, told Live Science via email that the circumstances of the current outbreak resemble a 2018-2020 outbreak that centered on the North Kivu province, which borders Ituri to the south.

This time around, several cases have been reported in both North and South Kivu provinces, parts of which are essentially partitioned between the DRC government and a Rwanda-backed rebel group, called M23. And there's been increasing violence among armed groups in Ituri in recent months, Walker said. Meanwhile, development assistance for healthcare in the area has fallen substantially in recent years. Together, these factors "will make access and coordination of a single response more difficult," he said.

Recent cuts to foreign aid are only making things worse, Dr. Manenji Mangundu, DRC country director for Oxfam, which is coordinating on-the-ground responses to the outbreak, told Live Science in an email.

"USAID [the U.S. Agency for International Development] was the main donor in the DRC and many aid organizations depended on its funding to deliver life-saving support in a country already devastated by conflict," Mangundu said. "When USAID was shuttered last year, eastern DRC lost around 70% of its humanitarian aid."

More funding cuts from other donors followed, leading to the closure of medical centers, declines in medical supplies and community health workers, and reduced capacity to deal with outbreaks.

"Funding cuts directly do not cause outbreaks, but they do weaken the very systems that are meant to prevent small crises from becoming larger crises," Mangundu said.

In Ituri, residents have been repeatedly displaced due to the conflict and must shelter in crowded schools and churches with limited access to clean water, sanitation and healthcare. Funding cuts only compound these existing problems, he said.

In this setting, it can also be difficult to convince people to adopt safety measures to limit the spread of Ebola, he added. For example, "communities remain attached to their deceased relatives and continue to handle the bodies, which increases the risk of transmission."

Lessons from past outbreaks

Walker noted that the international response to the current outbreak will shape how it evolves.

"The 2018-2020 Ebola response effectively sidelined the local Congolese health system, viewing it as too fragile or weak to be an effective partner," he said, citing his past research. So the response was largely orchestrated by outsiders to local communities, which fostered suspicion.

"One hopes," Walker concluded, "that there have been some hard lessons learned by the international community since the last major outbreak."

As global health leaders warn that this outbreak could swell to impact more countries, Mangundu emphasized that much more support is needed to snuff out the epidemic in the DRC.

"There is capacity in the country to respond, but there are not enough resources to help control and prevent the spread," he said. "We need to fund humanitarian aid and support the people of DRC at this time before a preventable crisis turns into one with far wider, global consequences."

This article is for informational purposes only and is not meant to offer medical advice.

A common asthma drug could be repurposed to help tackle hard‑to‑treat cancers, such as triple‑negative breast cancer, an early study suggests.

The research finds that cysteinyl leukotriene receptor 1 (CysLTR1), a protein found on many cells, may be hijacked by tumors to turn important immune cells into sleeper agents that work for the cancer instead of against it. Those immune cells, called neutrophils, would normally directly kill tumor cells, help to rally other immune cells against cancer, or boost the effects of certain cancer therapies.

However, research increasingly suggests that the cells are an important player in how cancers resist immunotherapy. Under certain conditions, they help build and maintain a tumor-promoting environment.

If the new study's finding is confirmed in future research, an existing medication could offer a way to target this receptor and thus reverse cancers' resistance to common immunotherapies. There's already a drug on the market that can block CysLTR1, called montelukast, which has historically been used to treat asthma and allergies.

The work suggests that "you can repurpose these drugs to revive or to reprogram those neutrophils to become immune stimulatory cells that basically sensitize tumors to immunotherapy," study co-author Dr. Bin Zhang, a professor of cancer immunology at Northwestern University Feinberg School of Medicine, told Live Science. The research, published Tuesday (May 19) in the journal Nature Cancer, could also help to explain why some patients don't respond to immunotherapy, a treatment that redirects the immune response toward cancer cells.

"There are not many options available for patients who are resistant [to immunotherapy]," Zhang said. "But now, using this drug, it seems like they [could] start to respond to the treatment."

Immune cells called to the dark side

CysLTR1 is an important actor in immune responses; it helps recruit immune cells to a site of infection and prompts the lungs to produce mucus and cough out any invading microbes, for instance.

The problem comes when that reaction gets out of hand. In asthma, blocking CysLTR1 can do wonders, alleviating symptoms like wheezing, breathlessness and allergy‑related nasal symptoms. The drug montelukast does just that, and it has been approved by the Food and Drug Administration (FDA) since 1998 to treat asthma and hay fever.

The new research suggests that CysLTR1 can also be co‑opted by tumor cells to cause neutrophils to adopt "tumor‑promoting" behavior. By releasing chemicals that tweak the behavior of immune cells — cytokines and cysteinyl leukotrienes — tumor cells encourage neutrophils to release powerful molecules that help cancer cells invade surrounding healthy tissue. They also help tumors ward off attacks from other immune cells that would normally seek out and help kill cancerous tissue.

"We identified this molecule plays a very important role in controlling neutrophils, which is one of the most abundant immune populations in the circulation, particularly in cancer patients," Zhang said.

When researchers blocked CysLTR1 in lab mice, by either turning the gene off or using montelukast, they found that they could slow tumor growth, increase the mice's survival time, and make previously resistant tumors respond better to immunotherapy drugs.

Blocking CysLTR1 worked across several tumor types in mice, including breast, colon and melanoma‑like cancers. It was particularly strong when combined with a common type of immunotherapy called "checkpoint blockades," causing once-resistant tumors to shrink under treatment.

This is important because some cancers, such as triple‑negative breast cancer, don't tend to respond well to checkpoint blockades, Zhang said. At least from preclinical models, we suggest that when checkpoint blockades and montelukast are combined together, "you see beautiful results reflected by increased survival" across multiple tumor types.

"It's a very amazing result," he said.

Turning science into treatment

In experiments with human cells, the team found that blocking CysLTR1 in human blood reduced neutrophils' ability to shut down cancer‑killing immune cells. It also stopped neutrophils from maturing into this tumor‑helping, immune‑suppressing state, suggesting that the same pathway the team saw in mice is also active in people. Using a genetic analysis, the team unraveled the chain of events that CysLTR1 triggers to switch into this "cancer-promoting" mode.

They then uncovered clues that this same mechanism had left traces in large cancer datasets. They found that patients whose tumors had more of the receptor tended to do worse overall and responded less well to checkpoint blockades.

Shakti Ranjan Satapathy, a postdoctoral researcher at Lund University in Sweden who studies this field but was not involved in the new research, said the study was "important and timely" and "moves the field forward."

Zhang is hopeful that the team will be able to launch a clinical trial on the back of their results."It's not easy, sometimes, doing a clinical trial, but in this case, it may be a little bit less challenging because those drugs are available," he said.

The team also suggests that doctors screen for this receptor to determine whether patients are likely to resist immunotherapy. "We are probably the first to demonstrate [CysLTR1 as] maybe a functional biomarker that could be linked to the patient prognosis and help predict the immunotherapy resistance," Zhang said. Still, there is a lot to be tested before this drug can be confidently rolled out in the context of cancer, he said.

"'Quickly move into trials' should not be confused with 'ready for routine cancer treatment,'" Satapathy cautioned. "Repurposing an approved drug still requires an appropriate dose, dosing schedule, patient selection strategy, safety monitoring, pharmacodynamic readouts, and evidence of benefit in combination with immunotherapy."

For one, montelukast is occasionally linked to substantial neuropsychiatric side effects when used for hay fever, including suicidal thoughts and mood changes, leading the FDA to raise a boxed warning in 2020. One alternative, Zhang said, might be to test whether the receptor could be targeted directly with an antibody, which could potentially cause fewer side effects, rather than a chemical, though further research will be needed to assess if this is the right path.

"Hopefully, we can have a real clinical impact," he said, "but that's too early to say."

This article is for informational purposes only and is not meant to offer medical advice.

The patient: A 59-year-old woman in Wisconsin

The symptoms: The woman sought medical care after noticing a rapidly growing mass in her right arm.

What happened next: Upon examination, doctors found a 0.8-by-0.8-inch (2 by 2 centimeters) mass in the patient's forearm that was firm to the touch. The mass could also be seen on an X-ray of the woman's arm, and the roughly oval-shaped lump appeared bright white on an MRI scan. This finding hinted that the mass might be a sarcoma, a type of cancer that starts in bone or soft tissue, such as cartilage, fat or muscle. Sarcomas are relatively rare; they make up only about 1% of cancer diagnoses.

To further examine the lump, doctors performed a core needle biopsy, which involves inserting a small, hollow tube into the tissue to collect a sample. They also collected fine needle aspirates, or biopsies of cells and fluids collected using a small needle and syringe.

The diagnosis: Analyses of the biopsied samples showed that the woman had myxofibrosarcoma (MFS), a type of cancer that develops in connective tissues beneath the skin, often in the limbs. MFS cases make up about 5% to 10% of soft tissue sarcomas; a few hundred new cases occur in the U.S. each year.

The cancer cells in the woman's biopsy were classified as Grade 2, or intermediate grade; in terms of the abnormality of the cells and expected speed of tumor growth, the cells were a 2 on a scale of 1 to 4, with 4 being the most abnormal and fastest growing.

The treatment: Following her biopsy, the patient reported that the mass in her arm had suddenly begun to shrink, and in two weeks, it could no longer be felt through her skin. Although the mass seemed to have disappeared, her medical team performed a procedure to remove the tissue where the lump had been "to ensure disease control," doctors wrote in a report describing the case.

They performed a wide local excision, meaning they removed tissue from the tumor site and a bit of healthy tissue surrounding it, to help prevent regrowth. However, the team spotted no viable cancer cells in the tissue they removed. The tissue showed scarring and inflammation that might be expected following an anti-cancer immune response, but the cancer itself had gone.

One year later, the patient remained cancer-free, the report said.

What makes the case unique: The woman experienced what's known as a spontaneous regression of malignancy, meaning the partial or complete disappearance of cancer without any treatment. Spontaneous regression can also sometimes occur after a patient receives a treatment that wouldn't be expected to effectively shrink a cancerous tumor.

Spontaneous regression is rare across all cancer types, but given that sarcomas are rare at baseline, there aren't many published descriptions of the phenomenon. In their report of the woman's case, which was published in April, the doctors found 32 previous reports of spontaneous regression of malignancy in sarcomas, including nine involving MFS.

Of the 32 cases of spontaneous regression, eight (25%) began after a diagnostic biopsy or some other physical trauma to the tumor, they found. Infections, such as pneumonia, appeared to be the trigger in three cases, and for most of the remainder, a specific trigger couldn't be identified.

The median time from biopsy to regression in these biopsy-triggered cases was less than a month. Regression due to infections had a median response time of five months, while the others regressed in about three months.

Half of the biopsy-associated cases saw complete tumor regression, while the others had near-complete or partial regression. Surgical resection was still performed in most of the cases, with some patients showing no signs of cancer cells in the resected tissue and others having some lingering cells.

The report authors hypothesized that physical disruptions to the tumor's structure during a biopsy releases tumor-related proteins into circulation that can then be spotted by the immune system. Simultaneously, the biopsy summons immune cells to the tissue by triggering a wound-healing process.

This chain of events may expose the tumor to the immune system while also spurring a local immune reaction at the tumor site. The scarring and inflammation evident in the patient's resected tissue may support that hypothesis.

That said, "the observation of a regressing sarcoma presents a clinical trap. It may tempt the clinician to cancel surgery," the case report authors wrote. "However, our systematic review reveals that while some regressions are complete, many are partial or transient. Furthermore, in the biopsy group, nearly 40% of resected specimens still contained residual tumor cells despite clinical regression."

They recommended removing the tissue where the tumor had been regardless of the regression, in case some cancer cells persist. The authors also told New Scientist that they hope to unravel exactly what happens in these rare regressions in order to replicate it through some sort of treatment.

For more intriguing medical cases, check out our Diagnostic Dilemma archives.

This article is for informational purposes only and is not meant to offer medical advice.

A strange divergence is happening in the diagnosis of colorectal cancer: Older people, who are most at risk from the disease, are seeing fewer cases while people under 50 are seeing more.

These diagnoses are often devastating, as younger people also tend to go longer between first experiencing symptoms and getting diagnosed, meaning most of their cancers are caught in a late stage that is more difficult to treat.

"Almost all my patients are my peers, many of whom have young kids or are pregnant themselves or navigating the challenges of just establishing their careers," Dr. Geoffrey Buckle, a gastrointestinal medical oncologist at University of California, San Francisco Health, told Live Science. "They're hit with these obviously extremely scary diagnoses."

But what's driving this rise in young people? Doctors and researchers think some change that occurred after the 1960s is to blame, likely a shift in people's environments or lifestyles. Perhaps offering a clue as to the culprit, recent research also suggests that, whatever the factor, it primarily affects cancers of the rectum and the lowest part of the colon.

The rise of colorectal cancer in young adults

There were about 158,850 new cases of colorectal cancer diagnosed in the U.S. in 2026, according to the American Cancer Society (ACS). Over 86,000 cases — more than half — occurred in people over 65. But those numbers represent a decline of 2.5% a year in that age group since 2013.

Doctors chalk up the decline in colorectal cancer in people 65 and older up to the success of screening, said Dr. Aasma Shaukat, a gastroenterologist at New York University Langone Health. During routine colonoscopies, which start at 45 years old for people at typical risk, doctors remove precancerous polyps and thus prevent that tissue from becoming cancerous.

At the same time over-65s have seen lower cancer rates, people between 50 and 64 have seen a 0.4% increase per year and people between the ages of 20 and 49 have seen an even more alarming jump of 3% each year. The rise is seen in every racial and ethnic group.

What that translates to, according to research published in ACS's CA: A Cancer Journal for Clinicians, are 24,640 new cases a year for people 49 and younger and 47,600 new cases a year for people 50 to 64.

Most of these cases are what doctors call "left-side" cancers, occurring in the lower colon, which descends down the left side of the body, and the rectum. Between 1999 and 2023, rectal cancer mortality rose two to three times faster than colon cancer mortality across all demographics, according to research presented in May at Digestive Disease Week 2026, a major gastroenterology conference.

Possible environmental factors at play

Cancers arise due to genetic errors, some of which occur randomly when cells divide. And the cells in the gut divide constantly: The entire lining of the colon is shed and replaced every week, Shaukat said. The body has mechanisms to repair the myriad DNA mistakes that happen during this turnover, but when the rate of errors increases too quickly or when repair mechanisms fail, that's when most colorectal cancer occurs.

The environment in the gut can affect both this error rate and the efficacy of repair. Researchers have found that there's a complicated feedback loop between the gut microbiome, meaning the community of microorganisms in the colon, and health factors such as diet, exercise and insulin resistance.

Inflammation also factors into this feedback loop. While inflammation is a necessary immune response that repairs damaged tissue with new cell growth, when it becomes chronic, dividing cells become prone to mutation and overproliferation — in other words, cancer.

The culprits for increased chronic inflammation are many, Dr. Theodore Levin, a researcher and clinical lead for colon cancer screening at Kaiser Permanente Northern California, told Live Science. But "these are all thoughts or hypotheses," he cautioned.

One is the rise in sedentary lifestyles and obesity, which contributes to insulin resistance and, in turn, disrupts the microbial colonies that live inside the intestines. These microbes aid digestion and release compounds that can either promote or reduce inflammation.

Childhood antibiotic use rose after the 1960s, which can also perturb the gut microbiome. Additionally, microbiome-disturbing dietary changes since the 1960s include a rise in sugar-sweetened beverages, Levin said, as well as the introduction of a greater number of ultraprocessed foods, which typically lack the fiber content of fresh fruits and vegetables. Fiber, he said, promotes a diverse gut microbiome that tends to tamp down inflammation. (Fermented foods do the same thing, research suggests.)

Researchers are also concerned about the ubiquity of plastics, Levin added.

Some lab research suggests that colorectal cancer cells can take up microplastic particles and that the takeup of those particles increases the cells' propensity to migrate — at least in a lab dish. That could hint that microplastics make cancer more likely to spread through the body. Some animal studies also find that microplastics hamper immune function, which could theoretically help cancer cells to escape the body's defenses.

Plastic particles might also carry carcinogenic compounds deep into the gut, Levin said. Research is still ongoing, but some evidence links chronic exposure to perfluorooctanesulfonic acid (PFOS), a type of "forever chemical" found in nonstick cookware and firefighting foams, to colorectal cancer risk. Experiments using mouse intestinal tissue finds that PFOS reduces a gut enzyme that protects against cancer while spurring the production of proteins that encourage tumor growth.

But researchers have not yet found "one smoking gun" to explain the rise, cautioned Michael Sapienza, the Chief Executive Officer of the nonprofit Colorectal Cancer Alliance. For example, the results of observational studies of forever chemical exposure and colorectal cancer rates are mixed, with some even finding that more PFOS in the blood actually correlates with fewer colorectal cancer cases.

So while the hypotheses are many, the evidence remains murky. Older adults are exposed to all of these environmental and lifestyle changes, too, so researchers also need to understand why their cancer rates aren't rising along with those in younger people. It could be that the removal of precancerous lesions during colonoscopies are masking what would otherwise be a similar rise in the over-65s. Or perhaps it's early childhood exposure that matters most, a risk factor that the oldest adults escaped.

Raising awareness of the symptoms

Scientists aren't entirely sure why cancers of the lower colon and rectum are rising faster than the "right-sided" cancers of the upper intestines.

The lower and upper parts of the colon are very different, Levin said, even arising from different parts of the embryo in the very earliest stage of development. Cancers on the right side and left side often show different genetic mutations. Left-sided colorectal cancer frequently arise from what researchers call chromosomal instability, or mistakes in how chromosomes split between dividing cells during replication, when cells make a copy of their DNA before dividing. Right-sided cancers are more prone to arise from problems with DNA repair during replication.

These differing pathways could help researchers link environmental and lifestyle factors with the changes that lead to colorectal cancer. But that research will take time. For now, gastroenterologists are hoping to raise awareness about the symptoms of the disease and make sure other doctors think to check younger patients for cancer.

Early symptoms include rectal bleeding, unexplained weight loss, anemia, abdominal pain, blood in the stool, changes in bowel habits and unexplained nausea and vomiting. Unfortunately, many early symptoms of colorectal cancer match those of much less serious conditions. For instance, rectal bleeding can be caused by hemorrhoids, and changes in bowel habits could arise from anything from stress to an infection.

Jenna Scott, 40, of Atlanta was 29 and pregnant when her symptoms started. She didn't get a diagnosis until she was 31. By that time, the cancer was metastatic, having spread to other organs. Scott remains in treatment today.

"I don't know if it would have been as aggressive if they had caught it a year-and-a-half earlier," she told Live Science.

Scott's initial symptom was rectal bleeding, but her doctor brushed it off as hemorrhoids caused by pregnancy. Another classic colorectal cancer symptom, weight loss, seemed like typical postpartum shifts on the scale. Health systems and organizations like the Colorectal Cancer Alliance are working to raise awareness among doctors in all specialties so that they check these symptoms out thoroughly in young people rather than explaining them away.

Although routine colon cancer screenings don't start until 45, patients should be pushy with their doctors to get checked out earlier if they have any telltale symptoms, Sapiena said.

"It doesn't mean you have colorectal cancer," Sapiena said of these symptoms. "But it does mean you need to be your own advocate" and seek screening ASAP.

This article is for informational purposes only and is not meant to offer medical advice.

An Ebola epidemic in Africa has become a public health emergency of international concern, the World Health Organization (WHO) announced on Sunday (May 17).

The Democratic Republic of the Congo (DRC) has reported more than 390 suspected Ebola cases and over 100 deaths in the outbreak, Dr. Jean Kaseya, the director general of the Africa Centres for Disease Control and Prevention, told BBC News on Monday. Two additional cases have also been reported in Uganda.

This particular outbreak is caused by the Bundibugyo virus, one of three species of virus known to spark large Ebola disease outbreaks. There are no licensed therapeutics or vaccines for Bundibugyo virus. However, prompt medical care to treat people's symptoms and stabilise their vitals can improve survival, according to the WHO.

The last two outbreaks of the Bundibugyo virus had case fatality rates ranging from 30% to 50%.

"We have more than 100 people already passed on, and we don't have a vaccine, we don't have medicine available to support," Kaseya told BBC News.

"This is my biggest worry because we need to see how to stop the transmission and we are working with the government of DRC and the government of Uganda to stop the transmission of this outbreak," Kaseya added.

At least six Americans were exposed to the virus while in the DRC, although it's unclear at this time whether any of them are infected, CBS News reported.

The outbreak doesn't meet the criteria for a pandemic, as COVID-19 did in 2020, according to the WHO. However, in its Sunday statement, the WHO described the outbreak as "extraordinary" and warned that it is potentially much larger than currently reported.

The WHO declaration indicates the outbreak has a high risk of cross-border spread and could require international cooperation to contain. It also enables the WHO to issue guidance about how countries should address the issue.

Ebola is an often fatal disease that spreads from animals, such as fruit bats and chimpanzees, to humans; people can get infected after close contact with the bodily fluids of infected animals. Ebola can also spread from person to person via contact with infected bodily fluids. Early symptoms include fever, fatigue, headache and muscle pain, which can make it difficult to distinguish from other common diseases, like malaria.

A healthcare worker was the first known suspected case and fatality in the current outbreak; their symptoms started on April 24. In total, at least four healthcare workers have died during the outbreak so far, highlighting gaps in control measures and the potential for health facilities to amplify the disease, according to the WHO.

Lab testing confirmed the virus behind the outbreak to be Ebola on May 15. Cases in the DRC have been reported across three different areas in the Ituri Province in the northeast of the country, which borders Uganda. The two confirmed cases in Uganda affected people who had recently traveled from the DRC.

Factors such as the DRC's humanitarian crisis, high population movement and its large network of informal healthcare facilities compound the risk of the disease spreading, the WHO cautions. The same factors came into play during a large Ebola epidemic that occurred in the eastern DRC between 2018 and 2020. That epidemic resulted in more than 3,300 confirmed cases and 2,299 deaths, but it was driven by the Zaire ebolavirus — a viral species for which there are vaccines.

There is ongoing conflict in the Ituri province, restricting where disease surveillance teams can travel, limiting the deployment of rapid response teams and compromising the secure transport of lab samples, according to the WHO. Health officials also fear that the disease could spread to even more countries in the region, with the DRC's neighboring countries considered to be at high risk. To the north and east, those countries include the Central African Republic, South Sudan, Uganda, Rwanda, and Burundi.

"The event requires international coordination and cooperation to understand the extent of the outbreak, to coordinate surveillance, prevention and response efforts, to scale up and strengthen operations and ensure ability to implement control measures," Tedros Adhanom Ghebreyesus, the WHO Director-General, said in the statement on Sunday.

In the aftermath of the hantavirus outbreak on the cruise ship MV Hondius, many of the 150 passengers are currently being monitored or undergoing up to six weeks of quarantine, based on the virus's lengthy incubation period. Public health authorities have emphasized that person-to-person transmission of Andes virus — the only type of hantavirus known to spread between humans — is rare and associated with "close and prolonged contact."

But there's no clear and consistent definition of what that means.

Some health agencies are using definitions of close contact from the COVID-19 pandemic to define exposure risk in this outbreak. In the case of the U.S. Centers for Disease Control and Prevention, that's a distance of 6 feet (1.8 meters) or less from a symptomatic patient in an enclosed space, for 15 minutes or more. But scientists and public health officials agree that Andes virus is a lot less contagious than SARS-CoV-2, the virus that causes COVID-19.

The World Health Organization says high-risk contacts include "intimate partners, household members, and persons with prolonged close indoor exposure."

When it comes to precautions healthcare providers should take while caring for patients, personal protective equipment (PPE), such as a high-quality face mask, is recommended.

"In terms of any kind of recommendations for taking care of patients, you'd err on the safe side," said Dr. Dean Blumberg, chief of the Division of Pediatric Infectious Diseases at the University of California, Davis (UC Davis). "That's why the recommendations are to use N95s [respirators designed to filter at least 95% of airborne particles] and to do airborne precautions for those patients."

Airborne diseases are those that spread when infectious particles remain suspended in the air and cause disease after being inhaled by others; COVID-19, tuberculosis and measles are examples of airborne diseases. Airborne spread may occur over short or long distances and may involve either small or large infectious particles that the infected person expels.

When it comes to Andes virus, it's known that people can get sick after breathing in tiny bits of infected rat droppings, urine or saliva floating in the air — which may have been disturbed while someone cleaned a room, for example. People have also caught the virus after dining indoors near an infected person. For some experts, that points to some degree of spread through the air. But if it does occur, that doesn't mean this mode of spread is super common.

"There's quite a bit of concern about this genotype that is transmitted from person to person, but in Argentina, it's been here for decades and the outbreaks are contained," said Juan Diego Pinotti, a postdoctoral researcher for Argentina's National Council of Research, based at the Institute of Animal Diversity and Ecology at the National University of Córdoba.

"What we know is that it's not common," Blumberg added. "Otherwise, there would be [more] person-to-person outbreaks in Argentina. And really just a handful of events have been described."

The largest documented Andes virus outbreak took place from late 2018 to early 2019 in Epuyén, a Patagonian town of around 2,400 people. The outbreak began when one person experiencing fever attended a birthday party with about 100 guests. Five people sitting near them at the party went on to develop symptoms in the following weeks, leading to a chain of infections, with 34 confirmed cases and 11 deaths by the outbreak's end.

Argentine researchers studying the outbreak identified three patients as "superspreaders," the source of 21 cases ‪—‬ over 60% of the outbreak. Laboratory investigations found these patients had liver damage, as well as higher viral loads than the other infected individuals.

The timing of when symptoms began seemed to be a critical factor in transmission: In more than half of the cases, transmission could be traced to a single day when the infected person first developed fever and then came into contact with another person, who later became ill.

While the Epuyén outbreak demonstrates Andes virus's ability to spread between humans under certain conditions, experts caution against overinterpreting its transmissibility.

"There were 94 other people at the party, and they didn't get the virus," Blumberg said. "And there were 82 healthcare workers who cared for the infected patients, many without using masks or any other PPE, and they didn't get infected either."

Then there's the case of a woman who, in 2018, carried Andes virus to Delaware after being infected in Argentina. Over 50 people were monitored after potentially being exposed to the virus, but none developed the infection.

Keeping the definition of "close and prolonged contact" somewhat vague might be most useful from a public health messaging standpoint, Blumberg said. "We don't know exactly the timing or the distance, and that's probably going to vary depending on the stage of the illness of the person who's infected and how symptomatic they are," he said.

The environment of a cruise ship — where passengers have significantly more close contacts than they might in daily life — is what likely allowed the virus to spread, he added.

"You're going to be at increased risk for every infection, including something like this that's not very transmissible," he said. "I think it's the cruise ship that really allowed this to happen in an unusual way."

This article is for informational purposes only and is not meant to offer medical advice.

Six years after COVID-19 first made headlines, an antiviral pill has finally been shown to stop users from developing the disease after being exposed to the virus.

The drug, called ensitrelvir, was originally approved for use in Japan as a treatment for COVID-19, and it has now been approved as a preventative treatment, too. Now, promising late-stage trial results have been published as regulators in the U.S. and Europe consider whether to follow suit, Nature reported.

While SARS-CoV-2 is no longer prompting global lockdowns, the virus still poses a significant threat to a large proportion of the population, especially older adults and people with compromised immune systems. But while antivirals like Pfizer's Paxlovid have been developed to reduce disease severity and viral load once an infection has started, nothing has so far proven effective at preventing the disease after exposure to the virus.

Now, ensitrelvir, developed by Japanese pharmaceutical company Shionogi, has been shown to significantly reduce the risk of developing the disease, according to research published Wednesday (May 13) in The New England Journal of Medicine.

The trial specifically focused on exposures from household contacts, a common source of SARS-CoV-2 spread. So if your roommate got sick, you could take ensitrelvir in addition to distancing yourself from them at home.

Ensitrelvir works by blocking a key enzyme that the virus relies on to make new copies of itself. This enzyme is also targeted by Paxlovid. But unlike Paxlovid, ensitrelvir was shown to significantly reduce the risk of developing COVID-19 symptoms compared to a placebo among those who had been exposed to the virus.

The newly published trial looked at more than 2,000 people who lived with people who got infected with SARS-CoV-2 between June 2023 and September 2024. Roughly half of the participants were given a five-day course of ensitrelvir while the other half were given a placebo. Neither the participants nor the researchers knew who had been given which pill, making the trial "double-blinded."

While 9% of those given the placebo within 72 hours of exposure developed COVID-19 symptoms, only 2.9% of those who took ensitrelvir became symptomatic.

The trial runners also tested participants for SARS-CoV-2 up to the tenth day out from exposure: Only 14% of those who received the drug tested positive — with or without symptoms — compared to 21.5% of those who received the placebo.

There was no real difference in side effects between the ensitrelvir and placebo groups; in fact, slightly fewer people in the ensitrelvir group reported adverse events (15.1% compared to 15.5%). Reported adverse effects included temporary and reversible reductions in "good" cholesterol and higher levels of fat in the blood.

The researchers note that their trial did not consider factors that might influence the degree of household transmissions, such as the size of the household and whether or not participants were social distancing. The medication was also not tested on pregnant women or those taking medications that could interact with the drug.

"This is really the first clear demonstration in a well-performed phase III placebo-controlled, double-blind trial that we actually have an agent that is easily administered orally and effective if taken in a timely fashion for protecting individuals who are exposed to COVID-19 in the household setting," first study author Frederick Hayden, a professor of medicine and pathology at the University of Virginia, told MedPage Today.

Beyond households, he said that the drug would likely also protect patients in the case of COVID-19 outbreaks at nursing homes and long-term care facilities. It's just that those uses weren't expressly included in the trial.

Ensitrelvir, known by the brand name Xocova, was approved by Japan's health ministry for treatment of mild-to-moderate COVID-19 infections in March 2024 and as a means of preventing the disease in March 2026. It has also been approved in Singapore.

Shionogi submitted the drug for U.S. Food and Drug Administration approval in September 2025. A decision by the U.S. regulator is expected in June, according to Medpage Today.

This article is for informational purposes only and is not meant to offer medical advice.

When a cluster of hantavirus infections struck the cruise ship MV Hondius, about two dozen American passengers were on board. At least seven disembarked before health authorities were informed of the outbreak and headed home to the United States; 17 others remained on the ship for several weeks and have only just been repatriated. Meanwhile, a few Americans who had never been on the ship may have been exposed to the virus while on board an international flight.

Officials with the World Health Organization (WHO) say they've been in consistent communication with the U.S. Centers for Disease Control and Prevention (CDC), coordinating plans for the American passengers and exchanging technical information about hantaviruses. But this is an unusual time for the CDC, and the agency is not behaving as it usually would in such outbreaks, Jodie Guest, senior vice chair of epidemiology at Emory University's Rollins School of Public Health, told Live Science.

The U.S. is no longer a WHO member state, and the CDC has endured deep staffing cuts at the hands of the second Trump administration. The agency has been slow to issue public statements about its efforts to manage the hantavirus outbreak, and on the few occasions they've spoken with the press, CDC representatives have often been vague or imprecise.

Live Science spoke with Guest — who led Emory's COVID-19 Outbreak Response Team within Georgia and advised Atlanta city officials during the mpox outbreak — about the country's management of this outbreak. We discussed whether the CDC, once considered the world's premier public health agency, may no longer be equipped to handle infectious disease outbreaks.

Nicoletta Lanese: What is different about how the CDC is responding to this outbreak compared with prior ones?

Jodie Guest: I definitely believe that the CDC's response is less visible than we would normally anticipate. CDC normally plays a leadership role and is extremely involved in the original investigation, as well as decisions about how to move people, etc., and WHO took the lead on that, in CDC's absence.

NL: WHO officials have said they're communicating with CDC leaders. But is there less communication than we'd expect?

JG: I can't speak to what communication they've had, but what I can say is that we were multiple weeks into this outbreak before CDC issued any sort of announcement about it. Additionally, it was only last Friday [May 8] that they put out a health alert to the HAN, the Health Alert Network, to clinicians in the United States. [HAN is the CDC's primary method of sharing time-sensitive, urgent public health information with officials, doctors and labs.]

While it's unusual to not have had that health alert sent out much earlier, I will say the risk to the general population is so incredibly low [in this instance]. That HAN is important to go out as a matter of procedure, but at the same time, we don't anticipate clinicians will be seeing people with hantavirus that are not already under surveillance.

The low transmission rate of the virus is definitely working in our favor, on that.

NL: What do you think is behind the CDC's delayed response?

JG: I think one of them is our removal from the WHO. So, when the U.S. left the WHO in January, that really changed our relationship, being at the table with leadership decisions and helping design protocols, surveillance, etc.

I do believe that CDC employees were there as the last disembarkment happened [on May 10 in the Canary Islands]. But generally, we would see the CDC taking the lead on how that disembarkment would happen, where they would go, how we would transfer people, and the overall international set of protocols.

There's certainly a huge amount of workforce reductions that have happened at CDC, as well as a kind of a back-and-forth with the workforce [being fired and rehired]. So some people have not been consistently employed; some people have been brought back. But there are generally about 18% fewer CDC employees than we previously saw, including outbreak investigators and specialists for things like cruise ship sanitation and port health.

NL: Thinking back to prior outbreaks, is there a good comparison to draw to this current situation? I was thinking of the Ebola cases in 2014, for instance.

JG: I do think that Ebola is probably the best example. There's a lot of differences between the two diseases, but from a response model standpoint, the CDC's posture for Ebola was an extremely large amount of global leadership. And at this point in time for hantavirus, I would say the international leadership is limited, and it's mostly domestic monitoring — which is extremely important; I do want to highlight that.

So I think it's reduced visibility and influence, as opposed to leading a global response.

NL: Given the U.S. is taking a back seat, do you think that's hindered the WHO's response at all?

JD: I think that there was some slow uptake at the beginning, and I don't know that that's anything other than hantavirus not being what you would anticipate on a cruise ship. You know, the original case was not tested for hantavirus; testing for hantavirus is not common and not available in all locations. It's not a routine clinical test. With all of those things, it doesn't matter who was leading the effort; that's going to delay everything. It's not going to be in your top diagnostic list of things to be looking for.

But I do think that there was some additional lag that happened that perhaps the CDC could have filled in. It's a counterfactual, so we will never know for sure. But I also believe that the WHO's efforts in their surveillance and their consistent communication has been excellent. They have been very, very communicative about what is happening, and they have been doing a wonderful job taking the lead on this.

NL: In the immediate term, do you feel the sluggishness we're seeing from the CDC places Americans in danger? Or is it more of a long-term issue?

JG: I think we have a response model problem. But at this point in time, I wouldn't say that this had any impact on the actual disease risk, including the care of the people who were passengers on that ship. So that's the great news. The immediate impact of these changes for the disease burden is really very, very low.

It's more about the visibility of response and strategic initiatives for the next thing that will happen that is most concerning. My biggest concerns are about our preparedness in times when we don't have an outbreak. Our systematic response in regards to how we're always looking for signals of something that is amiss — we want to make sure that is a fully staffed and fully capable group at the table with all the international leadership, all doing the same thing. Our surveillance systems are critical to the health of our population.

Big picture, I would say at the moment, we're less prepared for contagious pathogens and outbreaks than we normally anticipate being. Part of that is our withdrawal from WHO and not being a leader in the conversations but instead being a secondary method of getting information.

NL: Compared with our previous relationship with the WHO, what are we missing out on?

JG: Membership in WHO means that you get the early warning messages before they are available for public consumption. When you're not a member, you cannot be guaranteed that you have access to that. You don't have access to the immediate real-time surveillance and contact tracing data that you'd have had if you were a member.

It also means you're not part of the leadership of thought, and so you don't get to be part of the conversations about how we should disembark from this cruise ship, etc. We no longer have scientists who are embedded in the WHO-led teams that include virus sequencing, field investigations and things like that.

By no means do I think the WHO is actively keeping information from the CDC. I don't want that to be the message — but membership in WHO is critical. It's critical for thought leadership, but it's also critical for speed and depth of information and the flow of that information.

NL: Are there any pathogens you're particularly worried about regarding future outbreaks?

JG: I don't have any that I would name — you know, I would not have put hantavirus on a bingo card for 2026. And so, I wouldn't put a list together, but I would say that we are spinning out outbreaks like this more commonly, given our close contact with each other, our decreasing vaccine rates for some things, and just our global travel patterns. These factors are incredibly important to take into account, as well as climate change.

NL: Do you think the CDC could regain its capacity quickly, given investment, or could it take a long time to rebuild?

JG: I hope it will be in short order. There are extraordinary scientists that are still employed at CDC, who are the best of the best at work like this. My concern is it does take longer to build back something that was dismantled than it takes to keep something going.

I also have two other concerns. We've lost a lot of really important leadership at CDC and some very high-level experts, based on the current climate. That is unfortunate, to lose thought leaders. Then, going with that, the impact on the pipeline of new people going into public health — it is the exact time where we need everyone in public health to join us, but we do have a lot of concerns from students: "Will there be a career for me in this?" And the answer is absolutely yes, but we need to make sure we are showing them that.

In a moment when there is less investment in the public health infrastructure in the United States, you can understand why they would have questions.

NL: I assume that concern also extends to international students coming to the U.S. to train?

JG: Absolutely. When you make it harder to teach and to partner with other people in public health, that is going against what we know are the best practices. Public health is a team science. We need to all be doing this together to move the health of everyone forward. We cannot look at one particular area and say we're only going to focus on that without recognizing that the health of people everywhere affects all of us.

NL: One message leaders keep reiterating in this current outbreak is that "this is not COVID." Could you compare the two viruses?

JD: A couple of huge differences between the two: First of all, hantavirus is a known virus. We do have experience with it. It is also a rare virus. COVID was a novel virus [SARS-CoV-2] that we were learning about in real time in front of everyone. It also was not rare once it began; COVID is extremely transmittable from person to person.

What we call the R0 [pronounced R-naught], which is the reproductive number, is very high for COVID. It is very low for hantavirus. One infected person with the Andes strain [the type of hantavirus implicated in the cruise outbreak] will infect maybe 1.19 people, additionally. So the transmission rate is very, very slow, which is a good thing.

[In a previous outbreak, the median R0 across the whole outbreak was 1.19, while it was around 2.1 at the outbreak's start and 0.96 after containment measures were employed.]

The fatality rate of COVID at the beginning was, unfortunately, quite high, but it never reached the fatality rate of what we see with hantavirus, either.

Another comparison with COVID is, because so few people get [hantavirus], we don't need to be worried about mutational changes the way we saw with COVID. The more people that have it, the more ability a virus has to mutate, and we just don't have enough cases of hantavirus to be concerned about the instability of the virus and it mutating.

NL: During a past outbreak in Argentina involving transmission at a birthday party, the R0 of the Andes virus was estimated to be higher. What makes the difference there?

JD: The more general R0 [of 1.19] is aggregated across our traditional, although unusual [infrequent], outbreaks of Andes virus. The one at the birthday party in Argentina was a bit higher because of the close contact in the situation. You don't often see an outbreak like this, where multiple people are going to have that level of close contact.

I think that's the role that the cruise ship is also playing in this particular outbreak. Again, cruise ships are not where we would think about hantavirus, but given that it came onto a cruise ship, there was this closed environment where, particularly in the weather that they were in, where people were not outdoors all the time. And so you were inside, in close quarters, and more people ended up being a close contact than we would normally expect to see.

NL: With the Andes virus, what degree of interaction is a concern? And how is "close contact" defined?

JD: For hantavirus, it appears to be about a 24-hour window at the onset of symptoms that someone has enough virus that they're shedding to transmit to another person. So, it's a fairly small window.

But "close contact" in previous hantavirus outbreaks and this one so far does appear to be contact where you are sleeping in the same room with someone, sharing meals for long periods of time in a smaller space than the entirety of a cruise ship, for example, [or] if you are a health professional who has been taking care of a person during that time period. So it's about prolonged time together during that window when you're most likely to transmit the virus to another person.

NL: Would "prolonged" mean a couple of hours?

JG: I don't actually know that we have a better definition on hours. When we think of a person who shares a bedroom with someone else, those are long hours that you're together, but it doesn't necessarily have to be eight hours.

In the Argentina outbreak with the birthday party, they knew how long people were in this room at this birthday party, and there's actually even tracking of exactly where everyone was situated at the tables while they were consuming food, which is another great way to transmit if it's a respiratory illness and the room is closed. [The index patient in that case was reportedly at the event for 90 minutes and had a fever.]

All of those things are going to contribute to this close contact. Close contact outdoors is really different than close contact indoors.

NL: How are we confident that asymptomatic spread isn't a likely scenario?

JG: We've not seen any human-to-human transmission from someone who's been asymptomatic. So as long as people are remaining asymptomatic, their risk of transmitting it to another human appears extremely low, if not nonexistent.

It's what we would call just basic surveillance, "shoe leather" epidemiology. It's tracking all these cases [during outbreaks]. To wrap back to the HAN, this is one of the reasons why it's important that a health alert does go out; while we don't anticipate there would be cases that aren't related to the cruise ship, we would need to know if there are any.

So the monitoring tracks each individual person who you had contact with and then ranks the type of contact it is. Doing that monitoring while people are asymptomatic, as well as if and when they become symptomatic — it is that tracking during the asymptomatic time frame that helps us feel confident that we've not seen any transmission.

NL: So, in past outbreaks, it has always come back to a symptomatic person?

JG: Yes.

NL: Do you have any final messages you'd like to share?

JG: I will just highlight one more time that, while we may be somewhat conspicuously absent from the international efforts, this does not appear to have impacted the general health of Americans at this point in time. So that's the good news.

Editor's note: This interview has been lightly edited for length and clarity. Live Science spoke with Jodie Guest on May 12, 2026; developments in the hantavirus outbreak that took place after that date may not be reflected.

This article is for informational purposes only and is not meant to offer medical advice.

Climate change is likely to shift the distribution of virus-carrying rodents, potentially increasing the risk of spillover, when viruses make the jump from animals to humans.

This will likely expose populations to diseases that they haven't encountered before and raise the risk of outbreaks, researchers warn.

The hantavirus cluster on the cruise ship MV Hondius has put the rodent-borne disease into the global spotlight. While countries in South America, especially Argentina and Chile, have been dealing with hantavirus for decades, there's been a recent uptick in infections, according to the Argentine ministry of health. More than 100 cases of hantavirus disease were recorded between June 2025 and early May 2026, roughly double the number recorded in the previous year.

Hantaviruses are a family of rodent-borne viruses found across the Americas, Europe and Asia. "New world" hantaviruses cause hantavirus cardiopulmonary syndrome (HCPS), characterized by headache, fever and gastrointestinal symptoms, followed by potentially life-threatening respiratory problems. The Andes virus, responsible for the cluster of cases associated with the MV Hondius, is the only hantavirus known to be transmissible between people.

With a case mortality rate of up to 50%, HCPS is considered one of the most severe forms of hantavirus disease, while the infections that strike in Europe and Asia have lower fatality rates.

Climate change is affecting rodent host populations

Scientists studying hantavirus risk in southern South America have so far identified 11 genotypes linked to human disease across 13 native rodent species, said Juan Diego Pinotti, a postdoctoral researcher for Argentina's National Council of Research, based at the Institute of Animal Diversity and Ecology at the National University of Córdoba. Each strain of the virus has evolved within a specific rodent species, enabling that species to carry the virus while not falling sick from it.

The natural "reservoir" for Andes virus, the long-tailed pygmy rice rat (Oligoryzomys longicaudatus), typically lives in the humid forests and shrublands of the southern Andes in Chile and Argentina. The virus is spread to humans primarily through contact with the urine, feces, or saliva of an infected rodent.

Climate models predict that changing weather patterns over the next few decades may expand the long-tailed pygmy rice rat's habitat eastward, toward Argentina's Atlantic coast, where the vast majority of the country's people live.

"More intensive surveillance and testing are needed across provinces, because the virus might be reaching new areas without us finding out," Pinotti, who worked on the models, told Live Science.

El Niño-La Niña fluctuations may further reinforce this pattern. In central and southern Argentina, El Niño years usually bring increased rainfall, which stimulates vegetation growth, meaning rodents have access to abundant food sources and shelter, driving rapid population expansion.

"That in turn interacts with what the winters are like," said Veronica Andreo, a researcher for Argentina's National Council of Research, working at the Gulich Institute. "If the winter is more severe, fewer mice might survive. If it's a bit milder, more mice can survive and pass on to the next generation."

Beyond hantavirus: other viruses on the rise

A recent study focusing on a different family of rodent-borne viruses, known as arenaviruses, drew similar conclusions. New World arenaviruses, which include Guanarito virus in Venezuela and Colombia, Machupo virus in Bolivia and Paraguay, and Junin virus in Argentina, can cause severe hemorrhagic fevers with high hospitalization rates. Fatality rates range from about 5% to 30%, depending on the virus strain and the patient's overall health and healthcare access.

Researchers used machine learning to map how climate projections, changing rodent populations, and shifts in people's land use could alter the distribution and transmission of arenaviruses in South America over the next 20 to 40 years. They found that climate-induced shifts in temperature and precipitation, coupled with the expansion of agriculture, will likely increase spillover risk as viruses spread into new regions.

The researchers hope the models will help public health officials understand the need to prepare for outbreaks of these diseases as climate change drives more extreme weather patterns.

"These are high impact diseases, but they are fairly neglected in terms of how much research is ongoing about them, or whether they are on the radar of public health officials," said study lead author Pranav Kulkarni, a veterinary epidemiologist at the University of California, Davis (UC Davis) Weill School of Veterinary Medicine.

Notably, the Centers for Research in Emerging Infectious Diseases, part of the U.S. National Institutes of Health, would have been researching these diseases but was shuttered last year.

Continued surveillance is critical

As climate change reshapes disease risk, data gathering and surveillance will be crucial for improving outbreak preparedness. Better regional coordination and data sharing could help countries identify shifting hotspots earlier and build more effective public health responses, said Kulkarni.

"If we can come up with that sort of infrastructure, especially in countries which will probably be affected by this, then there would be more robust modeling, more accurate predictions, and a more informative way of creating health policy," Kulkarni told Live Science.

More research is needed to fully understand the diversity of viral genotypes and rodent species that exist in South America's southern cone, said Andreo. "We still need to understand how all the different reservoirs and viruses interact, and whether the viruses can jump from one reservoir to another," Andreo told Live Science. Some New World hantaviruses, such as the Laguna Negra genotype and the Lechiguanas genotype, are known to have multiple reservoirs.

Additionally, two new hantavirus genotypes have been identified in Argentina in recent years, added Pinotti.

"Always the most important thing is prevention — epidemiological surveillance and education of the population," Pinotti told Live Science. Yet, funding cuts to Argentina's health and science sectors have jeopardized disease surveillance programs, research capacity, and the ability to carry out large-scale, long-term studies into zoonotic and vector-borne diseases.

"When these teams see their operational capacity reduced," Andreo said, "the entire early warning network that makes it possible to detect outbreaks before they escalate is weakened."

This article is for informational purposes only and is not meant to offer medical advice.

A new artificial intelligence (AI) model can help doctors detect pancreatic cancer up to three years before physicians typically spot tumors on CT scans, a new study suggests.

The program, described April 28 in the journal Gut, was used to analyze almost 2,000 CT scans that had been previously cleared as "normal," bearing no signs of disease. The tool identified tiny irregularities in the structure of the pancreas that later developed into tumor tissue.

Early detection is the single biggest factor in pancreatic cancer patients' survival. Therefore, the model could potentially enable physicians to begin effective treatment while the disease is still curable, the study authors said.

A chance to detect cancer early

Pancreatic cancer is one of the deadliest cancers.

"The five-year survival rate [in the U.S.] is about 12% to 13% because of our inability to detect it at a time when therapeutic options could work their magic," study co-author Dr. Ajit Goenka, a radiologist and nuclear medicine specialist at the Mayo Clinic in Rochester, Minnesota, told Live Science. The early stages of pancreatic cancer often don't trigger any symptoms, so the disease is often advanced at the point of diagnosis.

Although doctors' ability to catch and treat many other cancers has improved in recent decades, no corresponding breakthrough has been seen in pancreatic cancer. Diagnosis typically involves a combination of tissue sampling and imaging tests, including CT scans. But by the time tumors are visible via these methods, the cancer is often terminal.

However, there may be earlier markers of the disease.

"The basic science research tells us that the process of cancer development is not something that starts six months earlier," Goenka said. "It starts 10 to 15 years earlier, which means that there was a signal in the pancreas and that signal was outside the purview of human detectability."

Leveraging AI to recognize patterns that humans cannot, Goenka and colleagues developed a tool to amplify that existing signal and identify early signs of disease in CT scans.

The model, dubbed Radiomics-based Early Detection Model (REDMOD), essentially converts the CT scan image into a mathematical puzzle. It first segments the organ, building a 3D model of the pancreas from the 2D images captured by the CT machine. Then, it evaluates the resulting structure pixel by pixel.

"It's taking each and every pixel in that image and it is quantifying the degree to which it differs from the rest of the organ, and then it's comparing that against the controls where you don't expect that change to be present," Goenka explained. "At the end of the day, it's mathematics. It converts that image into a mathematical representation and extracts those mathematical features."

The team tested the model on a sample of 2,000 existing CT scans, which were previously collected for medical issues unrelated to cancer and had all been signed off as normal. About one-seventh of the scans belonged to patients who later went on to develop pancreatic cancer.

The model successfully identified 73% of these early-stage cases, and on average, the scans the model analyzed had been taken 16 months before the person's actual diagnosis.

"The sensitivity gain over radiologists was nearly twofold across the spectrum, and when you look at even earlier — more than two years prior to diagnosis — that sensitivity gain was almost threefold," Goenka said. In other words, the AI tool correctly identified cancer cases earlier than radiologists did, and the earlier in time you look, the greater that performance gap grew.

Next steps

That said, the AI tool has room for improvement. "The radiologist was less likely to flag a healthy patient incorrectly," Goenka noted. The model correctly identified disease-free patients 81.1% of the time, compared with an average of 92.2% for human radiologists. "So there is a complementary role for both of them, for physician expertise combined with AI augmentation."

The study was very well designed and produced some extremely promising results, said Tatjana Crnogorac-Jurcevic, a professor of molecular pathology and biomarkers at Queen Mary University of London who was not involved in the work.

"Such early detection would make a huge change in the clinical workup of the patients," she told Live Science. "Because pancreatic cancer is fairly uncommon, general screening as we have now for colon and breast is not going to be feasible, but there are defined high-risk groups for which surveillance will be possible — individuals with a family history of pancreatic cancer, those with other cancer mutations, and patients with new-onset diabetes."

Goenka hopes the model could be routinely implemented in the clinic within the next five years, and the team is currently running clinical trials to further validate that this detection strategy works in practice.

Looking forward, combining this REDMOD with other diagnostic methods could yield even greater gains in early detection, Crnogorac-Jurcevic said.

"We are developing urine-based tests with exactly the same aim, and having an AI imaging tool to combine with our body fluid biomarkers would be fantastic," she said. "It's highly likely that they will be complementary, which would increase the sensitivity and accuracy of early detection massively."

This article is for informational purposes only and is not meant to offer medical advice.

A cluster of hantavirus cases struck the Dutch-flagged cruise ship MV Hondius as it traveled across the southern Atlantic, stopping at a number of destinations along the way.

American passengers who had been isolated on the ship have now been transported to Nebraska. Plus, several Americans who had disembarked the cruise at an earlier port are being monitored in other states.

Public health authorities' investigations are ongoing. Gaps in knowledge are expected during an unfolding investigation, and as those gaps are filled, we will update you here.

Here's everything you need to know:

• As of May 12, nine confirmed and two suspected cases of hantavirus infection have been associated with a cruise aboard the Dutch-flagged MV Hondius, according to the World Health Organization. The ship departed Argentina on its current voyage April 1. Three people have died.
• After disembarking at Tenerife Sunday (May 10), the remaining passengers and some of its crew on board the MV Hondius have returned on chartered flights to their respective countries. Fifteen American citizens and one British national have been taken to a quarantine facility in Nebraska, where they will be assessed for symptoms and exposure risk. Two people have been transported to Emory University's Serious Communicable Diseases Unit in Atlanta.
• Additionally, several dozen people disembarked the ship on St. Helena on April 24. These passengers include seven Americans, who are now being monitored across five states.
• Hantavirus infections in humans are relatively uncommon, but when they do occur, they can be deadly. Most hantavirus infections in humans stem from exposure to infected rodents. However, the hantavirus behind this outbreak — the Andes virus — is also known to be able to spread between people.
• This outbreak poses little risk to the general public, the WHO and U.S. CDC emphasize.

This blog is for informational purposes only and is not meant to offer medical advice. The blog is no longer live.

What is hantavirus, and how risky is this outbreak?

Hantaviruses are a family of viruses carried by rodents. Hantavirus infections in humans are relatively uncommon, but when they do occur, they can be dangerous, with fatality rates ranging between 1% and 50% depending on the type of hantavirus. No specific treatment exists to cure infections, but prompt medical care can improve patients' chances of survival.

While most hantaviruses cannot pass between people, one specific type, known as the Andes virus, can. The Andes virus is the type of hantavirus that laboratory tests point to being behind this cluster. Health authorities are now working to analyze the virus's DNA to compare its sequence to that of Andes viruses involved in past outbreaks.

The World Health Organization and the U.S. Centers for Disease Control and Prevention have said the risk posed to the public from this cluster remains low, although they continue to monitor the situation.

For more on the Andes virus, you can read health editor Nicoletta's story here. And for more background information on hantaviruses, broadly, you can read this story.

World Health Organization says risk to the public is "low"

The World Health Organization (WHO) just held a news conference to discuss the hantavirus cases.

The WHO has been working with collaborating centers to identify the type of virus behind the outbreak, as well as investigate suspected and confirmed cases and perform contact tracing. The agency has also been quick to quash fears that the outbreak could spark a global pandemic.

"This is not SARS-CoV-2 [the virus that causes COVID-19]. This is not the start of a COVID pandemic. This is an outbreak that we see on a ship," Maria Van Kerkhove, the WHO's interim director of epidemic and pandemic preparedness and prevention, said at the news conference.

"This is not the same situation we were in six years ago," she continued. "It [the Andes virus] doesn't spread the same way like coronaviruses do. It's very different. It's that close, intimate contact that we've seen, and most hantaviruses don't transmit between people at all."

"The Andes virus, which has been identified here ‪—‬ we've seen some human-to-human transmission," she added. "I want to reiterate [that] the actions that are being taken on board are precautionary to prevent any onward spread, and so there's a lot that is being done right now to be able to try to minimize the risk even further."

"Viruses don't care about politics"

Both Argentina and the U.S. recently withdrew from the World Health Organization (WHO). In the face of this outbreak, "I think they will reconsider their positions," said Tedros Adhanom Ghebreyesus, the WHO's director-general. "Viruses don't care about our politics, they don't care about our borders, and they don't care about all the excuses that we may have."

When asked whether U.S. health authorities are participating in the ongoing investigation, several WHO representatives confirmed that the U.S. Centers for Disease Control and Prevention is providing helpful technical support and expertise and communicating with WHO leaders daily.

Where did the infection come from?

WHO Director-General Tedros Adhanom Ghebreyesus told reporters at the news conference that the WHO is working with health authorities in Argentina to investigate where the first two people to contract the virus got infected. Those passengers, a husband and wife, marked the first two deaths associated with the outbreak.

Prior to boarding, "the first two cases traveled through Argentina, Chile and Uruguay, on a bird-watching trip, which included visits to sites where the species of rat known to carry Andes virus was present," Ghebreyesus said.

The Andes virus is transmitted to humans mainly through contact with the long-tailed pygmy rice rat (Oligoryzomys longicaudatus). People may pick up the virus through exposure to the rat's urine, feces or saliva. For instance, they may accidentally touch the rat's feces and then touch their face, or breathe in viral particles that get released into the air when rodent droppings get disturbed in the environment.

Monitoring of potential contacts

People who have potentially been exposed to the virus are being "actively monitored," according to Dr. Abdirahman Mahamud, director of the World Health Organization's (WHO) Health Emergency Alert and Response Operations. What that looks like depends on the country where the case contacts are currently located; some may be quarantined in facilities, while others may receive a daily visit from healthcare workers, for instance, he said.

The WHO recommends that contacts be monitored for six weeks, as the incubation period ‪—‬ the time between when someone is exposed to the virus and when symptoms begin —‬ of hantavirus infections can be that long. Known cases that are symptomatic are being isolated and cared for in hospitals.

Genetic sequencing underway

Genetic material from the confirmed hantavirus cases is now being sequenced. This will enable experts to compare the genetics of the hantaviruses involved in this cluster to those that caused past outbreaks.

As of yet, there's "no indication" that there's anything particularly unusual about the hantaviruses themselves, but it is notable that the outbreak is taking place on a cruise ship, said Anaïs Legand, the WHO's technical officer of viral hemorrhagic fevers. A ship is a unique environment where people from many places are in close quarters.

Deceased passenger remains on board

The body of the third person to die in the outbreak — a woman who passed away on board May 2 after developing pneumonia — is still being stored on the MV Hondius. WHO officials are in contact with the cruise operators about safe storage and eventual transport of the remains.

Viral videos of distressed passengers

When asked about videos of distressed cruise passengers circulating online, Maria Van Kerkhove, the WHO's interim director of epidemic and pandemic preparedness and prevention, confirmed that WHO officials had seen the videos.

"This is quite frightening for those that are on board," she added, noting that health authorities are coordinating with the ship's captain to ensure those on the ship receive the best medical and psychological care possible.

Additionally, once the medical status of everyone on board is assessed, the WHO will also coordinate with each person's home country to safely repatriate them.

Clarity on cruise itinerary

Various social media posts and videos have been casting suspicion on when the MV Hondius actually departed Ushuaia, Argentina. The WHO's website notes April 1 as the departure date, while the Africa CDC website states March 20. So I reached out to the cruise operator, Oceanwide Expeditions, about the discrepancy.

A spokesperson shared that, from March 20 to March 30, the ship traveled from Ushuaia to Antarctica and back. Then, from April 1 to April 24, it traveled from Ushuaia to the island of St. Helena. Then, between April 24 and May 4, it traveled from St. Helena to Cape Verde.

When asked if any potential hantavirus cases were associated with that first leg of the trip, the spokesperson directed me to the WHO's official statements. The earliest known symptomatic case was on April 6 and involved a man who had boarded the ship April 1.

Both the man and his wife — the second passenger to get sick — had traveled in Argentina, Chile and Uruguay prior to boarding, and officials currently suspect that that's when they got exposed. Both individuals have since died.

Catching a killer — how to trace a rare and deadly virus

Andes virus outbreaks are rare, with only a handful documented since the 1990s. This makes investigations into clusters of cases like those associated with the MV Hondius tricky. However, one outbreak that hit southern Argentina's village of Epuyen in 2018 may prove to be informative.

The Epuyen outbreak infected 34 people and led to 11 deaths due to hantavirus pulmonary syndrome, in which a hantavirus attacks the lungs.

According to a 2020 study published in The New England Journal of Medicine, the Epuyen cases stemmed from three separate superspreader events. The first occurred when the first infected person, or index patient, attended a birthday party with around 100 others.

The 68-year-old man, who was feverish and feeling poorly at the time, attended for about 90 minutes and passed the infection to several people who had been sitting near him. Additional cases followed as several of these individuals or their close contacts attended other events while sick.

In many cases, infected people passed on the virus on the first day they began feeling feverish, the study authors determined. That hints that the infection might be at its most contagious when those early symptoms emerge — meaning the close confines of a ship could be an ideal location for the virus to spread in that time window.

Airline crewmember being tested for hantavirus

Earlier today, the Dutch outlet RTL Nieuws reported that an airline crewmember had been admitted to Amsterdam University Medical Center (UMC) after having brief contact with an infected person from MV Hondius.

The infected person — the woman whose husband was the first to die on board — had felt ill when she disembarked on the island of St. Helena. Her condition worsened during a flight from St. Helena to Johannesburg, South Africa. She then attempted to board a flight from Johannesburg to Amsterdam, but "due to the passenger's health condition at the time, the crew decided not to allow the passenger to board the flight," KLM has said.

The woman subsequently died and her case was later confirmed to be a hantavirus infection.

During her brief time on the Amsterdam-bound plane, the sick passenger interacted with the flight attendant who is now at Amsterdam UMC with mild symptoms of illness. Doctors are expecting to receive the attendant's test results later today, which will reveal if she has a hantavirus infection, CNN reported.

(For background, sustained close contact is typically required for Andes virus infections to transmit between people, so it's unclear whether this brief encounter would be particularly risky.)

Trump admin axed Andes virus research

Ten research centers that made up the Centers for Research in Emerging Infectious Diseases (CREID) were terminated last year after their funder, the National Institutes of Health, deemed their work "unsafe" and "not a good use of taxpayer funding." It turns out that one of those centers had a pilot program aimed at studying the Andes virus, which has now been implicated in the MV Hondius outbreak, Scientific American reported.

The pilot program was aimed at learning more about the inner workings of the Andes virus, including how it spreads from rodents to people. Some $100,000 would have likely been dedicated to this project in Argentina, sources told SciAm.

In the long run, the goal of CREID's many projects was to better understand germs capable of jumping from animals to people in order to respond quickly and effectively to future outbreaks. While the Andes virus pilot program likely wouldn't have stopped this cruise ship outbreak, its loss could very well undermine scientists' broader efforts to understand hantaviruses and the threat they might pose in the future.

As always: Vet your sources

A word of advice from your friendly neighborhood health editor: As investigations into the hantavirus cluster continue, emerging data may be incomplete and the narrative of who did what (and when) could also be fuzzy. A degree of uncertainty is expected in the midst of an unfolding investigation, because if all was known, there would be nothing to investigate.

With that in mind, be wary of bad actors, particularly on social media, who take advantage of uncertainty to sow doubt or stir up conspiracies. I understand the impulse to seek out more information and to pose questions when something is unclear or underexplained — but that is distinct from spreading misinformation and disinformation.

In short, if a given social media user's main goal is to gain views and monetization, rather than to provide clarity and well-sourced expertise, their input is unlikely to serve you.

Arizona Department of Health Services gives a hantavirus update

About half a dozen Americans are among the passengers who have disembarked the MV Hondius amid the outbreak. One of those individuals is now in Arizona.

The Arizona Department of Health Services provided an update Thursday (May 7) at 3 p.m. local time. During a virtual news conference, they said they had received notice on May 5 that an Arizona resident had been on the cruise ship. That individual's county-level health department is now monitoring their symptoms, checking in daily about their body temperature and any other signs of illness.

The person is currently asymptomatic, and based on the information available, it doesn't seem likely that they had much, if any, close contact with the infected individuals on the ship, officials said. The local health department will determine if the person requires testing, and likely, that wouldn't happen unless they develop symptoms, said Kenneth Komatsu, a state epidemiologist with Arizona Department of Health Services. That's in part because an asymptomatic person could very well come back negative on a test, he noted.

If the individual were to eventually develop symptoms, testing, contact tracing and quarantining would follow, along with monitoring of household contacts, Komatsu and other spokespeople suggested.

I asked whether the U.S. Centers for Disease Control and Prevention (CDC) had provided guidance on how the department should handle the situation.

"As CDC is currently working at a fast pace to put out some recommendations and guidance, most jurisdictions that have any individuals potentially exposed, they've been in contact with CDC sometimes two, three times a day to answer our questions," said Dr. Joel Terriquez, medical director of the Bureau of Infectious Disease Services and the Bureau of Immunization Services with the Arizona Department of Health Services.

"Guidance is currently being developed and an official recommendation will be coming out soon," he added. Komatsu also confirmed that public-facing CDC guidance was forthcoming. When asked which CDC department was heading the effort, he pointed to the Division of Global Migration Health within the National Center for Emerging and Zoonotic Infectious Diseases.

The health department emphasized that the risk to Arizonans remains low. "We just want to make sure that the message is clear," Terriquez said. "This situation is very low risk to the general public."

Other cruise passengers in the U.S.

In addition to the person in Arizona who recently returned from a cruise on the MV Hondius, several people in Georgia and California are facing the same situation.

On May 7, the Georgia Department of Public Health told Live Science via email that it is "monitoring two Georgia residents who returned home after disembarking from the MV Hondius, the cruise ship at the center of a hantavirus outbreak. The individuals are currently in good health and show no signs of infection. They are following current recommendations from CDC."

Also on May 7, the California Department of Public Health told Live Science via email that the department is coordinating with local health officials to monitor returning travelers, as needed.

"There is no information that the California residents are ill or infected. In order to protect patient privacy, CDPH cannot disclose the travelers' residences or other information. At this time, the risk to public health in California is low," the statement concluded.

Seventeen Americans remain on the MV Hondius, The New York Times reported.

Dutch flight attendant tests negative for hantavirus infection

Good morning, everyone. We're back with some possible glimmers of good news, as the KLM Royal Dutch Airlines flight attendant who had been in contact with a woman who died from a hantavirus infection has tested negative for the virus, Reuters reports.

Both Reuters and the health newsletter Inside Medicine (which got the scoop) cite the World Health Organization (WHO) as their source, although we're still awaiting firsthand confirmation.

“As you know, the incubation period is long and although she is negative for now, she might turn positive in the future,” Tedros Adhanom Ghebreyesus, the WHO's director-general, told Inside Medicine via a text message.

"It's very much, we hope, under control": U.S. sets lowest emergency level response to the virus

Those were the words of President Donald Trump when asked if he'd been briefed on the virus.

"I think we're going to make a full report about it tomorrow," he continued. "We have a lot of people — a lot of great people are studying it. It should be fine, we hope."

The U.S. Centers for Disease Control and Prevention (CDC) has classified the situation as "Level 3," its lowest level of emergency response, ABC News reported Thursday (May 7). That grade of emergency response is typical for this stage of a disease cluster, and it means the agency is actively monitoring the situation.

U.S.' slow hantavirus response offers a troubling glimpse into future pandemic preparedness, experts say

The U.S. Centers for Disease Control and Prevention's (CDC) delayed response to the hantavirus cases suggests the U.S. is "ill prepared" for future health crises, including pandemics, The New York Times (NYT) reports.

“We should be able to deal collectively with a hantavirus outbreak much more quickly and effectively than this is happening,” Stephanie Psaki, a public health expert at Brown University and former coordinator for global health security in the Biden administration, told the NYT. "It can get much harder than this."

President Donald Trump signed an executive order to withdraw the U.S. from the World Health Organization (WHO) on Jan. 20, 2025, and officially withdrew Jan. 22, 2026. Consequently, the CDC is not immediately notified of updates from the WHO relating to emerging health threats, Dr. Daniel Jernigan, former director of the CDC's National Center for Emerging and Zoonotic Infection Diseases, told the NYT. Jernigan resigned from his post in August 2025.

The U.S.' decision to leave the WHO "makes both the United States and the world less safe," WHO officials wrote in a statement published Jan. 24, 2026.

When asked at yesterday's (May 7) news conference on the hantavirus cluster whether U.S. health authorities are taking part in the ongoing investigation, WHO representatives confirmed that the U.S. CDC was working with the WHO daily.

"Viruses don't care about our politics, they don't care about our borders, and they don't care about all the excuses that we may have," said Tedros Adhanom Ghebreyesus, the WHO's director-general.

Where is the cruise ship now?

The MV Hondius is currently about 200 miles (over 300 kilometers) off the west African coast, due west of the Mauritanian port city of Nouadhibou. Sailing northwest, it is expected to dock at Tenerife in the Canary Islands Sunday (May 10).

Health officials on the Spanish island are preparing to perform careful evacuations of the ship's passengers into an isolated, cordoned-off area.

What will happen when the ship arrives in Spain?

The MV Hondius is set to reach the Spanish island of Tenerife Sunday (May 10), the Associated Press reported May 8. The U.S. will send a plane to the Canary Islands to repatriate the 17 U.S. citizens on board the ship.

Measures are being put in place to ensure the ship's passengers do not come into contact with local residents during the evacuations from the cruise ship.

"They will arrive at a completely isolated, cordoned-off area," Virginia Barcones, Spain's head of emergency services, said at a May 7 news conference. "They will board vehicles that are isolated and under guard and will proceed to a section of the airport that will be completely cordoned off. They will board the aircraft and depart."

"I am saying this so that the people of the Canary Islands, the men and women living there, can rest assured that there will be absolutely no possibility of contact at any time," she concluded.

British authorities identify new suspected case

U.K. authorities have identified a new suspected case of hantavirus on the South Atlantic island of Tristan da Cunha, according to a May 8 statement by the U.K. Health Security Agency.

The individual, a British man, likely disembarked from the MV Hondius when it made a stop there on April 15. He is currently in the hospital while his spouse is isolating, U.K. officials said. The island's population is a little over 200 people.

"We shouldn't be alarmist; we should be realistic," hantavirus expert says

This is what Gustavo Palacios, a hantavirus expert and professor of microbiology at the Icahn School of Medicine at Mount Sinai in New York who documented a previous outbreak of the disease, told El País in a story published today.

Palacios led a study of the November 2018 to February 2019 Andes virus outbreak in the village of Epuyén, in Argentina's Chubut province. There were 34 confirmed cases and 11 deaths during that outbreak, with human-to-human transmission occurring during a "superspreader" birthday party that resulted in four generations of infections.

Palacios told El País that these findings were met with skepticism. "It's been a David versus Goliath story, trying to convince the global virology community" that there can be chain infections from the Andes virus, he said in a translated interview.

However, Palacios noted that the conditions of the 2018 Argentine outbreak are "quite different" from the currently unfolding situation.

"We must keep in mind that we know little about the Andes virus because it hasn't been studied much," he said. "We've never seen how it behaves on a ship."

Despite the lack of data, the conditions on the ship are theoretically worse than the 2018 outbreak in Argentina. "A ship is inherently a place that facilitates contagion," Palacios said.

Woman self-isolating in Alicante

A woman is self-isolating in the Spanish city of Alicante after traveling on a flight "close to" a woman who died with a hantavirus infection, Spain's health minister, Mónica García, wrote in a translated statement on X.

The woman "has reported mild symptoms compatible [with the disease] and is being preventively isolated while the National Microbiology Center analyzes the diagnostic samples that will be taken from her," García wrote.

"We reiterate that the risk for the general population remains very low," she concluded.

2 Singapore residents test negative for hantavirus

Two Singapore residents who were on board the MV Hondius have tested negative for hantavirus, Singapore's Communicable Diseases Agency has announced.

The two residents, a 67-year-old and a 65-year-old, had returned to Singapore from St. Helena on the same flight as a person who later died from the virus.

The agency conducted tests "with multiple samples collected from the individuals, and confirmed that hantavirus, including the Andes virus, was not detected," officials wrote.

However, due to the long incubation period of hantaviruses, those who test negative now can turn positive later. This means that the pair will remain in isolation.

"As a precaution, the two individuals will be quarantined for 30 days from the date of last exposure, and testing will be conducted again before release from quarantine," they continued. "They will then undergo phone surveillance for the remaining monitoring period of 45 days from the date of last exposure, which is the maximum incubation period for hantavirus exposure."

The agency says the risk to the general public in Singapore is low.

All passengers left on MV Hondius currently without symptoms, WHO says

That's according to Anais Legand, the World Health Organization's (WHO) technical officer, who is giving an update on how the WHO is running its contact tracing.

"They will be asked to take their temperature every single day for 42 days. They will be asked to check every day for other symptoms like feeling unwell or a headache," Legand said. "They will be provided with someone to contact. If they're not feeling well, it's up to the national authorities where people will go next."

Where did the cruise stop?

Since leaving Ushuaia, Argentina, April 1, MV Hondius has visited numerous islands.

The ship first visited South Georgia and Tristan da Cunha, before sailing on to St. Helena. They stopped at St. Helena April 24, with this being the final destination for some passengers on board.

The ship then continued on to Ascension Island, leaving April 27. The vessel arrived in Cape Verde waters, off the west coast of Africa, on May 3 but was denied plans to dock.

MV Hondius is now sailing to the Canary Islands, a Spanish archipelago off the west coast of Africa, where it is due to arrive by early Sunday.

Is hantavirus on the rise?

The answer is complicated: Cases of hantavirus infection did rise in parts of the Americas in 2025, according to a Dec. 19, 2025 report from the Pan American Health Organization (PAHO) and the World Health Organization (WHO). But the pattern is far from uniform across the rest of the world.

Argentina routinely experiences the highest number of hantavirus cases in the Americas, and hantavirus cases are also rising there. Argentina's ministry of health reported on May 5 that there have been 101 confirmed hantavirus cases since June 2025, according to the Associated Press (AP). That's an increase from the 69 cases (11 confirmed and 58 under investigation) in Argentina in 2024.

"Argentina has become more tropical because of climate change, and that has brought disruptions, like dengue and yellow fever, but also new tropical plants that produce seeds for mice to proliferate,” Dr. Hugo Pizzi, an infectious-disease specialist and epidemiologist at the National University of Córdoba in Argentina, told the AP. "There is no doubt that as time goes by, the hantavirus is spreading more and more."

The joint PAHO and WHO report found that Argentina and Brazil experienced "an increase in [hantavirus disease] lethality" in 2025, compared with recent averages. Bolivia and Paraguay have seen substantial increases in hantavirus infections compared with historical averages.

Between 1993 and 2023, there have been 890 cases of hantavirus disease in the U.S., of which 35% of cases were fatal. (The U.S. first started surveilling hantavirus infections in 1993.) It is unclear whether the incidence is increasing in the U.S., as data covering 2024 and 2025 is currently unavailable, according to the PAHO and the WHO.

The European Center for Disease Prevention and Control reported 1,885 confirmed cases of hantavirus infection across 28 European Union/European Economic Area counties in 2023. Along with 2020, 2023 marked the lowest case rate for the 2019-to-2023 period.

Hantavirus disease cases in East Asia, particularly in China and the Republic of Korea (South Korea), have declined in recent decades, according to the WHO.

Hantavirus evacuation has a short time window due to weather conditions

Spanish officials have told reporters that they have a fairly narrow weather window to get passengers off MV Hondius and onto their flights home.

"The only window of opportunity we have to carry out this operation is around 12 o'clock on Sunday morning and until conditions change from Monday," Alfonso Cabello, spokesperson for the government of the Canary Islands, told reporters today (May 8).

"Otherwise, the ship must leave and no operation could be carried out again in theory ... until the end of May," Cabello added, citing adverse weather conditions such as wind and swell.

If all goes well, the passengers will be flown back to their home countries under quarantine conditions soon after the vessel arrives Sunday (May 10).

US citizens on board will receive repatriation flight

The 17 American citizens who are currently on board the MV Hondius will receive a repatriation flight arranged by the U.S. Department of State, a spokesperson for the department told Reuters today (May 8).

"The Department of State is ​closely tracking the hantavirus outbreak on ​a Dutch cruise ship in the Atlantic Ocean and maintaining close contact with ​the cruise ship staff, Americans ​on board, and U.S. and international health ‌authorities," the spokesperson said in a statement.

The Department of State is in contact with the Americans on the ship and will provide consular assistance as soon as it docks at Tenerife, Spain, according to the spokesperson.

There is no vaccine for hantavirus, but research is promising

Currently, there is no effective vaccine against any hantavirus, and the future of research into vaccines against the virus family is uncertain, especially in the U.S.

Scientists at the U.S. Army Medical Research Institute of Infectious Diseases have been working on hantavirus vaccines since the 1980s, virologist Jay Hooper told Nature News. Hooper's team has already completed Phase I clinical trials of a vaccine that protects against the Andes virus ‪—‬ the only hantavirus type that has been shown to spread between humans ‪—‬ that has been linked to the MV Hondius cluster. But the team has not identified a region with enough cases to run the full clinical trial that would allow them to meet licensing requirements for a vaccine.

"Right now, we are pushing from the research side, but there is no strong external pull, so progress is slower than it could be. It is frustrating — like pushing a rock up a hill for years," Hooper said.

Scientists at the University of Bath in the U.K. are also working on a vaccine that targets the hantaan hantavirus, which is found primarily in East Asia. To date, they have tested their vaccine in laboratory and animal models, but they have yet to advance to Phase I trials in humans. And scientists at the University of Guelph in Canada are working to develop vaccines that prevent hantavirus cardiopulmonary syndrome caused by the Andes virus and other "New World" types.

But experts told NBC News that hantavirus vaccine research has repeatedly stalled, in part because outbreaks tend to affect impoverished countries where pharmaceutical companies aren't investing their resources.

"Our funding agencies don't put a lot of money into this, because it's likely not to cause the next epidemic or pandemic," Sabra Klein, a molecular microbiologist at the Johns Hopkins Bloomberg School of Public Health, told NBC News.

CDC will escort Americans on MV Hondius to quarantine in Nebraska

The U.S. Centers for Disease Control and Prevention (CDC) has dispatched staff to meet American passengers aboard the MV Hondius in the Canary Islands. From there, the passengers will be escorted back to the U.S. aboard a charter flight to quarantine. "One source said the charter is a specialized aircraft with a biocontainment unit, similar to those used during Covid-19 evacuations," CNN reported. The passengers will then quarantine in Nebraska, which hosts the federally funded National Quarantine Unit and the Nebraska Biocontainment Unit.

"Nebraska Medicine and UNMC [University of Nebraska Medical Center] remain in close coordination with national partners regarding the evolving situation with the hantavirus outbreak on the MV Hondius cruise ship," Nebraska Medicine said in a statement. "We cannot discuss specific communications at this time, but our specialized teams, including the Nebraska Biocontainment Unit and National Quarantine Unit, are staffed and ready, if needed, to safely provide care while protecting our staff and the community."

Other countries are scrambling to contain the outbreak as concerns grow about what will happen when the MV Hondius docks in Tenerife, part of Spain's Canary Islands. The ship is predicted to dock at the port city of Granadilla Sunday (May 10), but Oceanwide Expeditions, the ship's operator, has said this is subject to change. The company also stated that no symptomatic individuals are currently on board and that it has "preparations regarding our point of arrival, quarantine and screening procedures for all guests, and the onward travel plans for all guests and affected crew are being led by organizations from a number of countries."

Spain finds South African exposed to woman who died of hantavirus

In a translated X post, Spain's health minister, Mónica García, announced, "We confirmed that the second person who traveled on the plane at the same time as the Dutch woman from the MV Hondius cruise ship, who later died from hantavirus in Johannesburg, has been located."

According to García, the South African woman is currently asymptomatic in South Africa, after having stayed a week in Barcelona.

"According to the epidemiological investigation carried out, during her stay she stayed alone in a hotel and did not have close contacts," García posted.

Weekend updates

Live Science is signing off for the weekend, but our reporters and editors will continue to track the outbreak as it evolves. If anything major changes, we'll pop on here to let you know — but barring that, we'll be back to blogging at a regular clip on Monday (May 11).

If you have any questions about hantaviruses that you'd like us to address, reach out to ls-editors@futurenet.com with the subject line "Reader hantavirus question." (Questions without the appropriate subject line may be missed or deleted.)

WHO Director-General to people of Tenerife

On May 9, Tedros Adhanom Ghebreyesus, the director-general of the World Health Organization (WHO), shared a message with the residents of the Spanish island of Tenerife, where MV Hondius is anticipated to make port Sunday (May 10).

"It is not common for me to write directly to the people of a single community, but today I feel it is not only appropriate, it is necessary," he wrote. "I want to speak to you directly, not through press releases or technical briefings, but as one human being to another, because you deserve that."

"I know you are worried. I know that when you hear the word 'outbreak' and watch a ship sail toward your shores, memories surface that none of us have fully put to rest. The pain of 2020 is still real, and I do not dismiss it for a single moment. But I need you to hear me clearly: this is not another COVID. The current public health risk from hantavirus remains low. My colleagues and I have said this unequivocally, and I will say it again to you now."

Tedros continued by reiterating that there are no symptomatic passengers on board MV Hondius, that a WHO expert is on the ship, and that Spanish authorities have prepared a plan to safely disembark the passengers and crew. He thanked Prime Minister Sanchez for Spain's "act of solidarity and moral duty" in receiving the MV Hondius passengers and crew.

"I intend to travel to Tenerife to observe this operation firsthand, to stand alongside the health workers, port staff, and officials who are making it happen, and to personally pay my respects to an island that has responded to a difficult situation with grace, solidarity, and compassion. Your humanity deserves to be witnessed, not just acknowledged from a distance."

You can read Tedros's full statement on the WHO's social media platforms.

WHO update on May 9 — still eight cases

In a live social media update on Saturday, Maria Van Kerkhove, the WHO's interim director of epidemic and pandemic preparedness and prevention, clarified that the number of confirmed and suspected hantavirus cases associated with MV Hondius is still eight. There had been some discussion of a potential ninth case, but testing has now confirmed that case was negative, she said.

On Friday, the WHO said six of the eight cases have now been confirmed to be hantavirus, while the final two cases are suspected to be.

WHO update on May 9 — repatriation flights planned Sunday and Monday

In the live social media update on Saturday, Maria Van Kerkhove of the WHO said plans are in place to disembark the remaining passengers and crew from MV Hondius on Sunday, and that repatriation flights are planned to start transporting people home Sunday and Monday.

The disembarkment will involve MV Hondius anchoring offshore and small boats taking subsets of the passengers and crew from the ship to land. Everyone will undergo a thorough screening and "exposure assessment" to determine what degree of exposure they likely had to the infected passengers on board. Everyone on board remains asymptomatic as of May 9, Van Kerkhove said.

What will happen to the American passengers now that they're back in the U.S.?

Good afternoon, everyone. We're back with more updates regarding the cluster of hantavirus cases associated with the cruise ship MV Hondius.

Following their evacuation onto the Spanish island of Tenerife early Sunday (May 10), the ship's passengers are being repatriated via chartered flights. Seventeen American citizens and one British national have been transported to the U.S.

One member of this group has "mild symptoms," according to the U.S. Department of Health and Human Services (HHS), while another has reportedly tested "mildly" positive on a PCR test, which measures the amount of viral genetic material in a sample. These passengers have now been taken to a specialized facility at Emory University in Atlanta, according to the HHS.

Spain's secretary of state for health, Javier Padilla, noted that this passenger had previously had one inconclusive test and one negative test on board the MV Hondius. During the evacuation, though, each passenger was treated as a possible positive case out of caution.

The remaining passengers are being transported to specialized facilities housed at Nebraska Medicine and the University of Nebraska Medical Center. There, they will be evaluated for symptoms and interviewed about their degree of contact with infected passengers on the ship. The Nebraska Biocontainment Unit on-site is equipped to safely treat any passengers with symptoms. Hantavirus infections can be deadly, and they require prompt treatment to improve patients' chances of survival.

"If they weren't in close contact with someone who was symptomatic, then we're going to deem them 'low risk'" in terms of likelihood of exposure, Dr. Jay Bhattacharya, acting director of the U.S. Centers for Disease Control and Prevention (CDC), said in an interview with CNN. "If they were in close contact, we're going to deem them 'medium' or 'high risk.'"

Following that evaluation, passengers will be offered the option of staying in Nebraska or being safely transported to their home state, if "their home situation allows it," Bhattacharya continued. If transported home, those individuals would then be monitored by their state and local health departments with CDC support.

Bhattacharya noted that the protocols being followed in this situation are the same ones employed during a 2018 event in which one person in Delaware tested positive for the Andes virus, marking the first-ever case in the U.S.

Genetics of the virus appear very similar to past outbreaks, Spanish health minister says

"The first genetic analyses of the MV Hondius hantavirus confirm that it corresponds to the Andes variant that is already known and rule out relevant mutations," Spain's health minister Mónica García wrote in a translated statement on X. "Investigation is helping to reconstruct how transmission occurs and to strengthen epidemiological monitoring."

Tentatively, these initial results are good news, suggesting the virus is not rapidly evolving new abilities — gaining mutations that could make it more contagious, for instance.

"I hope it's fine" — President Trump says "we're in very good shape" on hantavirus

President Donald Trump was asked about the hantavirus during a maternal healthcare event today (May 11) in the Oval Office.

"Now the one thing with this one is that it's much harder to catch. It's been around a long time; people are very familiar with it," Trump said. "So, I hope it's fine. All I can do is what a president can do, which is actually somewhat limited."

"It seems like it is not easy to spread; in fact, in certain ways, it's very hard to spread," he added. "We've lived with it for years — many years — and we think we're in very good shape."

All about hantavirus

Wondering about the symptoms of hantavirus infections or how best to avoid the illnesses? We've just updated our short guide to hantavirus disease.

It includes details of how hantaviruses spread, where they're found worldwide, how infections manifest, what treatments are available, and how deadly the illnesses are.

For the general public, the risk of infection associated with the MV Hondius disease cluster remains quite low, and no particular precautions are recommended at this time. That said, the above article provides general information about how to avoid infection from both infected rodents and other people.

Cruise passengers now at Atlanta hospital

Two passengers who disembarked MV Hondius are now being treated at Emory University's Serious Communicable Diseases Unit in Atlanta, CBS News Atlanta reported.

The Centers for Disease Control and Prevention (CDC) notified the Georgia Department of Public Health that the passengers, who are a couple, were being transported to the containment unit. Video captured Monday morning showed the two patients arriving at the hospital.

A Health and Human Services official said at a news conference that one person was experiencing symptoms of illness but had so far tested negative for hantavirus. The second person is asymptomatic and so is being monitored for any new symptoms.

"Federal healthcare workers are taking every precaution needed in each of these cases, and there is no risk to the public at this time," the Georgia Department of Public Health said.

16 in Nebraska, two in Georgia

To recap: Eighteen passengers — 17 Americans and one British dual-national — who had been on board MV Hondius have now been transported to the U.S.

Sixteen remain in Nebraska, and all are asymptomatic, although one tested positive for hantavirus. The person who tested positive is in the University of Nebraska Medical Center's biocontainment unit, while the others are in its quarantine unit, CNN reported.

The two people described in our most recent post are now being monitored at Emory University's Serious Communicable Diseases Unit in Atlanta. Neither has tested positive for hantavirus, but one is showing symptoms of illness. Per CNN, the transfer to Emory was a part of a contingency plan acknowledging that the University of Nebraska Medical Center's facilities have limited space to hold people for monitoring.

At least 11 additional people are being monitored in seven states. That includes cruise passengers who disembarked before the ship was isolated at sea, as well as a few people who had possible exposures on an international flight.

That brings the total number of people being monitored in the U.S. to 29.

Reader questions, answered (1 of 3)

We received a few questions from readers! We'll answer them in this and the next couple of posts. If you have a question, email us at ls-editors@futurenet.com with the subject line "Reader hantavirus question."

What will happen to the MV Hondius passengers who have now been repatriated?

The answer may differ slightly from country to country, as each is in charge of its own containment protocols, although the World Health Organization (WHO) offers guidance on best practices.

In the U.S., the 18 passengers who were just transported to the country are currently being monitored in specialized centers. Any people who develop symptoms will be provided prompt medical treatment, as early treatment improves patients' chance of survival. After a few days of monitoring, officials will weigh whether those who remain asymptomatic and negative on hantavirus tests should complete their monitoring period at home or in medical facilities. The full monitoring period is 42 days, but it should be noted that it's counted from the last likely point of exposure to the virus.

Reader questions, answered (2 of 3)

What are the symptoms of hantavirus disease, and how can I avoid it?

The answer to those questions and more can be found in this article!

TL;DR, hantaviruses from the Americas — like the hantavirus implicated in this infection cluster — typically cause fever, muscle aches and fatigue at first, as well as chills, headache, dizziness and gastrointestinal issues. The disease can then quickly progress to coughing, shortness of breath, shock and fluid buildup in the lungs, which can ultimately be deadly. Prompt medical treatment is key.

The majority of hantavirus infections are caused by exposure to infected rodents and their pee, poop or saliva. Therefore, precautions that limit your exposure to wild rodents help cut your risk of infection.

Only the Andes virus, a specific type of hantavirus, is known to spread from person to person, and it's implicated in this outbreak. Your chances of encountering someone with an infection are low, but the article linked above describes measures for limiting person-to-person spread, as well.

Reader questions, answered (3 of 3)

Is there anything the general public should be worried about?

In the near term, likely not. From what scientists know about the nature of this virus — and from what we've learned in sequencing its genetic material during this event — the chances of this sparking a large, runaway outbreak are low.

It's worth emphasizing that not all viruses behave the same way, and they don't all carry the same "pandemic potential." Officials have repeatedly emphasized that the risk to the general public is low, adding that "This is not COVID" — and while that's a vague turn of phrase, it rings true in that we know more about this virus than we did about SARS-CoV-2 (the virus that causes COVID-19) when it emerged, and from what we know, the Andes virus isn't nearly as transmissible.

So, I wouldn't recommend being consumed with worry; I would suggest paying attention to the news as it comes and keeping that bigger picture in mind. If anything changes such that it dramatically shifts our impression of this virus for the worse, we'll let you know ASAP.

Now, in the longer term, this event could well raise some alarm bells.

The U.S. has far fewer CDC staff than it used to. It's withdrawn from the World Health Organization. It's axed research funding aimed at better understanding germs that can jump from animals to humans. These changes degrade not only the United States' ability, but the world's ability, to respond quickly to outbreaks. The U.S. has stood as a world leader and major investor in public health for many years, and we're still moving through the transition period of the country stepping down from that role. Scientists have warned that "The Big One," a pandemic to pale COVID-19, could be on its way — and it's that future, big outbreak that I'm personally worried about.

"We expect more cases," says WHO director-general

Dr. Tedros Adhanom Ghebreyesus, the director-general of the World Health Organization (WHO), has just finished a news conference with Spanish Prime Minister Pedro Sánchez in Madrid.

In response to questions from reporters, he said the gap between the first hantavirus case on MV Hondius and its identification means more cases are expected.

"We would expect more cases because, as you may remember, the index case, the first case in the ship, was on April 6," he said at the news conference. "And until the report was confirmed as infectious — that's around April 24 or 25 April — there was a lot of interaction actually with the passengers."

"As you know, the incubation period is six to eight weeks," he continued. "So because of the interaction, while they were still in the ship, especially before they started taking some infectious prevention measures ... we would expect more cases."

Nonetheless, Tedros was careful to reiterate during the conference that there was "no ⁠sign that ⁠we are seeing the start of ‌a larger outbreak."

A dozen hospital workers quarantined after possible hantavirus exposure

Twelve workers at Radboud University Medical Center (Radboudumc) in Nijmegen, Netherlands, have been placed into precautionary quarantine following improper protocol in the handling of a MV Hondius passenger's blood and urine, hospital officials wrote in a May 11 update.

Workers followed a standard procedure instead of a stricter protocol when taking the passenger's blood, while also not obeying the most recent international regulations in the disposal of the passenger's urine.

The hospital workers have been placed into preventive quarantine for six weeks as a precaution.

"Despite the fact that the chance of actual infection is very small, these measures have a major impact on all those involved," Bertine Lahuis, chair of the executive board of Radboudumc, said in a statement. "We regret that this happened in our umc [university medical center]. We will carefully investigate the course of events to learn from this so that it can be prevented in the future."

"Where is the CDC?" Experts troubled by the U.S. government's hantavirus response

President Donald Trump told reporters yesterday that the U.S. was "in very good shape" on hantavirus.

But public health experts are far from convinced, saying that the U.S. Centers for Disease Control and Prevention (CDC) has been missing in action, the Associated Press (AP) reports.

"The CDC is not even a player," Lawrence Gostin, an international public health expert at Georgetown University, told the AP. "I've never seen that before."

The CDC's actions thus far have drawn concern from some experts. The organization did little to act upon last week's developments until late Friday (May 8), and on Saturday (May 9), CDC officials ducked a direct answer to reporters over whether American passengers evacuated from the cruise ship could leave quarantine when they wanted, the AP reports.

This makes the hantavirus outbreak "a sentinel event" that speaks to "how well the country is prepared for a disease threat. And right now, I’m very sorry to say that we are not prepared," Dr. Jeanne Marrazzo, CEO of the Infectious Diseases Society of America, told the AP.

"I don't think this is a giant threat to the United States," Jennifer Nuzzo, director of Brown University’s Pandemic Center, told the AP. But the situation "just shows how empty and vapid the CDC is right now."

Spain confirms positive hantavirus case

A Spanish MV Hondius passenger that gave a "provisional positive" result yesterday has been confirmed positive for hantavirus, Spain's ministry of health wrote in a translated statement on X.

"The patient presented yesterday with a fever and light respiratory symptoms, although they are currently stable and without evident clinical deterioration," ministry officials added.

What do you mean by "symptoms"?

Contract tracing continues around the world as health officials work to find people potentially exposed to hantavirus by MV Hondius passengers. As that happens, we're likely to hear occasional reports of people experiencing "symptoms" and being admitted to hospitals for testing and treatment.

For clarity: People experiencing "symptoms" in this context may well have a different infection; until it's officially confirmed to be hantavirus, it's not worth getting too worried about. The early symptoms of Andes virus infections are fairly generic: fever, muscle aches, fatigue, chills, headaches, dizziness and gastrointestinal issues. In short, they can be flu-like, as can many other respiratory illnesses in their early stages.

A pertinent example is the KLM flight attendant who was briefly exposed to a confirmed hantavirus case, later developed "symptoms," and went to a hospital to be checked. (And that was a good thing to do, on her part.) She ended up testing negative for hantavirus.

We're likely to see more cases like hers before this situation wraps up, so just keep that in mind when you see a scary headline.

Nonetheless, the long incubation period of the virus means that those who test negative now could test positive days or weeks later; it's for that reason that MV Hondius passengers are being monitored for 42 days from their last exposure. We want people experiencing symptoms, alongside those who suspect they had contact with an infected passenger, to get periodically checked out at hospitals. In the event they do have a hantavirus infection, they'll get prompt treatment and be isolated from others before they continue the chain of transmission.

Where is the MV Hondius now? And who's still on board?

The MV Hondius cruise ship is currently passing Morocco as it makes its way to its final destination in Rotterdam, Netherlands.

There are currently 25 crew on board and two medical staff from the Dutch National Institute for Public Health and the Environment (RIVM), according to a new update from Oceanwide Expeditions, the cruise company that owns the ship. None of the staff on board are displaying symptoms associated with hantavirus.

"The vessel is expected to arrive in Rotterdam on either Sunday 17 or Monday, 18 May," the company statement says. "Upon arrival, all crew will disembark and follow quarantine procedures outlined by the Dutch authorities and RIVM."

Following disembarkment, there will be rigorous decontamination of the boat. Additionally, according to an update published yesterday (May 11), the body of the third person to die in the outbreak — a woman who passed away on board on May 2 after developing pneumonia — will also be removed from the MV Hondius.

Hantavirus-carrying rats expected to expand range

The rodent species that carries the Andes virus — the germ implicated in the MV Hondius outbreak — is expected to expand its range in Argentina in upcoming years. That's due, in part, to shifts in weather patterns driven by climate change.

Other rodents that carry viruses capable of infecting people, such as arenaviruses, are also expected to expand their ranges. As these critters seed new territories, the risk of outbreaks caused by these viruses may increase, in turn.

Read more in this news analysis written by Live Science contributor Naomi Mihara.

Illinois investigates unrelated potential hantavirus case

Good morning, everyone. We're tracking the cases of hantavirus associated with the cruise ship MV Hondius and will bring you updates as they arrive.

There have been no new developments on case numbers today — they remain at nine confirmed and two suspected cases reported by the World Health Organization (WHO) yesterday (May 12).

Elsewhere, the Illinois Department of Public Health has announced it is investigating a potential hantavirus case in an Illinois resident in Winnebago County. This suspected case is unconnected to the cluster on MV Hondius, as the individual, who is not seriously ill, is reported to have been potentially exposed to the virus while cleaning a home where rodent droppings were present.

The North American hantavirus is not the same as the Andes virus implicated in the MV Hondius cluster and does not spread between people.

"Typically, we see it [hantavirus] in cases like this one, where someone was cleaning an area where rats may have dwelled, and it may have aerosolized the either urine or feces from the rat that contain[ed] the virus," Dr. Alfredo Mena Lora, an infectious-disease specialist at Saint Anthony Hospital, told ABC7 Chicago.

Between 1993 and 2023, there have been 890 cases of hantavirus disease in the U.S., of which 35% of cases were fatal. (The U.S. started surveilling hantavirus infections in 1993.) It is unclear whether its incidence is increasing in the U.S., as data covering 2024 and 2025 is currently unavailable, according to the Pan American Health Organization and the WHO.

American doctor who tested positive speaks from biocontainment unit

Dr. Stephen Kornfeld, an oncologist and MV Hondius passenger who stepped up to manage the outbreak after the ship's doctor fell ill, spoke to CNN from isolation in the biocontainment unit at the University of Nebraska Medical Center (UNMC).

Kornfeld tested "mildly positive" for hantavirus, according to the U.S. Department of Health and Human Services. (This finding came from a PCR test, which measures the amount of viral genetic material in a sample, and may have returned a result at or just below the threshold of confident detection.)

Kornfeld remains asymptomatic, but he said that in early to mid-April, he and a number of passengers on MV Hondius fell ill with "what felt like a flu," with symptoms that included night sweats, chills, mild respiratory symptoms and fatigue.

"At the time, it felt like this was just some virus," Kornfeld told CNN. "And now, in retrospect, there is a question: Could it have been hantavirus? But it's just speculation; there's no way to really know."

Though he is awaiting further test results and updates from experts at UNMC, establishing a past infection "may not be that straightforward to interpret," Kornfeld added. "So it may never be known if that illness, which others also had, was hantavirus or a typical virus that circulates through a cruise boat."

"Membership in WHO is critical": Emory epidemiologist concerned about United States' outbreak readiness

Throughout this outbreak, public health experts have expressed concern about the United States' response. They've said that the Centers for Disease Control and Prevention has been slow to share information about the outbreak domestically, and that it's not at the helm of the international containment effort, as it usually would be.

I spoke with Emory University epidemiologist Jodie Guest about her assessment of this development and what it reveals about America's overall outbreak preparedness. She said that, in the current outbreak, America's response hasn't placed the general public at increased risk of hantavirus infection, so that's the good news.

But in the long run, she's worried about whether the country will be prepared to surveil and manage outbreaks driven by far riskier pathogens.

In our chat, we also discussed the attributes of the Andes virus that make it less likely to spark a big outbreak, compared to germs like SARS-CoV-2. You can read the interview here.

Dealing with a long incubation period

Symptoms of an Andes virus infection can take a long time to show up following exposure to the germ — about seven or eight weeks, at the longest. That length of incubation is relatively uncommon, though, and more often, people develop symptoms within four to 42 days of exposure. Various factors may affect when a given person becomes symptomatic, Scientific American reported today.

One likely factor is the way the person was exposed — for example, by touching their mouth with hands contaminated with infected rat pee, breathing in bits of infected rat poop, or kissing a person with an active infection. Additionally, the amount of virus, or viral load, someone is exposed to may affect how quickly sickness sets in, with higher viral loads associated with shorter incubation periods.

The Andes virus can circulate in the blood and begin to infect cells without immediately sparking a big immune response, which may help to explain why its incubation period is so long. You can read more about how that lengthy incubation period affects outbreak management at the link above.

Hantavirus outbreak, as told in graphs and maps

CNN has released maps of where MV Hondius stopped along its journey, noting when and where various passengers disembarked and where passengers were recently repatriated. Additionally, a chart details the numbers and nationalities of passengers who disembarked at the island of St. Helena on April 24, before the ship was isolated at sea and the World Health Organization was alerted to the infection cluster.

41 people in 12 U.S. states are being monitored for hantavirus

A total of 41 people are being monitored for hantavirus in the United States, the Centers for Disease Control and Prevention (CDC) said in a Thursday afternoon news conference, according to news reports. That total is up from the previously reported 29.

The individuals being monitored include the 18 MV Hondius passengers who returned to the U.S. on May 11 via a flight from the Canary Islands. They are now at specialized facilities in Nebraska and Georgia, Dr. David Fitter, the CDC's incident manager for the hantavirus outbreak, said during the conference.

According to USA Today, the other two groups of people that Fitter identified were seven passengers who left the ship prior to the World Health Organization being alerted to the outbreak, as well as 16 people who may have been exposed to a symptomatic person on a flight between the island of Saint Helena and Johannesburg. (That symptomatic person was the second known case in the outbreak and died shortly after arrival in Johannesburg.)

Although the CDC has not released specific information about where people in these latter two groups are being monitored, various state health departments have acknowledged that they have residents being monitored for hantavirus. USA Today compiled a map of states that have provided information about individuals who have potentially been exposed to hantavirus and are being monitored. The states include Washington, California, Arizona, Texas, Nebraska, Kansas, Minnesota, Georgia, Virginia, Maryland and New Jersey. There's also a potential case in Illinois that's known to be unrelated to the cruise ship; that individual was exposed to rat droppings while cleaning.

(Note that state health departments have not specified the cities or counties these individuals are in, to maintain their privacy.)

There are currently no confirmed cases of the Andes virus — the type of hantavirus implicated in the outbreak — in the U.S., according to the CDC. There is one person in the U.S. with an inconclusive test result that bears confirmation, the WHO has said. The virus does not pose a pandemic threat, Reuters reported, and health officials and experts have emphasized the general public's risk of infection is low. Given the virus's long incubation period, however, more cases might emerge in the next month.

'Not a major transmission crisis at all': Leading epidemiologist weighs in

Renowned epidemiologist Michael Osterholm — whom Live Science has previously interviewed about infectious disease risk and pandemic preparedness — says this outbreak is unlikely to spark the world's next pandemic.

In an interview with Center for Infectious Disease Research and Policy (CIDRAP) News, Osterholm emphasized that "respiratory person-to-person transmission is not new with the Andes hantavirus." It's been observed in at least three prior outbreaks since 1996. That said, in the grand scheme, this form of transmission is a relatively rare occurrence.

"There have been over 100 cases of hantavirus in Argentina this past year and no reports of person-to-person transmission. It’s a rare phenomenon, but it happens," Osterholm said. When person-to-person spread does happen, it likely involves superspreaders who, for whatever reason, transmit the bug at high rates, he went on.

He pointed to a case in 2018 in which a woman traveled to Argentina and then back home to Delaware, carrying the Andes virus with her. This was the first confirmed case of the Andes virus in the United States. Over 50 people potentially got exposed, but none fell ill — she wasn't a superspreader. Instances like hers raise the idea that not everyone has the same risk of spreading the virus to others, Osterholm said.

Later in the interview, he noted that people are currently focused on the 42-day incubation period of the virus. But, he said, the median incubation period is 18 days, meaning about half the cases would be anticipated in the first 18 days after exposure. Based on the timeline of the cruise, that hints there's unlikely to be many more additional cases related to exposure on board the ship.

"I believe the current outbreak is not a major transmission crisis at all," Osterholm said. You can read the full interview at the link above.

Scientists to investigate outbreak's original source

A study involving 20 countries is being launched to better understand how long Andes virus persists in the human body following infection and how long people remain contagious, ABC reported Friday.

Additionally, the World Health Organization is collaborating with partners in Argentina to investigate the movements of the first cases prior to boarding MV Hondius in order to pinpoint a potential source of infection. Argentine scientists will also head to Ushuaia, the port city where the ship departed, next week to collect and test samples.

Local officials in Ushuaia haven't detected any confirmed hantavirus cases there in the past or during this current outbreak, so they aren't convinced the exposure occurred nearby, according to ABC.

Editor's note: Further updates on the hantavirus cluster can be found on Live Science's live blog, which will provide the latest information on the ongoing investigation.

Confirmed and suspected cases of hantavirus infection have struck eight people on a cruise ship in the Atlantic Ocean, and now, laboratory tests have pointed to a specific kind of hantavirus at fault.

Hantaviruses are a large family of viruses carried by rodents, such as rats. It's relatively uncommon for them to cause infections in people, but when they do, they can be deadly — depending on the type of hantavirus at hand, fatality rates range between 1% and 50%. There is no specific treatment to cure hantavirus infections, but prompt medical care to manage symptoms can improve patients' chance of survival.

Once inside the human body, most types of hantavirus can't then pass to another person. However, "one of them is known to be able to transmit itself from one human being to another," Dr. Manuel Schibler, head of the virology laboratory at Geneva University Hospitals, said in a video translated from French to English. "It is called Andes virus."

Upon learning about the cluster of illnesses associated with the cruise ship and identifying hantaviruses as a possible culprit, health authorities, including the World Health Organization (WHO), already suspected that the Andes virus might be to blame. As of now, three people who became sick on the cruise have died, including one with a confirmed hantavirus infection; additionally, several other people are receiving care for suspected infections and two people in medical care have confirmed infections.

At a May 4 news conference, Maria Van Kerkhove, the WHO's interim director of epidemic and pandemic preparedness and prevention, said the agency was operating under the assumption that the Andes virus was behind the illnesses and taking necessary precautions to prevent further cases. That includes isolating suspected cases, since the Andes virus is the only hantavirus known to spread between people.

Now, the Centre for Emerging Viral Diseases of the Geneva University Hospital, a WHO collaborating center, has examined a clinical sample from one of the people infected on the cruise. The patient is being treated at the University Hospital of Zürich, where he was immediately placed in isolation upon arrival.

The patient had "responded to an email from the ship's operator informing the passengers of the health event, and presented himself to a hospital in Zurich, Switzerland, and is receiving care," the WHO posted May 6 on X. His case brings the total number of hantavirus cases associated with the cruise to eight, including three confirmed and five suspected infections.

The hospital staff followed the WHO's lead, also operating under the assumption that the patient had an Andes virus infection. "Our result has confirmed this hypothesis," Schibler said of their laboratory results, which were announced on May 6.

"It is clear we would have preferred it to be a hantavirus for which [human-to-human] transmission is not documented," Schibler said. "Unfortunately, that is not the case."

The silver lining is that, to scientists' knowledge, the Andes virus doesn't spread as easily as many major pathogens. "It is not a virus that is as transmissible through the respiratory tract as COVID or the flu. So that's rather reassuring information," Schibler said. Nonetheless, it will be important to remain vigilant and isolate any suspected cases efficiently, to limit additional spread as much as possible, he said.

Schibler and colleagues now aim to sequence the virus's genetic material to gather more information about its subtype, but this data likely won't affect the immediate care for patients with hantavirus infections, he noted.

On X, the WHO added that, in addition to the Geneva University Hospitals, South Africa's National Institute for Communicable Diseases detected Andes virus in clinical samples from the cruise ship passengers. (The WHO's statement doesn't note which patient's samples were analyzed by the National Institute for Communicable Diseases, but there is one patient with a confirmed hantavirus infection currently receiving care in Johannesburg.)

Investigations are ongoing and will include further analysis of the suspected and confirmed cases, the WHO has stated. Three people with suspected cases were evacuated from the ship on May 5 to be transported to the Netherlands for medical care. Van Kerkhove has said that the plan for the rest of the people onboard is to travel to the Canary Islands, where authorities will conduct a full epidemiologic investigation, disinfect the ship and assess the remaining passengers.

This article is for informational purposes only and is not meant to offer medical advice.

Editor's note: Further updates on the hantavirus cluster can be found on Live Science's live blog, which will provide the latest information on the ongoing investigation.

Two confirmed and five suspected cases of hantavirus infection have struck passengers of a cruise ship in the Atlantic Ocean.

Of the seven affected individuals, three have died and one is currently receiving intensive medical care, the World Health Organization (WHO) said in a May 4 statement. Hantavirus infections have been officially implicated in one of the deaths and in the intensive-care case. Three additional individuals are currently experiencing mild symptoms or are asymptomatic at this point.

What are hantaviruses?

Hantaviruses are a family of viruses typically carried and spread by rodents. People can catch the germs if they are exposed to the urine, droppings or saliva of infected animals, or rarely, if an infected animal bites them. One type of hantavirus, called the Andes virus, is capable of spreading from an infected person to other people, but such cases of human-to-human transmission have been rare. The specific type of hantavirus involved in the cruise ship cases has not been disclosed.

Hantaviruses can cause two types of serious infection: hantavirus pulmonary syndrome (HPS) and hemorrhagic fever with renal syndrome (HFRS). The former infection can take up to eight weeks to develop after exposure to the virus; it starts with fever, chills and fatigue and progresses to potentially deadly organ dysfunction and respiratory issues. The latter infection takes about two to four weeks to set in and causes fever, headache, gastrointestinal issues, kidney dysfunction and, sometimes, internal bleeding.

HPS is deadlier than HFRS, with a fatality rate of 38% in patients who develop respiratory symptoms of the disease. The fatality rate of HFRS varies depending on the specific hantavirus a person is infected with, with fatality rates ranging from 1% to 15%.

Treatments for hantavirus disease aim to manage a patient's symptoms; there is no cure for the infections.

"While there are no specific treatment nor vaccines for hantavirus infections, early supportive care and immediate referral to a facility with a complete ICU can improve survival," the WHO states.

What happened on the cruise?

So far, only one of the illnesses connected to the cruise has been confirmed to be a hantavirus infection, according to the cruise's operator, Oceanwide Expeditions. The company, which offers expedition-style voyages to the polar regions and sub-Antarctic, detailed the situation in statements released May 3 and May 4.

The affected vessel is the MV Hondius, which departed from Ushuaia in Argentina on April 1, was carrying a total of 147 individuals, including 88 passengers and 59 crew members. After departure, it traveled across the southern Atlantic, stopping in mainland Antarctica, South Georgia, Nightingale Island, Tristan da Cunha, St. Helena and Ascension Island. The ship is currently off the coast of Cape Verde.

"The extent of passenger contact with local wildlife during the voyage, or prior to boarding in Ushuaia remains undetermined," the WHO noted in its May 4 update. The agency has been told there are no rodents on the ship itself.

On April 6, a passenger developed fever, headache and mild diarrhea, and five days later, he died on board of respiratory distress. His cause of death could not immediately be determined and no laboratory tests were conducted.

On April 24, that deceased passenger and his surviving wife, both Dutch nationals, were dropped off on St. Helena to await repatriation to the Netherlands. She had gastrointestinal symptoms at the time. The following day, she boarded a flight to Johannesburg, South Africa, and her condition worsened, and she died upon arrival at an emergency department on April 26. As of May 4, her case was confirmed to be caused by a hantavirus via a laboratory exam, the WHO reported..

These two passengers had traveled in South America, including in Argentina, prior to boarding MV Hondius.

Meanwhile, on April 24, another passenger got sick with symptoms of fever, shortness of breath and signs of pneumonia. He was evacuated from Ascension Island to South Africa for treatment after his condition worsened. The passenger, a British national, remains in intensive care in Johannesburg and is in "critical but stable condition." Laboratory tests have confirmed that a hantavirus infected this patient.

Back on MV Hondius, another passenger died on May 2 after developing a fever on April 28. Her condition had progressed to pneumonia before she died.

Then, three additional people on board developed fever or gastrointestinal symptoms.

Maria Van Kerkhove, the WHO's interim director of epidemic and pandemic preparedness and prevention, gave an update on the situation on May 4. The patient in intensive care is improving, while two sick individuals onboard are being prepared for evacuation to the Netherlands for treatment, she said. The third sick individual is now asymptomatic.

"The situation is being closely monitored," Van Kerkhove said. DNA analysis of the viruses sampled from the confirmed hantavirus infections is taking place now, along with medical examinations of the people with suspected cases, contact tracing and investigations to determine the original source of infection, she said. Once the two sick passengers are evacuated, the plan is for MV Hondius to go to the Canary Islands so a full investigation of the outbreak and disinfection of the ship can take place.

Based on the information available about the outbreak and what is known about hantaviruses, the WHO judges the current risk to the general public as low.

Is human-to-human transmission to blame?

To date, the Andes virus, found in Chile and Argentina, is the only hantavirus with strong evidence of human-to-human transmission. "For other hantaviruses, transmission is believed to occur almost exclusively from rodents to humans," Luis Escobar, an assistant professor in Virginia Tech's Department of Fish and Wildlife Conservation, told Live Science in an email.

Escobar's lab researches the biogeography, ecology and evolution of infectious diseases, including hantaviruses. He noted that scientists don't yet understand which biological features of the Andes virus make it capable of spreading between people.

It's been difficult to pin down exactly how infectious the virus is to people, in part because public health authorities in Chile and Argentina have been quick to act in instances when human-to-human spread was suspected. Measures like contact tracing, isolation and monitoring have limited the virus's spread, meaning there's little data regarding its transmission between people.

"While it cannot be completely excluded that other hantaviruses [in addition to the Andes virus] might have some capacity for person‑to‑person spread, there is currently no convincing evidence that this happens," he told Live Science. "But research has been limited."

Current evidence does suggest that different flavors of hantavirus have distinct traits. For example, hantaviruses in North America and South America can infect a greater variety of rodent species than hantaviruses in Europe and Asia can. Although this flexibility doesn't necessarily make the viruses in the Americas more likely to infect people, it does suggest "a greater tendency to cross species boundaries," Escobar said. These differences among hantaviruses are an active area of study.

The WHO and other health authorities are still investigating the source of the cruise ship infections and whether human-to-human spread might be at play. If an Andes virus from South America is to blame, human-to-human spread wouldn't be a total surprise. However, if a different hantavirus is the culprit, that could be significant.

"I would be surprised if authorities were to find some evidence of human‑to‑human transmission caused by a hantavirus other than Andes virus," Escobar said. "Such a finding would fundamentally change our current understanding of hantavirus biology and would signal a much greater epidemic and pandemic risk than has ever been documented for this group of viruses."

"We are working under the assumption that it's the Andres virus," Van Kerkhove said in the May 4 update. At this juncture, the WHO's working hypothesis is that at least one of the two initial cases were infected before boarding the ship and that some degree of human-to-human transmission took place onboard between close contacts. That said, it's also possible that others who fell ill were exposed to the virus during one of the additional stops that the ship made on its journey, she said.

Editor's note: This article was last updated at 3:30 p.m. on May 5, 2026. The story was first published at 1 p.m. on May 4, 2026.

This article is for informational purposes only and is not meant to offer medical advice.

The force of a pumping heart changes how cancer cells function, halting their ability to multiply and spread, a new study shows.

The finding may help to explain why heart cancer is so rare, occurring in fewer than 2 in 100,000 people per year.

A protein called Nesprin-2 is key to this phenomenon. Found in the outer membrane of a cell's nucleus, the protein was already known to sense and respond to mechanical forces. Now, Nesprin-2 has been found to sense the force of heartbeats and stop cancerous cells from multiplying.

In addition to offering a possible explanation for why heart cancer is so rare, the findings could open the door for new therapies for other cancers, researchers concluded in the study, which was published April 23 in the journal Science.

We're going to "try to exploit this knowledge to develop a mechanical therapy for cancer," study author Serena Zacchigna, head of the Cardiovascular Biology Laboratory at the International Centre for Genetic Engineering and Biotechnology in Italy, told Live Science.

Zacchigna and colleagues are developing bands that can be strapped around tumors on the skin and then reproduce the force of a beating heart. Because metastatic skin cancer is one of the more common cancers to spread to the heart, this is a good first clinical case to look at, Zacchigna said.

Heartbeats subdue cancer

Both primary heart cancer, which starts in the heart, and secondary heart cancer, which spreads to the organ from other places, are fairly rare. The reason for this rarity is a long-standing mystery.

The mechanical load of heartbeats, meaning the physical force they exert, has been found to limit the ability of heart tissue to regenerate. So Zacchigna and her colleagues wanted to see if heartbeats might also stop cancerous cells from multiplying.

First, they implanted lung cancer cells into the hearts of lab mice to observe the cells' growth and spread. The hearts were either beating normally or were "unloaded," meaning they were attached to a blood supply but not actively pumping. Beating hearts seemed to stave off cancer growth, while the unloaded hearts saw a massive proliferation of cancerous cells.

The team ran a similar test with rat heart tissue grown in lab dishes. They found that tinkering with the amount of mechanical load in the tissue affected the behavior of lung cancer cells; the cancer grew and spread more when the mechanical load was reduced.

To understand what causes this phenomenon, the team took tissue samples from human patients whose lung, colon or skin cancer had spread to the heart and other organs. They mapped the gene activity of those cancer cells and zoomed in on their epigenetics, the markings "on top of" DNA that control which genes are switched on.

They found that certain epigenetic markers were tied to tumor growth and confirmed that heartbeats reduce these tumor-related markers. From there, they identified Nesprin-2 as a key player — switching off Nesprin-2 in "beating" heart tissue increased cancer proliferation.

These findings are the first to show that mechanical forces beyond the tumor itself affect the growth and spread of cancerous cells, Zacchigna said. The ability for mechanical forces to thwart cancer proliferation also appears to be a general mechanism, as "we saw that this signature is common to many cancer types," she said.

Possible treatments?

These findings are "of consequential importance," said Julie Phillippi, a chair of cardiothoracic surgery and head of the Cardiac Research Laboratory at the University of Pittsburgh, who was not involved in the research.

In an email, she told Live Science that the findings could also shed light on how to regenerate heart tissue in a targeted manner. And because heart cancer is so rare, "this work may have stronger impact in the context of cancers in other organs," she added.

The potential of using mechanical stimulation in cancer therapies is an "exciting idea to pursue," Phillippi said. But it requires a better understanding of how the properties of the tissue surrounding cancer cells affect their ability to sense mechanical forces.

With their new cancer-shaking bands, the team hopes to start a clinical trial within four years. For that, they'll need the first prototypes of these systems ready for human use, Zacchigna said. It will be key to identify the right time to implement the therapy and the patients who would benefit most, she noted.

A major challenge is to confirm this mechanical stimulation is a safe procedure, Zacchigna said.

"My fear is that by squeezing a tumor we may favor its dissemination," she said. "This is something we really have to rule out before moving forward."

Another approach could be to find drugs that can mimic the epigenetic effects of heartbeats, without the need for mechanical stimulation. The team is exploring that idea, too.

This article is for informational purposes only and is not meant to offer medical advice.

On a hot Saturday in San Antonio over 10 years ago, an 8-year-old boy was rushed to the hospital after days of fever, headache, vomiting and sensitivity to light. The child's mother, who lived near the Texas-Mexico border, had taken him to a series of clinics in Mexico, but his condition had worsened. The child was now unconscious and unresponsive to sound, light or other stimuli.

Doctors put the child on a ventilator and began a breakneck effort to find out what was wrong. What they discovered, swimming in the boy's cerebrospinal fluid, was an organism that left little room for hope: Naegleria fowleri, more popularly known as a "brain-eating amoeba."

It was the third case that Dr. Dennis Conrad, a pediatric infectious disease specialist, then at University Hospital in San Antonio, had ever seen in his career. The other two patients had died.

But Conrad had recently read that a new drug option, miltefosine, had been approved as an experimental treatment for N. fowleri infections. He added it to the boy's drug regimen, which already included other antimicrobial and anti-inflammatory medications.

"It's the kitchen sink," Conrad told Live Science. "It's a bad disease, and you just hit them with everything you can think of."

The child's prognosis was grim. He had been sick for five days before arriving in San Antonio, and most people who contract an infection with N. fowleri die about five days after symptoms start. According to the Centers for Disease Control and Prevention (CDC), there were 157 confirmed human cases of N. fowleri infection in the United States between 1962 and 2022. Four survived.

Elsewhere in the world, the numbers are similar. It's rare to become ill from an infection with this amoeba — and it's very, very rare to survive. But the few recent survivors may owe their recovery to miltefosine, the most recently recommended new medication for primary amebic meningoencephalitis (PAM), the disease caused by the amoeba. New drugs may be on the horizon as well. The question is whether they can reach patients before the damage is done.

'A bull in a china shop'

N. fowleri thrives in warm fresh water around 80 degrees Fahrenheit (26.6 degrees Celsius) or warmer, although it might manage to hang on in cooler temperatures, too, according to the CDC. It infects people purely by accident, when water is forced up the nose, driving the amoeba through a lacy bone called the cribriform plate to the olfactory nerve, which acts as a highway to the brain.

Immunocompromised people are at higher risk, said Dr. Juan Fernando Ortiz, a neurology resident at Corewell Health in Grand Rapids, Michigan, who wrote a journal article about treating the infections. Boys under age 14 make up a disproportionate number of cases, according to the CDC, perhaps because they're more likely than other groups to do things that push water up the nose, like jumping and diving. Most cases involve natural bodies of water, but cases have rarely been linked to treated water, such as in splash pads. In a few cases, people have gotten infected by using tap water in neti pots to rinse their sinuses.

The child Conrad and his colleagues were treating in August of 2013 had a tragically typical story of infection. He had spent the summer with his mother at an informal camp on the banks of the Rio Grande, where there was no running water. People bathed in the river, and the child enjoyed splashing in the shallows there.

Most likely, that's where he encountered the amoeba, which Conrad and his team now had to kill — before it could wreak more havoc than the child could survive.

PAM kills by massive destruction of brain tissue. The amoeba itself does some of the destruction directly, giving it the "brain-eating" moniker, but much of the brain damage is actually caused by the body's aggressive immune response to an intruder in the control system, Conrad explained. Parasites that evolve to live inside a body usually have ways of tamping down their host's immune response so they don't lose their meal ticket, Conrad said. But because N. fowleri has no need for a host, it has none of those adaptations. "It's a bull in a china shop," Conrad said.

Fortunately, there are only between zero and six N. fowleri infections in the U.S. each year, and there is no evidence that infections are becoming more common, said Dr. Julia Haston, a medical epidemiologist with the CDC's Waterborne Disease Prevention Branch. Although most cases occur in Texas, Florida and other Southern states, there have been more cases than usual in the northern U.S. in recent years, perhaps because climate change is warming waterways to the temperatures that the amoebas favor, Haston said, and a 2021 study found cases increasing in the Midwest as far north as Minnesota.

"The safest approach for people wondering whether they're at risk … is just to assume that Naegleria fowleri amoebae are in all fresh water," Haston said. "Lakes, rivers, any naturally occurring freshwater body."

A Hail Mary works

To battle the amoeba that was attacking the San Antonio patient's brain, Conrad and his team pulled out a then-novel treatment, miltefosine. The drug, an antimicrobial originally used to treat leishmaniasis, an illness caused by a tropical parasite — had shown promise against N. fowleri in studies, so the CDC had been distributing it for PAM cases. Miltefosine penetrates the blood-brain barrier and is relatively well tolerated by patients, Ortiz said. That's important, as many antiparasitic drugs also damage human cells, he added.

The doctors ordered the drug from the CDC. (Today, it's available commercially under the brand name Impavido.) It arrived 14 hours after the child was admitted.

The child lived.

But he was not unscarred. When the boy left the hospital, he could breathe on his own but not do much else. After months of rehabilitation, he regained some of his abilities, but his family still had to help him with basic self-care, Conrad said.

That same summer, however, a 13-year-old girl in Arkansas contracted the amoeba while swimming in an artificial pond. She received quick treatment, including miltefosine, and recovered. After six months of rehab, she had no lingering neurological effects from this brush with death, according to a 2015 case report describing her treatment.

She and the Texas boy were the first U.S. survivors of PAM since 1978. In 2016, a 16-year-old boy in Florida contracted PAM and received miltefosine; he also recovered fully.

However, not all PAM patients who have received miltefosine have survived. Even with the new drug, PAM has a fatality rate of over 97%, according to the CDC.

Each summer, a handful of new PAM cases pop up around the country, and doctors are continually working to improve their treatment. They're increasingly exploring strategies like cooling patients' body temperature to around 95 F (35 C), Conrad said, which some studies suggest might improve recovery from brain trauma.

There may be new pharmaceuticals on the horizon, too. Miltefosine can have toxic side effects on the kidneys and liver and isn't available in developing countries, said Jacob Lorenzo-Morales, a senior lecturer in parasitology and the director of the University of La Laguna Institute of Tropical Diseases and Public Health of the Canary Islands.

So Lorenzo-Morales and his team are looking for alternatives. One of the most promising is nitroxoline, an antibiotic used in Europe to treat urinary tract infections. Lorenzo-Morales and his team reported in the journal Antibiotics in August 2023 that in lab dishes, low concentrations of nitroxoline induced cell death in N. fowleri, without causing toxic effects on host cells. This drug has also been used to successfully treat one patient infected with a different brain-eating amoeba, Balamuthia mandrillaris.

Now, they're conducting animal studies and hope to present positive results at next year's international Free-Living Amoebae Meeting, a biannual meeting of amoeba researchers. Nitroxoline is already widely available worldwide, Lorenzo-Morales said, and because it is already approved for use, extensive clinical trials won't be necessary; doctors can begin using the medication off-label.

New alternatives

There are also efforts to find new medications that work against PAM. Some researchers are interested in developing mRNA vaccines against N. fowleri infection, with a 2024 study in the journal Scientific Reports using modeling of the amoeba's surface features to suggest what such a vaccine might look like. (The authors of that study did not respond to requests for an interview with Live Science.)

Lorenzo-Morales and his colleagues are also investigating the effects of a pigment called elatol, which is extracted from red algae. "We have isolated some key compounds from red algae that are very active against different free-living amoebas, including Naegleria, at concentrations that are even lower than the current treatments," he said.

However, the researchers are currently doing those tests in lab dishes. Moving testing to people will require funding from pharmaceutical companies. That can be difficult, Lorenzo-Morales said, because companies don't see a lot of potential for profit from a "rare" disease like PAM. However, he said, PAM still goes unrecognized far too often, he said, which may mean the potential market is bigger than pharmaceutical executives believe.

A race against time

Perhaps the most immediate hope for today's patients is simply recognizing the disease faster. The time to save someone with PAM is short, said Julia Walochnik, a professor of tropical medicine at the Medical University of Vienna who studies amoebic diseases. "If it's too late, it doesn't matter which drug is used; the patient will usually not survive," she told Live Science.

The late onset of treatment might be one reason why Conrad's 8-year-old patient sustained such serious brain damage while the other youth treated around the same time recovered more fully.

The test for the amoeba is simple: Take a sample of the fluid surrounding the brain and spinal cord and look for swimming single-celled organisms. But doctors may not think to order the test in time, because PAM looks like meningitis caused by much more common viruses and bacteria. Families of children who have died of the disease are increasingly working to raise awareness, which could hopefully spur quicker diagnosis and treatment. For instance, the Jordan Smelski Foundation for Amoeba Awareness, started by the parents of an 11-year-old boy who died of PAM in 2014, hosts educational events for doctors and the public.

Awareness is making a difference, Lorenzo-Morales said. "Every time we have been involved in a clinical case in the last four to five years, the diagnosis has been fast," he said. "That didn’t happen before."

Editor's Note: This story was originally published on July 26, 2024.

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A 63-year-old man known as the Oslo patient is "likely cured" of HIV after a stem-cell transplant remodeled his entire immune system.

Prior to this case, a handful of other HIV patients who received similar transplants had entered long-term remission from the infection. In those cases, the donated cells came from people unrelated to the patients, but in the Oslo patient's case, the transplanted cells came from his brother. His sibling happened to carry a genetic mutation that made him resistant to HIV, doctors reported Monday (April 13) in the journal Nature Microbiology.

The mutation, called CCR5 delta 32, disables a protein on the surface of immune cells that HIV often exploits to trigger infection. The patient's brother carried two copies of this mutation, which effectively locks the virus out of cells that would normally be its prime targets.

"A sibling has a 25% probability of being a match for a transplant, and the frequency of CCR5Δ32/Δ32 is around 1%" in northern European populations, study co-author Dr. Anders Eivind Myhre, a hematologist at Oslo University Hospital, where the patient was treated, told Live Science in an email. "So it is an unlikely scenario, and we were not aware of the donor's CCR5 status before the transplant."

"Like winning the lottery twice"

The Oslo patient had been diagnosed with HIV in 2006, at age 44. In 2010, he started antiretroviral therapy (ART), which suppresses the virus's ability to replicate in the body and thus prevents the infection from progressing to AIDS. The treatment drove the HIV in the man's blood down to undetectable levels, which also stops the virus from being transmitted through sex. The patient has maintained this level of "viral suppression" from August 2010 to the present.

However, in 2017, the patient became fatigued, and his blood cell counts plummeted. The next year, he was diagnosed with a type of bone marrow cancer called myelodysplastic syndrome, in which new blood cells made in the bone marrow fail to mature. Initially, the patient responded well to a drug for the condition and entered remission, but he later relapsed, prompting his doctors to seek a bone marrow transplant instead.

Also known as hematopoietic stem cell transplants, bone marrow transplants involve infusing healthy, blood-making stem cells into the body to replace diseased ones. These new stem cells multiply and give rise to new red and white blood cells, ultimately remodeling the patient's blood supply and immune system.

At that point, the patient was referred to Myhre's care at Oslo University Hospital, and the team there searched for a bone marrow donor who happened to carry the coveted CCR5 delta 32 mutation. They were aware of similar cases where patients with HIV and blood cancer had received transplants with the mutation and then entered long-term remission from both their conditions. (More recently, there have been a few reported cases of remission without CCR5 delta 32, or with only one copy.)

Unfortunately, the team's search failed to turn up a compatible donor with double CCR5 delta 32, so the patient's 60-year-old brother donated his bone marrow instead, to at least treat the cancer. But on the day of the procedure, the medical team discovered that the sibling happened to have two copies of CCR5 delta 32.

The patient has said "he feels like he has won the lottery twice," study co-author Dr. Marius Trøseid, a group leader, professor and infectious-disease specialist at Oslo University Hospital, told Live Science. "He was cured for his bone marrow disease, which could be fatal, and he's also now cured for HIV, most likely."

Following the transplant, the patient did experience a complication known as graft-versus-host disease. This happens when the transplanted cells give rise to new immune cells that then see the patient's body as "foreign" and attack the tissues. But he was treated for this complication with an immune-modulating medicine, and over time, the new immune system successfully took over.

Two years out, the new cells had completely replaced the patient's original immune cells in the blood, bone marrow and gut, the study authors found in a thorough analysis.

"Most likely, it's a cure"

Trøseid was asked to evaluate the Oslo patient's case following the transplant, when a question emerged about whether he could safely stop ART. Tests confirmed that the patient's immune system had been completely transformed, leaving no trace of HIV in the blood. The team collected 65 million CD4 T cells — the primary targets of HIV infection — and found that none carried virus capable of replicating.

So, 24 months after his transplant, the patient was cleared to stop ART. Since then, there's been no sign of viral rebound — and Trøseid and colleagues have been on the lookout.

They thoroughly analyzed lymph tissues in the patient's gastrointestinal tract, which serve as the main hiding place for HIV in the body, and found no trace of the virus. They also ran tests with the patient's immune cells, and found that they responded well to common viruses, like the "mono" virus and influenza viruses, but did not react to HIV.

"So they function well, but they do not recognize HIV," Trøseid said. "It seems like his new immune system has never met HIV and does not recognize it."

Taken together, these analyses suggest the Oslo patient's case represents a "likely cure," Trøseid noted, though conservatively, scientists prefer to label such cases "sustained remission" from HIV. There's no consensus as to when a given patient can officially be declared cured, but from a practical standpoint, the Oslo patient no longer needs to take daily medications to keep the virus at bay.

"What will happen when some of these cure cases reach very old age and the immune system starts to decline a bit for other reasons? We don't know," he added. "I think we will just need to see. But most likely, it's a cure."

Trøseid thinks the myriad tests they ran in this study could be useful benchmarks for future transplants, to help doctors judge when a patient is in long-term remission. Studying these patients could also help reveal new and better strategies for controlling the virus, which are still needed.

"It's one of several stepping stones on the way to a functional cure," Trøseid said of studying these transplant cases. A functional cure would sustainably suppress HIV in the body without needing to completely eliminate it, as the latter would be a more difficult feat to achieve.

ART is very effective at stopping viral replication, disease progression and transmission, but it must be taken consistently for life. This presents logistical and monetary challenges for many people with HIV, some of whom also struggle to access ART due to the stigma that comes with acknowledging an HIV diagnosis. And while bone marrow transplants offer one route to long-term remission, the harsh procedures carry a lot of risks and are generally administered only to patients who need them for another serious condition, like cancer.

"The number of people living with HIV worldwide is more than 30 million, so it's also not feasible" to give them all transplants, Trøseid said. "We need to find other strategies to cure or control the virus."

Trøseid noted that recent trials suggest that engineered antibodies may be a promising solution for controlling the virus without ART. And in Europe, an international consortium called EU2Cure has formed to help spur the development of these and other potential HIV cures.

"Hopefully, we can move the threshold a little bit with each trial," he said, "and eventually, get a functional cure where a large fraction of people can live for a longer time without taking meds."

This article is for informational purposes only and is not meant to offer medical advice.

The patient: A 58-year-old woman in Greece

The symptoms: The patient, who worked outdoors on a Greek island, developed pain around the center of her face that grew progressively worse. About two to three weeks after this pain began, she also developed a severe cough.

Shortly after that, "worms" came out of her nose when she sneezed, prompting her to seek medical attention, she told doctors.

What happened next: A report of the case doesn't describe how the patient was examined. However, it notes that an ear, nose and throat specialist surgically removed wriggling creatures from her maxillary sinuses, the large sinuses located on the sides of the nose. These critters included 10 larvae and one pupa (the insect life stage between the larval and adult stages).

Following this extraction, experts closely examined two of the larvae and part of a puparium, the pupa's protective outer casing in which it matures into an adult. One larva was pale yellow and about 0.6 inches (15 millimeters) long, while the other was light brown and 0.8 inches (20 mm) long. The puparium was black and wrinkled, and it contained remnants of the pupa, they noted.

The team visually examined the larvae and extracted DNA for analysis.

The diagnosis: This examination revealed the wormlike creatures to be the larvae of the sheep bot fly (Oestrus ovis). This parasite is typically found in the nasal passages and sinuses of sheep and goats. Notably, the outdoor area where the woman works is located next to a field with grazing sheep, the report authors wrote.

Parasitic fly infections are generally known as "myiasis," so the woman was diagnosed with "O. ovis nasal myiasis with pupation."

The treatment: In addition to having the larvae and pupa surgically removed from her sinuses, the woman was given nasal decongestants. With these two treatments, she made a "complete recovery," according to the report.

What makes the case unique: Human cases of O. ovis myiasis have been reported in the past, but these infections have typically affected the eyes, rather than the nasal passages.

"O. ovis bot flies infrequently affect humans, most often depositing larvae in the conjunctival sac," which is located between the eyelid and eyeball, the report authors noted. More rarely, the flies have been reported to deposit larvae into people's nostrils, mouths or ear canals, they added.

Historically, it was thought that O. ovis couldn't develop for very long in humans, making it to only the first larval stage, known as L1. But in recent cases, older larvae, including L2 and L3, have been identified, the report authors wrote. Pupation, the point at which larvae mature into "teenagers," follows the L3 stage.

"The patient we report had a severely deviated nasal septum and appears to have been inoculated with a large larval burden," they noted. "From a purely anatomic perspective," the authors hypothesize that the high number of larvae combined with the woman's septum deviation prevented said larvae from exiting her nose. This permitted the larvae to progress to the L3 stage and, in one instance, pupation, they concluded.

When infecting sheep and goats, adult female O. ovis deposit larvae (also called maggots) in and around the host animals' nostrils. The larvae then travel into the nasal passages and sinuses, where they may mature for months before exiting the nostrils. Once out, they burrow into the ground and enter the pupa life stage for several weeks. Once mature, the adult fly breaks free of its puparium and emerges from the ground.

On occasion, L3 larvae can get stuck in the nasal passages of their host animals, but they don't typically pupate at that point. Instead, they usually dry up, liquefy or calcify, and their remains can sometimes trigger secondary bacterial infections.

The maggots die because the sinuses don't provide a favorable environment for them to enter the pupal stage. As such, "pupation of O. ovis larvae within any mammalian host is considered biologically implausible," the authors noted. Nonetheless, it happened in their patient.

The authors suggest that some "unidentified anatomic or physiologic factors" must have allowed pupation to occur in the woman's case. Alternatively, the strange occurrence may reflect an evolutionary adaptation that could enable the species to complete its life cycle in humans, they mused.

"In either scenario, additional cases and data are needed to understand this phenomenon, but clinicians should be aware of the potential for human bot fly infections in endemic areas," they concluded.

For more intriguing medical cases, check out our Diagnostic Dilemma archives.

This article is for informational purposes only and is not meant to offer medical advice.

The patient: A 20-year-old man in China

The symptoms: The patient had gotten a red cross tattooed on his neck, just below his voice box. But three months later, the ink vanished.

The man developed lumps on both sides of his neck, which grew gradually. Indented scars appeared where the ink had once been, along with ulcers made of dead tissue that were filled with a pinkish mixture of serum and blood. These types of growths are known as "necrotic" ulcers.

The patient went to the hospital about five months after his tattoo appointment. He was prescribed antibiotics and topical corticosteroids, but his symptoms did not improve.

What happened next: When doctors physically examined the patient, they identified hard and swollen lymph nodes on both sides of his neck, just below his jaw. They also examined a large necrotic ulcer on the middle of the base of his neck, finding that the crusted mass had spread to the deeper layers of his skin.

MRI showed the lump on each side of the man's neck was approximately 1.6 by 1.2 inches (4 by 3 centimeters), while a central mass below the large necrotic ulcer was 1.9 by 1.4 inches (4.9 by 3.5 cm). An enhanced CT scan revealed blood clots in the two jugular veins closest to the midline of the neck.

The doctors then used fine needles to take biopsies of the necrotic ulcer, which revealed dead cells, immune cells and scar tissue. This did not point to what triggered the necrosis. But because the medical team was concerned by the scan results and the pace at which the man's condition was progressing, the patient was immediately sent to surgery, the doctors wrote in a report of the case.

The team removed the ulcer and masses and tied off the clotted jugular veins to prevent blood flow. The patient's neck was then reconstructed using tissue from his thigh.

The diagnosis: The team ran immunohistochemical tests on the biopsy samples, in which they used antibodies to check for specific antigens, or immune-response-triggering substances. The results were negative for both Epstein-Barr virus, the germ that causes mono, and tuberculosis, but a type of cell that forms benign tumors was detected.

"These findings collectively supported a diagnosis of necrotizing granulomatous lymphadenitis," the doctors wrote. "Granulomatous" refers to a condition in which clusters of immune cells form a wall around persistent infections or foreign materials.

Necrotizing granulomatous lymphadenitis is an immune response mounted against a bodily injury — in this case, the man's cross tattoo. The doctors also noted in their report that heavy metals, such as mercury and cadmium, and red organic dyes in tattoo pigments can sometimes trigger delayed immune responses. However, none of the vanished tattoo pigment was detected in the surgically removed lesions, so they couldn't examine its contents directly.

The treatment: Following surgery and a bout of short-term hormone therapy, the man made a full recovery, the doctors reported. (They did not specify the type of hormone treatment he was given or why it was necessary.)

What makes the case unique: Tattoos can come with potential health risks, such as allergic reactions and skin infections. In a study of 226 people who had reactions to tattoos, granulomatous reactions were relatively common, making up 48% of the inflammatory responses reported.

The doctors noted that this man's case is only the second known reported case of necrosis following a tattoo. In the other known case, the patient experienced necrobiosis lipoidica, a rare inflammatory skin condition in which the collagen in the skin degrades, and early granuloma annulare, characterized by a raised, ring-shaped rash.

The man's necrotic ulcer was also particularly aggressive, the doctors noted, and it was unusual in how deep into the skin it had spread.

The doctors suggested three potential causes for the man's severe necrosis. First, the chronic inflammation and otherwise-heightened immune response triggered by the tattoo could have raised his risk of blood clotting. Alternatively, the enlarged lymph nodes on the sides of his neck may have compressed the jugular veins and thus slowed blood flow. A final possible explanation is that the walls of his veins began to erode due to the chronic inflammation.

In all, "this report expands the spectrum of tattoo-associated pathology," the doctors wrote in the report. Given that this is the second known case, though, it's likely a very rare outcome.

For more intriguing medical cases, check out our Diagnostic Dilemma archives.

This article is for informational purposes only and is not meant to offer medical advice.

Alzheimer's disease, the most common form of dementia, has beaten back potential treatments for decades. Past research suggested it was a complicated, multifactorial disease in which a patchwork of biological and lifestyle factors combined to increase or decrease risk.

But a new study published in January in the journal Nature suggests the risk of developing the disease is determined largely by one key gene, called apolipoprotein E (APOE). Lifestyle and environmental factors can dial the risk up or down modestly in people with susceptible gene variants, but those who have protective versions of the APOE gene are extremely unlikely to develop Alzheimer's. And a staggering 99% of the population carries at least one disease-fueling version of the gene.

The findings raise the possibility that gene therapy targeting APOE could dramatically reduce the risk of Alzheimer's for a large swath of people who are at risk of developing the disease, thus paving the way for one of the first widely used gene therapies, experts told Live Science.

There are more than 900,000 people in the United States who have the highest-risk form of APOE, said Nolan Townsend, CEO of gene therapy company Lexeo Therapeutics, which is developing a therapy targeting the gene.

"There's been no gene therapy to date that's tried to address a population of that size," Townsend told Live Science.

An elusive treatment

For decades, there were no good treatments for Alzheimer's disease. No medicines actually slowed the disease's progression until the advent of anti-amyloid antibodies like donanemab, which clear the characteristic amyloid plaques that are a hallmark of the disease. But these drugs, touted as the first disease-modifying treatments for the condition, have severe side effects, including swelling and microbleeds in the brain. The patients most at risk from Alzheimer's are also most vulnerable to these side effects.

At first glance, the APOE gene wouldn't seem very relevant to Alzheimer's disease. The main role of the protein it codes for is to ferry fat molecules through the bloodstream. However, the APOE protein also closely interacts with what is considered the best-known molecular culprit in Alzheimer's: the protein amyloid-beta, which aggregates into plaques that destroy connections between neurons and trigger inflammation.

There are three versions of the APOE gene ‪—‬ APOE2, APOE3 and APOE4 ‪—‬ and each codes for a slightly different version of the protein. For decades, researchers thought that APOE2 was a protective variant, while APOE4 increased the risk of the disease. APOE3 was thought to neither increase nor decrease the risk.

But in past work, APOE2 was underrepresented; the allele is present in less than 1% of the population. In the new Nature study, which looked at data from 450,000 people, the gene trio's true contributions were revealed. APOE3 is not neutral, the study found; rather, it increases Alzheimer's risk, albeit to a much lesser extent than APOE4 does. Carrying two copies of APOE2, meanwhile, made people almost immune to developing Alzheimer's.

It's not clear why, but other research in lab dishes shows that the highest-risk variant of APOE impairs the processing of fats in support cells called glia and that this can trigger dysfunction and neuro-inflammation. APOE4 also seems to increase cell death and impairs how well cells react to oxidative stress, a state of imbalance between antioxidants and reactive chemicals called free radicals. It also impairs synaptic plasticity, or the ability to adaptively strengthen or weaken connections between brain cells.

The study authors concluded that APOE3 and APOE4 together are responsible for between 72% and 93% of Alzheimer's disease cases.

"Without strong underlying risks from APOE ε3 [APOE3] and ε4 [APOE4], almost all AD [Alzheimer's disease] and half of all dementia would not occur," the study authors noted in the paper.

That finding is buttressed by other work hinting that APOE2 is strongly protective. A 2020 study found that someone with two copies of APOE2 has a 200 times lower risk of developing Alzheimer's than someone with two copies of APOE4. Carrying just one copy of the APOE2 gene lowers the risk 80-fold.

The research raises the possibility that people with higher-risk variants might stave off the disease if they had one or two copies of the APOE2 version of the gene.

Gene therapy for the masses

That's where gene therapy comes in.

Gene therapies have transformed the lives of people with rare genetic disorders, such as the muscle-wasting disease spinal muscular atrophy (SMA) and a progressive form of blindness called retinal dystrophy. In these cases, the therapy involves delivering a copy of a healthy gene into a tissue that lacks it.

But these treatments target tiny populations; SMA, for example, affects about 1 in 15,000 live births in the United States. Some gene therapy approaches are customized for just a single patient.

By contrast, the study estimates that about 28% of the population carries at least one copy of the highest-risk versions of the APOE gene that could potentially benefit from this drug.

Mayur Parmar, a pharmacologist at NOVA Southeastern University in Florida, has conducted studies of APOE2 gene therapies in mice.

"As we have learned in recent years, APOE4 plays an important role in terms of amyloid beta, tau, neuroinflammation, and oxidative stress. It can be a potential target, Parmar told Live Science. APOE2 therapies could work by suppressing these effects, he added.

Now, these ideas are being put to the test. New York City-based Lexeo Therapeutics plans three safety and dosing clinical trials to increase protective APOE gene variants and reduce harmful APOE gene variants in people with the highest-risk gene APOE4/APOE4 gene combination who have early Alzheimer's disease.

The first phase of their research is a combined safety and dosing study that incorporates the protective APOE2 gene variant into the brains of people with early Alzheimer's. A second study, which has not yet reached the human testing phase, will instead add a version of APOE2 that has the ultrarare Christchurch mutation, a rare variant found in the brains of people who show no Alzheimer's symptoms despite having severe amyloid plaque buildup.

Researchers think the Christchurch variant is like a souped-up version of APOE2 that will offer even more neuroprotection. Finally, the team is planning a trial combining the addition of APOE2 with using tiny snippets of RNA to suppress APOE4 gene expression, which they hope will enhance the therapeutic effect.

The company's initial safety testing showed that the therapy was well-tolerated and reduced tau levels in most of the 15 participants recruited. Only topline results from the study have been published, although Townsend said that long-term cognitive data from the trial will eventually be released.

The ability of APOE gene therapies to target multiple disease pathways could offer patients significant benefits, but it will be tough to prove. Pharmaceutical companies like Lexeo must choose a clinical outcome, like better memory preservation or less amyloid buildup, to demonstrate to regulators that their therapies work. The most obvious signs that a therapy works are detected through behavioral and cognitive testing, but trials pegged to those outcomes are massive in scope and cost, said Townsend. That's because it can take years for the effects of a promising treatment to manifest and because such testing is quite expensive on its own.

The pharma companies that developed anti-amyloid antibodies bypassed this need because the U.S. Food and Drug Administration (FDA) agreed to view reduced amyloid load in the brain as a proxy for cognitive improvement. However, this approach has been controversial because of the uncertain link between these molecular changes and cognitive benefits, and Townsend said the regulatory environment for genetic therapies is less permissive.

"There's uncertainty in the regulatory frameworks and landscape to get to an accelerated approval of a genetic-focused approach in this area," Townsend said.

Crossing the barrier

Another challenge is getting the gene into the brain cells that need it. Adeno-associated viruses (AAVs) have been the vector of choice for gene therapy. Viruses such as AAV9 can bypass the blood-brain barrier and access the brain. But scientists are still working out how to deliver AAV gene therapies to maximize blood-brain barrier penetrance.

Gene therapies can be injected directly into the brain, but this approach isn't perfect either. An earlier gene therapy that used this approach to deliver neuroprotective nerve growth factor (NGF) into patients with mild to moderate Alzheimer's disease passed safety tests but didn't improve symptoms. Parmar said follow-up work showed the NGF therapy didn't reach cholinergic neurons in the basal forebrain, the brain cells that needed it most. The vector failed to travel well within brain tissue, and the trial didn't use tools that would have helped the clinicians assess whether they had injected the right areas of the brain.

Lexeo has instead delivered its gene therapy into patients' cerebrospinal fluid, which circulates through the spinal cord — a technique that bypasses the blood-brain barrier and improves brain-wide delivery. The injection is a 40-minute outpatient procedure, Townsend said, and will meet their goal to "bathe the brain in the vector."

The new study showing the negative effects of APOE3 opens the door to expanding the target population for these gene therapies, Townsend said.

"If the approach for suppressing E4 [APOE4] works, then there's no reason why there could not be a parallel approach to suppressing E3 [APOE3]," Townsend said.

No silver bullet

Ultimately, gene therapies targeting APOE variants have excited the field because they could potentially benefit a vast number of people.

But no lone treatment is likely to be sufficient, said Dr. Shanshan Wang, an anesthesiologist at the University of California, San Diego. Wang is working on a separate gene therapy that she thinks may help protect damaged neurons. That's because even if APOE does have an outsize role in Alzheimer's risk, it's not the whole story.

"When you think about cancer treatment or any other disease treatment, do you just use one therapy?" Wang said. Cancer treatment has thrived on targeting multiple disease facets simultaneously. "It's always combinatory."

In a single year, the secretary of Health and Human Services (HHS), Robert F. Kennedy Jr. (RFK Jr.), has done such comprehensive damage to the extraordinarily successful HIV prevention program as to leave the country almost defenseless against a brewing HIV pandemic, right when elimination seemed possible.

These unprecedented actions have stunned and frightened many who work in the field. But I know from past personal experience that strong science promoted by strong advocacy can return us to the path of HIV elimination.

I saw the AIDS epidemic play out firsthand. In my final year of medical school in 1983, I did a month-long practice internship at the San Francisco General Hospital AIDS ward, the first in the country. The cause of acquired immunodeficiency syndrome (AIDS) was unknown. No test or treatment existed, and the modes of transmission were controversial.

Gay men were the primary risk group. The number diagnosed with AIDS was exploding exponentially, and everyone died slow, lingering, excruciating deaths. Patients were blinded and emaciated, vomiting and asphyxiating and covered with sores, often abandoned by neighbors, family and friends out of the terror of contagion.

Stonewall had come and gone, Harvey Milk had been assassinated, and now fundamentalist preachers thundered from the pulpit that AIDS was God's justified vengeance on sinners.

Then there was the soft-spoken, low-expenditure, laissez-faire approach, with the implication that AIDS was nature's way of culling out undesirables.

Soon after my time on the AIDS ward, the cause of AIDS was identified: human immunodeficiency virus (HIV).

Supported by science, AIDS activists refused to accept that HIV was an inevitable death sentence and launched a hard-hitting campaign demanding research on treatments. Within years, there was a proliferating alphabet soup of anti-HIV medications, which ultimately ensured that most of those infected could live near-normal life spans.

Success produced a paradox: Increased years of potential infectivity meant an expanding epidemic. In 2010, I was working for the CDC on HIV prevention in Kenya, with a tiny role in an ongoing giant multi-national study examining whether it was possible to use anti-HIV treatment to stop HIV transmission. In a meeting room in the local public hospital, I was speaking to a group of health care workers who were going to carry out this study and others.

Almost all were women. They were being paid the standard princely salary of about $300 a month. They were our study workers because they came from the community most at risk. One-in-four women in their age group were HIV infected. Access to anti-HIV medication was fiscally and logistically limited. Only a third of those who needed treatment actually received it. That meant an unknown number of the women to whom I was speaking were ultimately going to die the same death as those in the San Francisco AIDS ward. But they went out to the villages and did the hard work to enroll study subjects and bring home the data.

Because of these women and others across the globe, the resulting 2016 scientific publication became one of the most cited and influential studies in medicine. For the first time, it demonstrated that HIV transmission was not inevitable. It could be stopped cold through anti-HIV treatment. Zero transmission — IF appropriate treatment is received.

Fast forward a decade, and RFK Jr., is an HIV skeptic, suggesting that a conspiracy of persons with personal ambitions had diverted attention away from other potential causes of AIDS, such as a "toxin." He's also claimed, without evidence, that anti-HIV medications were based on "phony, crooked" studies that killed people.

In 2025, five of the 11 branches of the CDC's Division of HIV Prevention were abolished and the employees laid off. All the CDC's HIV websites were taken down. After being restored by court order, the web page on treatment now contains the header, "This page does not reflect biological reality and therefore the Administration and this Department rejects it." A similar header appeared on the HIV prevalence page, but some brave CDC soul managed to insert an explanation why the data was frozen in 2023: "the branches that produced HIV incidence estimates... were eliminated." RFK Jr. cancelled $759 million in HIV research grants, and proposed that responsibility for HIV be transferred from the CDC and all other agencies to a new Administration for a Healthy America under his direct control, with a funding reduction of 80%. Pending that reorganization, a half-billion dollars in budget cuts from HIV treatment were put before Congress.

All this came at the moment when the tools to end the HIV epidemic seemed to be in our hands. New cases had been cut by more than 90%, and maternal-to-child transmission had been eliminated completely.

Now, instead of having resources to finish the job, states are implementing or considering a host of expenditure reduction measures: treatment waiting lists, reduced formulary options, work requirements, low income requirements, an end to reimbursement for the lab assays needed to know if the medications were working.

Similar cutbacks are happening globally, as the U.S. withdrew assistance from international HIV prevention. With our domestic defenses being stripped away and an increased threat of foreign exposures, viral spread will obviously accelerate to infect far more than the current 1-in-300 Americans. Those new cases will infect others. Inevitably, HIV will escape from its risk groups to create a generalized pandemic in the U.S.

1983 redux?

Thanks to almost 50 years of hard work by AIDS activists in San Francisco, village health workers in Kenya, laboratorians across the world, along with so many others, the choices now seem clear: With appropriate treatment, we can bring the HIV epidemic to a halt before it becomes a pandemic, allow the infected to live near normal lives, and provide great cost-savings for society. Or, with lack of treatment, we can have uncontrolled transmission, a spreading epidemic that becomes a pandemic, tormented deaths for individuals, and great costs for society.

In this choice, perhaps the term "1983" should take on the same resonance for health that George Orwell once gave the term "1984" for politics. For HIV, do we really want to return to the hopelessness of 1983? Or do we defy inevitability, use strong advocacy backed by strong science to restore our defenses, stop the HIV resurgence before it starts, and put an end to the epidemic before it becomes a pandemic?

Opinion on Live Science gives you insight on the most important issues in science that affect you and the world around you today, written by experts and leading scientists in their field.

Colorectal cancer — cancer of the large intestine or rectum — is now the leading cause of cancer deaths in people under 50 in the U.S., a new study finds.

Colorectal cancer incidence and mortality have been increasing in people under 50 each year since 2013 and 2004, respectively, according to research published March 2 by the American Cancer Society (ACS). This rise in early onset diagnoses is driven by advanced-stage disease. (Colorectal cancer is also known as bowel cancer.)

"The trend is very serious," study co-authors Rebecca Siegel, Nikita Sandeep Wagle and Dr. Ahmedin Jemal told Live Science in a jointly written email. Siegel is senior scientific director of cancer surveillance research at the ACS; Sandeep Wagle is principal scientist of cancer surveillance research at the ACS; and Jemal is senior vice president of surveillance, prevention and health services research at the ACS. "Colorectal cancer is the only common cancer [in people] under 50 with rising mortality," they wrote.

Incidence is also increasing among adults aged 50 to 64, with the disease being diagnosed at more advanced stages. This is thought to be linked to the similarly increased mortality in this age group, the authors wrote in the study.

The trend in people under 65 is in marked contrast to the decreasing rate of new bowel cancer cases and deaths in adults ages 65 and over. Because most cases are in people 65 and over, this declining trend is masking an opposing pattern among the younger cohorts, the authors wrote in the study.

A troubling trend

Colorectal cancer is the second-leading cause of cancer deaths globally and mainly affects people 65 and over. But colorectal cancer "can no longer be called an old person's disease," Jemal said in a statement. Indeed, a 2025 analysis revealed that colorectal cancer cases were simultaneously rising in people under 50 and either stabilizing or declining in 50- to 74-year-olds in 14 countries, including the U.S., Canada, Australia and England.

But in the new study, the researchers compiled data on the number of new colorectal cancer cases from 1998 to 2022 alongside the number of colorectal cancer deaths from 1930 to 2023, while zooming in on slightly different age cohorts. The data were drawn from the National Cancer Institute and the Centers for Disease Control and Prevention (CDC).

By narrowing the age ranges examined, the team found that the rise is occurring not just in people under 50 but also in people up to 65 years old. "The increase in colorectal cancer is not just in young people, per se," the study authors told Live Science.

This phenomenon is called the "birth cohort effect," meaning that when an individual was born is more closely related to disease risk than when they were diagnosed. This confirms "a real uptick in disease because of something we're doing or some other exposure," Siegel said in a statement.

However, it remains unclear what is causing this trend, the authors wrote in the study.

"Long-established risk factors for colorectal cancer were identified based on cancer in older adults who were exposed to different risk factors than those in more recent generations," Siegel, Sandeep Wagle and Jemal told Live Science. For example, for all ages combined, almost 14% of colorectal cancer is attributable to smoking, but people under 50 are less likely than older adults to have smoked, they said.

Since the second half of the 20th century, individuals have been exposed to new environmental factors that may raise cancer risk, such as microplastics and ultraprocessed foods, they said. Research has also previously found colorectal cancer is associated with high antibiotic exposure and processed meat.

Colorectal cancer screening saves lives

The team estimated there will be 158,850 new cases of bowel cancer in 2026. Of those, 47,600 will be in 50- to 64-year-olds and 24,640 will be in those under 50. Over 55,000 people of all ages are projected to die from the disease this year. Of those, 7% will be in those under 50 and 24% will be in people aged 50 to 64.

With most people under 50 being diagnosed with an advanced stage of the disease, which is harder to treat, earlier diagnosis is essential, Siegel, Sandeep Wagle and Jemal told Live Science.

"Earlier diagnosis can also be achieved by increasing awareness of symptoms for colorectal cancer like blood in stool, abdominal pain, diarrhea, or fatigue, which can often be mistaken for other health issues," they said. "Earlier attention to symptoms could help shift diagnoses toward earlier, more treatable cancer"

Screening also allows for earlier detection and removal of precancerous lesions in the bowel; which accounts for 79% of averted colorectal cancer deaths. Current ACS guidelines state average risk individuals — those without a personal or family history of the disease — should begin colorectal cancer screening from age 45. Medicare covers various screening tests from this age, including a stool DNA test and colonoscopy. There are no specific ACS guidelines for high risk individuals, but they may require earlier and more frequent screening.

However, the researchers found that only 37% of 45- to 49-year-olds are up-to-date with their colorectal cancer screening. With half of deaths in people under 50 being in 45- to 49-year-olds, this means that many colorectal cancer deaths in this cohort could be prevented, Siegel, Sandeep Wagle and Jemal said.

This article is for informational purposes only and is not meant to offer medical advice.

In the three decades between 1993 and 2024, measles in the U.S. was relatively rare — a few hundred cases each year, at most. But suddenly, the disease has become so entrenched in American life that it sometimes fails to make headlines when a new outbreak erupts.

As of March 2026, measles has been continuously circulating around the U.S. for more than a year, starting with an outbreak in Texas that lasted from January to August 2025. Before that outbreak was declared over, an outbreak on the Utah and Arizona border began in August and is ongoing. An outbreak in South Carolina began in September, drastically increased in January 2026, and continues.

Thirty states have had measles cases this year; 47 have seen cases since the start of 2025. Health officials across the U.S. have confirmed 1,300 infections already this year as of March 6, putting the country on track to surpass 2025’s numbers, which were the highest in 35 years.

We study outbreak preparedness and response at Brown University's Pandemic Center, and we view the return of measles in the U.S. as a grim signal of what's to come.

Low levels of vaccination across the country mean measles outbreaks will continue to occur, needlessly hospitalizing and killing the unvaccinated. But beyond these harms, the disease's resurgence serves as a serious warning about the country's capacity to manage infectious disease threats of all kinds.

An eliminated disease returns

Measles' return is no mystery: At its root is the falling vaccination rate.

Around 90% of the U.S. population has received the MMR vaccine, which protects against measles, mumps and rubella, and in some regions of the country, the rate is below 60%. Since about 2019-2020, that overall number has dropped below the 95% needed for herd immunity. It is necessary to keep that rate nationally, but maintaining herd immunity at the local level is equally important in order to prevent measles from finding pockets of unvaccinated communities.

Countries that remain free of continuous transmission for 12 months are deemed to have eliminated measles — a designation the U.S. achieved in 2000. The Pan American Health Organization was scheduled to decide in April whether the U.S. should lose that designation, but the organization postponed its meeting until November.

Current trends suggest that both the U.S. and Mexico, which has also been battling the disease, may lose this status — as Canada did in November 2025. All three countries have seen their vaccination rates fall below the 95% threshold, and their outbreaks may share epidemiological links.

A serious, long-term threat to US health

By any measure, the ongoing U.S. measles outbreaks signal that the disease has returned in a way that will have serious adverse health consequences. In 2025, three people died from measles in the U.S. That is more than in any year since the disease’s elimination 25 years ago.

Of the country's 2,283 confirmed measles cases in 2025, 11% were sick enough to be hospitalized. In South Carolina, where most measles cases have been reported in 2026, hospitals don't have to report when patients are admitted due to measles complications, so the actual number of hospitalizations due to measles could be much higher.

People who recover from measles can experience complications such as pneumonia, which can lead to death, or encephalitis, which can later lead to deafness or intellectual disabilities from the brain swelling. The virus can also affect the immune system, making people more susceptible to other infections over the long term, even ones they've had before.

In rare instances — though more likely if someone is infected as a child — measles patients can develop a progressive dementia known as subacute sclerosing panencephalitis, or SSPE, anywhere from two to 10 years after their infection. SSPE always leads to death. This past year, a school-age child in Los Angeles died of this condition years after being infected with measles as an infant, before they were old enough to be vaccinated.

Measles is an economic scourge

Recurring outbreaks of measles in the U.S. will mean high economic costs. Countries have pursued measles elimination in part because of the clear economic benefits of stopping domestic transmission of the virus.

Studies have found that the cost of containing measles outbreaks is often as much as tens of thousands of dollars per case. One outbreak in Washington state in 2018-2019, which involved 72 cases — a small outbreak compared with what states are reporting now — cost US$3.2 million for the public health response, medical expenses and productivity losses. The Common Health Coalition found that a sustained 1% drop in MMR coverage would cost the U.S. billions across health care systems and the economy.

An opening for infectious disease

As concerning as recent outbreaks of measles have been, they herald a larger systemic problem.

How a country controls measles can be viewed as a proxy for how well it would control many other diseases. That's because the steps for stopping the spread are the same: deploying vaccines to prevent infections, detecting and isolating cases when they occur, identifying exposed contacts of infected people and making sure they stay home if they're likely to be contagious, and treating sick people safely.

But besides measles, we've already seen infections that were once controlled, like whooping cough, that rose sharply in 2024 and remained high in 2025 compared with before the COVID-19 pandemic.

That's because controlling the spread of many infectious diseases depends on the public's trust in the basic components of public health. Declining MMR vaccine coverage reveals underlying challenges in public support for vaccines. Public confidence in the current Centers for Disease Control and Prevention is also eroding, according to polling from 2023 to early 2026 by the health policy organization KFF. Less than half of the people polled trust the government even "a fair amount" to provide reliable vaccine information.

These growing cracks in the country's public health armor will complicate efforts to protect Americans from future disease threats — whether an outbreak, a pandemic or a biological attack.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

A single gene mutation protects against Alzheimer's disease in people destined to get the disease very young — and now we know why.

The gene mutation affects a protein called reelin that directs brain cells to shred the probable culprits in the disease — toxic amyloid plaques and tau tangles. The mutation makes reelin work much more efficiently, new research reveals.

The finding could point the way towards transformative therapies for the condition, experts said.

"I would never have expected that it would be so protective that it actually negates the effect of a dominant early onset Alzheimer's disease mutation," Dr. Joachim Herz, a neuroscientist at the University of Texas Southwestern Medical Center who was not involved in the new research, told Live Science. "That I would never have in my wildest dreams predicted."

A tale of two genes

Unpacking how the protective mutation worked began with a population that faced the opposite problem: an extraordinarily harmful mutation that accelerates Alzheimer's disease.

For decades, people in the lush valleys near Medellin, Colombia, had faced premature memory loss.

Neurologist Dr. Francisco Lopera grew up in the region. While he was still a medical student, he came across his first case, a 47-year-old man displaying memory symptoms usually seen in elderly people with dementia. Lopera traveled across the region, determined to map where people were facing early memory loss. He ultimately identified thousands of people affected by a rare genetic form of Alzheimer's disease. The condition was autosomal dominant, meaning that anyone carrying at least one copy of the mutated presenilin 1 (PSEN1) gene would, like clockwork, lose their memories in their mid-forties.

Lopera's work in mapping this affected population was invaluable to dementia research, but his most important contribution came just a year before he died in 2024. He co-authored a paper in the journal Nature Medicine that detailed the case of a patient he met in his travels across Colombia. This patient had the PSEN1 gene mutation but lived well into his 60s before developing Alzheimer's. This was the neurological equivalent of a house that stays standing for decades despite cracks in its foundations that should give way.

Lopera discovered that this man's resilient brain was strengthened by another mutation, dubbed COLBOS after the research centers in Colombia and Boston that characterized it.

Improving efficiency

The new research, published in December 2025 in the Journal of the American Chemical Society, has identified exactly how the COLBOS mutation protected the patient's brain for decades.

When the COLBOS variant was first identified in 2023, scientists noted that the mutation altered how a cell signaling protein called reelin functioned. The protein promotes the formation of new connections between brain cells, prevents the toxic tau protein from becoming activated, and prevents amyloid plaques from building up in the brain.

COLBOS altered how reelin binds to another signaling molecule called heparan sulfate, a sugar found on the cell surface of virtually all cell types in humans, including neurons. But how reelin's binding ability affected Alzheimer's progression remained unclear. In the new paper, molecular biologist Chunyu Wang and colleagues at the Rensselaer Polytechnic Institute in New York mapped this process.

Wang's study relied on a technique called surface plasmon resonance, which reveals. how strongly a free-floating molecule — in this case, reelin — binds to a molecule anchored to a sensor surface — in this case, heparan sulfate. Wang's team saw that the COLBOS mutation acted like a molecular glue, strengthening the bonds between the two molecules, suggesting it could cause reelin to accumulate at the surface of neurons in the brain.

This change explained why COLBOS was able to ward off Alzheimer's. When reelin binds to heparan sulfate, the protein becomes localized to the surface of brain cells, where its anti-Alzheimer's signaling is most effective. Here, reelin can more easily ward off cognitive decline by slowing key Alzheimer's disease processes, such as the phosphorylation of the tau protein, said Wang. Phosphorylation destabilizes the normally ordered structure of tau, causing toxic tangles to build up in neurons.

Herz mapped out much of the reelin pathway 20 years ago in a series of papers. Herz's work was in mice, and although his team predicted reelin mutations could be neuroprotective, it was only through Lopera's tireless clinical work that the theory was proven.

Uphill battle

Unfortunately, as Lopera noted, the COLBOS mutation could only delay rather than prevent people with rare Alzheimer's mutations from getting the disease. Herz's theory is that patients with PSEN1 mutations exhibit malfunctions in organelles called the endolysosomal compartments. These are like cellular shredders that chop up troublesome proteins like tau and amyloid. He added that the COLBOS mutation makes the process of feeding these proteins into the shredders more effective.

But as the brain ages, Herz said, the shredder's defects become harder to overcome, despite reelin's effects, leading to Alzheimer’s.

The findings could have useful implications for future Alzheimer's therapies that delay or prevent disease in the vast majority of patients, including ones without high-risk PSEN1 mutations. Wang pointed to recent research that showed reelin-producing neurons are some of the first to die in Alzheimer's disease. Without these neurons, less reelin is made, toxic waste builds up, and Alzheimer's disease accelerates.

Wang hypothesized that if they could get reelin to act more efficiently at brain cell surfaces, even with less reelin present, that could protect such people from further symptoms. Wang is currently discussing with a colleague at Rensselaer the development of a gene therapy that enhances reelin signaling based on these findings.

Wang pointed out that even if researchers could delay Alzheimer’s by a fraction of the two decades that the COLBOS mutation granted to the Colombian patients, it would be by far the biggest disease improvement ever realized with Alzheimer's. Current drugs on the market for the condition may extend independent living by two to three years, tops, he said, so "20 years is amazing."

The patient: A 64-year-old woman in New South Wales, Australia

The symptoms: The woman was admitted to the hospital after experiencing abdominal pain and diarrhea for three weeks. She also had a persistent dry cough and night sweats.

A CT scan of her lungs showed opaque areas where the tissue had thickened, likely due to inflammation or an infection that caused the air spaces in the lungs to fill with fluid, pus or a buildup of white blood cells. The woman also had lesions, or areas of damaged tissue, in her liver and spleen.

When doctors sampled fluid from the patient's lungs, they found an unusually high percentage of eosinophils, a type of infection-fighting white blood cell. At that time, they diagnosed the woman with a rare lung condition called eosinophilic pneumonia and prescribed a daily dose of the steroid prednisolone, which relieved some of her symptoms. They noted that the cause of the lung infection was unknown.

What happened next: Three weeks later, the woman returned to the hospital with a cough and a fever, despite still taking prednisolone, and the lesions on her organs had not healed.

Further tests failed to identify the cause of her respiratory distress. Tissue sample cultures showed no signs of bacterial or fungal infection. Blood work showed that her immune system wasn't producing antibodies to various parasitic flatworms, such as blood flukes (Schistosoma) or liver flukes (Fasciola). Nor was there any evidence of these parasites in her fecal samples.

Doctors advised the patient to continue taking prednisolone and also prescribed her ivermectin, a treatment for parasitic worms, as she had informed the doctors that she'd traveled to countries where such parasites are common.

But her respiratory symptoms did not go away, and they worsened when she attempted to reduce the prednisolone dosage. Her condition continued unchanged for several months.

The diagnosis: About a year after her initial hospital visit, the woman began to develop signs of depression and had episodes of forgetfulness. Physicians ordered an MRI of her brain and detected a lesion on the right frontal lobe. They then performed an open biopsy to expose and examine the damaged area. That's when they discovered "a stringlike structure" inside the lesion, which they identified as a living parasitic worm called a helminth, according to a report of her case.

The worm was bright red and measured about 3 inches (80 millimeters) long and 0.04 inches (1 millimeter) thick.

The treatment: Doctors removed the helminth from the woman's frontal lobe and examined the surrounding tissue, where they found no more parasites. They gave her ivermectin for two days, this time in combination with a four-week course of albendazole, a broad-spectrum drug for treating helminth infections, to kill any lingering parasites in her organs.

Albendazole is absorbed by the central nervous system more quickly than ivermectin is, and these drugs have previously been used together to treat nematode infections in humans and snakes. The patient also received a 10-week course of the corticosteroid dexamethasone, to prevent additional inflammation.

Six months after the surgery and three months after the end of the dexamethasone course, the lesions in the patient's lungs and liver were gone, her white blood cell count was normal, and her neuropsychiatric symptoms had improved.

What makes the case unique: The doctors identified the helminth as a third-stage larva of Ophidascaris robertsi, a type of parasitic nematode native to Australia. The adult worms reproduce inside carpet pythons (Morelia spilota), but the nematode can infect other animals during the larval stages of its life cycle.

Carpet pythons were common near the woman's lakeside home, and although she did not recall having any direct contact with snakes, she often foraged wild greens for cooking. She likely became infected after touching or eating plants contaminated by O. robertsi eggs, the case report authors suggested. After the eggs hatched, the larvae migrated to her organs.

The longevity of this larval infection wasn't unusual, as laboratory rats can host O. robertsi larvae for more than four years, according to the report. However, no human infection by this parasite had ever been documented, nor had the parasite's larva ever been found in the brain of its host.

For more intriguing medical cases, check out our Diagnostic Dilemma archives.

This article is for informational purposes only and is not meant to offer medical advice.

People with obesity are 70% more likely than those without the condition to be hospitalized with or die from severe infections, according to a new study of over half a million people.

The research found that 1 in 10 deaths attributed to infections worldwide were in people with obesity. This link persisted even in people with obesity who did not have metabolic syndrome or diabetes. And it showed up regardless of socioeconomic status or physical activity levels, researchers reported Feb. 9 in the journal The Lancet.

"People with obesity may find it harder to fight off infections," study senior author Mika Kivimäki, an epidemiologist at University College London, told Live Science. "Extra body fat can affect the immune system in several ways, including impairing lymphatic function, reducing lung function, and increasing long-term low-grade inflammation." The lymphatic system helps to maintain a balance of fluids in the body, as well as to train and ferry immune cells around.

An earlier study by different researchers, published in August 2025, found that using semaglutide — the active ingredient in drugs like Ozempic and Wegovy — reduced users' risk of severe infections by 10%. That finding might also hint that obesity and infection susceptibility are linked and, perhaps, suggest that the risk can be lowered.

The connection between obesity and the dangers of infection were made prominent during the COVID-19 pandemic, the new study found. In 2021, 15% of all infection hospitalizations and deaths were linked to obesity. That connection between obesity and COVID-19 severity motivated Kivimäki and his team to investigate whether the coronavirus was uniquely dangerous for people with obesity or whether the danger extended to all types of infections.

They turned to the UK Biobank, a large database of genetic sequencing and linked medical records from U.K. adults, as well as two similarly large studies from Finland: the Finnish Public Sector study and the Health and Social Support study. Together, these databases included over 540,000 people.

In the Finnish cohorts, participants self-reported their heights and weights, which could be used to calculate a body mass index (BMI). BMI is a rough estimate of body composition often used in large-scale population studies. The UK Biobank participants had more precise measurements done with a body-composition device, and they also had their waist circumferences measured. (Some researchers have argued that these types of metrics should replace BMI, as they're more useful for predicting health outcomes.)

In the study, people with obesity included those with a BMI of 30 or higher; a waist circumference of over 40 inches (102 centimeters) in men or over 35 inches (88 cm) in women; or a waist-to-height ratio of 0.6 or more. Obesity was linked to a 70% greater chance of hospitalization with or death from infection, once adjusted for age and sex. This relationship held across different definitions of obesity and across all bacterial, viral, fungal and parasitic infections.

The results also showed that the greater the degree of obesity, the greater the risk.

People with a BMI of 30 to 34.9 had a 50% higher risk of infection, hospitalization or death, compared with people with BMIs under 30. But people with a BMI of 35 to 39.9 had twice the risk, and people with a BMI of 40 or above had three times the risk. In participants with follow-up measurements of obesity after their first baseline measurement, those who lost or gained weight saw their severe infection risk drop or rise in turn.

The nature of the study did not enable the researchers to prove causation or tease out precisely how obesity might raise these risks, Kivimäki said.

That said, evidence suggests that fat tissue and the immune system are enmeshed; the precursor cells that can turn into fat cells can act like immune cells, and some fat cells also excrete pro-inflammatory substances, said Nikhil Dhurandhar, a professor of nutritional sciences at Texas Tech University who was not involved in the new research.

Previous studies have found not only that weight can influence infection risk but also that certain pathogens are linked to the development of obesity, Dhurandhar told Live Science. The evidence that certain germs drive increases in fat has mostly been gathered in lab animals so far, while the human data is less conclusive.

Obesity can contribute to immune dysfunction that makes it harder for the body to fight infection, Dhurandhar added. Because of this dysfunction, people with obesity may not respond as well to vaccination as do people with weights categorized as overweight or normal, leaving them vulnerable. Obesity is tied to a lack of sensitivity to the hormone leptin, which helps regulate body weight and appetite and also has an immune-protective role, he said.

Dhurandhar said the 1 in 10 infection deaths linked to obesity in the study shouldn't be considered easily preventable by weight loss, because it is very difficult to lose weight and keep it off.

"Obesity is a disease," he said. "It's a chronic disease. It's not a matter of willpower; it’s not a matter of discipline."

However, the emergence of drugs like semaglutide, collectively known as GLP-1 agonists, may make weight loss easier for some people. The effect of these medications on risks from infection remains to be seen, Kivimäki said.

While trials hint that these medications reduce the risk, people taking these drugs also often lose muscle mass along with fat, which could have negative effects on the immune system. Muscle tissue provides an amino acid called glutamine that powers some immune cells, and also produces the anti-inflammatory compound interleukin-6.

"In our future research, we want to better understand why obesity raises the risk of severe infections," Kivimäki said, "and, importantly, what can be done to reduce that risk."

This article is for informational purposes only and is not meant to offer medical advice.

For most of modern medical history, scientists have framed infectious disease as having two possible outcomes: recovery or death. You either get better, or you do not survive. But this binary has never fully captured reality.

For a substantial number of people, illness does not simply end — it lingers, reshaping and even permanently altering their life trajectories.

Vaccines are critical tools for avoiding these debilitating outcomes, not only because they help prevent individuals from getting sick, but because they also prevent the multitude of post-infectious conditions that can arise months or years later. By undermining the public's confidence in vaccines and cutting research funding, the second Trump administration is not only increasing the risk of infections, but expanding the population left with chronic post-infectious disease — at the very moment science should be mobilized to prevent, diagnose, and treat both.

The COVID-19 pandemic forced the concept of post-infectious conditions into public view.

Long COVID — marked by persistent fatigue, exhaustion after exercise and effort, cognitive dysfunction ("brain fog"), headaches, and a host of other multisystemic symptoms — affects an estimated 10% to 20% of adults and children after their initial infections. For many, these symptoms are not mild annoyances but life-altering disabilities, disrupting their ability to work, attend school, or participate fully in daily life.

While long COVID may feel unprecedented, it is far from novel. What is new is our collective awareness that such a condition exists, and our opportunity to intervene.

History tells a consistent story: major infectious disease outbreaks are often followed by waves of chronic illness in a subset of survivors. After the 1889-1890 pandemic, often called "Russian influenza," physicians documented prolonged post-viral syndromes that they termed "influenza exhaustion." Affected patients reported months to years of fatigue, muscle pain, anxiety, sleep disturbances, depression, and neurologic symptoms. The phenomenon was so widespread that entire medical texts were devoted to describing it.

A few decades later, the 1918 H1N1 influenza pandemic left an even darker legacy. In its wake emerged encephalitis lethargica, a devastating post-infectious condition marked by encephalitis (brain inflammation) and catatonia, a condition that leaves a person unresponsive to the world around them. It also came with profound neurologic impairment and coma-like states in some of those affected.

Between 1919 and 1927, the British Ministry of Health recorded nearly 16,000 cases, with an estimated mortality rate approaching 50%. Of those who survived, only a small fraction fully recovered; many were left with lifelong disability. Children were disproportionately affected — in 1924 alone, more than 1,000 schoolchildren in England had developed the condition, two-thirds of whom never returned to their baseline health.

This pattern repeated throughout the 20th century. During the poliovirus epidemics that swept the Northern Hemisphere, most infected individuals experienced only mild illness, while others developed paralytic disease. But the story did not end with acute infection. Years or even decades later, some polio survivors, regardless of the initial severity of their infection, developed post-polio syndrome. This was marked by progressive muscle weakness, severe fatigue, debilitating pain, and, in some cases, paralysis. The unpredictability of who would be affected, and when, remains one of polio's most unsettling features.

More recently, survivors of the 2002-2004 SARS outbreak experienced what is now known as "Long SARS," with persistent pulmonary disease, muscle wasting, sleep disturbances, fatigue, and cognitive impairment lasting a year or more. SARS, a close relative of SARS-CoV-2, foreshadowed the post-viral syndrome that would follow COVID-19.

And after the 2014-2016 West African Ebola epidemic, many survivors reported chronic eye complications, musculoskeletal pain, neurocognitive deficits, and profound fatigue, despite having already survived a virus with a fatality rate exceeding 40%.

Across time, geography, and pathogens, the lesson is strikingly consistent: surviving an infection does not always mean recovering from it. Knowing that history repeats itself, it becomes clear that prevention is not just a tool for avoiding acute illness, but our most powerful strategy for preventing chronic disease. Simply put, vaccines are indispensable.

Vaccination does more than reduce hospitalizations and deaths. By preventing infection in the first place, vaccines can also prevent the downstream risk of long-term medical problems that we still cannot reliably predict, treat, or reverse. The only proven way to eliminate the risk of post-infectious chronic illness is to avoid the infection altogether.

Yet public confidence in this foundation has been steadily eroded. Conflicting messages from the Health and Human Services Secretary Robert F. Kennedy Jr., politicized health decisions, and policies that stray from evidence have left families — especially those with children — struggling to know whom to trust. This confusion does real harm. It weakens vaccine uptake, increases circulation of preventable diseases, and sets the stage for future waves of chronic illness.

Modern medicine did not become extraordinary by accident. It became extraordinary because scientists and doctors embraced data, rigorous study design, and prevention. Vaccines are among its greatest achievements — not only because they save lives today, but because they spare lives from being permanently altered tomorrow.

While any medical intervention carries a degree of risk, the risks associated with vaccines are minor, and their profound benefit on human health is unmatched.

We are at a pivotal moment, with an unprecedented ability to unify and advance the study of post-acute conditions. Modern technology and communication now make it possible to interrogate their biology in ways that were previously unimaginable. If we have learned anything from more than a century of pandemics, it is this: history does repeat itself. Abandoning vaccines and evidence-driven medicine will not make us freer or healthier. It will, quite simply, make us sicker.

Opinion on Live Science gives you insight on the most important issues in science that affect you and the world around you today, written by experts and leading scientists in their field.

This article is for informational purposes only and is not meant to offer medical advice.

A vaccine designed using "DNA origami" activated more of the key immune cells needed to fight HIV than did traditional vaccines built upon protein scaffolds, a new mouse study found.

"DNA origami" refers to a precisely engineered, three-dimensional scaffold made of folded DNA that can hold and display viral antigens — bits of viruses that the immune system can recognize and attack.

The new mouse study's results, published Feb. 5 in the journal Science, suggest a "potential breakthrough" that could "transform the way we think about active immunotherapies and vaccine design," study co-author Mark Bathe, a professor of biological engineering at MIT, said in a statement.

Why could this origami approach be transformational? The answer may lie in how the DNA-based vaccines are seen by the immune system, compared to traditional vaccines.

How the DNA origami vaccine works

Conventionally, vaccines have relied on weakened or killed viruses to rouse immune cells to make antibodies against proteins found on that virus's surface. By binding to the proteins, the antibodies block the virus from invading human cells and flag the germ for destruction by other immune cells.

This process imparts immunity by prompting the body to make "memory B cells," which linger and get activated much faster if the same pathogen is encountered again.

But nowadays, rather than using whole viruses, many vaccines use only the surface antigens attached to synthetic, virus-like particles. These nanostructures mimic the size and geometry of viruses but cannot cause infection.

Most virus-like particles used today are built using protein scaffolds that the immune system sees as "foreign," so they trigger an "off-target" antibody response against the scaffold itself. In some contexts, this may dilute the responses against the antigen, previous studies suggest.

In the new study, scientists replaced the protein scaffolds with a DNA-based scaffold and, by doing so, sharply reduced those off-target responses. This new vaccine design produced up to three times more of the important memory B cells than state-of-the-art protein nanoparticle vaccines did.

John Moore, an HIV researcher at Weill Cornell Medicine who was not involved in the work, described the study as "elegant." It clearly demonstrates how eliminating scaffold-related immune responses pushes the immune response "in the right direction," he told Live Science.

He cautioned, however, that it remains to be seen whether the same degree of immune focusing will occur in humans.

An edge on the competition?

HIV evades the immune system by constantly reshaping its surface proteins so that antibodies that work against one strain often fail against others. That is why HIV vaccine design has been "incredibly challenging," said Adam Wheatley, an immunologist at the University of Melbourne who was not involved in the study.

What the vaccine needs to produce are "broadly neutralizing antibodies" against the virus, he said. These antibodies lock onto parts of the virus that barely change from strain to strain.

One example of such an antibody is called VRC01, which has been identified in a small number of people living with HIV whose bodies produce broad antibody responses. VRC01 targets a vulnerable region on HIV's outer envelope called the CD4-binding site. This is the "key" the virus uses to enter human immune cells, and it doesn't differ much between strains.

The challenge is that B cells that are capable of producing VRC01-like antibodies are extraordinarily rare in the human body, said Raiees Andrabi, an immunologist at the University of Pennsylvania who was not involved in the work. Activating those elusive cells "becomes an engineering problem," he told Live Science.

To target these rare B cells, the researchers carefully engineered the vaccine using an HIV antigen on the DNA scaffolding. Developed about a decade ago, the antigen they used mimics the CD4-binding site and selectively binds the rare B cells' receptors, thus initiating the production of broadly neutralizing antibodies.

The researchers got the idea to combine the antigen with DNA origami after testing the origami approach in an experimental COVID-19 vaccine. They'd found that the immune system showed virtually no response to the DNA scaffold.

"This property seemed especially useful for a case like HIV, where the B cells of interest are exceptionally rare," first study author Anna Romanov, an immunology researcher at MIT, said in the statement.

They hypothesized that delivering the antigen on a silent scaffold could reduce the competition with other irrelevant B cells, thereby boosting the "on-target" response against HIV. And in the study, they found the silent-scaffold approach had indeed amplified the B cells that produce broadly neutralizing antibodies. (That said, they have not yet assessed how many broadly neutralizing antibodies actually get made; that should be addressed in future work.)

"We were all surprised" that DNA origami outperformed the standard virus-like particles used in eliciting the desired B cell responses, Bathe said.

In general, it's unclear how bad it is for the body to generate an immune response against the scaffold, Wheatley said. But in the case of HIV, the desired B cells are so rare that even a modest off-target response seems to undermine the response against the target antigen.

The road ahead

The engineering of the DNA-origami vaccine was not straightforward; early versions produced weak immune responses. That was partly because, after injection, those vaccines failed to reach specialized immune cells inside the lymph nodes, where B cells train.

To correct this, the team redesigned the DNA particles to pack the HIV antigens more precisely and tightly. This enabled them to be carried into the right regions within the lymph nodes. The researchers also added a molecule to help activate T cells — immune cells help the critical immune response grow. This T-cell recruitment happens naturally with protein-scaffold vaccines.

"I think it is quite striking how efficiently they modified their DNA scaffold in a number of ways to get it to work," Wheatley said. "I guess the major utility of it is [that] it's really tunable."

Beyond HIV, the study authors suggest that DNA origami could be applied to make vaccines against other rapidly mutating viruses, such as influenza, where the effectiveness of the vaccine might be improved by focusing the immune response it triggers.

However, it remains to be seen how well this technique will translate to humans. HIV vaccination is "very difficult" and might have multiple components to help develop the immune response over time, Andrabi explained, adding, "It's not just going to be one or two shots."

However, he said, "they have figured out the first step."

A vaccine designed to fight HPV-driven head and neck cancers has shown promising results in a lab study in human tissues and mice.

If proven effective in humans, the therapeutic shot could complement standard cancer therapies, and its design may help scientists build better vaccines for other diseases.

Human papillomavirus (HPV), the virus behind most cases of cervical cancer, also causes several other cancers, including oropharyngeal cancer (throat cancer). In the U.S., about 70% of oropharyngeal cancers are linked to HPV. While over 100 strains of HPV exist, only 12 types are considered "high-risk" for causing cancer; almost all cases of HPV-related throat cancer are caused by the high-risk HPV strain 16.

The vaccine Gardasil 9 can prevent HPV infections and thus reduce the risk of these cancers down the line. But for people who already have HPV-related tumors, treatment still relies on surgery, radiation and chemotherapy. Combining a cancer vaccine with these conventional therapies could enhance their effectiveness by teaching the immune system to fight the cancer.

Now, scientists have engineered a cancer vaccine whose components are arranged in a unique structure. Similar to preventive vaccines, cancer vaccines train the immune system to recognize specific proteins — in this case, a protein found on HPV-positive tumors — and often contain ingredients called adjuvants that rev up the immune response. Rather than preventing the disease in the first place, though, cancer vaccines are generally used to treat the disease and help prevent its recurrence.

In lab studies of HPV-positive head and neck cancer, this new, carefully crafted vaccine slowed tumor growth and improved survival in mice, according to a study published Wednesday (Feb. 11) in the journal Science Advances.

Dr. Ezra Cohen, a head and neck cancer specialist at UC San Diego Health who was not involved in the study, said that if the vaccine works in humans, it could complement standard therapies.

"One can imagine a multi-modality approach to render a patient disease-free and then the vaccine to prevent recurrence," he said. But he cautioned that results in lab animals and isolated tissues don't always translate to humans. "The real test is in people," he told Live Science in an email. "But strong preclinical data, like these, make the chances of success in clinical trials higher."

In this case, the vaccine's underlying design is notable.

"The key finding is that the structure of the vaccine makes a significant difference," Cohen said. "Successful vaccination is not just about selecting the correct antigens [target proteins] but placing those antigens in the right sequence with other vaccine elements."

The vaccine uses spherical nucleic acids (SNAs) — globe-shaped DNA particles that enter immune cells and bind to targets more effectively than linear DNA does. Each SNA nanoparticle within the vaccine consists of a fatty core surrounded by an adjuvant and a fragment of an HPV protein from the tumor cells. The adjuvant mimics bacterial DNA and is recognized by the immune system as "foreign."

The researchers tested three designs, changing only how the HPV fragment was positioned. One version hid it inside the nanoparticle, while the other two versions had the HPV fragment on the surface of the particle, attached at different ends of the fragment's structure, known as the N terminus and the C terminus.

The version with the fragment attached to the surface via its N terminus triggered the strongest immune response, the team found. This design led killer T cells — immune cells that destroy infected, damaged and cancerous cells — to produce up to eight times more interferon-gamma, a key antitumor signaling protein. This made them more effective at killing HPV-positive cancer cells.

In mouse models of HPV-positive cancer, the vaccine significantly slowed tumor growth. Additionally, when tested in tumor samples collected from HPV-positive cancer patients, the N-terminus vaccine killed two to three times more cancer cells compared with the other two vaccine designs.

"This effect did not come from adding new ingredients or increasing the dose. ​It came from presenting the same components in a smarter way," study co-author Dr. Jochen Lorch, the medical oncology director of the Northwestern Medicine Head and Neck Cancer Program, said in a statement.​

"The immune system is sensitive to the geometry of molecules," he said. "​By optimizing how we attach the antigen to the SNA, the immune cells processed it more efficiently."

Looking ahead, study co-author Chad Mirkin, inventor of SNAs and director of Northwestern's International Institute for Nanotechnology, hopes this approach could help scientists redesign older vaccines that initially seemed promising but failed.

"This approach is poised to change the way we formulate vaccines," Mirkin said in the statement. "We may have passed up perfectly acceptable vaccine components simply because they were in the wrong configurations. We can go back to those and restructure and transform them into potent medicines."

This article is for informational purposes only and is not meant to offer medical advice.

The patient: An 18-year-old in Louisiana

The symptoms: The teenager, who was training to be a welder, developed a cough and was hospitalized with pneumonia and respiratory failure a week later. He was intubated at the hospital, meaning a tube was placed into his airway and attached to a machine to help him breathe.

The teen was six months into his welding apprenticeship, which involved working four hours per day, four days per week. He was otherwise healthy and reported being a nonsmoker with no history of excessive drinking.

What happened next: The doctors ordered a blood test, which revealed an infection with a bacterium in a related group of microbes known as the Bacillus cereus group. At that point, the doctors did not know which specific bacterial species within that group had caused the infection. But most often, B. cereus group bacteria cause intestinal infections, like food poisoning, not lung infections.

Although very rare, the teen's combination of symptoms, occupation and geographic location had previously been documented in cases involving welders in Louisiana and Texas. The knowledge of this rare phenomenon enabled the medical team to quickly identify the likely cause of his symptoms, they wrote in a report of the case.

The diagnosis: The patient was suspected to have welder's anthrax, an anthrax-toxin infection that presents as pneumonia in metalworkers. This severe respiratory disease is exceptionally rare, with only eight documented cases before this patient. All previous cases involved welders or metalworkers. Of those eight patients, only two recovered.

Anthrax is normally contracted following contact with the spores of Bacillus anthracis — a bacterium included within the B. cereus group. In the body, the spores produce anthrax toxin, thanks to anthrax-toxin genes they carry in their DNA.

Exposure to the spores can happen through a cut or scrape or if someone eats infected animal products or breathes contaminated air. The latter, known as inhalation anthrax, is the most lethal form of the condition, according to the Centers for Disease Control and Prevention (CDC).

Welder's anthrax is unusual in that it is caused by a different Bacillus species. Historically, it was thought that only B. antracis could produce anthrax toxin, but in recent years, it's been discovered that some other bacterial species within the B. cereus group share the disease-causing genes normally found in B. anthracis.

The fumes produced through welding are known to increase the risk of developing lung infections. The patient previously conducted shielded metal arc welding, which uses an electric current to join metal plates and produces more fumes than other welding types do.

The treatment: Before waiting for the final diagnosis, the doctors gave the patient four powerful antibiotics — vancomycin, meropenem, ciprofloxacin and doxycycline — that treat some of the most severe bacterial infections, including pneumonia.

Then, in partnership with the CDC, the medical team administered the anthrax antitoxin obiltoxaximab 34 hours after the initial diagnosis. This antitoxin, which in this case was obtained from the U.S. Strategic National Stockpile, targets the protective antigen of B. anthracis, the bacterium that causes the typical form of anthrax.

This case marked the first time obiltoxaximab had been used to treat welder's anthrax; a different antitoxin, raxibacumab, was administered in the one previous case where the patient received an anthrax antitoxin.

The patient recovered quickly after receiving obiltoxaximab, and his breathing tube was removed three days later. The doctors continued to treat him with antibiotics, and they also drained the fluid that had built up around his lungs — a common occurrence in patients with pneumonia.

The Louisiana State Public Health Laboratory tested the patient's blood and found he had been infected with Bacillus tropicus, a bacterium within the B. cereus group.

After 26 days of hospitalization, the patient was discharged with a personalized antibiotic regime. He had fully recovered by his three-month follow-up appointment.

What makes the case unique: There have been only nine known instances of welder's anthrax since the first recognized case in 1994. Only three patients have survived the illness, of which two received an anthrax antitoxin.

This new case is also unique because of the patient's young age; the age range of all previous patients was 34 to 56 years old. Additionally, the patient had been welding for only six months, whereas some individuals who had contracted the disease in the past had been welding for a decade or longer.

In an investigation of the case, the Louisiana Department of Health collected 245 soil and surface samples from the man's workplace and found that 11.4% were positive for anthrax-toxin genes. Limited airflow and ventilation, inconsistent use of personal protective equipment and eating in the work area were risk factors for the patient contracting the disease, the authors wrote in the case report.

However, notably, no one else at the patient's worksite became ill.

"The reason that this previously healthy young man was the only worker to become ill, despite the detection of anthrax toxin genes in multiple environmental samples from his worksite, is unclear," the authors wrote.

For more intriguing medical cases, check out our Diagnostic Dilemma archives.

This article is for informational purposes only and is not meant to offer medical advice.

Brain-training exercises may reduce the risk of dementia if they involve speedy thinking, whereas exercises involving memorization or reasoning have no effect on dementia risk, a two-decade-long trial suggests.

The finding could prompt researchers to design video games to help preserve users' cognitive function as they get older, some experts say.

As people age, their probability of developing Alzheimer's disease or another form of dementia increases, and these conditions affect nearly half of people in their 80s and 90s, Art Kramer, a psychologist at Northeastern University who was not involved with the new study, told Live Science. There is currently no cure for these disorders, but researchers are exploring interventions to reduce the risk of dementia. Some available drugs can help slow cognitive decline in early stages of the disease, but they're far from silver bullets.

Now, a trial that began in the late 1990s is pointing to non-pharmaceutical interventions that might help ward off dementia.

Weeks of training meant years of protection

At the study's start, 2,021 participants ages 65 and older enrolled in the long-term randomized controlled trial, whose results were published Feb. 9 in the journal Alzheimer's & Dementia. These participants were split into four groups. One group performed speed-training exercises, which required them to divide their attention between two tasks at once. The other three groups completed memorization exercises in which they used mnemonics; reasoning exercises that involved spotting patterns and using them to solve problems; or no cognitive exercises at all, as a point of comparison.

Participants in the three training groups completed up to 10 60- to 75-minute-long sessions over five or six weeks. Some participants also returned for up to four 75-minute-long "booster" sessions one to three years later.

Twenty years after the study began, the trial runners determined that only the speed-training exercises were linked to a reduced risk of Alzheimer’s disease and dementia. The effect was more pronounced in the booster group.

"If you were in the speed training group and you had the booster sessions, you had a 25% lower risk of having a diagnosis of dementia [by the end of the trial]," said study co-author Marilyn Albert, a neuroscientist at John Hopkins University. By comparison, dementia was just as common in the other two training groups as it was in the comparison group, suggesting the memory and reasoning tasks had no protective effect.

The trial results raise the question as to whether speed-training cognitive exercises, including certain brain-training video games or apps, could help guard against dementia.

"There are hundreds of those that exist in the marketplace" and claim to be designed to boost brain health, Kramer said. "When these things get commercial, sometimes people make claims that go beyond the data, so you always worry about that," he cautioned. But still, he argued that these games could theoretically achieve a similar effect to the speed-training cognitive exercises tested in the trial.

Albert, meanwhile, is hesitant to suggest that video games could recapitulate the effects seen in this study.

"Speed-of-processing training isn't a whole lot of fun. It's hard," she told Live Science. She argued that the most important factor of the speed-training exercises, which may be missing from video games, was that they were adaptive. They involved looking for objects in the center and at the edges of a computer screen to find two that match; the exercise would refresh faster and with more objects as performance improved.

This adaptation wasn't an element of the memory and reasoning exercises, which may explain why those didn't lead to a significantly reduced risk of dementia, Albert said.

One strength of the trial was that it included a large group of participants, a quarter of whom belonged to minority groups. "People who are Black or Hispanic have a higher risk of dementia," Albert said, arguing that their representation in the study may make the results more generalizable.

The next step is to investigate whether the exercises prompted any specific brain changes that delayed neurodegeneration.

"We need to understand the mechanisms, because if we did, then we could better design the interventions," Albert said. Kramer suggested following up with MRI scans to see how cognitive exercises alter brain anatomy in human participants.

He noted that scientists can train lab animals, such as rodents, to perform similar training exercises. "And then you can do things that are a bit more invasive," he added, such as changing the lab mice's genetic makeup to understand what genetic factors are at play.

In the meantime, scientists already know of other lifestyle factors that are tied to a lower risk of Alzheimer's disease and other forms of dementia, Albert noted. These include engaging in regular physical activity and maintaining blood pressure within the normal range. Someday, perhaps brain-training exercises will also become a common method to stave off dementia — especially since, in the trial, it took only a few weeks of training to protect the participants for 20 years, Albert said.

This article is for informational purposes only and is not meant to offer medical advice.

A first-of-its-kind trial demonstrates that AI-assisted mammography can improve the outcomes of patients with breast cancer, particularly those with aggressive disease.

While many people have only recently begun to use artificial intelligence (AI) in their everyday lives, the technology's use in medicine began about a decade ago, especially in the field of image-based diagnostics. Researchers have been training AI programs to recognize tumors and other signs of disease in various medical imagery, such as X-rays, MRIs, and tissue biopsies mounted on slides.

These images have been taken primarily from patients whose diagnoses were already known, in "retrospective" studies. Knowing the diagnosis enabled doctors to provide feedback to the AI, confirming that it correctly identified cancer or determined an image was cancer-free. These studies have shown that AI could be an invaluable tool in diagnostic medicine.

However, to know if an AI tool can really diagnose cancer and make a difference to patients, you need to have a "prospective" study — one in which patients who are diagnosed using the AI tool are then followed for several years to determine their health outcomes.

Now, researchers in Sweden have conducted a gold-standard trial to assess the use of AI in mammography screening. Results from the Mammography Screening with Artificial Intelligence (MASAI) trial, published Jan. 31 in the journal The Lancet, showed that mammography reading supported by AI can improve screening performance while reducing radiologists' workload.

This is the first time AI has been shown to improve the outcomes of patients with breast cancer.

Spotting cancer earlier

The practice of regularly screening patients has significantly reduced the incidence of late-stage cancer and breast cancer deaths in much of the world. But even with regular mammograms, some cancer may go undetected.

These "interval cancers" are not detected at an initial screening but get diagnosed within the next two years, or between two screening rounds. They are often missed because they are masked during the initial screen due to breast-tissue density or the tumor disguising itself as normal tissue. Or sometimes, they can develop very quickly between screening dates.

These cancers are invasive, spreading into nearby healthy tissues, and typically aggressive, resulting in worse patient outcomes. Declines in interval cancer rates are the best way to confirm that a screening method works, meaning it drives down late-stage cancer diagnoses by spotting more cases earlier.

"If you want to improve the efficacy of screening, then the interval cancer rate is a very good surrogate measure of breast cancer mortality," senior study author Dr. Kristina Lång, a breast radiologist and clinical researcher at Lund University in Sweden, told Live Science. "So if we can lower the interval cancers, it will likely have a positive impact on patient outcomes."

The MASAI trial included more than 100,000 women between the ages of 40 and 80 living in Sweden. It used a commercially available AI system that was trained on more than 200,000 examinations from medical institutions all over the world.

In a comparison group, mammograms were read by two radiologists, as is the standard in Sweden. In the AI-assisted group, the AI system analyzed mammograms for suspicious findings and provided a risk score of 1 to 10. Cases with a score of 1 to 9 were subsequently read by a single radiologist, while a score of 10 would be read by two radiologists. The AI system was also able to highlight the suspicious findings within the image so the human radiologists could easily review them.

The AI-supported screening identified more clinically relevant cancers than unassisted mammography did. "Clinically relevant" cancers are those that have the potential to progress and thus require medical intervention.

It also reduced the number of interval cancer diagnoses within the two years following the screen. This shows that the AI program was more effective at identifying cancers that might normally be missed by a human radiologist, allowing medical treatments to start earlier.

Reducing false positives

While cancer screening is mostly beneficial, there are some potential downsides, such as false positives and overdiagnosis. When a patient is called back for a recheck after a screening but does not have cancer, "that can be a really stressful experience," Lång said.

The latter situation, overdiagnosis, refers to situations where a screen detects a cancer that will ultimately cause no harm to the patient. Such cancers grow so slowly that they won't cause symptoms within a patient's lifetime or increase the chance of death. Overdiagnosis can subject healthy patients to unnecessary cancer treatments.

The goal of AI-assisted mammography is to improve the ability of the screening test to find cancer while mitigating these potential negative effects — and the study found that AI-assisted screening did not increase the risk of false positives and that it improved the detection of clinically relevant cancers.

Along with improving cancer detection, AI-assisted screenings could address the consistent shortage of radiologists available to provide cancer screening.

"In some places, you're lucky to find one radiologist to read the mammograms," said Dr. Richard Wahl, a radiation oncologist at Washington University in St. Louis who was not involved in the study. "If you don't have the expert radiologists, women can't benefit like they should from screening programs."

Additionally, as the few radiologists available work more hours, their performance decreases. But AI doesn't get tired, and its performance doesn't decline at the end of the workday.

"The workforce issue is real, and this [study] could have an impact," Wahl said. "I think people will gradually be interested in having AI-aided interpretation as a second set of eyes."

Lång and her team will be starting a screening trial in Ethiopia in March, during which they will use AI to support the rapid assessment of breast cancer using bedside ultrasounds within a screening program.

"The problem in these settings where they don't have a screening program is that many women come in with late-stage disease, and there are no radiologists there," Lång said. With AI support, Lång hopes to improve access to accurate screening and thus enable earlier diagnosis of breast cancer in these limited resource settings.

This article is for informational purposes only and is not meant to offer medical advice.

Around 90% of people are infected with Epstein-Barr virus at some point in their lifetimes. For most of them, the virus causes a mild, transient illness or no symptoms at all. But for a subset of people, Epstein-Barr can eventually contribute to chronic illnesses, such as lupus and multiple sclerosis, or to the development of cancer.

Now, new research uncovers 22 human genes that might make an Epstein-Barr infection more likely to turn into a chronic condition.

Researchers can't yet definitively say whether these genes directly make Epstein-Barr more dangerous, or whether they are part of an underlying immune suppression that allows the virus to persist at higher levels in the body than usual. But the new study should provide a jumping-off point, said Jill Hollenbach, a professor of neurology at the University of California, San Francisco, who was not involved in the study.

"My lab is already looking into the results and thinking about what we can learn from this and what other avenues of research it suggests," Hollenbach told Live Science. Hollenbach wrote a commentary of the new study accompanying its Jan. 18 publication in the journal Nature.

Nearly two dozen genes

Epstein-Barr virus can cause mononucleosis, better known as mono, a temporary illness notable for producing extreme fatigue. But even once the symptoms of mono disappear, the virus lies latent in the body, mostly in the immune system's B cells, which remember and defend against specific germs.

For most people, this latent Epstein-Barr virus causes no problems. But in other people, the virus persists at a higher, more active level. In these cases, it can raise the risk of certain nasopharyngeal cancers and lymphomas, and may fuel autoimmune disorders such as multiple sclerosis. Chronic, active Epstein-Barr has also been linked to heart and lung disease.

To understand why only some people seem to experience these chronic effects, Ryan Dhindsa at the Baylor College of Medicine and colleagues turned to an underexplored source of information: human DNA biobanks. These biobanks collect full gene sequencing data and health records for hundreds of thousands of individuals. In sequencing the human genome, they also happen to scoop up the DNA of any viruses that happen to be in residence inside cells.

"Typically, when we're analyzing human genome sequence data we ignore the reads that don't map back to a human reference genome. We just kind of throw them away," Dhindsa told Live Science. "Here, we decided maybe we could go through those reads that we normally throw away and see if we could recover viral DNA."

By combing through tossed-aside Epstein-Barr sequences from 750,000 people in the UK Biobank and the U.S. National Institutes of Health's All of Us biobank, the researchers were able to identify individuals — about 11% of the total — who had very high levels of Epstein-Barr DNA. They found that these high levels of viral DNA were associated with health conditions previously linked to Epstein-Barr, including diseases of the spleen and Hodgkin lymphoma.

The presence of viral DNA was also associated with conditions thought to be linked to Epstein-Barr, although less definitively: rheumatoid arthritis, chronic obstructive pulmonary disease (COPD), and lupus. Other associations in the data reinforce even less well-studied connections, including links between Epstein Barr and heart disease, kidney failure, stroke and depressive episodes.

In addition, the researchers found 22 genes tied to a higher likelihood that someone would be in the 11% of people with chronic Epstein-Barr. Many of these genes were in a region of the genome called the human leukocyte antigen (HLA) locus, which is known to code for the immune cells that present antigens — immune-response-triggering foreign molecules — to other immune cells.

"It seems like these variants changed the way an individual's immune response actually presents Epstein-Barr virus to the immune system," Dhindsa said, possibly making it harder for the body to suppress viral replication. That said, the data has only shown a link between these genes and persistent infection — more research is needed to prove cause-and-effect.

In people with high levels of Epstein-Barr, the researchers also saw variations in genes that regulate the immune system. One, the SLAMF7 gene, typically encodes for a cell-surface protein that helps the immune system's natural killer cells attack tumors. Another, called CTLA4, encodes for a receptor on T cells that helps keep the immune system from attacking the body.

"They found some really interesting results," Hollenbach said.

She and her team are now interested in looking deeper at the mechanisms that link the genetic variation to the immune response to Epstein-Barr. Meanwhile, Dhindsa and his colleagues are interested in using biobank data to search for other viruses that have long-term impacts on human health. Some examples are the cancer-causing viruses Merkel cell polyomavirus and human T-cell lymphotropic virus type 1.

The researchers are also eager to expand their methods to more diverse global datasets of human genes. While the All of Us dataset includes participants from a variety of backgrounds, the U.K. Biobank is predominantly made up of people of European ancestry.

"We need to be able to look at genetic differences across more representative samples in future work," he said.