Colorectal cancer rates have been rising in people under 50 since the mid-1990s. These early-onset cancers tend to be more aggressive and resistant to treatment than cancers in older adults — and now, scientists may be learning why.

A new study published Thursday (Oct. 29) in the journal Nature Medicine compared colorectal tumors from people between 29 and over 90 years old, and it revealed key differences between young and old patients.

The new findings might, in turn, help scientists uncover new ways to fight colorectal cancer in young people, said study co-author Ana Anderson, a professor of neurology at Harvard Medical School and a core faculty member of the Gene Lay Institute of Immunology and Inflammation at Brigham and Women's Hospital.

"I believe that our study is essentially a turning point now in the field," Anderson told Live Science. "Because up until now, we've had more questions than answers."

Many questions surround early-onset colorectal cancer, as the disease is rising in people under 50 even as it falls in older populations. It's now the leading cause of cancer death in the U.S. for people under 50, and its numbers are even on the rise among children and adolescents.

Beyond questions about what's driving this uptick in cases, another mystery has been why this disease is so deadly in young people.

"The clinical data suggests that the disease in the younger patients is more aggressive overall," Anderson said. "The patients, being very healthy otherwise, do not do well with treatment."

To investigate that mystery, Anderson collaborated with Dr. Kimmie Ng, an oncologist at the Dana-Farber Cancer Institute, and Dr. Ramnik Xavier, a gastroenterologist at the Broad Institute and Mass General Brigham. They used a method of analyzing RNA in cells that allowed them to work with frozen and banked tumor tissue. RNA, a cousin of DNA, reflects the genes that are active in cells. In all, the team analyzed 189 tumors: 54 from patients under 50 and 135 from patients over 50.

With that many samples, the researchers could look at gradual differences tied to each age group, instead of just comparing tumors between the younger and older groups overall. That enabled them to pinpoint subtle differences, Anderson said.

For starters, younger people had a higher proportion of connective tissue cells in their tumors than they did of malignant cancer cells. That pattern was flipped in patients of older ages. Having a smaller proportion of malignant cells might sound good, but connective tissue in tumors can secrete compounds that suppress the immune system, Anderson said. That helps protect the tumor from immune cells that might otherwise target its cells for destruction.

These connective tissue cells can also physically block chemotherapy drugs from getting to the cancerous cells. This could be one reason younger patients' cancers resist treatment, the researchers suggested.

Based on patterns of gene activity in the tumors, the researchers suspect that younger patients' cancer cells also show distinct activity related to cell-to-cell communication. That may help the cells migrate through the body more easily than cancer cells in older patients do. In other cancers, this kind of gene activity has been linked to more aggressive tumors and a greater chance that the disease will spread, or metastasize, Anderson said.

The study's results also turned up an intriguing mystery: the presence of lots of long noncoding RNA. These strands of RNA contain more than 200 building blocks, called nucleotides, that don't provide instructions for building proteins. Coding RNA, in contrast, is ferried to protein-building factories in cells to be used as blueprints.

Scientists don't know what much of this long noncoding RNA does in the body, nor do they understand what it is doing in the tumors specifically. However, they hope to find out.

Anderson and her team are already working on manipulating the RNA they found inside cancer cells in petri dishes. In time, this line of research could supply another piece of the puzzle, helping scientists understand why colorectal cancer is so aggressive in young people.

"It's a new avenue for research into this disease that we previously had no idea about," Anderson said.

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

A proposed change to decades-old guidance on hepatitis B vaccination would lead to a dramatic increase in chronic hepatitis B virus (HBV) infections among young people, a new modeling study predicts.

Previously, the Centers for Disease Control and Prevention (CDC) recommended that all newborns be vaccinated against HBV within hours of birth ‪—‬ a strategy known as "universal birth-dose vaccination." But in December 2025, the Advisory Committee on Immunization Practices (ACIP) advised ending this recommendation, and the CDC accepted that advice.

The new guidance would recommend birth doses only to babies whose mothers tested positive for HBV or whose HBV status was unknown. The guidance suggests that mothers who test negative should instead ask their doctors about whether their child needs a birth dose — an approach the CDC calls "shared clinical decision-making." The new recommendation states that babies who forgo the birth dose should be at least 2 months old before starting the HBV vaccine series.

Health experts widely criticized the proposed change when it was announced, and for the moment, its implementation has been put on pause by legal action. The modeling study, published Oct. 19 in the journal Annals of Internal Medicine, predicts what would happen if it came to pass.

"Overall, this modeling study has many strengths and I think presents an accurate projection of how the vaccine recommendations may impact future chronic HBV in the U.S.," Dr. Norah Terrault, a transplant hepatologist at the University of Southern California Keck School of Medicine who wasn't involved in the study, told Live Science in an email.

When caught in infancy or early childhood, over 90% of HBV infections become chronic. About 15% to 25% of people with chronic HBV go on to develop liver scarring (cirrhosis), a form of liver cancer called hepatocellular carcinoma, or another chronic liver disease. So, an uptick in chronic HBV infections would translate to an uptick in these harmful liver conditions.

Increases in infection

"Not every pregnant person is tested for hepatitis B," said study co-author Dr. Amir Mohareb, an infectious-diseases physician-investigator at Massachusetts General Hospital and Harvard Medical School. For those who are tested, there's a chance their results are inaccurate or that they're not provided the right care after testing positive. "Something can be missed at any step in the care process, so the vaccine dose at birth provides protection," he said.

Mohareb and his colleagues built a simulation model using published data, including the current prevalence of HBV and the screening rate among pregnant people. The team also factored in the HBV test's sensitivity, the share of children who are fully vaccinated by age 2, and the risk of developing chronic HBV infection in different age groups. They made estimates of how often children are exposed to the virus through contact with infected household or community members.

HBV is "very, very transmissible," Mohareb said. It can spread from mother to child at birth or through exposure to tiny amounts of bodily fluids, like blood from a scratch, after birth. So, even if a baby does not get HBV from their mother, if they are unvaccinated, they can still get from another family member or from other children.

With this data, the researchers tested what would happen if vaccination were postponed to 2 months of age for babies whose mothers tested negative. Among babies born in 2026, 19% more would have chronic HBV infections by age 20, compared with universal birth-dose vaccination, they found.

In this scenario, the babies would still start the HBV vaccine series, albeit two months later than usual. However, the CDC's proposed recommendation offers more wiggle room; it says that parents should consult with their children's doctors to "decide when or if their child will begin the hepatitis B vaccine series" at all.

The researchers ran a stimulation to compare these two scenarios: one where kids get their first shot two months late and one intended to capture this looser "shared clinical decision-making" scenario.

"Other vaccines whose recommendations employ similar language had uptake as low as 25%," Mohareb noted. This aspect of their modeling has some uncertainty, he emphasized, since it's unknown exactly how the public will respond to such loosening of the guidance.

The researchers assumed that about 87% of kids would complete the vaccine series by age 2 under the deferred strategy, while only 50% would under the shared decision-making strategy. That 50% coverage, in turn, would increase chronic HBV infections acquired by age 20 by 83%, and about 50% and 70% of those born under that guidance would be susceptible to HBV infection at age 20.

That's about 1.8 million people in this age group per year, compared with fewer than 250,000 under universal birth-dose vaccination. "This represents a population that is at risk for acquiring HBV via sex, drug use etc — behaviors more prevalent among young adults," Terrault said.

A "missed opportunity to protect against infection"

To test the robustness of the findings, Mohareb's team varied the most uncertain inputs across wide ranges and ran the model 1,000 times. In every simulation, the birth-dose strategy led to fewer chronic infections than either alternative.

These conclusions seem "robust" because "they are the same conclusions no matter how we change the numbers of the model," Mohereb noted. Though of course "the specific magnitude of change depends on how many people defer vaccination," he said.

The new study does not specifically show how many additional cases of liver disease or cancer would result from the uptick in HBV infections. But Terrault said that the risks of liver failure, cirrhosis and liver cancer "would be anticipated to increase due to the missed opportunity to protect against infection."

Mohareb stressed that he is in no way opposed to the principle of shared decision-making between doctors and patients. "They should always make the decision together," he said. "But we rely on our public health agencies not to tell us that we should be making decisions with the patient, but rather to tell us what policy would make us healthier as a country."

Childhood HBV infections in the U.S. dropped from more than 25,000 cases a year in 1985 to fewer than 100 reported cases in 2024. This steep decline is credited to HBV screening during pregnancy, antibody treatment for babies born to HBV-positive mothers and universal birth-dose vaccination.

"Certainly without following a universal dose vaccination recommendation there would be a lot more hep B infections early in life," Dr. Brian McMahon, a hepatologist and the director of the Liver Disease and Hepatitis Program at the Alaska Native Medical Center, told Live Science in an email.

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

More children, teens and very young adults are being diagnosed with colorectal cancer in the United States, and new research suggests they often experience aggressive forms of the disease.

While diagnosis rates are rising, the disease is still rare among young people. Colorectal cancer, which affects the lower intestines and rectum, is largely a disease of age: 55% of all colorectal cancers are diagnosed in people over 65, and only 16% occur in people ages 49 or younger, according to a 2026 study published in the flagship journal of the American Cancer Society. Only a few hundred cases per year are diagnosed in people under age 21 in the U.S.

Nevertheless, the numbers of cases in the very young are rising, even as colorectal cancer rates decline or hold steady in older individuals. This increase coincides with an overall rise in colon and rectal cancer rates in people under 50.

The reasons for this schism aren't entirely understood. People over 50 receive routine colonoscopies in which precancerous polyps are removed, and that likely accounts for much of the decline in colorectal cancer diagnoses in older adults. But researchers suspect that environmental factors, such as ultraprocessed foods and sedentary lifestyles, might be behind the growing rates in young people.

"Most of the research has really focused on the gut microbiome," the community of bacteria and other microbes that live in the gut, said Dr. Christopher Lieu, a professor of medical oncology at the University of Colorado Anschutz and a medical adviser to the nonprofit Colorectal Cancer Alliance.

Microbiome disruptions may spur inflammation, which, in turn, may trigger DNA mutations that cause cancer. But these mechanisms are complicated, Lieu told Live Science, and there likely isn't one simple reason young people's microbiomes may be getting disturbed.

"It's going to be extraordinarily more complex than that," he said.

Aggressive disease in young people

What researchers are starting to learn is that colorectal cancer in people in their early 20s or younger tends to be a more aggressive disease than that often seen in older people.

"We do feel like it is a bit of a distinct disease than what we're seeing in older adults," said Dr. Erica Arnold, a pediatric surgery research fellow at Nationwide Children's Hospital in Columbus, Ohio. In October, Arnold presented new research on colorectal cancer in people ages 21 or younger at the annual meeting of the American Academy of Pediatrics.

Arnold and her colleagues analyzed the cases of 84 patients diagnosed between 2012 and 2023. They found that the median age of diagnosis was 16 years old and the median duration of symptoms before diagnosis was only 12 weeks long.

Only about 20% of the patients had a close relative with colorectal cancer, suggesting that for many of these young people, the disease did not necessarily emerge due to hereditary factors.

Eighty percent of the study participants were diagnosed with Stage III or Stage IV disease, meaning the cancer had already spread locally and to lymph nodes or to other, distant organs when the patients were diagnosed. For comparison, in colorectal cancer patients of all ages, 60% are diagnosed in Stage III or IV, according to the Centers for Disease Control and Prevention (CDC).

In addition, Arnold said, one-third of the patients in their study had cellular markers of particularly aggressive cancer.

"Some of that might be related to delays in diagnosis," Lieu said, "but if you want my honest opinion, it does suggest that these cancers are developing differently."

The study's data was not nationally representative, but a recent analysis of CDC data has also found that colorectal cancer rates in youth are on the rise. In 1999, the diagnosis rate in kids ages 10 to 14 was 1 in a million. By 2020, it had risen to 6 in a million. For teens between 15 and 19, the rate of diagnosis went from 3 in a million to 13 in a million in that same time frame.

Unclear causes

There is no definitive reason for this rise, Lieu said. Research on the microbiome has suggested that processed food, antibiotic exposure in childhood, stress, reduced exercise and other lifestyle factors may contribute to this increased risk of colorectal cancer.

Some microbes may play a particularly strong role, at least in some cases of colorectal cancer. For instance, a specific variant of the common gut bacterium Escherichia coli is strongly associated with colorectal cancer; the variant carries a genetic segment and produces compounds that are toxic to genes. But this variant alone cannot explain all colorectal cancer cases in young people. Nor is it clear why the gut microbiome might be undergoing a shift in the first place.

"It may be a combination of food, antibiotic use and environmental exposures," Lieu suggested.

Regardless of the exact causes behind the cases, Arnold's new research pointed to the symptoms that deserve closer scrutiny in young people. Among the 84 patients in the study, 75% reported experiencing back and abdominal pain before their diagnosis, 45% had changes in their bowel movements, 43% experienced unexplained weight loss and 38% had rectal bleeding.

These are classic colorectal cancer symptoms, Arnold said, but they might be overlooked in this young age group because these same symptoms can have more common causes.

Parents should know that in most cases, stomach pain and gastrointestinal disruptions in kids are not caused by colorectal cancer, Lieu said, calling the cancer an "extraordinarily rare event." Nevertheless, pain or gastrointestinal upset that doesn't ease or that worsens over time needs a checkup, and symptoms like weight loss and blood in the stool are very unusual in kids and deserve extra attention.

"It's just important to investigate it to make sure we're catching colorectal cancer earlier rather than later in these patients," Arnold said.

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

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A gene variant called APOE4 dramatically increases the risk of late-onset Alzheimer's disease, the most common form of dementia. Now, emerging research is revealing APOE4's true role in the condition, and a new study pinpoints a possible way to treat it.

Historically, scientists studying Alzheimer's disease have focused on two proteins that accumulate in patients' brains: amyloid-beta and tau. However, there's a "third thing that people didn't pay attention to, until recently," said study co-author Li-Huei Tsai, a neuroscientist at MIT. That third thing is the accumulation of droplets of fat, or lipids, in the brain, she told Live Science.

The APOE gene makes proteins responsible for transporting fat around cells throughout the body and brain. A version of the gene called APOE4, which increases the risk of late-onset Alzheimer's three- to 12-fold, makes proteins that are less efficient at this function, Tsai said. But how APOE4 affects different brain cells was not clearly understood.

Tsai's team has been working to close that gap for about a decade.

"APOE4 can influence many different cell types," she emphasized. "It's not just one cell type."

Zeroing in on the clues

In past laboratory research, Tsai's team found that APOE4 causes a buildup of cholesterol in astrocytes, star-shaped brain cells that support the function of neurons. Genetic analyses suggested that the gene variant may mess with how these cells process fat.

Another study zoomed in on oligodendrocytes, cells that help insulate neurons' outgoing wires with a fatty material called myelin. This material helps neurons send messages more efficiently. APOE4 caused the oligodendrocytes to accumulate cholesterol. So, in lab mice, the team used a drug to help the cells get rid of that extra cholesterol, and it improved the cells' ability to make myelin and the mice's performance on cognitive tests.

In their latest research, published Thursday (Oct. 15) in the journal Cell Stem Cell, Tsai's team dug into the question of why APOE4 causes fat to accumulate in the first place.

They used stem cells to grow APOE4-carrying oligodendrocytes and then turned specific genes on or off, to see if they increased or decreased the formation of fat droplets. This screening pointed to a major group of genes involved in cell-to-cell communication, called the Wnt signaling pathway. This included a key gene called DKK1, which acts as a brake on this signaling system.

Disabling DKK1 — essentially lifting the brake — reduced the concentration of fat droplets in the cells, the team found.

In brain tissue samples from organ donors with APOE4, the team also found signs of low Wnt signaling. This finding "establishes a very strong link" between the signaling pathway and formation of fat droplets, said Rosie Jackson, a cell biologist at the University of Dundee who was not involved in this study.

APOE4's effects across the brain

The researchers then investigated exactly how Wnt signaling was disrupted in oligodendrocytes.

APOE4 seemed to decrease the cells' supply of a protein that helps relay Wnt signals. That helpful protein was being broken down by an enzyme whose levels had been boosted by the APOE4. In mice, the team used a drug to block that extra enzyme, and the treatment ultimately restored normal Wnt signaling, reduced fat buildup, and helped the cells make myelin properly.

This could change how scientists think about treating Alzheimer's disease, Jackson said. It "opens up a new wave of potential therapeutics" that could target the accumulated fats, rather than going after only amyloid-beta and tau, she said.

"I think that this is becoming a really common idea in the field — that we're going to need multiple medications that target slightly different elements," she told Live Science. "And targeting lipids will be a really important part of that."

That said, the findings have not been confirmed in humans yet.

"It's very encouraging that facilitating lipid clearance and lipid movement is a potential therapeutic avenue," said study co-author Joel Blanchard, a neuroscientist at the Icahn School of Medicine at Mount Sinai. The question is how we can do that in a safe and effective manner in humans, he said.

Blanchard has led other research that underscores APOE4's effects beyond fats and myelin. The gene variant may affect cells that support blood vessels in the brain by driving scarring and contributing to amyloid-beta buildup. It may also mess with the "trash collectors" inside astrocytes, again leading to a buildup of harmful proteins.

While cells with other versions of the APOE gene can put a lot of energy toward breaking down the proteins, APOE4-carrying cells put all their energy toward fat storage, Blanchard said.

But more research is needed to understand how to fix the problem, he said. Hopefully, targeting fat storage "could rescue not just one thing but multiple things that go wrong in the course of Alzheimer's disease," he told Live Science.

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

Flu season in the U.S. typically starts around late October or early November and peaks between December and February. But new data reveals that the current flu season is starting slightly earlier than normal.

According to the Centers for Disease Control and Prevention (CDC), around 3.4% of respiratory samples tested for flu came back positive for the week of Sept. 26. That's around seven times the rate compared with the same week in 2025.

The positive tests are coming mainly from Western states, including California, Washington and Arizona. Regardless of where you're located in the U.S., though, most people are recommended to get their annual flu shot in September or October, and the same goes for this flu season.

The annual flu shot is the best way to prevent hospitalization and death from seasonal influenza. Nearly everyone ages 6 months and older is recommended to get a flu vaccine, and older adults have several special options, including a high-dose shot, a vaccine containing an extra immune-stimulating ingredient called an adjuvant, and a brand-new mRNA vaccine.

Given that flu season is off to an earlier start this year, our latest poll asks whether you plan to get vaccinated or have gotten vaccinated already. Tell us your thoughts in the comments below.

Flu season is off to an early start in some parts of the U.S., data shows.

In a typical year, U.S. flu activity starts building in late fall — typically in October or November — and peaks between December and February. This year, flu activity is currently low but rising nationwide: During the week ending Sept. 26, 3.4% of respiratory samples tested by clinical labs were positive for flu, according to Centers for Disease Control and Prevention (CDC) data.

That's about seven times the rate that was seen at the same point last year. About 0.5% of samples tested positive during the week ending Sept. 27, 2025.

"This particular year, it appears to be starting early — like right now," Dr. William Schaffner, a professor of preventive medicine and infectious diseases at Vanderbilt Health in Tennessee, told Live Science. Patients at clinics in his area are already testing positive for flu, he said.

The early uptick in flu is mostly unfolding in Western states, including Washington, California and Arizona. In Washington, for example, the share of emergency department visits diagnosed as flu climbed from 0.25% in the week ending Aug. 29 to 1.34% in the week ending Oct. 3, according to CDC emergency department data. That's a more than fivefold increase over six weeks.

Where the flu took off first isn't a warning sign in itself, Schaffner noted.

"There's nothing unusual about flu starting in the West Coast and moving east," he said. Recent seasons have more often begun in the Southeast or Midwest, he noted, but "it can start almost anywhere."

Leading with H1N1

Nowadays, seasonal flu is caused by three subtypes of flu viruses: two subtypes of influenza A, called H1N1 and H3N2, and the Victoria lineage of influenza B. (A second subtype of influenza B used to circulate but is now thought to be extinct.)

Last season, a fast-spreading version of H3N2 known as subclade K dominated. The CDC classified the 2025-2026 season as highly severe for children, as at least 195 children died of flu-related causes.

Schaffner likens influenza A and B to siblings. "They're very related, but they each have their own individual characteristics," he said. Influenza A strains usually cause the biggest outbreaks early in the season, while influenza B strains "kind of smolder along" and account for most cases toward the end, he noted.

This year, H1N1 has taken the initial lead. Of the influenza A samples that public health labs subtyped during the week ending Sept. 26, 96% were identified as H1N1, according to CDC data. That doesn't mean H1N1 will continue to dominate throughout the season; it just gives a snapshot of what's happening now.

The dominant strain matters because flu is "a moving target," said Dr. Paul Offit, director of the Vaccine Education Center at Children's Hospital of Philadelphia. The virus constantly mutates — especially hemagglutinin, the protein on the virus's surface that it uses to latch onto human cells. Hemagglutinin is the main target of flu vaccines.

An early start to the season doesn't guarantee it'll be a severe one, either. In its 2026-2027 season outlook, the CDC projected that this season will likely be moderate, although it has only low-to-moderate confidence in that forecast.

When to get vaccinated

Everyone 6 months and older is recommended to get an annual flu vaccine.

Influenza is especially dangerous for children under 5, adults 65 and older, people with chronic health conditions and pregnant people, as these groups are more prone to severe infections. Serious cases of flu can lead to complications such as pneumonia, sepsis, and brain or heart inflammation, and in some cases, they can be deadly. Tens of thousands of people die of flu each season in the U.S.

For flu vaccination, timing matters. The CDC generally doesn't recommend vaccination in July or August for most adults, because the shot's protection can wane over the course of a season. But with flu arriving early, "October is the ideal time to get vaccinated, and even more so right now," Schaffner said.

When circulating strains' features differ from those captured in the vaccine, "that usually predicts a more difficult season," Offit said. That said, it's too early to know if this year's flu shots are a good match for the circulating flu viruses.

Protection begins building right after you get the shot, but it takes up to about two weeks to reach full strength.

How much protection a flu vaccine offers varies by season, depending partly on how well its formulation matches the strains that circulate. Offit said that protection against symptomatic illness varies by age group and that the vaccines are "a little more effective" at preventing more severe illness. In terms of flu cases that prompt people to seek medical care, the shot has been 29% to 56% effective over the past decade, the CDC estimates.

While the vaccines are less reliable at preventing mild cases of flu, Schaffner said, they work best at "keeping you out of the hospital, keeping you out of the intensive care unit, and keeping you out of the cemetery."

The CDC's 2026-2027 guidance keeps its recommendation of an annual flu vaccine for everyone 6 months and older, with high-dose and adjuvanted shots preferred for adults 65 and older. (Adjuvanted shots contain an extra ingredient to help rev up the immune system.)

There's also a new option: In August, the Food and Drug Administration approved mFlusiva, the first mRNA flu vaccine, for adults 50 and older. (You can find out where mFlusiva shots are available near you using Moderna's vaccine finder.) With the mRNA shot, "you're less likely to get symptomatic disease," Offit told Live Science.

Traditional flu shots contain purified pieces of the virus itself, Schaffner explained. With mRNA, the vaccine contains a "blueprint" of those proteins — essentially a set of genetic instructions that the body's cells then use. In mFlusiva's case, those instructions code for hemagglutinin (the protein on the virus's surface that it uses to latch onto human cells) from each of three flu subtypes, Offit said. The mRNA then breaks down in the body, Offit noted. It "cannot influence human genetic material," Schaffner emphasized.

Whether this early start gives way to a heavy flu season should become clearer in the coming weeks, as the CDC's weekly surveillance reports will show whether cases keep climbing beyond the West.

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

Cases of dengue fever are surging in Florida, spurring several counties to declare a state of emergency.

The state has seen 497 reported cases so far this year. Of those, 252, or about 51%, were caught locally, rather than brought to the state by travelers. The Florida Department of Health confirmed one woman's death from dengue fever in early September, marking the state's first known dengue death in almost a century.

Prior to the past few years, most dengue cases reported in Florida were the result of travel. In other words, people caught the disease in other countries and then traveled to Florida, where their case was then diagnosed. At 245, the number of travel-related cases reported this year is not unusually high, Caroline Waddell, a public health researcher at the University of Florida, told Live Science in an email. However, the number of cases caught from local mosquitoes is more than five times higher than at this point in the year compared with any of the previous four years, she said.

Why are local dengue cases especially high this year? Live Science spoke with experts to find out.

A growing global health concern

Dengue fever is caused by the virus Orthoflavivirus denguei, which spreads from mosquitoes to people through the pests' bites; it doesn't spread from person to person. Aedes aegypti and Aedes albopictus mosquitoes transmit the virus to humans, and the same species can also carry the viruses behind yellow fever, Zika and chikungunya.

About 100 million to 400 million dengue infections happen annually worldwide, with about 800 cases reported in the U.S. historically, although that number has increased recently. Only about 1 in 4 people exposed to the dengue virus develop symptoms, which can include fever, headache, body aches, nausea and rash. About 1 in 20 cases become severe, and immunocompromised people, children, older adults and pregnant people are especially susceptible to these serious infections.

Severe symptoms can include abdominal pain, vomiting, difficulty breathing and bleeding of the gums or nose. The most severe forms of the infection can lead to leaky blood vessels, severe bleeding, shock, organ dysfunction and death. There is no specific treatment for dengue, so care focuses on managing symptoms and maintaining patients' vital signs.

Dengue has escalated as a global health concern in the past few decades. Between 2000 and 2019, global cases of dengue increased tenfold; between 1990 and 2021, dengue-related deaths doubled. Scientists say this surge is likely driven by climate change, since rising temperatures expand Ae. aegypti mosquitoes' range, in turn exposing more people to the insects' bites. Plus, warmer conditions speed up mosquitoes' life cycles and the dengue virus's replication rate, thereby boosting transmission.

International travel also factors into these rising case counts. In 2023, dengue spikes around the world were attributed to the resurgence of global travel following the COVID-19 pandemic.

Zooming in on Florida

As the global picture has worsened, dengue cases in the U.S. have also increased.

Nearly 3,800 cases were reported in 2024 ‪—‬ an increase of more than 300% above the annual average for the previous 10 years. The uptick was tied to a rise in travel-associated cases, reflecting the wider global surge, as well as to warming temperatures that brought dengue-carrying mosquitoes to new regions of the U.S.

Each year, Florida experiences dengue outbreaks in the southernmost parts of the state, such as Miami and the Florida Keys, Panpim Thongsripong, a disease ecologist at the University of Florida, told Live Science. Historically, outbreaks in Miami typically totaled around 50 or fewer cases. But then a 2019 outbreak resulted in over 200 cases, and from 2022 to 2024, outbreak totals have ranged from about 500 to 675 cases.

The outbreak currently unfolding in Florida centers on Hillsborough County, which is farther north and includes Tampa. This is unusual, Thongsripong said, as this region of the state normally sees just a few sporadic cases. Hillsborough County has reported 223 of the state's 252 locally acquired cases this year, and it's where the one dengue-related death took place.

Florida's health department regularly traps mosquitoes and tests them for viruses. So far this year, 20 pools of mosquitoes have tested positive for dengue across seven counties, and 19 of those positive pools were sampled from the greater Tampa area. In 2025, only four mosquito pools throughout the state tested positive, and in 2023, one mosquito pool did.

"Finding positive mosquito pools is rare in Florida because dengue is not endemic to the state," said Keira Lucas, deputy executive director of the Collier Mosquito Control District. "In many ways, it can be like looking for a needle in a haystack," she told Live Science.

Routine mosquito trapping is a relatively inefficient method for detecting viruses, though, Lucas said. As such, detecting dengue-positive mosquito pools may indicate that a large amount of transmission is already unfolding. "Since approximately 75% of dengue infections are asymptomatic, the virus can circulate within a community without being readily detected for some time," Lucas explained.

In addition to Hillsborough, neighboring Pasco and Pinellas counties have declared local states of emergency over dengue.

An unlucky combination of factors

So what's driving the unusual dengue activity this year?

In the past, Florida's local dengue outbreaks tended to be concentrated in the South, which saw moderate rainfall, warmer temperatures and more travel-related dengue cases compared with the rest of the state, according to a 2022 study in the journal Insects. With the outbreak concentrated farther north this year, that could suggest changing climatic patterns are making additional parts of the state especially hospitable to mosquitoes and the virus. That wouldn't necessarily explain why Tampa is seeing more local cases than Miami this year, but it could nonetheless be a factor in the overall trend.

For the virus to persist in local mosquitoes, dengue still needs to be reintroduced periodically through travel-related cases. Because the virus is not yet endemic to the state, it doesn't regularly circulate in local mosquitoes; however, a somewhat predictable "dengue season" has been emerging that coincides with upticks in international travelers carrying the virus to Florida.

This year, though, the high number of locally acquired dengue cases suggests a shift from predominantly imported infections toward outbreaks spurred by local Florida mosquitoes. Scientists hypothesize that climate change could increase local transmission in Florida even more in the future.

This year, Florida has also been enduring its most intense drought in over a decade. In theory, that might be expected to limit mosquito populations because the pests need water to breed, Lucas said. However, when it's dry, people tend to run their sprinklers more, creating mosquito breeding grounds when puddles form or containers fill up, she noted. This could bring mosquitoes closer to people, as it creates opportunities for them to breed.

Ae. aegypti mosquitoes are especially well adapted to living alongside humans, as they prefer to breed in human-made containers. Droughts can also drive dehydrated mosquitoes to bite more as they hunt for fluids.

"It's almost like an unlucky [combination]," Thongsripong said. "Everything coming together at the right time and right place, and boom, you have the conditions for an outbreak to occur."

The true number of dengue cases may be even higher than reported, Waddell said. The cases captured in the data include infected individuals who went to a doctor to get tested. Because many infections are mild or asymptomatic, additional people may have contracted the virus but never got counted.

What can be done

It's too early to definitively say what factors have increased Florida's dengue cases this year, Thongsripong said, as scientists are still gathering information. Despite the unknowns, she thinks the health and housing infrastructure in the U.S. will stop dengue from becoming too dangerous here.

To get dengue under control, it's key for government-level mosquito control efforts to coordinate and for the public to be aware of the virus, Lucas said. The mosquito control district coordinates with the health department for the latest data to best target where to spray larvicide, which kills mosquito offspring before they can bite people, she said.

It's important for people to use mosquito repellent when going outside, Thongsripong said, as well as to empty water from objects that can collect water and become a mosquito breeding ground, such as pets' water bowls, plant saucers, buckets or discarded tires.

Due to this year's strong El Niño, Florida is expecting a rainier winter, which could mean even more mosquitoes than usual, Lucas noted. That, in turn, could fuel additional dengue cases.

"Cases with September onsets are still being reported," Waddell said, "so we're not out of the woods."

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

Mpox is an infectious disease caused by a poxvirus, meaning a virus in the same family as smallpox. The infection was formerly known as monkeypox.

Historically, mpox was endemic to Africa, and the virus consistently spread in the continent's central, eastern and western regions. In 2022, an unprecedented global outbreak spurred the widespread transmission of mpox in places that had seen only sporadic cases in the past.

Today, many countries affected by that outbreak — including Germany, Portugal and the United States — are still contending with local mpox transmission. Here's what to know about the virus, how it spreads and how to prevent infection.

What to know about mpox in the U.S.

Mpox is still spreading at low levels in the United States and may soon be considered endemic to the country. While case counts have fallen dramatically since the peak of the global outbreak in summer 2022, some people are still advised to get vaccinated against the virus.

Who should get vaccinated for mpox?

The mpox vaccine currently used in the U.S. is called JYNNEOS. One dose is about 35% to 86% effective, while the complete two-dose series is 66% to 90% effective. (The effectiveness varies, in part, because some studies include people with HIV and people without HIV, and inadequately treated HIV can undermine the body's response to vaccines.)

The JYNNEOS vaccine is not currently recommended for routine use in the general population because, beyond vulnerable groups, the risk is not high enough to warrant a universal vaccination strategy. The current outbreak is primarily affecting men who have sex with men, and those sexual networks are the primary targets for JYNNEOS vaccination.

However, not all men who have sex with men need to be vaccinated, according to the Centers for Disease Control and Prevention (CDC). Instead, vaccination is recommended for a specific subset of the group, including those who, in the last six months, have had more than one sex partner, have had sex at commercial sex venues, or have been diagnosed with other sexually transmitted diseases.

Nonbinary and transgender people with these risk factors are also recommended to get two doses of JYNNEOS, as are any sexual partners of anyone in the above groups.

Vaccines are also recommended after a suspected exposure to mpox, as they can help prevent or reduce the severity of the infection.

"For those who are eligible and have not yet completed vaccination, now is a good time to talk with a healthcare provider about getting protected," Dr. Demetre Daskalakis, chief medical officer of Callen-Lorde, an LGBTQ+ community health center in New York City, told Live Science in an email.

With the exception of laboratory researchers who work with mpox, people who have received two doses of JYNNEOS are fully vaccinated and do not need a booster, he said. And if a person has caught mpox in the past and recovered, they do not need to get a vaccine, he added.

About the virus

The poxvirus family also includes smallpox, which has been eradicated worldwide. Mpox and smallpox cause some similar symptoms, but mpox tends to be far milder than smallpox. However, the viruses are closely related enough that vaccines designed to prevent smallpox can also protect against mpox.

Mpox was initially named monkeypox because the virus behind the disease was discovered in captive monkeys in Denmark. But monkeys are not the main hosts of the virus in the wild; rodents and small mammals mostly found in West and Central Africa likely are. Health officials changed the name to mpox in 2022.

There are two major branches of the mpox family tree, called clade I and clade II. These clades were historically thought to have very different death rates, with clade I being the deadlier of the two. The case-fatality rate (CFR) of clade I has been estimated to range from 1.4% to over 10%, depending on the outbreak, while the CFR for clade II has been estimated at between 0.1% and 3.6%.

However, as both clades have spread beyond Africa, data suggests that the CFR for clade I may be lower than once thought, said Joel Wertheim, a professor of medicine in the Division of Infectious Diseases and Global Public Health at the University of California, San Diego.

The features of a given outbreak — such as the surrounding health infrastructure, patients' access to timely medical care, and the population's underlying risk factors for severe disease — likely play a big role in determining the virus's death toll, Wertheim told Live Science. In short, rather than being an immutable feature of the virus itself, the CFR is dependent on the underlying health of and resources available to a given population.

How mpox spreads

Mpox can spread from infected animals to humans through the animals' bites or scratches. Additionally, people can get the virus when they come into close contact with animals and/or their bodily fluids during hunting, skinning, trapping, cooking, eating animals or handling carcasses, the World Health Organization (WHO) notes.

The virus also spreads from person to person, primarily through very close contact, including intimate contact during sex. The virus typically enters the body through broken skin, the respiratory tract or mucous membranes (thin tissues found in the eyes, nose, mouth, anus and genitals), spreading via bodily fluids such as spit, mucus or blood. People can also pick up the virus via objects, such as clothing or linen, that are contaminated with the bodily fluids of an infected person.

The virus can spread through small respiratory droplets expelled during speaking or breathing. However, this is thought to be a less-common transmission route than close contact. There is also evidence that asymptomatic spread sometimes occurs, though it's unclear how frequently that happens.

Mpox can spread from mother to baby during pregnancy or birth. This route of infection can result in pregnancy loss, stillbirth, death of the newborn, or complications for the mother.

Symptoms of mpox

Symptoms of mpox typically appear within a week of a person being exposed to the virus, but they can sometimes take up to 21 days to develop. Once they emerge, symptoms last about two to four weeks, although the illness can linger longer in people with weakened immune systems.

Common symptoms include rash (see images), fever, sore throat, headache, muscle aches, back pain, swollen lymph nodes and low energy. Often, mpox rashes first appear on the face and then spread to other parts of the body; however, if a person becomes infected during sex, the rash may instead start around their genitals. The rashes begin as flat, discolored patches of skin and then progress into raised bumps, blisters, and large, pus-filled pimples that eventually scab over and fall off.

Some people with mpox develop painful swelling of the rectum (proctitis), while others have pain and difficulty when peeing (dysuria) or when swallowing.

Mpox rashes can make people vulnerable to bacterial skin infections, which can cause abscesses or other serious skin damage. Additional complications of the illness include pneumonia, infection of the cornea that can cause vision loss, and vomiting and diarrhea that causes dehydration or malnutrition. Mpox can also lead to blood infections, the intense immune reaction sepsis and, rarely, brain infections (encephalitis) or heart inflammation (myocarditis).

Children, pregnant people, and people with weakened immune systems, including from HIV infection, have a higher risk of serious illness and death from mpox.

Mpox prevention measures

Beyond vaccination, other strategies to decrease the risk of mpox infection include washing hands frequently, avoiding contact with contaminated objects and materials used by people with mpox, avoiding contact with other people's scabs or rashes, and using condoms, although they may only reduce, not eliminate, the risk of mpox exposure during sex.

Mpox treatment

Mpox treatment aims to manage a person's rashes and pain while also preventing complications. "Early and supportive care is important to help manage symptoms and avoid further problems," according to the WHO.

There is no antiviral drug approved for use in mpox, although some are available for emergency use in various countries. For example, the U.S. allows the use of certain smallpox medicines for mpox.

Severe mpox infections also may be treated with vaccinia immune globulin intravenous, which contains antibodies taken from the blood of people who were immunized against smallpox.

People who have recently been exposed to mpox can be given an mpox vaccine to reduce the severity of their symptoms or to prevent the illness altogether. This approach is known as post-exposure prophylaxis, or PEP.

"Post-exposure vaccine should be given as soon as possible, ideally within 4 days of exposure; administration 4 through 14 days after exposure may still provide some protection against monkeypox," the CDC states.

Mpox spread across the world in 2022, triggering tens of thousands of cases in countries where the infection was once rarely seen. Although the disease has since fallen out of news headlines, mpox (formerly called monkeypox) continues to circulate. Now, recent data suggests that the viral illness may soon be endemic to the United States, meaning it will circulate in the country consistently.

Previously, mpox cropped up sporadically in the U.S. via travelers who had visited African countries where the disease is endemic, as well as imported, infected animals that spread the virus to people. Cases have fallen substantially since the peak of the outbreak in 2022, but they haven't disappeared. A report published in August found that there were 2,800 cases in 2024 and over 2,500 in 2025, with only a small fraction being tied to travel. Nearly all of the viral samples analyzed were descendants of the strain that sparked the 2022 outbreak. In short, once the virus arrived, it never went away.

"There's no set threshold for what constitutes endemicity of monkeypox virus (MPXV) in the United States," Ryan Standford, an epidemiologist in the Centers for Disease Control and Prevention's (CDC) Poxvirus and Rabies Branch and co-author of the report, told Live Science in an email. "But each year provides further evidence of this transition."

Why is mpox still spreading in the U.S., and what can be done to snuff it out? It's likely that too few people have received two doses of the mpox vaccine JYNNEOS, which together are 66% to 90% effective. But beyond low vaccination, there may be other, less-understood factors that are contributing to the continued spread, experts told Live Science.

"We don't quite know how it's able to persist at such low numbers across the entire country," said Joel Wertheim, a professor of medicine in the Division of Infectious Diseases and Global Public Health at the University of California, San Diego.

At the same time, public health efforts around mpox have dwindled. Without a sustained effort on that front, it's unlikely the disease will be eliminated from the U.S.

"We have vaccines, testing, and a much stronger understanding of the disease than we did in 2022," Dr. Demetre Daskalakis, chief medical officer of Callen-Lorde, a LGBTQ+ community health center in New York City, told Live Science in an email. "Our focus now should be making sure those tools remain accessible, especially for communities that continue to face ongoing risk," said Daskalakis, who coordinated the nation's mpox response during the previous presidential administration.

"People at increased risk should know that mpox has not disappeared."

Who is at risk of mpox in the U.S.?

In the U.S., mpox is predominantly affecting men who have sex with men, and current vaccine recommendations are aimed at this group and their sexual partners. Mpox mostly spreads from person to person through close contact, and transmission during sex is playing a major role in the ongoing spread in the U.S.

Men who have sex with men are not more prone to mpox infection than anyone else. Rather, this transmission pattern stems from the outbreak beginning within a specific sexual network and then continuing to persist within the same network. "The mpox virus rediscovered the same transmission network that HIV had explored decades earlier," Wertheim said.

In a paper published in 2025, Wertheim and colleagues described the transmission dynamics of mpox in New York City during the 2022 outbreak. Similar to how HIV previously spread, mpox triggered "densely connected" clusters of infection. Then, as people in the network gained immunity via infection and vaccination, the cases petered out, decreasing to the persistent trickle we see now.

Wertheim noted that he's not surprised that mpox has remained largely confined to the same network, rather than leaping into new groups.

"From an evolutionary, ecological perspective, it's not hugely successful," Wertheim said. "It's sort of barely hanging on as an STI."

Why is mpox still circulating?

So if mpox is not hugely successful and we have a vaccine, how has the virus continued to circulate? One big factor is that too few at-risk people have been vaccinated, experts said.

The CDC's Center for Forecasting and Outbreak Analytics has crunched the numbers to see what percentage of that at-risk group needs to have immunity to stop mpox transmission, Daskalakis said. The at-risk group is estimated by counting the men who have sex with men who are either taking HIV-preventing medicines or have HIV, and then adding 25% to that total to account for additional people in the same sexual network. That estimate comes out to about 2 million people.

To prevent an outbreak bigger than the one in 2022, between 21% and 35% would have to have immunity through vaccination or a past infection. If over 50% of the group had immunity, that would mean there's a "very small probability" of sustained local transmission, the CDC's modeling suggested.

The current case counts suggest we haven't hit the 50% mark, or a total of roughly 1 million complete vaccinations or past infections.

Data from the August report on mpox seems to support the idea that too few people are vaccinated. That said, information about vaccination status was missing for about 62% of the reported cases. Among the remaining cases, 76% were unvaccinated, while 10% had gotten one dose and 14% had gotten two.

In a subset of 860 cases, the effect of vaccination was striking: Unvaccinated people had nearly 10 times higher odds of hospitalization due to mpox than fully vaccinated people did.

Waning public health attention

It's difficult to pin down exactly how many at-risk people are vaccinated, given that that data is no longer tracked at the national level. "My understanding is that there's no mandatory reporting on mpox vaccination data," Wertheim said.

The CDC previously monitored national vaccination trends, comparing the number of people vaccinated to the overall at-risk population. But that tracking stopped in early 2024, when about 23% of the at-risk population had been fully vaccinated.

Some states, such as New York, previously mandated that clinicians provide their state health department data on the number of people given mpox vaccines. But that reporting is now voluntary, a spokesperson for the New York State Department of Health told Live Science in an email.

Meanwhile, "as the emergency phase faded from public attention, awareness and risk perception may have declined," Daskalakis said. Public health messaging about the virus and vaccination has also waned.

"In recent weeks, HHS [the Department of Health and Human Services] has pulled down some of the plain-language guidance, which is not helpful in supporting messaging," Daskalakis noted. This decision to remove online resources about mpox reflects the federal government's current stance against addressing issues that affect LGBTQ+ health, he told Live Science.

Complicating factors

Although JYNNEOS substantially lowers the risk of severe mpox infection, the vaccine is not perfect, said Rachel Roper, a professor of microbiology and immunology at East Carolina University.

The virus typically enters the body through broken skin, the respiratory tract or mucous membranes (thin tissues found in the eyes, nose, mouth, anus and genitals). The mpox vaccine is good at generating systemic immunity, but it's not as good at guarding against the virus's immediate effects at those mucous membranes, said Roper, who studies poxviruses and vaccines against them.

Because mpox is largely spreading through sexual contact that involves those membranes, that slight gap in protection may also help to explain some of the ongoing spread, she suggested.

Plus, "there are also some data supporting asymptomatic infection as a possible route of transmission, making it more difficult to eliminate local transmission of mpox," Daskalakis said.

What can be done?

Given that mpox is already well established within some sexual networks in the U.S., "preventing endemicity entirely may be increasingly difficult," Standford told Live Science.

And notably, some federal funding cuts could undermine efforts to address mpox, Daskalakis said. These include cuts to Medicaid, mental-health services, housing programs, and HIV services such as the Ryan White HIV/AIDS Program.

Thankfully, looking at current mpox trends, "there's no indication we're returning back to 2022 levels," Wertheim told Live Science. So far in 2026, just under 1,000 mpox cases have been reported, according to the CDC. Month over month, the number of cases is generally trending downward. So, at a glance, the current situation seems better than it was in 2025, he said.

"We sort of seem to be on this razor's edge between endemicity and extinction," he said. "And it's not really clear which way it'll go."

Tipping the virus toward extinction will require healthcare providers to be informed and equipped to spot and manage cases, Daskalakis said. And communicating the importance of vaccination is key.

"One lesson from 2022 was that trusted messengers matter," he said. "We [at Callen-Lorde] work closely with LGBTQ+ communities and make information and vaccination opportunities available in settings where people already receive care." The clinic integrates conversations about mpox vaccination into routine health visits, sexual health services, HIV prevention programs and community outreach activities.

Beyond vaccinating at-risk populations, educating patients about how mpox spreads and how to reduce their risk is also key, Standford noted. "Vaccination coverage is a very important factor, but it is not the only one," he said.

Tipping mpox toward extinction will also require enough investment to maintain the disease surveillance, vaccination, testing and treatment capacity that the federal government helped to expand in 2022, Daskalakis said. The vaccine itself is now commercially available to clinics and in adequate supply, he emphasized.

"The fact that we're seeing ongoing circulation underscores the need for sustained prevention efforts rather than viewing mpox as a resolved public health issue," he said. "Infectious diseases don't disappear simply because public attention shifts."

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

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About 1 in 8 cancer cases are caused by infections with viruses, bacteria or parasites, a new study finds, suggesting that one of the most effective ways to reduce cancer rates might be to prevent common infections.

In a new analysis published Sept. 28 in the journal The Lancet Oncology, researchers mapped the global impact of 12 cancer-causing pathogens. They estimate that infections drove about 2.3 million new cancer cases in 2024, or about 12% of all cancer cases diagnosed that year.

The study highlights that a large fraction of cancer cases could be avoided if these underlying infections were prevented, Dr. Prashant Mathur, director of India's National Centre for Disease Informatics and Research, who was not involved in the study, told Live Science in an email.

"When combined with other risk factors such as tobacco use, alcohol consumption, appropriate diet, physical activity, and environmental pollution, it is estimated that about 50 to 60 percent of all cancers in India are avoidable," he said. Past studies suggest that similar figures hold on a global scale.

In the new study, the researchers used the Global Cancer Observatory's GLOBOCAN database, which combines data from various cancer registries to estimate that about 20 million new cancer cases were diagnosed in 2024. The team combined that information with other published data examining the prevalence of different infections in people with specific cancers. This enabled them to estimate how many cases were attributable to each infection.

Their analysis focused on 12 pathogens tied to cancer, including human papillomavirus (HPV), hepatitis B and C, HIV and Epstein-Barr virus (EBV), the virus behind mononucleosis. The resulting breakdown revealed that just four pathogens accounted for roughly 92% of the cancer cases caused by infections.

A bacterium called Helicobacter pylori, which infects the gastrointestinal tract, accounted for 760,000 cases, primarily gastric cancers. The other three leading cancer triggers were viruses. HPV accounted for 750,000 cases, including cervical, penile, throat and mouth cancers. The liver-attacking hepatitis B virus was responsible for 360,000 cases and EBV drove 260,000 cases. (EBV is known to increase the risk of throat cancers, as well as certain lymphomas and stomach cancers.)

The scale of the burden contrasts with gaps in prevention. In 2024, just 31% of eligible adolescent girls worldwide received at least one dose of the HPV vaccine, well below the 90% target, the World Health Organization reports. The degree of protection provided by the vaccine is striking in countries that have achieved higher coverage.

"We have now achieved the critically important milestone of cervical cancer starting to disappear in countries that quickly achieved vaccination rates of over 80 percent," said Dr. Rebecca Perkins, an obstetrician-gynecologist at Tufts University School of Medicine who was not involved in the study. "Research from Australia, England, and Finland have shown zero cases of HPV-related cancers or deaths in young adults who received vaccination by age 13," Perkins told Live Science in an email.

But these successes are concentrated in wealthy nations. The Lancet study found that low- and middle-income countries bear 77% of the global infection-driven cancer burden. For example, about 81% of HPV-linked cancers occurred in these countries.

Perkins pointed out that shifting from the standard two-dose HPV vaccine series to a single-dose regimen using the same vaccines could make mass campaigns easier worldwide by lowering costs and eliminating the need to track patients for follow-ups. The single-dose approach has been backed by recent trials.

In the U.S., progress has been uneven across states with some boasting high vaccination rates and others lagging behind. One barrier is that some children's caregivers feel the shots are unnecessary or that their kids are too young to receive it. "The biggest misconception from families is that the HPV vaccine is not needed or that it can wait," Perkins noted. "The reality is that you can't vaccinate too early, only too late."

There is also a highly effective vaccine for hepatitis B, and health officials recommend giving children their first dose as soon as possible after birth. (The U.S. Centers for Disease Control and Prevention recently made the decision to stop recommending universal vaccination at birth, which experts say could raise the country's rates of hepatitis B infections and related cancers.)

While the challenge with HPV and hepatitis B is getting their vaccines into widespread use, there isn't an approved vaccine for EBV yet.

"The biggest hurdle has been the complexity of the virus," said Claire Shannon-Lowe, a tumor virologist at the University of Birmingham in the U.K. who was not involved in the study. "Unlike many other viruses that use just one or two virus proteins to enter cells, EBV uses multiple proteins ... and it hides inside cells for our entire lifetime."

Epstein-Barr infections are also incredibly common, with up to 95% of people infected by adulthood; most people infected with the virus don't develop a related cancer, but it's still a major contributor to the global cancer burden. The germ has also been tied to several autoimmune diseases, which may help spur the development of a vaccine, Shannon-Lowe suggested.

"With the increased impetus following EBV's association with multiple sclerosis and lupus, we may finally have a potential vaccine in sight that could not only prevent virus infection but could help treat EBV-associated cancers," she said.

For H. pylori, meanwhile, researchers are pursuing population-wide testing for and treatment of the infection to help prevent gastric cancer, while vaccine development remains an area in need of further investment.

The true scale of the infection-related cancer burden may be even larger than the study suggested. Some of the registries used in the new research cover only about 19% of the global population, and only 2% of Africa's population. More high-quality data is needed to fill in these gaps.

For Mathur, though, the bottom line is that cancer prevention makes economic sense.

"Studies have clearly demonstrated that the return on investment of prevention on cancers is much higher than on its treatment in the long run," he said. "Preventive aspects must be strengthened for long-term gains."

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

Scientists have identified an inherited genetic mutation that greatly increases the risk of lung cancer, even in people who have never smoked.

The mutation involves the EGFR gene, which helps control cells' growth, division and survival. People who had never smoked and who had the genetic mutation — called EGFR T790M — were 62 times more likely to develop lung cancer than nonsmokers without the mutation, according to the new study, published Thursday (Sept. 17) in the journal Science.

By comparison, people who smoked but didn't carry the mutation were four times likelier to develop lung cancer than nonsmokers, so the mutation alone carried a higher risk of the disease.

Among people in the study who smoked and carried the mutation, T790M increased their cancer risk 11-fold compared with other smokers.

This is a "very important finding," said Chris Amos, a genetic epidemiologist at the Baylor College of Medicine who wasn't involved in the study. "The prevalence of the T790M variant and its impact on lung cancer risk has previously been poorly understood."

The study included over 3 million people of European ancestry, and the mutation showed up in 1 out of every 15,850 people. Given that it's relatively rare, it likely doesn't account for a large percentage of overall lung cancer cases, Dr. Stephen Chanock, director of the Division of Cancer Epidemiology and Genetics at the National Cancer Institute, who wasn't involved in the study.

However, Amos argued that it is important to test whether a patient has this mutation when they have a family history of lung cancer in nonsmokers, or when their relatives are known to have the mutation. Having the T790M mutation not only influences a person's risk of lung cancer, but also affects treatment decisions for those who already have cancer, he said.

Combining genetic, geographic and historical data

For the study, researchers analyzed DNA and health data from over 3.3 million people who used 23andMe's at-home genetic testing kits and who gave consent for their personal data to be used in research.

Two of the largest public genetic databases to date — called All of Us and the UK Biobank — contained just 19 and two individuals with the T790M mutation, respectively. But the 23andMe cohort included 641 individuals with the mutation, giving the researchers enough data to run reliable statistical analyses.

On average, people who had the mutation had about 25 times the odds of developing lung cancer compared with people who didn't have the mutation. That statistic includes both smokers and nonsmokers. T790M was not linked to any other type of cancer or noncancerous lung condition.

When the researchers looked at where the study participants were born, they found that the T790M mutation was much more common among those born in the Southeast, especially in Alabama, Mississippi and Tennessee. In those three states, the mutation showed up in 1 out of every 2,078 people who'd contributed data to 23andMe.

By referring to historical records, the researchers pieced together when and how the mutation likely spread. They think settlers from the British Isles first brought it to the U.S. in the early 1700s. Later, families with the mutation moved to southern Appalachia, where they were relatively isolated —‬ so the variant got passed down again and again within that area and became unusually common there.

The concentration of people with the T790M mutation in the Southeast‬ may help to explain why this region of the U.S. experiences elevated lung cancer rates, Chanock said. Statistics suggest that people in the region also have higher smoking rates than the U.S. average: approximately 20% of adults in Appalachia report smoking, compared to 16% of adults elsewhere in the U.S. So it's possible that those two factors interact.

Ongoing and future studies

Certain populations with a history of smoking are recommended to get screened annually for lung cancer using low-dose CT scans. A key question, Chanock said, is when and how often people with the T790M mutation should be screened.

The study found that people with T790M developed lung cancer about five years earlier than people without the mutation, on average. That finding highlights the "need to begin screen[ing] at an earlier age and irrespective of smoking status," Amos said.

A clinical trial is now underway to evaluate CT-based lung cancer screening in people with the mutation. The trial will also determine whether lung cancer risk increases with age in this population.

The researchers recommended that future studies unpack why the T790M mutation increases the risk of lung cancer, as well as investigate environmental risk factors that might interact with this genetic risk. Exposure to particulate-matter pollution in the air is one key factor to explore, they suggested. Future work could also look for other genetic mutations that might contribute to the inherited risk of lung cancer.

"Time will tell" whether additional lung-cancer-linked mutations will be identified, Chanock said. But personally, he fully expects scientists to find other very rare mutations that contribute to the risk.

"It is likely there are other variants of EGFR that increase lung cancer risk, but these may be even rarer than the one studied in this publication," Amos said. Finding these variants is important because it could enable people who carry them to proactively manage their risk for developing lung cancer, he said.

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

In women's reproductive years, their brains are exposed to high levels of sex hormones, and their neurons may come to depend on those hormones to function optimally. But leading up to and after menopause, the ovaries produce far less estrogen and progesterone, raising concerns that this drop in hormones may contribute to women's dementia risk.

"We think that the loss of those hormones at menopause renders those neurons more vulnerable to age-related cellular decline and pathologies like Alzheimer's," said Karyn Frick, a neuroscientist and professor of psychological and brain sciences at the University of Wisconsin-Milwaukee.

So, if falling hormone levels are a risk factor for dementia, could replacing those hormones help stave off the disease?

While the idea sounds logical on its face, studies that have looked at hormone replacement therapy (HRT) for dementia prevention have had mixed results. There are early hints that restoring estrogen during early menopause may protect brain health, but ultimately, more gold-standard clinical trials are needed to know for sure, experts told Live Science.

Support for estrogen protecting the brain

The idea that estrogen could help ward off dementia is plausible. Women are more likely to develop Alzheimer's disease than men are, and scientists think the loss of estrogen during menopause may be partly to blame, said Jennifer Bruno, an instructor of psychiatry and behavioral sciences at Stanford University.

Lab and animal studies buttress the idea that estrogen could protect brain health.

In the brain, estrogens act as neuromodulators, or chemical messengers that alter how neurons behave. Estrogen also helps neurons keep their shape. Estrogen loss in female mice triggers a drop in the number of dendritic spines ‪—‬ the small, bud-like bumps on neurons that receive chemical messages.

Researchers think that estrogen may help prevent the formation of the abnormal proteins — including one called amyloid beta — that accumulate, disrupt communication between neurons and ultimately kill cells in Alzheimer's disease. Amyloid beta is produced when a larger protein is cut the "wrong" way by an enzyme, Frick explained. Estrogen promotes the "normal" cutting of this protein, thus reducing amyloid beta, studies in lab mice show.

And estrogen may limit the buildup of a second Alzheimer's-related protein, called tau, by preventing the chemical processes that cause the tau proteins to clump together. This helps prevent the formation of tau tangles, a hallmark of Alzheimer's disease.

The hormone may also support brain health indirectly by improving sleep quality.

"It's well documented that menopausal women have difficulty sleeping, whether it's due to hot flashes or insomnia," Frick said. Estrogen can ease those nighttime hot flashes, thus helping menopausal women get more, less-fragmented sleep. Deep rest may help the brain clean out toxic proteins, while research shows sleep deficiency is linked to Alzheimer's disease.

Mixed results with estrogen-only HRT

HRT for menopause comes in two main forms: treatments that include only estrogen, and combined therapies with both estrogen and progesterone. The treatment has a complicated history.

HRT was popular in the 1990s but fell out of favor after results from the Women's Health Initiative study were published in 2002. That study identified various risks tied to both estrogen-only and combined HRT options, some of which have since been overturned by newer data.

That said, the Women's Health Initiative study found that estrogen-only HRT came with an increased risk of endometrial cancers, and later analyses have backed up this idea. That's why today, clinical guidelines recommend that women who have not gotten a hysterectomy take combined HRT, while estrogen-only options are reserved for those who have had their uterus removed. (The added progesterone counteracts estrogen's thickening effect on the uterine lining.)

For the subset of women who take estrogen-only HRT, observational data published in August showed that this form of the treatment was linked to a reduced risk of dementia. The study, published in the journal Neurology, found that women who took estrogen-only HRT were less likely to show Alzheimer's-related changes in the brain than women who didn't take any HRT.

Estrogen-only HRT was also tied to better clinical outcomes: Treated women were less likely to be diagnosed with dementia, were less likely to show clinical and functional cognitive decline, and had better scores on memory tests, on average, compared with untreated women. These findings drew on two large, separate groups of older women, reporting data from 21,400 people in total, but they didn't include data on when each woman started HRT.

Whereas earlier studies of HRT and dementia risk relied on doctors' ratings of patients' symptoms, the Neurology study measured levels of Alzheimer's-related proteins in the brain after death. That's a more "definitive" marker of disease, said Bruno, a co-author of the study. However, the research was observational, so it can't say whether estrogen-only HRT directly causes the better brain outcomes the team observed, she stressed.

Although the Neurology study's findings are promising, they don't necessarily match the results of other studies of estrogen-only HRT and dementia. For example, a slightly larger observational study, published in 2023, found that estrogen-only HRT was associated with an increased dementia rate.

In that research, most of the women took a type of estrogen called estradiol, while Bruno's study included a greater variety of estrogens. That may have been the difference in the two studies' results, but teasing that out would require further study. Meanwhile, the conflicting findings muddy the waters of what estrogen-only HRT can do for brain health.

Does timing matter?

One big finding from the Women's Health Initiative study was that starting HRT — either estrogen-only or combined — after age 65 was associated with worse cognitive function and increased dementia risk, said Yuko Hara, director of aging and Alzheimer's prevention at the Alzheimer's Drug Discovery Foundation.

The same may not be true for people who start HRT earlier. For context, menopause starts around age 51 to 52, on average, and it's preceded by perimenopause, a transitional period when hormone levels begin to drop, typically around the mid-40s.

An observational study published in August in the journal Alzheimer's & Dementia found that starting HRT between ages 46 and 56 was linked to a reduced risk of dementia. That study did not differentiate between estrogen-only and combined treatment; it lumped all of the data together.

The protective link was especially strong in three groups: women with "surgical menopause," triggered by the removal of one or both ovaries; carriers of a certain variant of a gene called APOE that raises Alzheimer's risk; and women who had a relatively short time between their first period and menopause.

A 2024 meta-analysis of randomized controlled trials also found that HRT had a cognitive benefit for women with surgical menopause; that finding was tied mostly to estrogen-only therapies.

However, outside of that specific group, the idea of early HRT protecting brain health is far from settled.

Who might benefit, if anyone?

When it comes to using hormone replacement to protect brain health, the evidence isn't yet strong enough to recommend any kind of HRT as a way to protect the brain in all women, Hara said. Women who had one or both of their ovaries surgically removed are the exception to this rule.

"This is a distinct clinical population because the procedure can cause an abrupt, early loss of estrogen, rather than the gradual hormonal decline that occurs with natural menopause," Hara said.

For most women who have gone through natural menopause, "there is not enough evidence to recommend [HRT] specifically for preventing cognitive decline or dementia," she said.

HRT is not currently prescribed to prevent dementia — it is prescribed to ease menopause symptoms, such as hot flashes, night sweats and sleep disturbances. To settle the science on HRT and the brain, what's really needed is a well-designed clinical trial that follows women from perimenopause to postmenopause, Bruno said. That would reveal the effects of HRT on brain health and dementia risk more reliably than the studies done so far.

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

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Artificial intelligence (AI) algorithms that hunt for cancer may do a better job when they approach the analysis as if they were a human pathologist, a new study suggests.

Many AI systems analyze preselected regions of a tissue sample, or they split a whole pathology slide into patches of a fixed size. By contrast, a pathologist searches more dynamically, panning across the tissue, zooming in and out, and pausing over areas that raise red flags. A whole slide can contain billions of pixels, while the evidence of cancer may occupy only a tiny patch.

Study co-author Zhi Huang, an assistant professor of pathology and laboratory medicine at the University of Pennsylvania, compared the process to a search-and-rescue helicopter. "You don't start by inspecting one square meter of ground," Huang told Live Science. You scan the landscape first and then swoop in for a closer look.

In the new study, published in July in the journal Nature, Huang and colleagues demonstrated that cancer-detecting AI might work better when it takes this humanized approach.

Training AI to hunt for cancer

AI algorithms called vision language models (VLMs) struggle with the first step that Huang described — that initial, cursory scan. That's in part because many pathology AI systems learn from what pathologists leave behind at the end of that search: a labeled image pointing out where the cancer is or an official diagnosis.

Instead, the researchers trained their new AI on pathologists' search behavior. They called this approach to training "Pathology-CoT," short for "chain of thought." It turns observable actions, including where pathologists move around and zoom in on an image, into training data.

To collect the data, the team created a tool that recorded how pathologists moved around a slide and changed magnification. The raw logs, gathered from eight pathologists, were messy, as a given pathologist might drift across a slide, overshoot their intended region of focus or fiddle with magnification to adjust it to their liking.

To clean up the data, the researchers filtered out those incidental movements, focusing on moments that appeared to represent deliberate attention, such as lingering over one view or making a sustained pan. Then, they compared those regions with eye-tracking data to check that the software was capturing where pathologists were actually looking.

For each region a pathologist inspected, the VLM also drafted a short rationale explaining why the region was worth examining and what features were visible; human pathologists could then accept, edit, or reject the rationale, creating additional training data for the AI. In one example, the AI flagged a portion of a slide as potentially metastatic and suggested zooming in to look for atypical cells. Other inspected regions were flagged as healthy tissue.

Ultimately, the researchers used this training method to build a new tool called Pathology-o3. It scans a slide at low resolution, uses a model trained on pathologists' behavior to choose regions worth a closer look, then sends higher-resolution views of those regions to a VLM for analysis.

Putting it to the test

Huang said the goal of the new study was not to show that Pathology-o3 worked better than specialized AI models that are specifically built to detect specific types of cancer; those models are often trained disease by disease. Rather, the researchers wanted to see whether their new training approach could help a general-purpose AI navigate a pathology slide more effectively.

They compared Pathology-o3 to other general-use AI systems, such as OpenAI's o3, and asked the algorithms to examine slides containing lymph node tissue. These slides were collected from colorectal cancer cases and some contained metastatic cancer, which human pathologists had already labeled.

The algorithm correctly identified slides that were positive for cancer 100% of the time. However, of the slides it identified as positive, 15.5% were actually negative. By comparison, OpenAI o3 correctly identified slides that were positive for cancer 87.5% of the time. Of the slides it identified as positive, 53.3% were actually negative.

The researchers designed Pathology-o3 to err on the side of flagging something for another look, rather than potentially missing cancer. That might help to explain the rate of false positives, Huang said.

Whether that rate of false alarms is acceptable depends on how Pathology-o3 is used, said Mohammad Asadi, a data scientist at Stanford University who was not involved in the research. It's not precise enough for the AI to diagnose patients on its own, but it could still be useful for a system to point a human toward regions of a slide that are worth double-checking. It may be an advantage that the approach shows the pathologist a specific region to inspect rather than declaring an entire slide suspicious, he said.

The researchers tried repeating the test on an independent dataset that the algorithms hadn't seen before to see how well it worked on unfamiliar slides. Pathology-o3 correctly identified slides that were positive for cancer 97.6% of the time. Of the slides it identified as positive, 37.1% were actually negative. The finding is an example of how AI performance can change when the data source changes, even when the medical task stays the same.

Asadi explained this result suggests the system can still work with slides from a different source. But that result does not yet show that using this tool would make pathologists more accurate or efficient in practice.

Can it help pathologists?

The researchers applied their training approach to several existing VLMs, finding that the models' performance consistently improved after the training. That suggests that the navigation data from pathologists was useful across settings, Asadi said.

For Huang, that is the most important result. "The takeaway isn't our system," he said. "It's that the missing ingredient has been sitting in hospitals this whole time."

The study did not compare Pathology-o3 directly with human pathologists, but the researchers said that wasn't their aim.

"The right question isn't whether it beats a pathologist," Huang said. "It's whether a pathologist working with it catches more [cancer cases] and works faster." The current study did not address the latter question, either, but the team's next experiment is designed to test pathologists on the same cases with and without Pathology-o3, measuring what they catch and how long they take to do so.

The system's most plausible use is as a prescreening tool, Asadi said, but he stressed that the research has not yet shown that doctors who use it become faster or more accurate. Asadi wants an even tougher test: trials conducted across multiple hospitals that measure not just accuracy and speed but also pathologists' workloads. He wants the trails to assess the burden of false alarms from the AI algorithms and whether doctors recognize when the AI is wrong.

Importantly, cancer diagnoses can require information from multiple slides, stains and a patient's medical history, while the current system just reads one slide at a time. "I wouldn't claim it should diagnose on its own," Huang said.

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

Yellow fever is appearing in regions that haven't seen cases of the disease in years, largely as a result of climate change.

Historically, the virus ravaged cities across the Americas, Europe and Africa, until a vaccine was introduced in 1937 and its range shrunk significantly. But now, as climate change creates favorable conditions for virus-carrying mosquitoes, scientists are seeing outbreaks in unexpected areas.

"Yellow fever is a highly deadly disease," Dr. Joelle Ivy Rosser, an infectious-disease researcher at Stanford University, told Live Science, "so any environmental pressures that increase the likelihood of future yellow fever virus outbreaks … is highly concerning."

How is climate change contributing to this pattern, and could it get worse in the future?

How rising temperatures impact yellow fever

Yellow fever is a mosquito-borne disease caused by the Orthoflavivirus flavi virus, better known as yellow fever virus (YFV). The infection causes fever, muscle aches, headaches and vomiting. About 15% of cases become severe, with patients showing jaundiced skin and eyes, bleeding from the mouth, eyes, nose and stomach, or organ failure.

Devastating yellow fever epidemics spread in the 17th to 19th centuries, before the development of a vaccine. Nowadays, an estimated 31,000 to 82,000 yellow fever deaths occur each year; severe cases have an estimated fatality rate of 20% to 50%.

Most yellow fever infections are a result of spillover from nonhuman primates; mosquitoes bite monkeys that carry the virus, such as howler monkeys, and then the infected mosquitoes bite humans. Several types of mosquitoes carry the virus, but the species Aedes aegypti is the main vector for yellow fever in cities, where high population density can make outbreaks especially severe.

Although there is an effective vaccine for yellow fever, cases have been on the rise in the past three decades. This led the World Health Organization (WHO) to set out a strategy in 2017 for eliminating yellow fever epidemics by 2026 through outbreak prevention and containment.

Climate-change-driven warming and extreme weather events may have heightened yellow fever risk over the past few decades, experts say. Rising temperatures make mosquitoes bite more because heat makes their metabolisms more active, said Dr. Seth Judson, an infectious-disease physician-scientist at UCLA. Warming also cuts down the virus's extrinsic incubation period, meaning the time it takes for the virus to replicate in a newly infected mosquito and then get passed on to another person, he told Live Science.

Weather patterns and deforestation

Changing weather patterns play a role, too. In 2017-2018, Brazil saw its first yellow fever outbreak in a city in almost a century. That outbreak, primarily in Belo Horizonte and São Paulo, was likely a result of drought, according to one study.

While heavy rainfall creates a breeding ground for mosquitoes, in this case, drought pushed forest-based mosquitoes — as well as YFV carriers like marmosets and howler monkeys — closer to cities as the animals searched for water. Drier conditions can also prompt dehydrated mosquitoes to bite more as they search for fluids, study co-author Jamie Caldwell, a disease ecologist at Princeton University, told Live Science.

"Extremes of weather in either direction" — very wet or very dry — "can exacerbate mosquito-borne disease transmission," Rosser said.

Parts of Africa and South America that were considered low-risk for yellow fever have already been seeing new outbreaks, Judson said, so maps of yellow-fever-affected areas have had to be updated. In research that's been released as a preprint but not peer-reviewed yet, Judson found that yellow fever is reemerging in an area of the Colombian Andes where it hadn't been reported since 1940.

Experts are paying particular attention to the edges of cities, where urban centers meet the forest. The risk of yellow fever transmission from monkeys to humans via mosquitoes is rising at these edges due to both climate change and deforestation.

"Humans are expanding the agricultural frontier and encroaching on forests where yellow fever mosquitoes … are found," Gabriel Parra-Henao, a biologist with the WHO, told Live Science in an email. "[This] results in more people being exposed to their bites."

Similar patterns have been seen with other mosquito-borne infections, such as malaria.

Could yellow fever return to the U.S.?

Climate change is expected to bring yellow fever to new areas. One study predicts that, under the most severe climate change scenario, nearly a billion people could face their first exposure to the mosquitoes that can carry YFV in the next century. While that worst-case scenario may not be the most likely, the mosquitoes' ranges are still expected to expand under less-severe conditions.

Europe is predicted to face the largest increase in exposure to Ae. aegypti mosquitoes compared to the rest of the world, and the U.S. and Canada are predicted to see increases too. In the U.S., the mosquito species already lives in a number of states, including Florida, Mississippi, Arizona and New Mexico. However, warming would increase the chances of mosquitoes surviving in locations further north, such as Philadelphia and New York, which suffered major yellow fever outbreaks in the past. One model predicts Ae. aegypti could spread as far north as Chicago by 2050.

Although the mosquito lives in the U.S. already, yellow fever cases are exceedingly rare within the country because the virus is not present in local populations. That's because of an international campaign that the U.S. spearheaded in the 20th century, which involved researching YFV, eradicating mosquito breeding grounds, and vaccinating people widely.

"If yellow fever virus reestablished itself in our local Aedes aegypti population, then that would be very concerning," Rosser said.

One way yellow fever could return to the U.S. would be via people carrying the virus home with them after traveling to regions where the disease regularly circulates. Local mosquitoes could then catch the virus by biting those infected people, and then pass it on to others.

For local transmission to take hold, "there needs to be significant numbers of infections [passed to locals], and infections among travelers," Judson said. "But … it's in the realm of possibility."

With climate change driving resurgences of yellow fever in more places, and more regions of the U.S. becoming hospitable to the mosquitoes, that reintroduction scenario may become more likely. But some scientists think that even if North American cities saw yellow fever outbreaks, the outcome would likely not be devastating. Infrastructure in wealthier cities could be the difference between a disaster and a manageable health concern.

"There's access to medicines and vaccines; we pipe water to our homes, so we don't have standing water around," Caldwell said. "So it is a concern, but it's never going to be the next COVID."

Other experts noted that diligent surveillance of yellow fever infections can help public health officials prepare. In places where yellow fever is circulating in forest primates, forest conservation can limit contact among humans, wildlife and the mosquitoes that spread diseases among them. It's also crucial to make vaccines widely accessible to people who live in the virus's endemic regions and to travelers who visit those regions.

The WHO's yellow fever campaign is set to conclude at the end of this year, and its next steps are unclear. There's ongoing discussion of what comes next, Judson said, with questions about whether the control of yellow fever outbreaks will rely more on national strategies than on international coordination via the WHO.

Whatever happens, this is a time for heightened awareness of the virus, Judson said.

"We think of yellow fever as this historic disease," he said. "I think many people don't realize that we're still seeing significant yellow fever outbreaks. … It's really important to be aware of the risks and think about how we prepare for that."

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

Two people in Lancaster County, Pennsylvania, have died of measles, marking the first measles-related deaths in the United States this year.

Neither individual was vaccinated against the disease, the Pennsylvania Department of Health (DOH) reported Tuesday (Aug. 25). Their deaths mark the first measles fatalities in the state in 35 years.

"To protect the privacy of the individuals and their families, DOH will not release any additional details that could personally identify these individuals and their families," DOH officials said in the statement.

Since the start of the year, there have been 393 confirmed cases of measles in Pennsylvania across 28 counties. Nationwide, 2,813 cases have been reported so far this year, according to the Johns Hopkins U.S. Measles Tracker. The 2026 nationwide total already exceeds the total number of measles cases reported in 2025, when 2,289 cases were reported, including over 240 hospitalizations and three deaths, according to Centers for Disease Control and Prevention data.

These totals represent both measles caught within the U.S. and imported cases from people who caught the infection elsewhere. Imported cases make up a relatively small proportion of the overall total, with most cases coming from local transmission, according to the tracker.

The two deaths in Pennsylvania come as the nation's vaccination rate for measles continues to fall among kindergarteners and as the proportion of kindergarteners with vaccine exemptions is rising. The U.S. is likely to lose its "measles elimination status" later this year, which would mean the same outbreak strain had been consistently circulating in the country for over 12 months. Essentially, this suggests that although the U.S. officially eliminated measles in 2000, the disease is likely back in regular circulation.

According to the tracker, nearly all of the measles cases reported this year — 96% — have been among unvaccinated people or people with unknown vaccination status. Two doses of either the MMRV vaccine (which protects against measles, mumps, rubella and chickenpox) or the MMR vaccine are about 97% protective against measles infections. (Both vaccines offer the same protection against measles, but the latter excludes protection against varicella, or chickenpox. Kids who receive the MMR shot get a separate chickenpox vaccine.)

Measles infections can cause rash; fever; cough; runny nose; and red, watery eyes. About 1 in 5 unvaccinated people who catch measles are hospitalized, and there's a risk of developing complications like pneumonia or brain inflammation. In the U.S., 1 to 3 in 1,000 people with measles die of the disease. Those who survive the infection can develop long-term health problems, such as neurological disease or "immune amnesia," where the immune system loses ability to fight off pathogens it's encountered in the past.

"Because measles was largely eliminated in the Commonwealth for more than three decades, people are not familiar with this disease and don't fully understand the potential severity of the illness," Dr. Debra Bogen, Pennsylvania's secretary of health, said in the statement. "We want to ensure every Pennsylvanian has the information they need to protect themselves, their loved ones and their communities."

The best way to protect against measles is to get fully vaccinated, DOH representatives said in the statement.

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

Vaccination against human papillomavirus (HPV) has drastically reduced cervical cancer rates among women who got the vaccine. But as doctors celebrate that news, they're warning of an ongoing uptick in other HPV-related cancers that is mostly affecting men.

Throat and mouth cancers, broadly known as oropharyngeal cancers, linked to HPV are on the rise, mostly in middle-aged and older men, data suggests. These cancers affect the back of the throat along the tonsils and the base of the tongue. A 2023 study of the U.S. found that cases of HPV-related oropharyngeal cancer had more than tripled between 1988 and 2004, with the bulk of that trend driven by male patients. This trend continues worldwide today, with one Danish study finding another tripling between 2000 and 2017.

So what's driving this trend, and what can be done?

How is HPV related to cancer?

HPV is an umbrella term that includes many viruses; those that cause cancer are known as "high-risk HPV." These high-risk strains spread during sex, including oral sex, making the leap from one body to another through tiny cuts in the skin or mucous membranes.

About 80% of sexually active adults will contract the virus in their lifetimes, usually within a few months to years of starting to have sex, according to the National Cancer Institute; about half of those cases are high-risk HPV. Most people's immune systems clear the virus within a year or two, but in some people, HPV lurks in the body and causes DNA damage that can turn cells cancerous.

There are 12 types of high-risk HPV, which are known to cause anal cancer, cervical cancer, oropharyngeal cancer, penile cancer, vaginal cancer and vulvar cancer. Two strains, known as types 16 and 18, are the most likely to cause cancer.

Anal cancer, penile cancer, vaginal cancer and vulvar cancer rates are all rising, too, although oropharyngeal cancer is more common than any one of these.

Why are throat and mouth cancers on the rise?

According to data from the U.S. Centers for Disease Control and Prevention, an average of 13,600 cases of oropharyngeal cancers likely caused by HPV are diagnosed in men each year. By contrast, there are 2,400 newly diagnosed cases in women per year. The number of cervical cancer cases likely caused by HPV each year is currently around 11,100.

Thanks to widespread vaccination and screening, Australia is expected to eliminate cervical cancer by 2035, and other countries are progressing toward that target too. Rates of cervical cancer have also dropped in young women in the United States, with declines of over 50% in the states with the highest vaccination rates in 2016-2021, compared with 2000-2005, before the vaccine was introduced.

The adoption of HPV vaccination among both male and female patients should lead to an eventual decline in oropharyngeal cancers, as it has in cervical cancer. But because HPV can lurk in the body and wreak havoc long after a person is initially exposed, risks for older individuals who were not vaccinated as young people still persist.

About 80% of oropharyngeal cancer cases are in men, and 40% are in people over the age of 65, who became adults after the sexual revolution of the 1960s. At that time, having multiple sexual partners became more common, but this was well before the first HPV vaccine, Gardasil, became available in 2006.

As people with chronic HPV infections age, the immune system may do a poor job of keeping the virus in check, said Electra Paskett, a cancer epidemiologist at The Ohio State University College of Medicine. Other factors, such as chronic stress, may also play a role in the immune system losing grip on the germ. That's likely why a virus contracted decades ago can cause cancer in middle-aged or older people.

Why men?

Men are likely more susceptible than women to oropharyngeal cancer for a few different reasons.

One study of patients in Baltimore found that men were more likely than women to have oral HPV infections, with their degree of risk tied to their number of recent oral and vaginal sex partners. Performing oral sex was linked to oral HPV infection in men in the study but not women. In addition, men were slower to clear these HPV infections than women, perhaps indicating immune system differences that make men more prone to chronic HPV of the throat and mouth.

Are there ways to screen for HPV oropharyngeal cancers?

When it comes to throat and mouth cancer, "we just don’t have any good screening, diagnostics or interventions like we have developed for cervical cancer," said Dr. Diane Harper, an HPV expert at the University of Michigan Medical School.

For example, Pap smears detect precancerous cells in the cervix, allowing doctors to remove them before they turn fully cancerous, and HPV tests look directly for the virus's genetic material. But it's not possible to take swabs or biopsies of the back of the throat without causing serious discomfort and damage, Harper told Live Science.

Due to the lack of screening, most cases of oropharyngeal cancer are diagnosed after a patient develops symptoms, like a lump in their throat or neck, Paskett told Live Science. Luckily, HPV-linked oropharyngeal cancers respond well to treatment: The five-year disease-free survival rate is 85% to 90%, meaning the vast majority of patients respond to treatment and survive their cancer. Additionally, the recurrence rates are lower than in oropharyngeal cancers that aren't linked to HPV.

However, the treatment is "grueling," Paskett said, with side effects from radiation including mouth sores, nausea, loss of appetite and weight loss.

Should more men get vaccinated?

People who have been vaccinated against HPV have lower rates of oropharyngeal cancer. The HPV vaccine is approved for people ages 9 to 45, but doctors recommend vaccination for people under age 26. That's because, for older adults who became sexually active before vaccination was available, an HPV shot may not reduce their cancer risk. The vaccines help only before HPV infection occurs.

However, Harper said, patients ages 26 to 45 who haven't been vaccinated yet should talk to their doctors about their sexual history and current sexual activity to decide if the shot might benefit them.

As for patients older than 45, clinical trial data suggests that the vaccine is safe for all ages and effective for anyone who hasn't already had HPV. While the pharmaceutical company Merck tested the Gardasil vaccine on patients up to age 26, another vaccine — GlaxoSmithKline's Cervarix — was tested in people up to 80 years old. Although Cervarix isn't available in the U.S., the results of those clinical trials suggest that in general, HPV vaccination is safe and effective for older adults too, Harper said.

Say a person has had few sexual partners and is expected to be monogamous for life, but they suddenly find themselves divorced or widowed after age 46. That person might consider getting the HPV vaccine series before reentering the dating pool, Harper suggested.

"It really is an individual decision and depends [on] how risk-averse people are to the consequences of HPV," she said. Insurance might not cover the shot because it is not officially approved for that over-45 age group. But sometimes, Harper recommends that her older patients still get it if they are willing to pay out of pocket.

By comparison, she said, the decision is much easier for young people.

"For parents, I beg — I beg [you] to please consider vaccinating both your girls and your boys," she said. "If you do it at the age of 15 or younger, they only need one shot," she added. Recent clinical trials show that one dose of the vaccine, if delivered before the age of 16, is as effective as two. That said, official recommendations still suggest that patients get two doses of the vaccine if they start the series before age 15, and potentially three doses if they start later.

Those choices made during a person's childhood could have a huge impact on their health down the line. "We're hoping, 30 years from now, we'll be able to say, 'Wow, oropharyngeal cancer just plummeted.'"

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

A severe case of COVID-19 can "reawaken" dormant viruses in the body, even in people with otherwise healthy immune systems, a new study finds.

These reactivated viruses include Epstein-Barr virus (the "mono" virus, or EBV), cytomegalovirus (CMV), herpes simplex virus (HSV) and anelloviruses. That final group of viruses can be found in the vast majority of people, but they have never been definitively shown to cause human disease.

However, in this study, the reactivation of these seemingly benign anelloviruses was linked to persistent physical disability from long COVID, researchers reported Aug. 5 in the journal Nature.

Anna Cliffe, an associate professor of microbiology, immunology and cancer biology at the University of Virginia who wasn't involved in this study, praised the work as "one of the largest and most carefully done studies of its kind."

The findings suggest that severe COVID-19 may wake up dormant viruses, and "once awake, they may add to the inflammation that makes COVID-19 worse," Cliffe told Live Science in an email.

What's more, "if our findings on Anelloviridae and long COVID are validated, then it would really create a lot of urgency around better understanding these viruses and developing antivirals for them," study co-author Dr. Esther Melamed, a neuroimmunologist at the University of Texas at Austin, told Live Science.

Viral reactivation

The study tracked 1,154 adults who'd been hospitalized with COVID-19 cases of varying severity, following them for a year. The researchers gathered blood samples and nasal swabs, as well as lung fluid samples from the ventilated patients. These samples were taken at six time points during the first month, and then at three, six, nine and 12 months.

The team ran tests to look for viral RNA, a genetic cousin of DNA, as a sign that these lingering viruses were reactivating during and after their infection with SARS-CoV-2, the virus that causes COVID-19. The results showed that many dormant viruses awakened during the acute infection, particularly members of the herpes family — EBV, CMV and HSV — and anelloviruses.

Each virus followed its own timeline of reactivation, with EBV and anelloviruses appearing early, and CMV and HSV later. And each was linked to its own set of immune and metabolic changes and clinical complications in the patients.

This widespread viral reactivation occurred even in people whose immune systems were not weakened. Nearly half of the patients in the study — 550 out of 1,148 — had at least one virus reactivate.

After the acute infection had passed, a percentage of the patients developed debilitating symptoms of long COVID, including fatigue and a reduced ability to complete everyday tasks, like dressing or walking. In these patients, anelloviruses were more likely to remain active after the acute phase of the COVID-19 infection.

Cliffe said the study had several strengths, including the year-long follow-up with repeated sampling. She highlighted that the team also replicated their main findings in a separate group of patients whose blood samples were included in a Mount Sinai biobank.

How COVID could reawaken viruses

The idea that herpesviruses can reactivate in healthy people, not just in those with weakened immune systems, is not new, Cliffe said. Previous research has shown that astronauts and Antarctic researchers, "who are about as healthy and rigorously screened as people get," can experience this reactivation and then shed multiple herpesviruses during periods of acute physical and psychological stress.

Viral reactivation may happen when the immune system lets down its guard, Melamed thinks. Viruses from past infections hide in different cells across the body, and usually, the immune system "sort of stands as the guard at the door, preventing them from waking up and getting out of those cells," she said.

But when the body encounters a huge stressor ‪—‬ such as a severe infection, an important exam, sleep deprivation or surgery ‪—‬ the immune system has to redirect its attention, Melamed explained. "When the guard walks away from the cell, then these viruses have the opportunity to wake up and do whatever they want," she said.

Cliffe suggested another possible mechanism. "For HSV-1 [which mostly causes cold sores], our own lab's work has shown that inflammatory signals the body produces during illness can directly wake the virus up from latency in neurons," she said. They've found that a molecule that signals the immune system, called IL-1, triggers HSV-1 activation in neurons by making the cells super excitable.

"Other groups have separately shown that IL-6," another immune-signaling molecule, "can do something similar in animal models," she said.

Cliffe cautioned that detecting viral RNA shows that a gene in the virus is switching on, but that metric isn't as convincing as finding whole new infectious particles in the body. That said, she noted that the authors did try to address this limitation with additional layers of evidence. For instance, they found both RNA of EBV and antibodies against it, as well as higher quantities of specific immune cells the virus is known to hide in, she said.

The other major caveat of the study, which the authors acknowledged, is that the link between virus reactivation and worse clinical outcomes is a correlation, not proof of the cause.

"The next step is to do prospective interventional trials to test whether antiviral medications for these reactivating viruses could help improve outcomes for people," Melamed said. They would explore this in both severe COVID-19 and long COVID.

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

Four lemurs that had close contact with people, including one via a "lemur yoga" class, caught a human herpesvirus and subsequently died, a new study shows.

The virus at fault was herpes simplex virus type 1 (HSV-1), which is extremely common in humans. In people, the infection usually causes no symptoms or produces cold sores. In primates, though, the infections can often be deadly — in this case, all four lemurs developed encephalitis, or inflammation of the brain, and died.

This is the first time that an HSV-1 infection has been confirmed in lemurs via a molecular analysis — namely, PCR tests like a doctor might use to diagnose a person's infection. Human herpesvirus infections have been documented in lemurs in the past, albeit rarely, and those reports used laboratory methods other than molecular analysis.

These recent cases highlight the dangers of close contact between animals and humans, scientists say.

"We've evolved these kissing behaviors that have resulted in pretty effective transmissions [of HSV-1] to the point where you look at infection rates of humans and they're very high," study co-author Dr. Jim Wellehan, a professor at the University of Florida's College of Veterinary Medicine, told Live Science. But when HSV-1 infects lemurs, the consequences can be far more severe, he emphasized.

Lethal "lemur yoga"

In the study, published in July in the Journal of Zoo and Wildlife Medicine, Wellehan and colleagues confirmed HSV-1 infections in two ring-tailed lemurs (Lemur catta), one black-and-white ruffed lemur (Varecia variegata) and one ruffed-lemur hybrid (Varecia rubra x Varecia variegata). All four lemurs were privately owned.

The problem isn't limited to lemurs. HSV-1 has previously caused fatal disease in other captive and wild primates, including marmosets, saki monkeys, gibbons and other monkeys. That said, these cases of human herpesviruses jumping to primates have been uncommon.

"Herpes, as viruses, have amazing host fidelity," Wellehan said in a statement. "They don't do big host jumps very often."

The four cases in the study occurred over an eight-year period in the U.S. One of the four infected lemurs had been used in a "lemur yoga" program. "People are doing yoga, and there's lemurs wandering around," Wellehan said in the statement. "It's not good for the lemurs."

That animal's infection was almost certainly related to its close contact with humans during these yoga sessions, Wellehan said, although the study cannot prove that transmission occurred during a particular yoga session. The other three lemurs were exotic pets and also had close contact with humans.

From cold sores to brain disease

HSV-1 and its close relative HSV-2, which mostly causes genital herpes, require relatively close contact to spread. HSV-1 is most often transmitted through contact with saliva or skin surfaces in or around the mouth, or with cold sores. Most adults have HSV-1 and many have no notable symptoms. It is possible to spread the virus even when symptoms aren't present.

That makes frequent, direct contact between humans and lemurs particularly concerning, the researchers said.

The four examined lemurs showed a range of symptoms, including lethargy, loss of appetite, mouth and throat ulcers, and breathing problems. One ring-tailed lemur developed prolonged, repeated seizures and died two days after initially being seen by veterinarians.

After the lemurs died, researchers examined their tissues under a microscope. In the brain, they found inflammation and destruction of the tissue, along with intranuclear inclusions, which are abnormal structures inside cells that can occur during herpesvirus infections.

The researchers then used various tests to identify the presence of HSV-1 in the body, detecting the virus's genetic material and proteins in the animals' brain cells. This provided additional evidence that the germ had caused the encephalitis.

In two of the lemurs, oral or mucous swabs collected while the animals were alive tested positive for HSV-1, while the testing of the other two occurred after death. The results from living animals means that similar samples could potentially help veterinarians diagnose infections before death in the future, rather than confirming the infection postmortem.

While humans and HSV-1 have had a long evolutionary relationship, lemurs and HSV-1 have not.

"This is a virus that's highly endemic in our species," Wellehan said. "Fortunately for lemurs, this isn't something you can catch from breathing in the same airspace, as [HSV-1] requires a more direct contact. But this is the story of a pathogen jumping into a new host, which is the story of evolution in the history of life."

The researchers noted that, while the lemurs in these cases were privately owned, accredited zoos have strict biosecurity measures designed to reduce the chance of pathogens passing between people and animals.

The cases illustrate a broader lesson about the risks of putting humans and captive primates into unusually close contact, Wellehan said. "It may be fun, but it's not [in] a lemur's best interest."

What do you know about chimpanzees and great apes? Test your smarts with our primate quiz.

Between outbreaks of explosive diarrhea leading to nationwide lettuce recalls and cases of Salmonella tied to eggs and jalapeños, foodborne diseases in the United States have been hitting the headlines hard this summer.

But is the U.S. really contending with more foodborne infections than usual this year, or does the extensive news coverage just make it feel that way?

Live Science spoke with researchers to find out. Here's what the experts wish people knew about the recent outbreaks.

What is Cyclospora, and how many people have been infected?

Cyclospora cayetanensis is a single-celled parasite that, when ingested, can cause an intestinal illness known as cyclosporiasis. Symptoms of the infection include watery diarrhea, nausea and cramping. It's rarely fatal, but its symptoms can be severe; specific antibiotics can clear the infection.

There are currently several unrelated outbreaks of cyclosporiasis in the United States, most of which have not been linked to specific sources of contamination. Across all of the outbreaks combined, 10,468 lab-confirmed and a further suspected 12,255 cases were reported in the U.S. between May 1 and Aug. 4.

Health officials have linked the largest of the outbreaks to iceberg lettuce sourced from central Mexico and supplied by Taylor Farms. A recall of the affected produce was issued July 17. As of Aug. 5, over 6,300 cases of cyclosporiasis across 15 states have been linked to this outbreak, resulting in 278 hospitalizations and two deaths.

However, despite the large number of cases involved, the outbreak linked to lettuce does not necessarily represent a cause for alarm.

"This particular outbreak traces back to a single independent farm in central Mexico that Taylor Farms estimates supplies under 1% of the U.S. iceberg [lettuce] supply," Jessica Steier, a public health scientist, told Live Science by email. "One contamination event, on one farm, growing product that gets shredded and distributed nationally through food service is enough to produce thousands of illnesses and isn't necessarily a trend."

Considering the total number of Americans and the volume of lettuce consumed annually each summer, "you're looking at a very small fraction," she said. "For the large majority of Americans, the risk right now is very low."

Furthermore, the exposures to the contaminated lettuce are likely behind us, she noted. Cyclosporasis symptoms can take two weeks to show up, and the nation's capacity to test for the parasite is limited. Those factors mean the case counts are catching up.

How does the Cyclospora situation compare with previous years?

The Centers for Disease Control and Prevention (CDC) has confirmed more than 10,000 domestically acquired cases of cyclosporiasis since May 1, with another 12,000-plus awaiting confirmation, compared with roughly 2,000 to 3,000 in a typical full year, Steier said. "This is the largest documented cyclosporiasis outbreak in US history," she told Live Science.

Although the primary Cyclospora outbreak has been tied to lettuce, how that lettuce became contaminated is not yet known. Exposure typically occurs as a result of irrigation water that is contaminated with tiny amounts of human waste bearing the parasite or improper sanitation for workers during growing, harvesting or handling, according to the State of Rhode Island Department of Health.

Cyclosporiasis was first detected in the United States in 1985 — the illness was seen in four travellers who had returned to New York from Haiti and Mexico. The first U.S. outbreak occurred in Illinois in 1990; there were just 21 clinically defined cases associated with contaminated tap water. The next recorded outbreak occurred in Florida in 1995, with just 45 cases; the following year, there was a single outbreak of more than 1,400 cases across 20 states linked to raspberries imported from Guatemala.

As a result of these outbreaks, in 1999 the disease became nationally notifiable, meaning new cases are reported to the CDC. On average, there have been around 3,600 cases of cyclosporiasis in each of the past few years.

Steier attributes the growing trend in Cyclospora cases to Americans eating more fresh produce year-round, with much of it grown in ‪—‬ and imported from ‪—‬ tropical and subtropical regions where the parasite is commonly found. In 1990, when the U.S. had its first cyclospora outbreak, imports accounted, respectively for only around 35% and 10% of the nation’s fresh fruit and vegetable availability; today, those figures have risen to around 60% and 35%. Additionally, tests that detect the pathogen have been improved, so there's a greater rate of diagnosis.

Is there one Cyclospora outbreak, or many?

Part of the problem is that some news coverage "keeps reporting a singular number that keeps increasing, which is not useful," Steier said. "Almost every story leads with a number, and almost none explain what it's counting."

There are many metrics being reported, including the CDC's confirmed national case count, the confirmed cases in the 15-state outbreak, the cases still awaiting confirmation, travel-associated cases, and various states' totals, which sometimes combine probable and confirmed cases.

If you conflate all those counts, Steier cautioned, "we create the appearance of one massive outbreak, which is not necessarily the case." In other words, "Cyclosporiasis reported in 47 different states is not the same thing as an outbreak in 47 states, and media coverage doesn't reflect that distinction."

Ellen Shumaker, a food safety scientist at North Carolina State University, said by email that "Clear and frequent communication with the public is really important in outbreaks like these, to make sure consumers are getting accurate information and have clear steps of what to do."

Shumaker also noted that these outbreaks highlight the need for better traceability for foodborne illnesses. Such improvements are expected to come in July 2028, from which point the U.S. Food and Drug Administration (FDA) will require companies to maintain more detailed records tracking food products across the supply chain, linked to critical events such as harvesting, processing or packing. This change — which was pushed back from its original implementation date of January this year to give the industry more time to adapt — is expected to not only enable much faster tracing but also allow product recalls to be more targeted around contaminated lots, thereby helping to minimize food waste.

What is Salmonella, and what outbreaks are ongoing?

Recent weeks have also seen two prominent outbreaks of Salmonella infection, or salmonellosis. Salmonella is a group of bacteria that can infect the intestinal tract, causing diarrhea, stomach pains and, sometimes, vomiting.

The first of the two outbreaks led to a recall of white shell eggs and brown, cage-free shell eggs sold by Midwest Poultry Services with best-by dates between July 20 and Aug. 17. The recalled eggs — sold under the brand names Country Morning, Cal-Maine Sunups, Brookshire's, Simple Truth and Kroger — were shipped to Arkansas, Louisiana, Mississippi, New Mexico, Oklahoma and Texas.

According to the FDA, although Midwest Poultry Services was identified as a common egg source by the traceback investigation, this producer does not account for all of the illness in the outbreak. In fact, as of July 24, there have been 98 confirmed cases across 17 states, including 26 hospitalizations and no deaths. Investigations to determine if there are other illness sources ongoing.

A second Salmonella outbreak has been tied to fresh jalapeños from the Mexican state of Sinaloa. These were sent by Coast Citrus Distributors to food service companies, restaurants, distributors and wholesalers across the United States.

Taylor Fresh Foods has issued a recall for multiple products made with jalapeños with “Best If Used By” dates up to and including Aug. 16. These include products sold at Hannaford, Kroger, Stop and Shop and Hannaford, Target, Trader Joe’s, Walmart and Whole Foods stores.

The Food Safety and Inspection Service has also issued a public health alert for meat and poultry products containing jalapeños that may be contaminated with Salmonella. These include products sold at Albertsons, Dillons, Hannaford, H-E-B, Kroger, RaceTrac, Randalls, Tom Thumb, Walmart and Wawa stores.

This second outbreak has been linked to 345 confirmed cases of Salmonella across 27 states as of Aug. 10, with 36 hospitalizations and no deaths.

Are there more Salmonella cases than usual?

The number of Salmonella infections this year is not abnormal, according to Steier.

Last year, for example, an outbreak of Salmonella infections tied to eggs distributed by County Eggs LLC led to 105 cases across 14 states in August; June saw 134 cases across 10 states as the result of an outbreak linked to the August Egg Co.; and 21 people were infected by contaminated home deliveries from Metabolic Meals across 13 states.

Looking at the big picture, "ninety-eight cases tied to recalled shell eggs and 345 tied to jalapeños are unremarkable for a pathogen that causes something like 1.35 million infections in this country every year," Steier said.

Salmonella may be getting more attention than usual, she added, "because Cyclospora has everyone on high alert."

Dr. Zoe Weiss, a clinical microbiologist at Tufts Medical Center in Boston, added that COVID-19 pandemic may have also had a lasting effect on people's reactions to infectious disease.

"The average person is just more aware of infectious diseases and has a more sophisticated understanding of disease spread," she said.

How can consumers stay safe?

The key thing for consumers to do is to keep checking the relevant product recall lists, such as those for lettuce, eggs and jalapeños, and not eat any of the recalled products.

Cyclospora is only really eliminated by cooking, and cannot be rinsed off lettuce. When it comes to Salmonella, Steier stresses that recalled eggs should be thrown out or returned, not “cooked more carefully.”

"Please don't panic — and please don't come away thinking you need to avoid lettuce or other produce beyond what has been recalled," she added, noting that the recalls related to specific products and not, for example, lettuce in general.

"What worries me is the collateral damage," she added. "Product sales have taken a hit, lettuce especially, and most Americans were not eating enough vegetables to begin with. Swearing off produce is a real cost to your health in exchange for protection you’re not actually getting."

Editor's note: This is a developing story and may be updated.

Michigan has reported two deaths in its ongoing Cyclospora outbreak, a wave of parasitic infections that has affected over 11,000 people in the state.

Since early May, 193 people in Michigan have been hospitalized with cases of Cyclospora cayetanensis infection, called cyclosporiasis. The parasite can enter the body when someone consumes food or water contaminated with the organism, and the cases in Michigan have been linked to iceberg lettuce sourced from central Mexico.

These two deaths are the first reported in the Michigan outbreak, as well as the first deaths documented in any of the ongoing Cyclospora outbreaks in the United States.

Multiple outbreaks have been detected in the country in recent months, but not all have been linked to a specific source of exposure, such as lettuce. Since May, the Centers for Disease Control and Prevention has confirmed over 6,700 cases of cyclosporiasis acquired within the U.S. (In some states, case counts are typical of what's usually seen this time of year, while in others, case counts are higher than normal.)

Regarding the deaths in Michigan, "according to medical records, both individuals had significant underlying health conditions that may have been impacted by cyclosporiasis and dehydration," the state's Department of Health and Human Services (HHS) said in a statement. "No additional information will be provided on these two cases."

Cases of cyclosporiasis range from mild to severe, with severe cases being more likely in young children, older adults, and people with weakened immune systems. Symptoms include loss of appetite, fatigue, low-grade fever, vomiting and diarrhea. The infection is treated with antibiotics, which block the parasite's ability to multiply.

In mild cases, the infection can sometimes resolve on its own, but without treatment, the symptoms can linger for over a month. Severe and prolonged infections can raise the risk of dehydration due to vomiting and diarrhea. Severe dehydration can then cause various complications, such as electrolyte imbalances and hypovolemia (severe fluid loss).

While these complications can be dangerous — causing kidney failure or shock, for instance — cyclosporiasis is not usually life-threatening. For instance, over 2,200 cases were reported in the U.S. between 2011 and 2015, but there were no associated deaths.

"Death resulting from cyclosporiasis is uncommon in the United States," Michigan HHS representatives noted in the statement.

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

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.