Roughly 1 in 8 child flu deaths in the U.S. so far this year have been linked to brain damage, according to a report released by the Centers for Disease Control and Prevention (CDC).

The U.S. is experiencing its most severe flu season in more than a decade, Live Science previously reported. More than 19,000 people have died including 68 children, at least nine of whom had flu-associated brain complications, according to a CDC Morbidity and Mortality Weekly Report published on Feb. 27.

In January, the CDC received anecdotal reports of children becoming critically ill and dying with influenza-associated encephalopathy or encephalitis (IAE), a spectrum of neurological syndromes. Encephalopathy is a group of conditions that cause brain dysfunction while encephalitis causes brain swelling, according to the Cleveland Clinic. IAE symptoms include seizures, decreased level of consciousness, hallucinations and personality changes lasting more than 24 hours, according to the report.

The CDC doesn't normally track cases of IAE, so it's not clear whether the number of cases reported this season is higher than in previous years. However, they did warn doctors to be on the lookout for IAE.

"It is not known whether cases observed in the 2024–25 season vary from expected numbers," the CDC report authors wrote. "Clinicians should consider IAE in children with influenza and abnormal neurologic signs or symptoms."

Related: How do people die of the flu?

Flu is among the deadliest viruses in the world. While it kills around 1.8 people per 100,000 infections, flu infects enough people that thousands die from it every year in the U.S. Nervous system injury, including IAE, is one of the main causes of flu fatalities among children, according to a 2021 study published in the journal Medical Science Monitor.

To investigate anecdotal reports of IAE, the CDC contacted state health departments for data on influenza-associated deaths in children across flu seasons between 2010 and 2025. Flu can spread all year round, but there are more cases in the fall and winter (the flu season), with activity peaking between December and February, according to the CDC.

The CDC found that as of Feb. 8 in the 2024-2025 season, 68 children had died with flu, with IAE documented in nine (13%) of those cases. That compares to a rate of 9% across all years, but it varied season to season and peaked at 14% in the 2011-2012 season, according to the report.

While the CDC couldn't identify whether the current rate of IAE was abnormal, the report highlighted the importance of vaccination and recommended flu shots for all eligible people aged 6 months or older so long as influenza viruses are circulating.

"Influenza vaccination is an important tool for preventing influenza and its associated complications," the report authors wrote.

Flu vaccine uncertainty

Early data suggest that this year's flu shots have dramatically reduced seasonal flu hospitalizations. However, uncertainty hangs over the next vaccination round for the 2025-2026 season.

Flu mutates quickly. So every year, manufacturers use strains circulating in the Southern Hemisphere to predict the strains most likely to circulate in the coming season and create updated versions of the flu vaccine targeted to those strains. A U.S. Food and Drug Administration (FDA) advisory panel normally meets around this time of year to decide which strains should be included in the vaccines for the next season. That meeting was scheduled for Mar. 13 but was canceled without reason, Reuters reported on Feb. 28.

There is concern among experts that the cancellation could disrupt the production of flu vaccines, which could mean higher rates of serious illness and death, Live Science previously reported.

An FDA spokesperson told Reuters on Feb. 28 that it would make recommendations to manufacturers public in time for updated vaccines to be available for the 2025-2026 season.

This is the second time a vaccine advisory panel has been disrupted since Robert F. Kennedy Jr. took over as head of the U.S. Department of Health and Human Services, Reuters reported. Kennedy Jr. is a notable vaccine skeptic, though he's denied being anti-vaccine.

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

A person in Maine has died from an infection with a rare tick-borne virus, according to health officials.

On Wednesday (April 20), the Maine Center for Disease Control and Prevention (Maine CDC) announced that a resident of Waldo County, in south-central Maine, had died from Powassan virus. The virus is spread through the bite of an infected deer tick (Ixodes scapularis), groundhog tick (Ixodes cookei) or squirrel tick (Ixodes marxi), according to the U.S. Centers for Disease Control and Prevention (CDC).

Powassan virus is rare in the U.S., with only about 25 cases reported in the country per year since 2015, the Maine CDC said. (Prior to 2015, the virus was even less common, with only about 10 cases per year between 2011 and 2014, according to data from the CDC.) Maine has reported 14 total cases since 2010. Cases usually occur in the northeastern and Great Lakes regions of the United States during the late spring through mid-fall, according to the CDC.

"Ticks are active and looking for a host to bite right now," Nirav D. Shah, director of the Maine CDC, said in the statement. "I urge Maine people and visitors to take steps that prevent tick bites."

Related: The deadliest viruses in history

Many people infected with Powassan virus don't experience symptoms, but for those who do, the disease can be serious, according to the CDC. Initial symptoms can include fever, headache, vomiting and weakness.

Some people with Powassan virus can develop an infection of the brain (encephalitis), or of the membranes surrounding the brain and spinal cord (meningitis). Symptoms of these potentially serious conditions can include confusion, loss of coordination, difficulty speaking and seizures. About 10% of people with severe disease die from the infection, according to the CDC.

In the Maine case, the patient developed neurologic symptoms and died while in the hospital, the statement said.

There is no specific treatment for the infection. People with severe disease usually need to be hospitalized and receive supportive care, including breathing support, hydration and anti-inflammatory medicines to reduce swelling in the brain, according to the CDC.

The best way to prevent infection with Powassan virus is to prevent tick bites. According to Maine CDC, strategies to prevent tick bites include: avoiding wooded and bushy areas with tall grass (tick habitats) and staying on the middle of trails whenever possible, using insect repellent and treating clothing with the repellent permethrin, as well as performing tick checks, especially after visiting tick habits.

The increase in Powassan virus cases in the U.S. in recent years are likely due to the expansion of the range for deer ticks (also called black-legged ticks). Factors such as increased temperatures and humidity, as well as a rise in deer and mice populations, have contributed to the expansion of the tick population, Live Science previously reported.

Originally published on Live Science. 

A mysterious neurological disease in young Californian black bears (Ursus americanus) is making them behave like pet dogs, cozying up to humans in a friendly manner.

Though it sounds cute, this abnormal behavior dramatically worsens the bears' chances of surviving in the wild.

The bears, which are all around 1 year old, appear to be suffering from a form of infectious encephalitis — inflammation of the brain tissue that can be caused by viruses, bacteria, fungi and parasites, as well as part of an autoimmune response. But veterinarians are unsure exactly what is causing the problem or how fast it is spreading among the population. 

Symptoms include a prominent head tilt, lethargic movements, muscle tremors, seizures, walking in circles and being significantly underweight, as well as a surprising fearlessness towards humans. 

Related: The 10 weirdest medical cases in the animal kingdom

"Infected bears come to our attention because they approach people in a peaceful, friendly and non-aggressive manner," said Ann Bryant, executive director of the BEAR (Bear Education Aversion Response) League who has been involved in rescuing infected bears. "Their behavior is similar to a dog, not a bear."

In the last year, four individuals have been found with the disease — the highest number of cases since it was first detected in 2014, according to the California Department of Fish and Wildlife (CDFW).

The black bear population in California has increased from between 10,000 to 15,000 individuals in 1982 to between 30,000 to 40,000 today, according to the CDFW. As a result, veterinarians aren't too worried about the impacts of the disease on the overall population. 

Fearless youngsters 

Although cases of encephalitis are rare, the symptoms have made it quite easy to spot infected bears.

"The first bear I personally rescued was diagnosed with encephalitis in March of 2018," Bryant told Live Science. "She walked into a school and entered a classroom where she sat down among the children, behaving very much like a friendly dog."

In 2019, another infected bear was caught on video trying to climb onto a snowboard alongside its rider. The young male was eventually rescued after the snowboarder and his friends played with him and fed him sandwiches. However, friendly behavior doesn't mean it's safe for humans to be around the bears.

"Bears approaching people who might then treat the animal as if they are tame could easily present a danger," Bryant said. "I would not be comfortable with a member of the public trying to handle one of these, or any, bears."

Instead, if anyone comes across bears displaying symptoms of encephalitis they should report it to the CDFW, Bryant said.

These two particular bears now reside in rescue centers, where they must receive constant medical care to keep the brain inflammation under control, but most other bears aren't so lucky.

The most recent bear found to have the disease, which was discovered in February lying in the back of a truck parked on a residential property, was majorly underweight and covered in fleas, and had to be put down because of its poor physical condition, according to the Sacramento Bee. 

Unfortunately, this sad fate has befallen the majority of infected bears, who are not able to take care of themselves and appear to have been abandoned by their mothers.

On the increase? 

Veterinarians with the Nevada Department of Wildlife (NDOW) first discovered the encephalitis in bears around Lake Tahoe on the Californian border in 2014, according to the CDFW. 

Since then the CDFW has recorded eight cases in California, although the actual number may be higher. Half of the confirmed cases have been detected in the last year, but this doesn't necessarily mean it is on the increase. 

"My opinion is that this is not on the increase," Bryant said. "But more studies are now finally being done so we are more aware of it." 

The disease also doesn't appear to be transmissible between individual bears, Bryant said. This is encouraging for the rest of the population but has left researchers confused as to what is causing it.

"The worst part about this threat to our bears is that we don't know for sure what causes it," Bryant said. "The unknown is troubling."

Unknown origin 

Infected bears are taken to the CDFW's Wildlife Investigations Laboratory, where they can either be treated or, more likely, euthanized due to their poor physical condition. 

"Bears that die or are euthanized are necropsied to determine the cause of death," Brandon Munk, senior wildlife veterinarian at the CDFW's Wildlife Investigations Laboratory, told Live Science. "Evaluation of the tissues can confirm whether an animal had encephalitis or not."

Although the vets can identify the disease, determining the cause of the encephalitis has proved much harder.

"The brain inflammation is likely what causes the symptoms," Munk said. "Beyond that, we do not know the specific mechanisms that may be at play."

Potential pathogens have been identified as the cause of the encephalitis, but none have been confirmed so far. 

"We have identified five new viruses from black bears, some of which are being pursued further as possible causes of the encephalitis," Munk said. "We are also working with a research lab to further evaluate whether a protozoan parasite might be the cause."

However, it is also possible that there is more than one pathogen responsible for the encephalitis, Munk said.

Originally published on Live Science.

COVID-19 may cause dangerous neurological problems, including delirium, brain inflammation, nerve damage or stroke, according to a new study.

What's more, the study authors reported seeing a concerning increase in patients at their hospital with a rare and sometimes fatal neurological condition called acute disseminated encephalomyelitis (ADEM). All of the patients with ADEM had confirmed or suspected COVID-19, suggesting that the pandemic may be leading to an increase in this condition, the authors said.

The findings add to a growing body of evidence linking COVID-19 to brain effects, and suggest that doctors should be "vigilant and look out for these complications" in COVID-19 patients, study co-senior author Dr. Michael Zandi, a neurologist at the National Hospital for Neurology and Neurosurgery in London, said in a statement.

It's unclear exactly how frequently brain complications occur in COVID-19 patients, but the  study included only hospitalized patients who were referred to the hospital's neurology team, meaning the study likely included some of the most severe cases.

The study authors analyzed information from 43 patients ages 16 to 85 with neurological complications who were treated at National Hospital for Neurology and Neurosurgery, part of the University College London Hospitals NHS Foundation Trust. Of these, 29 had a positive COVID-19 test and the rest were probable or suspected cases of COVID-10 based on symptoms and results from other tests such as chest X-rays and CT scans.

There were 10 cases of so-called transient encephalopathies, or temporary brain dysfunction, with symptoms of delirium, such as confusion and disorientation. One patient had symptoms of psychosis, including visual and auditory hallucinations. Most of these patients eventually made a complete recovery without specific treatments.

Separately, eight patients had strokes, typically due to blood clots. Previously, researchers found that COVID-19 may increase the risk of blood clots. These patients tended to have poor outcomes, with none making a full recovery, and one patient died after their stroke.

Eight additional patients developed nerve damage, often due to Guillain-Barré syndrome, a rare autoimmune response that typically occurs after an infection, such as a respiratory or gastrointestinal infection.

Twelve of the patients developed brain inflammation, and most of these were also diagnosed with ADEM. One of the patients in this group died. Usually, ADEM is seen in children, but the patients with ADEM in this study were all adults. Before the pandemic, the research team typically saw one adult case of ADEM a month at their hospital, but during the pandemic, that increased to one case per week.

The researchers did not find SARS-CoV-2, the virus that causes COVID-19, in samples of patients' cerebrospinal fluid (the fluid around the brain and spinal cord), suggesting that the virus had not directly attacked the brain in these patients. In some of the patients, there was evidence from brain scans (and in one case, a brain biopsy) that suggested that the brain inflammation was caused by an immune system reaction.

"Our study advances understanding of the different ways in which COVID-19 can affect the brain, which will be paramount in the collective effort to support and manage patients in their treatment and recovery," said study co-first author Dr. Rachel Brown, of the University College London Queen Square Institute of Neurology. 

More studies are needed to understand what causes these brain effects and whether they will lead to long-term health problems, the authors concluded. 

Originally published on Live Science.  

West Nile virus (WNV) is an infectious disease transmitted to people via the bite of an infected mosquito, most often during warm-weather months. Mosquitoes contract the virus from biting an infected bird. 

Most people (about 8 in 10) infected with West Nile virus have no symptoms at all. Only about 20% of infected people develop West Nile fever, a typically mild, flu-like illness. 

Less than 1% percent of infected people may become seriously ill. This severe form of  infection, called West Nile virus neuroinvasive disease, can cause swelling in the brain and, in rare instances, can be life-threatening. 

Related: The 9 Deadliest Viruses on Earth

WNV neuroinvasive disease may lead to encephalitis (inflammation of the brain) or meningitis (inflammation of the membranes surrounding the brain and spinal cord), according to the Centers for Disease Control and Prevention (CDC). About 10% percent of people with neuroinvasive disease die, according to CDC statistics.

Where did the West Nile virus come from?

The virus was first isolated in 1937, from a woman in the West Nile district of Uganda; from that region, it spread to other countries in Africa, Asia, Europe and the Middle East, according to the Baylor College of Medicine in Houston. 

A strain of the virus made its way to New York in the summer of 1999, possibly due to migratory birds, and this eventually led to a large WNV outbreak that had spread throughout the continental U.S. by 2003, according to the Illinois Department of Public Health. 

About 2,650 cases of WNV were reported in the lower 48 states in 2018, and the majority of people became ill between July and September of that year, according to the CDC. Roughly two-thirds of cases were neuroinvasive disease, the serious form of the illness, suggested an analysis by the CDC.  

Related: 7 Common Summer Health Concerns

Reported cases of West Nile virus may be heavily weighted toward people with neurological symptoms, because these individuals are more likely to seek medical attention, said Dr. Sharone Green, an infectious disease specialist at UMass Memorial Medical Center in Worcester. 

The seven states with the highest number of neuroinvasive cases in 2018 included California, Illinois, Nebraska, Texas, Pennsylvania, Michigan and New York. WNV cases are linked to warm weather, typically first appearing in late spring and ending after the first hard frost in fall. 

Causes and risk factors

West Nile virus can infect humans, birds, mosquitoes, horses and a few other mammals. 

The virus is spread by the bite of infected female mosquitoes (primarily the Culex species). The Culex mosquito is commonly found throughout the U.S. and has a tendency to bite between dusk and dawn, Green told Live Science. 

Mosquitoes pick up the virus when they feed on infected birds, especially crows, jays, ravens and magpies, which are particularly susceptible to WNV, according to the University of California, San Francisco. 

Most people infected with West Nile virus avoid getting sick or they develop only mild symptoms. The more-serious, neurological symptoms occur when the virus crosses the blood-brain barrier and directly invades nerve cells in the brain and spinal cord, Green said. This may result in meningitis, an infection of the covering of the brain and spinal cord, or encephalitis, an infection of the brain. 

Related: Going Viral: 6 New Findings About Viruses

Neuroinvasive WNV can also very rarely lead to acute flaccid paralysis, a type of sudden limb paralysis caused by a spinal cord infection, Green said. This paralysis may affect only one limb, such as an arm, or just one side of the body, she said. 

People over age 60 are at greatest risk of developing serious complications from WNV, the CDC reports. Individuals with medical conditions, such as cancer, diabetes, high blood pressure or kidney disease, also are at increased risk. 

A very small number of people may develop WNV from blood transfusions or organ transplants. (All donated blood is currently tested for the virus, but organ donors may not be tested, says the CDC.) 

In a few reported cases, the virus may have been passed from mother to baby during pregnancy or breastfeeding, but these cases are extremely rare, according to the American Academy of Family Physicians.

Symptoms

Symptoms of West Nile fever, the mild form of the infection, may resemble the flu. They may include: 

• Fever
• Headache
• Fatigue
• Body aches
• Muscle pain
• Nausea
• Vomiting
• Diarrhea

Sometimes, swollen lymph glands or a skin rash on the back, chest or stomach may accompany the fever. Symptoms of mild or severe WNV typically show up three to 14 days after the individual is bitten by an infected mosquito, and the effects may last anywhere from a few days to several weeks.

Most people recover completely from West Nile fever. But some people may develop chronic fatigue or mild memory problems afterward, Green said.

Symptoms of the severe form of WNV may include:

• Sudden high fever (above 102 degrees Fahrenheit, or 39 degrees Celsius)
• Severe headache
• Stiff neck
• Confusion
• Muscle weakness
• Numbness and paralysis
• Vision loss
• Tremors or seizures
• Coma

Recovery from neuroinvasive disease might take weeks or months, because people may need rehabilitative therapy to relearn basic skills, such as walking or feeding themselves, Green said.

Diagnosis and treatment

The most definitive test for West Nile virus is a spinal tap (lumbar puncture), Green said. This test analyzes a sample of fluid surrounding the spinal cord to determine whether the virus is present. 

Blood tests can also detect high levels of antibodies, proteins produced by the immune system when fighting a virus. 

There is no specific treatment for West Nile virus, and most treatments given are considered supportive, meaning they ease symptoms, Green said. Treatment for neuroinvasive disease usually involves a stay in the intensive care unit, where a person with breathing problems may need a ventilator or medication to control seizures, she said. 

How to prevent West Nile virus

There is no vaccine to prevent West Nile virus in people, but there is one for horses. To prevent infections in people, it's important to decrease the number of mosquitoes found around the house, Green said. Other tips for avoiding bites and reducing mosquito exposure include: 

• Applying insect repellent. Use products containing DEET, picaridin or oil of lemon eucalyptus. Spray permethrin, an insecticide, onto clothing and outdoor gear for additional protection.
• Limiting outdoor activities between dusk and dawn, when Culex mosquitoes bite most frequently. Wear shoes, socks, long-sleeved shirts and long pants outside.
• Eliminating standing water, where mosquitoes breed. Empty water from wading pools, flower pots, pool covers and containers.
• Fixing screens with holes in them to keep mosquitoes out.

Additional resources: 

• Find out how many cases of West Nile virus occurred in your state, according to CDC data.
• Read more about West Nile virus around the globe from the World Health Organization. 
• Read "On the Trail of the West Nile Virus," an account of an early U.S. outbreak published in Smithsonian Magazine. 

Eastern equine encephalitis (EEE), also referred to as triple E, is a viral illness transmitted to humans and horses by the bite of an infected mosquito. The insects pick up the virus from biting an infected bird. 

Most people infected with the virus will not develop any symptoms from it, and mild forms of the illness, known as systemic infection, may resemble the flu. But about 5% of people who become infected may develop an extremely rare and potentially life-threatening infection that can cause swelling and inflammation of the brain, known as encephalitis, according to the Centers for Disease Control and Prevention (CDC).

In the United States, an average of seven human cases of encephalitic EEE were reported each year between 2009 and 2018, according to the CDC. Although only a handful of cases are reported annually, about 30% of people who develop severe encephalitic EEE die from the disease and many experience ongoing neurological problems after they recover from it, according to data from the CDC. 

Related: The 9 Deadliest Viruses on Earth

As its name suggests, Eastern equine encephalitis tends to occur in the eastern portion of the United States, but the illness also occurs in the south along the Gulf Coast and in the Great Lakes region. 

Globally, there are four variants of the virus, but only one is endemic to North America and the Carribbean. It's also the one that causes the most human cases of EEE. The other three varieties are found in Central and South America and primarily cause equine illness, according to the CDC.  

In the U.S., most cases are seen east of the Mississippi River between July and September, said Dr. Brian Chow, an infectious disease specialist at Tufts Medical Center in Boston. States with the highest numbers of reported cases of EEE between 2009 and 2018 include Florida, Massachusetts, New York, North Carolina and Georgia. Every year, cases begin popping up when the weather gets warm and mosquitoes thrive, from late spring to early fall, according to the CDC. 

What causes Eastern equine encephalitis? 

The EEE virus is transmitted by the bite of infected female mosquitoes. These mosquitoes are commonly found in marshlands and swampy areas and often feed on birds, Chow told Live Science. 

Birds act as reservoirs for the EEE virus and can become infected without showing signs of the illness. These reservoirs then pass the virus on to mosquitoes, which can spread it to horses and other mammals, including humans, he said. 

The virus was first identified in horses in 1933, and was isolated from human central nervous system tissue in 1938, according to the online Encyclopedia of Entomology. Horses and humans are the most susceptible to the virus.  

Related: Going Viral: 6 New Findings About Viruses

Once the virus is inside the body, it can replicate and travel in the bloodstream. In rare cases the virus crosses the blood-brain barrier and infects the brain, resulting in swelling of brain tissue, or encephalitis. 

The EEE virus is not contagious. It's not spread by person-to-person contact, nor is it spread from people to animals or from animals to people, according to the New York State Department of Health. 

People older than 50 and younger than 15 seem to be at greatest risk of developing severe EEE infection, according to CDC statistics. Those with weakened immune systems — from undergoing cancer treatment or receiving an organ transplant, for example — are also at a higher risk. 

Symptoms

Symptoms of the mild form of the infection may resemble the flu, with a sudden high fever, chills and aches in the muscles and joints, and the illness may last up to two weeks, Chow said. 

The severe form of EEE also starts out with flu-like symptoms. But about four days after these symptoms first appear, signs of a brain infection may show up, Chow said. These symptoms may include confusion, excessive drowsiness and a bad headache, and the complications can worsen quickly, leading to seizures, coma and sometimes death, he said. 

EEE is one of the most severe mosquito-transmitted diseases in the United States; approximately 1 in 3 people with the severe form of the disease die from it, usually within 10 days of the first appearance of symptoms, according to the CDC. But even those who survive this serious infection may be left with brain damage, intellectual impairment, paralysis and personality disorders. 

Diagnosis and treatment

Doctors can use a spinal tap (lumbar puncture), in which they analyze a sample of fluid surrounding the spinal cord, to detect whether the EEE virus is present. Physicians may also use other diagnostic tests, such as a CT scan or an MRI of the brain, to reveal signs of inflammation, as well as blood tests to detect high levels of antibodies, which are proteins produced by the immune system when it's fighting a virus.

Although there is a vaccine to prevent Eastern equine encephalitis in horses, there is no vaccine to prevent the brain infection in people. 

Related: 10 Things You Didn't Know About the Brain

Hospitals tend to see the severe cases of EEE, and treatment is aimed at reducing the severity of symptoms as the viral infection runs its course, Chow said. Treatment for the severe form of EEE usually involves a stay in the intensive care unit, where the patient is placed on a ventilator for breathing problems and may be put in a medically induced coma. 

Medications may be given to treat seizures or help relieve brain inflammation. But once the virus enters the nervous system, there are often lingering neurological consequences, Chow said. Most of the deaths linked with EEE are due to swelling and pressure inside the brain and spinal cord. 

How to avoid Eastern equine encephalitis

Mosquitoes have limited range and usually travel only a mile or two from where they breed, Chow said. States where EEE activity is known to occur typically monitor and test the mosquito populations for the virus during warm-weather months and may spray insecticides in communities identified as hotspots for infected mosquitoes. 

Spraying insecticide helps to reduce the threat of EEE, but it does not eliminate the risk of the illness. People should also take the following steps to protect themselves from mosquito bites: 

• Use insect repellent. Choose repellents with DEET, picaridin or oil of lemon eucalyptus. Permethrin is an insecticide that can be sprayed on clothing to ward off mosquitoes. 
• Limit outdoor activities between dusk and dawn, the peak feeding times for mosquitoes. When mosquitoes are most active, keep skin covered outdoors by wearing shoes, socks, long-sleeved shirts and long pants. 
• Remove standing water, which can be a breeding ground for mosquitoes, Chow said. Empty standing water from kiddie pools, flower pots and buckets. 
• Repair holes in screens on windows and doors. 

Additional resources:

• Find answers to frequently asked questions about EEE, from the CDC. 
• Here's how EEE may affect kids, from Boston Children's Hospital.
• Learn about other mosquito-borne viral brain diseases in the U.S., from Mount Sinai Health System. 

A flight attendant in Israel is in a coma after getting the measles, according to news reports.

Israeli health officials told CNN that the 43-year-old woman has encephalitis, or inflammation of the brain, and has been in a "deep coma" for 10 days. She is unable to breathe on her own and is on a respirator.

The measles virus, though most well-known for its telltale rash, can cause serious complications. Such complications are most common in children younger than 5 and adults over 20, according to the Centers for Disease Control and Prevention (CDC).

The most common serious complication of measles is pneumonia, the CDC says: Up to 1 in 20 children with measles gets pneumonia, and it is the most common cause of death from the disease.

Much rarer is encephalitis, which affects 1 in every 1,000 children with measles, according to the CDC.

The flight attendant had been vaccinated against measles; however, she had received only one dose of the vaccine, according to CNN. Health officials didn't start recommending that children receive two doses of the vaccine until 1989, when it was discovered that one dose was more than 90% effective at preventing measles, but two doses boosted the effectiveness to 97%.

Dr. Amesh Adalja, a senior scholar at The Johns Hopkins Center for Health Security in Baltimore, previously told Live Science that adults who received only one dose of the measles vaccine as children could consider getting a second dose.

Health officials said it's not yet clear where the flight attendant, who works for the Israeli airline El Al, contracted the disease. It may have been in New York or Israel — there are ongoing outbreaks in both locations — or on board a flight. Officials do not believe she spread the virus to anyone on a flight.

• The 9 Deadliest Viruses on Earth
• 5 Dangerous Vaccination Myths
• 27 Devastating Infectious Diseases

Originally published on Live Science.

At least 10 people in India have died from a rare virus known as Nipah virus, according to news reports.

The deaths occurred in Kerala, a state in southern India, according to the BBC. Two other people have tested positive for the virus and are critically ill, and an additional 40 people have been put into quarantine after having contact with those who died, the BBC reported.

Nipah virus infection is an emerging disease that was first identified in 1999 during an outbreak among pig farmers in Malaysia and Singapore, according to the Centers for Disease Control and Prevention (CDC).

The virus is thought to naturally infect fruit bats (of the genus Pteropus), but it can also infect pigs and other domesticated animals, as well as humans, according to the World Health Organization (WHO). The virus can also spread from person to person. [10 Deadly Diseases That Hopped Across Species]

Nipah virus can cause an inflammation of the brain known as encephalitis, according to the CDC. Symptoms can include fever and headache, followed by drowsiness, disorientation and confusion. People who are infected with the virus may fall into a coma within 48 hours of showing symptoms, the CDC says.

The virus can be highly lethal, with an average fatality rate of around 75 percent, according to the WHO.

Human infections with Nipah virus in India and Bangladesh have been linked with eating raw date palm sap contaminated by fruit bats, and contact with bats, the CDC said.

There's no drug to treat the illness and no vaccine to prevent it. "We are now concentrating on precautions to prevent the spread of the disease since the treatment is limited to supportive care," Rajeev Sadanandan, Kerala's health secretary, told the BBC today (May 21).

Editor's note: This article was updated on May 22 at 12:30 pm ET with new information on the number of deaths tied to the outbreak.

Original article on Live Science.

When a Massachusetts man arrived at the hospital, he had trouble speaking and walking. Doctors soon suspected that he had a potentially life-threatening condition: inflammation in his brain or the tissue surrounding it.

But to squelch the inflammation, they needed to know the cause. Tests for dozens of viruses, bacteria and fungi — typical culprits for brain inflammation — kept coming back negative.

Doctors didn't discover the cause until after the man's death, according to a new report of the case, published yesterday (March 19) in the journal JAMA Neurology. The culprit was the Powassan virus, a rare virus carried by ticks in the northeastern and Great Lakes regions of the United States. Just 100 cases of Powassan virus infections have been reported in the United States in the last 10 years, according to the Centers for Disease Control and Prevention (CDC).

The Powassan virus can infect the central nervous system and cause dangerous inflammation, the CDC says. About 10 percent of Powassan virus cases are fatal. 

Because the disease is so rare, there is no standard way of diagnosing it. This man's case was even more complicated because he was taking a cancer medication that affected his immune system. As a result, standard lab tests that look for antibodies against viruses wouldn't work, because the man wasn't producing those antibodies. [10 Bizarre Diseases You Can Get Outdoors]

But there is one genetic test that can be useful in these situations: a test that screens for potentially any virus, bacteria or other pathogen that may be causing an illness, rather than looking for a single microbe at a time, the researchers said. This test, known as an "unbiased sequencing assay," ultimately helped diagnose the man with Powassan virus, according to the report, led by Dr. Isaac Solomon, a neuropathologist at Brigham and Women's Hospital in Boston.

A mysterious case

The man, who was in his 60s, had lymphoma, which is a cancer of the immune system. For treatment, he was taking a medication called rituximab, which acts on the immune system.

Problems began in December 2016, when the man went to the emergency room with a fever and pain in his testicles. Tests showed that he had orchiepididymitis, or inflammation in the testes. Doctors gave him an antibiotic and sent him home.

But three days later, he returned  to the hospital with speaking and walking problems and trouble using his arms. This time, doctors gave him three different antibiotics and an antiviral medication, suspecting that he had an infection causing inflammation in his brain (encephalitis) or the tissues surrounding his brain (meningitis).

A week later, the man's condition worsened, and he became much less alert. He appeared to have a severe brain injury; he wasn't opening his eyes in response to doctors' commands. An MRI showed that the man had excess fluid in his brain along with other signs of brain injury.

Doctors tested the man for numerous infectious diseases, including Lyme disease, syphilis, toxoplasmosis, herpes, mumps and West Nile virus infection. All the tests were negative.

Unfortunately, the man continued to get worse, and he died after two weeks in the hospital, according to the report.

A search after death

After the man's death, the doctors continued to search for source of the mysterious ailment. Ultimately, they used several different tools to identify the Powassan virus. (The results of these tests weren't available until after the patient's death.)

One was called "metagenomic next-generation sequencing," a type of unbiased test in which researchers sequence all of the DNA and RNA in a sample. Given that most of this genetic material is from the patient himself, this approach is like looking for a needle in a haystack. (In this case, the "needle" is the strand of viral or bacterial DNA/RNA that's causing the disease.)

Eventually, the researchers found genetic material from the Powassan virus and concluded that the man had died from encephalitis caused by this virus.

The findings "support the utility of unbiased pathogen-detection assays capable of detecting a wide variety of infectious agents" in cases in which doctors can't seem to find the cause of a patient's encephalitis, the researchers wrote.

Original article on Live Science.

A newborn baby in Iowa died this week from an infection with the virus that causes cold sores, which she likely contracted from a kiss, her doctors say. But how does this happen?

The baby, Mariana Reese Sifrit, was healthy when she was born July 1, according to ABC News. Six days later, Mariana's parents got married, and just hours after the wedding, Mariana looked sick — she became lethargic and stopped feeding, and her parents took her to the hospital, according to ABC.

Doctors diagnosed Mariana with meningitis, which is a swelling of the membranes that cover the brain and spinal cord. They said her meningitis was due to an infection with herpes simplex virus 1 (HSV-1), the virus that causes cold sores. Both parents tested negative for the virus, and her doctors said Mariana likely caught the virus from a kiss from someone who came to see the newborn, according to ABC. Mariana died Tuesday (July 18).

"Just keep your babies isolated," Mariana's mother, Nicole Sifrit, advised parents when she spoke with the ABC affiliate WQAD-TV. "Don't let people kiss your baby. Make sure they ask before they pick up your baby," Sifrit said. [7 Baby Myths Debunked]

In newborns, catching HSV-1 infection from a kiss is "unusual but not unheard of," said Dr. Otto Ramos, medical director of the Division of Pediatric Infectious Diseases at Nicklaus Children's Hospital in Miami. That's because people with HSV-1 infection — either with or without cold sores — can shed the virus and transmit it to others, said Ramos, who was not involved in Mariana's case and so cannot comment on the case directly.

However, in most cases of HSV-1 in infants, Ramos said, the baby catches the virus from its mother during delivery, and in 60 percent of such cases, the mother had no signs or symptoms of infection, Ramos told Live Science.

Indeed, according to a study published in March in the journal The Lancet Global Health, about 85 percent of newborns with herpes simplex infection catch the virus during delivery, while only 10 percent catch the virus after birth from someone with an infection. The other 5 percent catch the virus in utero.

Herpes simplex viruses can cause serve complications in newborns, and left untreated, the infection results in death in 60 percent of cases, The Lancet study said. These viruses can infect the brain, leading to a condition called herpes encephalitis, which can result in seizures, intellectual disabilities, vision and hearing loss, according to the March of Dimes. The viruses can also infect multiple organs at the same time, including the liver, lungs and kidneys, and about 30 percent of infants with these widespread infections die, the March of Dimes said.

About 1 of every 3,500 babies born in the United States, or less than 1 percent, contracts herpes simplex virus each year, according to the March of Dimes.

Ramos said newborns are particularly vulnerable to herpes simplex virus infections because their immune system is not mature enough to thwart the virus. "The baby doesn’t have an immune system that can fight it off," Ramos said.

New parents should be extremely careful not to let people with any kind of infection have close contact with their baby, Ramos said.

"You have to be very careful and very vigilant that no one who has any kind of infection is around the baby," Ramos said. "People should not be kissing babies if they have any kind of infection," he said.

To prevent HSV-1 infections in babies after birth, the National Institutes of Health says that people with cold sores should not come into contact with newborn infants. Parents and caregivers with cold sores should wear a mask and wash their hands carefully before coming into contact with their baby, the NIH said. Good handwashing is also important for anyone who has contact with a newborn, Ramos said.

Original article on Live Science.

A man in Brazil died of rabies in May after a vampire bat bit him.

The man, who lived in the northeastern Brazilian city of Salvador, was one of many people in the area bitten by bats. Brazilian news agency Agência Brasil reported that the bloodsucking bats have bitten 40 people since March.

Vampire bats were not thought to prey on humans, but Brazilian researchers recently found that one species of vampire bat (Diphylla ecaudata) had expanded its palate beyond birds, to human blood. 

These bats can carry and spread the rabies virus, and indeed, the man who died caught rabies from the bat that bit him. But what happens when a person gets rabies, and how does the virus kill? [27 Devastating Infectious Diseases]

The rabies virus can have a long incubation period, said Dr. Amesh Adalja, an infectious-disease physician and a senior associate at the Johns Hopkins Center for Health Security, who was not involved in the Brazilian man's care. In some cases, it can take months after a person is infected with the virus for symptoms to appear.

The length of the incubation period depends, in part, on where a person is bitten, Adalja told Live Science. The rabies virus travels through a person's nerve cells until it reaches the central nervous system and enters the brain, so it will take longer to get there if a person is bitten on the toe than, say, the face.

Once the virus gets to the central nervous system, a person will have general symptoms associated with viral infections, such as a fever and a headache.

But rabies is different from other infections, because as this infection gets worse, a person experiences changes in personality, including alterations in how he or she thinks, along with agitation and delirium, Adalja said. People infected with rabies may also develop hydrophobia, or a fear of water. These severe symptoms generally begin about two weeks after a person experiences the initial symptoms of the infection, Adalja said.

The changes occur because the virus causes inflammation in the brain, a condition known as encephalitis, Adalja said. This inflammation can disrupt neurotransmitters in the brain, altering how brain cells communicate with each other.

Severe brain inflammation can lead to seizures, coma and ultimately death, Adalja said.

If a person has been bitten by an animal that could be rabid, it's important to immediately seek medical attention, Adalja said. The infection can be nipped in the bud using "post-exposure prophylaxis" — in other words, giving someone the rabies vaccine after he or she has been bitten.

Post-exposure prophylaxis is extremely effective, Adalja said, but it's essential that patients get the treatment before symptoms start.

Once a person starts having symptoms, rabies is nearly impossible to treat, and is fatal. Only one type of treatment, called the Milwaukee protocol, has ever been shown to work to treat rabies and save the lives of people infected, Adalja said. That treatment involves putting a person in a medically induced coma and giving the individual antiviral drugs. But the treatment has been used in only a handful of cases, and there is significant debate in the medical community about whether it is effective.

About 59,000 people worldwide die from rabies each year, according to the Centers for Disease Control and Prevention. On average, there are one to three rabies cases reported yearly in the U.S.

Originally published on Live Science.

A young woman's weeklong bout of "strange behavior" was caused by a rare disease in which the immune system attacks the brain, according to a new report of the woman's case.

The 27-year-old woman went to the emergency room in Colorado after a week of feeling ill. She had began experiencing short-term memory loss and anxiety, and later developed agitation, hallucinations and involuntary movements, the doctors who treated her wrote in their report.

Prior to that week, the woman had been healthy. She told the doctors that she hadn't drank alcohol, smoked tobacco or used any drugs, according to the report, published Nov. 30 in The New England Journal of Medicine.

When a person comes into the emergency room with an "altered mental status," doctors must consider a wide range of possible causes, which run the gamut from neurological conditions, to trauma, to psychiatric illnesses, to body-wide diseases, according to the report. [Here's a Giant List of the Strangest Medical Cases We've Covered]

The doctors ran tests and carefully evaluated the woman's symptoms, eventually ruling out that the problem could be an infection, or the result of a toxin or a metabolic disorder.

The woman's age, sex and the involuntary muscle movements suggested that she might have had a rare type of encephalitis, or inflammation of the brain, called anti-NMDA receptor encephalitis, according to the report. The NMDA receptor, or N-methyl-D-aspartate receptor, is found on cells in the brain.

Anti-NMDA receptor encephalitis is an autoimmune disorder, said Dr. Susan Mathai, who treated the woman and was the lead author of the case report. In autoimmune disorders, the immune system attacks a person's own body. In anti-NMDA receptor encephalitis, the immune system makes antibodies that attack the NMDA receptor in the brain, said Mathai, who is also an assistant professor of medicine who teaches pulmonary science and critical care at the University of Colorado School of Medicine.

When this attack happens, it causes inflammation in the brain, which, in turn, can cause neurological symptoms, such as seizures and a loss of muscle-movement control, Mathai told Live Science.

Although the disease is rare, it's "not as rare as people think," Mathai said. She noted that there have been multiple cases at the University of Colorado, and that this autoimmune disorder is "increasingly being recognized as a cause of encephalitis." About 4 out of 5 people with anti-NMDA receptor encephalitis are women, according to the report.

Tests and treatment

To test for the condition, the doctors took a sample of the woman's spinal fluid. They found that it contained the antibodies, which confirmed she had the disease.

It's not entirely clear what causes a person to develop the autoimmune disorder. However, scientists think certain tumors may play a role.

Ovarian teratomas, which are a type of noncancerous tumor that grows on the ovaries, are the most common type of tumor found in patients with the disorder, according to the report.

In general, it's thought that certain proteins in these tumors trigger the immune system to create the antibodies that attack the NMDA receptor, Mathai said. 

Indeed, when the doctors looked at the woman's ovaries, they found such a tumor on her left ovary, and removed it, according to the report.

Tumor removal is an important part of treating the autoimmune disease, according to the report.

Doctors also need to remove all of the problematic antibodies from a person's blood. To do so, the woman in the case underwent plasmapheresis, a procedure to purify the blood, for five days, the doctors wrote. She was also given medications to suppress her immune system, in order to stop the production of more antibodies.

The woman has fully recovered from the illness, the doctors noted in the report.  

Originally published on Live Science.

Catching the mosquito-borne virus chikungunya usually leads to fever and severe pain, but a new study shows it may also lead to inflammation in the brain, and even death in some people.

In the study, researchers looked at an epidemic of the virus on Reunion Island, in the Indian Ocean near Madagascar, that lasted from 2005 to 2006 and sickened 300,000 people. As a result of their infections, 24 people developed encephalitis, which is inflammation of the brain, and four of these people died from their infection.

Encephalitis from the chikungunya virus was most common among babies younger than 1, and people ages 65 and older, according to the study.

The researchers noted that the encephalitis rates in these groups were "much higher than the rates of encephalitis in the United States in these age categories, even when you add together all the causes of encephalitis," study author Dr. Patrick Gérardin, of Central University Hospital in Saint Pierre, Reunion Island, said in a statement.

Chikungunya virus is transmitted to people by mosquitoes. The most common symptoms of an infection are fever and joint pain, as well as muscle pain, joint swelling and rash, according to the Centers for Disease Control and Prevention (CDC). Most people recover within a week of becoming infected, but for some people, the pain and other symptoms may continue for months or even years, the researchers said. [The 9 Deadliest Viruses on Earth]

There is currently no vaccine to prevent chikungunya, or medicine to treat infection with the virus, according to the CDC. People who catch the virus are typically treated with fever-reducing medications and painkillers, Gérardin told Live Science. If people develop arthritis as a result of infection with the virus, they are given anti-inflammatory drugs, he said.

Outbreaks of chikungunya have occurred in many regions of the world, including Africa, Asia, and the Caribbean islands, the researchers said. And in recent years, the disease has been spreading to new areas. As of September 2015, more than 7,000 cases had been reported in Mexico, according to the CDC.

"Since there is no vaccine to prevent chikungunya and no medicine to treat it, people who are traveling to these areas should be aware of this infection and take steps to avoid mosquito bites, such as wearing repellent and long-sleeves and pants if possible," Gérardin said.

In 2014, a Florida manbecame the first person to become infected with the virus in the U.S. (previously, other people had been diagnosed with chikungunya in the U.S., but they had contracted the virus while traveling elsewhere).

This year, 571 cases of chikungunya virus disease have been reported so far in 42 U.S. states, including cases contracted both here and elsewhere. And 196 cases have so far been reported in Puerto Rico and the U.S. Virgin Islands in 2015, according to the CDC.

When the researchers followed up with the people in the new study, three years after the outbreak, they found that an estimated 30 to 45 percent of the 24 people who had developed encephalitis went on to develop persisting disabilities. (The  researchers were not able to calculate the exact percentage as some people were lost to follow up.)

Among the children who had been infected as infants and developed encephalitis, these disabilities included behavioral changes and problems with thinking and memory skills, the researchers said.

"The consequences of this encephalitis seem to be particularly harmful in newborns," Gérardin said.

Among the adults who were infected with the virus and developed encephalitis as a result of the infection, the disabilities included dementia and epilepsy, according to the study, published today (Nov. 25) in the journal Neurology.

Follow Agata Blaszczak-Boxe on Twitter. Follow Live Science @livescience, Facebook & Google+. Originally published on Live Science.

Three people who received organ transplants from the same donor all developed serious brain problems shortly after their operations. The mysterious symptoms turned out to be due to a little-understood parasite that infected the donor before she died, according to a new report of the case.

The donor was a 43-year-old woman who died from a stroke, and her kidneys, heart and liver were all transplanted into patients in February 2014. But two months later, a man who received a kidney from the woman developed a fever, and showed changes in behavior, suggesting a brain problem.

Doctors were concerned that the man had contracted an infection from the donor, which happens in about 1 to 2 percent of U.S. transplants. The physicians tracked down the two other transplant patients — one who received the liver, and another who received both the donor's heart and other kidney. The patient who received the liver transplant had already seen a doctor because of tremors and problems walking, and the heart and kidney transplant patient had been admitted to the hospital for brain inflammation known as encephalitis.

"All three [transplant] recipients developed severe neurological complaints within a few months of the transplant," said study researcher Dr. Rachel Smith, a medical epidemiologist at the Centers for Disease Control and Prevention. [The 9 Most Interesting Transplants]

Doctors tested the patients' blood, urine, stool and cerebrospinal fluid for a number of infections, but all the tests were negative.

The patient with the kidney transplant got progressively worse over the next few months, and died in May.

During that patient's autopsy, doctors tested the man's tissue for infections, and the test was positive for a parasite called Encephalitozoon cuniculi, which belongs to a group of single-celled organisms known as microsporidia. Subsequent tests showed that both the donor and the two surviving transplant recipients also were infected with the parasite.

Most patients with this parasite have gastrointestinal symptoms such as diarrhea, and it's rare for them to have only brain symptoms, Smith said. Usually, microsporidia infection leads to disease only in people with compromised immune systems. That group includes transplant patients, who must take medications that suppress the immune system to prevent their bodies' from rejecting the new organ.

But this parasite "may be more common than we think," Smith said. It's difficult to diagnose, and whether it ever causes symptoms in healthy people, or goes away on its own, is not known. It may be that the organ donor carried the parasite in her body for a long time without ever having symptoms, Smith said.

Still, the parasite is rare in transplant patients, and it's unlikely that doctors would begin routinely testing organ donors for microsporidia at this time, Smith said. The parasite is a challenge to diagnose, and doctors are not certain what a positive result means in terms of patient safety, she said.

"There's always this tension between making sure that transplants are safe and making sure that no more people die on the waiting list than is already happening," Smith said. "Anytime we say that there should be another test done on donors, it needs to have a very obvious value added to the safety component of this."

Both of the surviving transplant recipients were given a drug called albendazole, and their neurological problems went away. More research is needed to better understand how to treat and diagnose these infections, Smith said.

Smith presented the findings this month at IDWeek, a meeting of several organizations focused on infectious diseases.

Follow Rachael Rettner @RachaelRettner. Follow Live Science @livescience, Facebook & Google+. Original article on Live Science.

He spawned millions of fuzzy toys, garnered media attention on everything from his cod-liver diet to his lack of mates and even inspired his own song before his untimely death in 2011.

He was Knut the polar bear, the star of the Berlin Zoo.

Now, new research shows how the adorable white beast really died.

It turns out that Knut was killed by an autoimmune disorder called anti-NMDA receptor encephalitis, a kind of brain inflammation. Past work implicated encephalitis in his death, but hinted that a virus or bacteria was to blame.

The new discovery suggests that a disease previously identified only in humans could be a leading cause of encephalitis deaths in other animals, study co-author Alex Greenwood, a veterinary physiologist at the Leibniz Institute for Zoo and Wildlife Research in Berlin, said in a press briefing. [See Images of the Adorable Polar Bear Knut]

A life full of drama

The twists and turns of Knut's life captured the popular imagination. His mother Tosca rejected him at birth (Dec. 5, 2006), and his brother, who was born the same day, died just four days later. So the zookeeper Thomas Dörflein bottle-fed Knut, forming a deep bond with the cub. Videos of Dörflein swimming and snuggling with Knut were Internet sensations.

"You had this immediate charismatic contact between human and animal," Greenwood said.

When Dörflein died suddenly of a heart attack in 2008, it was as if Knut was orphaned again. And Knut had a difficult time as a grown bear. He was rejected by potential mates and constantly fought with other polar bears and was separated from them.

Even his death was spectacular. On March 19, 2011, Knut had a seizure and collapsed, falling backward into his pool, dying in front of hundreds of zoo visitors.

Encephalitis

A tissue sample taken from Knut shortly after his death revealed he had encephalitis, with a 2014 study hinting at an infectious virus as the cause. But a closer analysis revealed antibodies, or immune cells, to the influenza virus, but no actual flu virus particles present. None of the inflammation seemed tied to an active infection, the researchers said.

"We basically had ruled out any pathogen imaginable with a very comprehensive search using all the most modern methods and next-generation sequencing and all the classic methods of serology, and we just didn't find anything," Greenwood said. (Serology refers to the study of body fluids, often the identification of antibodies in blood serum.)

But when Harald Prüss, a neurologist at the German Center for Neurodegenerative Disorders (DZNE) Berlin and Charité, read the report on Knut's death, he thought the case sounded a lot like the human disease he treats in his clinic, known as anti-NMDA receptor encephalitis. [Top 10 Mysterious Diseases]

The rare disease occurs when antibodies, the immune cells designed to recognize foreign agents, bind to glutamate (NMDA) receptors in the brain, causing them to malfunction. Anti-NMDA receptor encephalitis affects about one in 200,000 people, and initially causes fever, headaches and psychosis before progressing to motor problems, seizures and death if undiagnosed and untreated. It is the major cause of encephalitis in humans when no virus or bacteria can be blamed, yet it was only discovered in 2007.

Luckily, the disease can be mostly reversed if caught early enough, Prüss said in the briefing.

"We usually try with high-dose steroids during the first days, and then in some patients, plasma exchange — plasmaphoresis — is quite efficient in removing these antibodies," Prüss said.

The team analyzed Knut's brain and found signs of NMDA antibodies at his glutamate receptors, the researchers report today (Aug. 27) in the journal Scientific Reports. It's not clear exactly why his body began to attack his brain, but in humans, a recent case of influenza or herpes can sometimes trigger the body's friendly fire, Prüss said.

Widespread animal disease

The new results raise the possibility that anti-NMDA receptor encephalitis is relatively common across the animal kingdom. So theoretically, zoo animals and even some endangered species in the wild could potentially get treatment, Greenwood said.

Of course, animals can't talk, so veterinarians only suspect encephalitis when they start to have seizures or motor problems. Veterinarians would likely give sick zoo animals a cocktail of antivirals, antibiotics and immune-suppressing drugs as soon as they show those symptoms, to try to eliminate the antibodies, Greenwood said.

Follow Tia Ghose on Twitter and Google+. Follow Live Science @livescience, Facebook & Google+. Original article on Live Science.

Three people in Germany who worked as squirrel breeders and who all died from brain inflammation may have contracted a new strain of virus from their squirrels, according to a new report of the cases.

The new virus strain belongs to a group of viruses called bornaviruses, which typically infect animals such as horses, sheep and birds. Researchers have debated whether this group of viruses can cause disease in people.

The new findings suggest such viruses do cause disease, and moreover, raise the question of whether this virus "represents an emerging threat" to people in the area, according to a recent statement from the European Centre for Disease Prevention and Control.

The three squirrel breeders who died were all men in their 60s and 70s. They were friends with each other and met on a regular basis. They bred variegated squirrels, which are sometimes kept as exotic pets. At least two of the men had experienced scratches and bites from their squirrels, the report said.

Between 2011 and 2013, all three men developed encephalitis, which is inflammation in the brain, and is usually caused by a virus. They experienced fever, chills and weakness, and later, confusion and difficulty walking. All three men were hospitalized and treated in intensive care units, but each eventually went into a coma and died within two to four months of their first symptoms, the report said.

Tests for the usual causes of encephalitis did not initially reveal the culprit. But a more detailed genetic test of one of the squirrels owned by the breeders identified a new type of bornavirus, which the researchers call VSBV-1.

Further study identified this virus in the brain tissue of all three patients, and antibodies to the virus were found in the blood and spinal fluid of one of the men, pointing to the virus as the likely cause of the men's fatal brain inflammation, the researchers said.

"VSBV-1 is likely to be a previously unknown zoonotic pathogen transmitted by the variegated squirrel," the researchers, from the Friedrich Loeffler Institute in Germany, wrote in the July 9 issue of the New England Journal of Medicine. [10 Deadly Diseases That Hopped Across Species]

However, the new study does not definitively prove that this virus caused the encephalitis, the researchers noted.

Still, until more research is done, "feeding or direct contact with living or dead variegated squirrels should be avoided as a precautionary measure," the ECDC said.

Many questions remain, including where the virus naturally "lives" and how it is transmitted. In addition, people with unexplained encephalitis could also be tested for the virus, the researchers said.                                    

 Follow Rachael Rettner @RachaelRettner. Follow Live Science @livescience, Facebook & Google+. Original article on Live Science.

There were fewer reported cases of West Nile virus in the United States in 2013 compared with the previous year, according to a new report from the Centers for Disease Control and Prevention.

In 2013, there were 2,469 reported U.S. cases of West Nile virus, compared to 5,674 cases reported in 2012, when there was a large outbreak of the disease, the CDC said.

Of the cases reported in 2013, 1,267 were severe, defined as causing inflammation in the brain or surrounding tissues. Cases peaked in early September, and 90 percent of the people infected with the virus became ill between July and September, the report said.

Among the severe cases that caused neurological symptoms (called "neuroinvasive" cases), more than half (51 percent) occurred in just six states: California, Texas, Colorado, Illinois, North Dakota and Oklahoma. The states with the highest rates of neuroinvasive cases relative to their populations were North Dakota, South Dakota, Nebraska and Wyoming. [10 Deadly Diseases That Hopped Across Species]

Still, severe cases of West Nile remain rare: In 2013, the rate of neuroinvasive cases was four cases per 1 million people.

West Nile virus is most commonly spread by mosquitoes. About 70 to 80 percent of people infected with the virus show no symptoms, but about 20 percent develop a fever and other symptoms — such as headaches, body aches and vomiting — and less than 1 percent develop neurological illness, according to the CDC.

Because most people infected with West Nile do not develop symptoms, or do not feel sick enough to go to the doctor, the number of actual cases is likely much higher than the number of reported cases, according to the CDC. Taking into account underreporting, there may have been between 38,000 and 88,000 actual West Nile cases in the United States in 2013, the report said.

The number of West Nile cases varies from year to year due many factors — including the weather, number of birds that host the virus (when it's not in mosquitoes), the abundance of mosquitoes that spread the virus and human behavior such as the use of insect repellent — all of which can affect when and where outbreaks occur, the CDC said.

"This complex ecology makes it difficult to predict how many cases of disease might occur in the future and where they will occur," the report said.

To prevent infection with West Nile and other diseases spread by mosquitoes and ticks, the CDC recommends that people use insect repellant and wear protective clothing.

Follow Rachael Rettner @RachaelRettner. Follow Live Science @livescience, Facebook & Google+. Original article on Live Science.

A South Carolina woman who died from rabies she contracted from bats in her home might have been saved if she had been told of rabies risks associated with bats, according to a new report of her case.

The 46-year-old woman, who died in December 2011, was the first person to die from rabies in South Carolina in more than 50 years, according to the report published today (Aug. 15) by the Centers for Disease Control and Prevention (CDC). She had sought information from a local county animal control service on having bats removed from her home, but was not advised of the rabies risks associated with bats.

"Lack of referral to guidance concerning health risks associated with bats living in the home was possibly a missed opportunity to prevent rabies infection," CDC researchers wrote in the report.

Shots of rabies vaccine prevent the infection from taking hold after someone is bitten by an animal carrying the virus. People who have seen bats in their homes are generally advised to seek treatment because bats have small teeth, and bites that occur during sleep can go unnoticed. The vaccine is almost always effective if given before rabies symptoms appear.

The South Carolina woman awoke one summer night to find a bat in her room. She shook the animal out of her curtains, and it flew off through a window, her family later said. [10 Deadly Diseases That Hopped Across Species]

In December, she went to the hospital with shortness of breath, excessive sweating and chills. Her symptoms were similar to those of heart disease, and she had had heart problems in the past, so she was transferred to another hospital to be examined by her cardiologist.

But a few hours after her arrival at the new hospital, she stopped breathing and was transferred to the intensive care unit, where she was put on a ventilator for several days. Her condition worsened, and her organs started to fail.

Five days after she was admitted to the hospital, additional interviews with her family revealed that she had seen bats in her home the previous summer. Her doctors sent samples of her skin and saliva to the CDC to be tested for rabies.

The tests came back positive, but it was too late to administer the vaccine to the woman, who died several days later. The family members, and anyone at the hospital from the ambulance personnel to administrative staff who reported possible contact with the patient were given vaccine shots.

The rabies virus that had infected the woman was a strain found in Mexican free-tailed bats, the CDC investigations showed.

The number of human deaths from rabies in the United States has declined over the past century, to as low as one or two yearly in the 1990s. Bats are responsible for the majority of cases. Since 1995, more than 90 percent of people who got rabies in the United States contracted it from bats. 

The rabies virus infects the central nervous system, and causes inflammation in the brain and, ultimately, death. The early symptoms of rabies in people are fever, headache and general weakness or discomfort, and can be mistakenly attributed to other illnesses.

Therefore, the CDC researchers recommended considering rabies in any progressive encephalitis (inflammation of the brain) that doesn’t have clear cause.

The woman's case "highlights the importance of strong partnerships among public health officials and diverse non–health-care partners," the report said.

People who see bats in or around their homes might reach out to a variety of groups, including animal control, law enforcement or wildlife agencies, and it is important that these entities have strong partnerships and clear communication so that they can appropriately refer people exposed to bats for risk assessment and treatment, the report said. 

Email Bahar Gholipour. Follow LiveScience @livescience, Facebook & Google+. Original article on LiveScience.

In Laura Ingalls Wilder's "Little House on the Prairie" books, she describes her sister Mary going blind from scarlet fever. But brain and spinal cord inflammation likely caused Mary's blindness, a new study suggests.

The findings, published today (Feb. 4) in the journal Pediatrics, came from poring over the symptoms Wilder described in memoirs and books.

"Since I was in medical school, I had wondered about whether scarlet fever could cause blindness, because I always remembered Mary's blindness from reading the 'Little House' stories and knew that scarlet fever was once a deadly disease," said study co-author Beth Tarini, a pediatrician at the University of Michigan's C.S. Mott Children's Hospital, in a statement.

Wilder wrote several books describing her life as a pioneer in the mid-1800s. In one, she describes her sister Mary going blind at age 14 in 1879.

At the time, scarlet fever was one of the deadliest scourges for young children. The fever occurs when the bacteria that cause strep throat run rampant in the body, causing a rash, fever, bone and joint pain, and, in serious cases, kidney and liver damage.

To find out what caused Mary's blindness, Tarini and her colleagues investigated local newspapers, the author's memoirs and letters.

They found that Wilder described her sister's disease as a "spinal sickness" and that local newspaper reports said a "hemorrhage of the brain had set in [sic] one side of her face became partially paralyzed."

Those symptoms were more consistent with a disease called meningoencephalitis, an inflammation of the spinal cord and brain, which can result from several viruses.

"Meningoencephalitis could explain Mary's symptoms, including the inflammation of the facial nerve that left the side of her face temporarily paralyzed," Tarini said in a statement. "It could also lead to inflammation of the optic nerve that would result in a slow and progressive loss of sight."

It's not clear why the editors of the book tied Mary's blindness to scarlet fever, but one possibility is that the disease was such a well-known and feared scourge at the time, the researchers suggest.

Follow LiveScience on Twitter @livescience. We're also on Facebook & Google+. 

In 2010 at the Wuppertal Zoo in Germany, brain inflammation killed one female polar bear, Jerka, and sickened her male companion, Lars, whom veterinarians were able to save.

Brain-swelling disease, or encephalitis, can be caused by many pathogens. But after investigating samples from Jerka, Lars and nine other polar bears researchers believe they have identified the culprit: a mishmash virus that originated in zebras.

The bear-killing virus appears to have emerged when a portion of equine herpes virus transferred a portion of its genetic code — one known for its role in causing disease that affects the nervous system — into a second equine herpes virus, researchers say. (Equine refers to members of the horse family, which includes zebras.)

This conclusion raises many questions. For starters, when and where did this new virus emerge? And, is this recombination, or mixing, what enabled the virus to jump species and cause a fatal disease?

And, of course, how did the polar bears at Wuppertal Zoo catch the virus?

The zebras are housed 223 feet (68 meters) from polar bears and are not cared for by the same zookeepers. But the two parent viruses have also been associated with fatal encephalitis in other zoo species, such as gazelles and guinea pigs. The researchers are now exploring whether or not wild mice and rats could be carrying the virus.

"These viruses do not seem to respect species boundaries and in fact, we don't really know whether they have any," said study researcher Klaus Osterrieder from the Freie Universität Berlin in a statement.

Samples from a polar bear that had died years earlier at another zoo tested positive for the same recombinant virus. This indicates the virus had jumped between species more than once.

The research, led by Alex Greenwood, of Leibniz Institute for Zoo and Wildlife Research Berlin, was published online today (Aug. 16) in the journal Current Biology.  

Follow LiveScience on Twitter LiveScience @livescience. We're also on Facebook & Google+.