Health & Medicine: 1)Influenza outbreak declared on Stevenson Memorial Hospital; 2) Lifelong drugs for autoimmune diseases don’t work well. Now scientists are trying something new; 3)What happens when your immune system hijacks your brain

1)Influenza outbreak declared on Stevenson Memorial Hospital

Courtesy Barrie360.ocm

By Julius Hern, November 14, 2025

The Simcoe Muskoka District Health Unit declared an influenza outbreak on Stevenson Memorial Hospital (SMH) in New Tecumseth Friday Afternoon.

It relates directly to the medical/surgical unit of the hospital, of which the inpatient unit has been closed to visitors at this time, unless a designated care partner has been determined as required or a patient is palliative.

SMH says that wearing a mask will be required at all times in the unit, and those pieces of personal protection will be provided by the hospital.

It also says that all close contacts have been notified and enhanced cleaning, infection prevention, and control measures have been implemented. That includes additional influenza testing.

2) Lifelong drugs for autoimmune diseases don’t work well. Now scientists are trying something new

Courtesy Barrie360.com and The Associated Press

By Lauran Neergaard, November 16, 2025

Scientists are trying a revolutionary new approach to treat rheumatoid arthritis, multiple sclerosis, lupus and other devastating autoimmune diseases — by reprogramming patients’ out-of-whack immune systems.

When your body’s immune cells attack you instead of protecting you, today’s treatments tamp down the friendly fire but they don’t fix what’s causing it. Patients face a lifetime of pricey pills, shots or infusions with some serious side effects — and too often the drugs aren’t enough to keep their disease in check.

“We’re entering a new era,” said Dr. Maximilian Konig, a rheumatologist at Johns Hopkins University who’s studying some of the possible new treatments. They offer “the chance to control disease in a way we’ve never seen before.”

How? Researchers are altering dysfunctional immune systems, not just suppressing them, in a variety of ways that aim to be more potent and more precise than current therapies.

They’re highly experimental and, because of potential side effects, so far largely restricted to patients who’ve exhausted today’s treatments. But people entering early-stage studies are grasping for hope.

“What the heck is wrong with my body?” Mileydy Gonzalez, 35, of New York remembers crying, frustrated that nothing was helping her daily lupus pain.

Diagnosed at 24, her disease was worsening, attacking her lungs and kidneys. Gonzalez had trouble breathing, needed help to stand and walk and couldn’t pick up her 3-year-old son when last July, her doctor at NYU Langone Health suggested the hospital’s study using a treatment adapted from cancer.

Gonzalez had never heard of that CAR-T therapy but decided, “I’m going to trust you.” Over several months, she slowly regained energy and strength.

“I can actually run, I can chase my kid,” said Gonzalez, who now is pain- and pill-free. “I had forgotten what it was to be me.”

‘Living drugs’ reset rogue immune systems

CAR-T was developed to wipe out hard-to-treat blood cancers. But the cells that go bad in leukemias and lymphomas — immune cells called B cells — go awry in a different way in many autoimmune diseases.

Some U.S. studies in mice suggested CAR-T therapy might help those diseases. Then in Germany, Dr. Georg Schett at the University of Erlangen-Nuremberg tried it with a severely ill young woman who had failed other lupus treatment. After one infusion, she’s been in remission — with no other medicine — since March 2021.

Last month, Schett told a meeting of the American College of Rheumatology how his team gradually treated a few dozen more patients, with additional diseases such as myositis and scleroderma — and few relapses so far.

Those early results were “shocking,” Hopkins’ Konig recalled.

They led to an explosion of clinical trials testing CAR-T therapy in the U.S. and abroad for a growing list of autoimmune diseases.

How it works: Immune soldiers called T cells are filtered out of a patient’s blood and sent to a lab, where they’re programmed to destroy their B cell relatives. After some chemotherapy to wipe out additional immune cells, millions of copies of those “living drugs” are infused back into the patient.

While autoimmune drugs can target certain B cells, experts say they can’t get rid of those hidden deep in the body. CAR-T therapy targets both the problem B cells and healthy ones that might eventually run amok. Schett theorizes that the deep depletion reboots the immune system so when new B cells eventually form, they’re healthy.

Other ways to reprogram rogue cells

CAR-T is grueling, time consuming and costly, in part because it is customized. A CAR-T cancer treatment can cost $500,000. Now some companies are testing off-the-shelf versions, made in advance using cells from healthy donors.

Another approach uses “peacekeeper” cells at the center of this year’s Nobel Prize. Regulatory T cells are a rare subset of T cells that tamp down inflammation and help hold back other cells that mistakenly attack healthy tissue. Some biotech companies are engineering cells from patients with rheumatoid arthritis and other diseases not to attack, like CAR-T does, but to calm autoimmune reactions.

Scientists also are repurposing another cancer treatment, drugs called T cell engagers, that don’t require custom engineering. These lab-made antibodies act like a matchmaker. They redirect the body’s existing T cells to target antibody-producing B cells, said Erlangen’s Dr. Ricardo Grieshaber-Bouyer, who works with Schett and also studies possible alternatives to CAR-T.

Last month, Grieshaber-Bouyer reported giving a course of one such drug, teclistamab, to 10 patients with a variety of diseases including Sjögren’s, myositis and systemic sclerosis. All but one improved significantly and six went into drug-free remission.

Next-generation precision options

Rather than wiping out swaths of the immune system, Hopkins’ Konig aims to get more precise, targeting “only that very small population of rogue cells that really causes the damage.”

B cells have identifiers, like biological barcodes, showing they can produce faulty antibodies, Konig said. Researchers in his lab are trying to engineer T cell engagers that would only mark “bad” B cells for destruction, leaving healthy ones in place to fight infection.

Nearby in another Hopkins lab, biomedical engineer Jordan Green is crafting a way for the immune system to reprogram itself with the help of instructions delivered by messenger RNA, or mRNA, the genetic code used in COVID-19 vaccines.

In Green’s lab, a computer screen shines with brightly colored dots that resemble a galaxy. It’s a biological map that shows insulin-producing cells in the pancreas of a mouse. Red marks rogue T cells that destroy insulin production. Yellow indicates those peacemaker regulatory T cells — and they’re outnumbered.

Green’s team aims to use that mRNA to instruct certain immune “generals” to curb the bad T cells and send in more peacemakers. They package the mRNA in biodegradable nanoparticles that can be injected like a drug. When the right immune cells get the messages, the hope is they’d “divide, divide, divide and make a whole army of healthy cells that then help treat the disease,” Green said.

The researchers will know it’s working if that galaxy-like map shows less red and more yellow. Studies in people are still a few years away.

Could you predict autoimmune diseases – and delay or prevent them?

A drug for Type 1 diabetes “is forging the path,” said Dr. Kevin Deane at the University of Colorado Anschutz.

Type 1 diabetes develops gradually, and blood tests can spot people who are brewing it. A course of the drug teplizumab is approved to delay the first symptoms, modulating rogue T cells and prolonging insulin production.

Deane studies rheumatoid arthritis and hopes to find a similar way to block the joint-destroying disease.

About 30% of people with a certain self-reactive antibody in their blood will eventually develop RA. A new study tracked some of those people for seven years, mapping immune changes leading to the disease long before joints become swollen or painful.

Those changes are potential drug targets, Deane said. While researchers hunt possible compounds to test, he’s leading another study called StopRA: National to find and learn from more at-risk people.

On all these fronts, there’s a tremendous amount of research left to do — and no guarantees. There are questions about CAR-T’s safety and how long its effects last, but it is furthest along in testing.

Allie Rubin, 60, of Boca Raton, Florida, spent three decades battling lupus, including scary hospitalizations when it attacked her spinal cord. But she qualified for CAR-T when she also developed lymphoma — and while a serious side effect delayed her recovery, next month will mark two years without a sign of either cancer or lupus.

“I just remember I woke up one day and thought, ‘Oh my god, I don’t feel sick anymore,’” she said.

That kind of result has researchers optimistic.

“We’ve never been closer to getting to — and we don’t like to say it — a potential cure,” said Hopkins’ Konig. “I think the next 10 years will dramatically change our field forever.”

3)What happens when your immune system hijacks your brain

Courtesy Barrie360.com and The Associated Press

By Lauran Neergaard and Shelby Lum, November 21, 2025

“My year of unraveling” is how a despairing Christy Morrill described nightmarish months when his immune system hijacked his brain.

What’s called autoimmune encephalitis attacks the organ that makes us “us,” and it can appear out of the blue.

Morrill went for a bike ride with friends along the California coast, stopping for lunch, and they noticed nothing wrong. Neither did Morrill until his wife asked how it went — and he’d forgotten. Morrill would get worse before he got better. “Unhinged” and “fighting to see light,” he wrote as delusions set in and holes in his memory grew.

Of all the ways our immune system can run amok and damage the body instead of protecting it, autoimmune encephalitis is one of the most unfathomable. Seemingly healthy people abruptly spiral with confusion, memory loss, seizures, even psychosis.

But doctors are getting better at identifying it, thanks to discoveries of a growing list of the rogue antibodies responsible that, if found in blood and spinal fluid, aid diagnosis. Every year new culprit antibodies are being uncovered, said Dr. Sam Horng, a neurologist at Mount Sinai Health System in New York who has cared for patients with multiple forms of this mysterious disease.

And while treatment today involves general ways to fight the inflammation, two major clinical trials are underway aiming for more targeted therapy.

Still, it’s tricky. Symptoms can be mistaken for psychiatric or other neurologic disorders, delaying proper treatment.

“When someone’s having new changes in their mental status, they’re worsening and if there’s sort of like a bizarre quality to it, that’s something that kind of tips our suspicion,” Horng said. “It’s important not to miss a treatable condition.”

With early diagnosis and care, some patients fully recover. Others like Morrill recover normal daily functioning but grapple with some lasting damage — in his case, lost decades of “autobiographical” memories. This 72-year-old literature major can still spout facts and figures learned long ago, and he makes new memories every day. But even family photos can’t help him recall pivotal moments in his own life.

“I remember ‘Ulysses’ is published in Paris in 1922 at Sylvia Beach’s bookstore. Why do I remember that, which is of no use to me anymore, and yet I can’t remember my son’s wedding?” Morrill wonders.

Inflaming the brain

Encephalitis means the brain is inflamed and symptoms can vary from mild to life-threatening. Infections are a common cause, typically requiring treatment of the underlying virus or bacteria. But when that’s ruled out, an autoimmune cause has to be considered, Horng said, especially when symptoms arise suddenly.

The umbrella term autoimmune encephalitis covers a group of diseases with weird-sounding names based on the antibody fueling it, such as anti-NMDA receptor encephalitis.

While they’re not new diseases, that one got a name in 2007 when Dr. Josep Dalmau, then at the University of Pennsylvania, discovered the first culprit antibody, sparking a hunt for more.

That anti-NMDA receptor encephalitis tends to strike younger women and, one of the bizarre factors, it’s sometimes triggered by an ovarian “dermoid” cyst.

How? That type of cyst has similarities to some brain tissue, Horng explained. The immune system can develop antibodies recognizing certain proteins from the growth. If those antibodies get into the brain, they can mistakenly target NMDA receptors on healthy brain cells, sparking personality and behavior changes that can include hallucinations.

Different antibodies create different problems depending if they mostly hit memory and mood areas in the brain, or sensory and movement regions.

Altogether, “facets of personhood seem to be impaired,” Horng said.

Therapies include filtering harmful antibodies out of patients’ blood, infusing healthy ones, and high-dose steroids to calm inflammation.

Stealth attack on the brain

Those cyst-related antibodies stealthily attacked Kiara Alexander in Charlotte, North Carolina, who’d never heard of the brain illness. She’d brushed off some oddities — a little forgetfulness, zoning out a few minutes — until she found herself in an ambulance because of a seizure.

Maybe dehydration, the first hospital concluded. At a second hospital after a second seizure, a doctor recognized the possible signs, ordering a spinal tap that found the culprit antibodies.

As Alexander’s treatment began, other symptoms ramped up. She has little clear memory of the monthlong hospital stay: “They said I would just wake up screaming. What I could remember, it was like a nightmare, like the devil trying to catch me.”

Later Alexander would ask about her 9-year-old daughter and when she could go home — only to forget the answer and ask again.

Alexander feels lucky she was diagnosed quickly, and she got the ovarian cyst removed. But it took over a year to fully recover and return to work full time.

What could cause memories to vanish?

In San Carlos, California, in early 2020, it was taking months to determine what caused Morrill’s sudden memory problem. He remembered facts and spoke eloquently but was losing recall of personal events, a weird combination that prompted Dr. Michael Cohen, a neurologist at Sutter Health, to send him for more specialized testing.

“It’s very unusual, I mean extremely unusual, to just complain of a problem with autobiographical memory,” Cohen said. “One has to think about unusual disorders.”

Meanwhile Morrill’s wife, Karen, thought she’d detected subtle seizures — and one finally happened in front of another doctor, helping spur a spinal tap and diagnosis of LGI1-antibody encephalitis.

It’s a type most common in men over age 50. Those rogue antibodies disrupt how neurons signal each other, and MRI scans showed they’d targeted a key memory center.

By then Morrill, who’d spent retirement guiding kayak tours, could no longer safely get on the water. He’d quit reading and as his treatments changed, he’d get agitated with scary delusions.

“I lost total mental capacity and fell apart,” Morrill describes it.

He used haiku to make sense of the incomprehensible, and months into treatment finally wondered if the “meds coursing through me” really were “dousing the fire. Rays of hope?”

A growing list of culprits

The nonprofit patient advocacy group Autoimmune Encephalitis Alliance lists about two dozen antibodies — and counting — known to play a role in these brain illnesses so far.

Clinical trials, offered at major medical centers around the country, are testing two drugs now used for other autoimmune diseases to see if tamping down antibody production can ease encephalitis.

More awareness of these rare diseases is critical, said North Carolina’s Alexander, who sought out fellow patients. “That’s a terrible feeling, feeling like you’re alone.”

As for Morrill, five years later he still grieves decades of lost memories: family gatherings, a year spent studying in Scotland, the travel with his wife.

But he’s making new memories with grandkids, is back outdoors — and leads an AE Alliance support group, using his haiku to illustrate the journey from his “unraveling” to “the present is what I have, daybreaks and sunsets” to, finally, “I can sustain hope.”

“I’m reentering some real time of fun, joy,” Morrill said. “I wasn’t shooting for that. I just wanted to be alive.”