5 Common But Embarrassing Symptoms You Should Definitely Talk to Your Doctor About

'Chickenpox Parties' Never A Good Idea, Warns Doc – Risk Skin Infections, Pneumonia And Deadly Brain Swelling Disease

DOCTORS are warning parents that 'chickenpox parties' are never a good idea.

The gatherings - which aim to expose children to the virus to 'get it over with' - put kids at risk of "serious complications", such as bacterial skin infections, pneumonia and life-threatening brain swelling.

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Chickenpox parties could put children and adults at risk of nasty complications, GPs warnedCredit: Getty

The caution comes after the owner of a children's daycare centre discovered that some parents were secretly planning to hold at 'party' at the venue, putting healthy kids in contact with a child with chickenpox.

The plan was branded as "dangerous" and "irresponsible" by other parents, while the owner described it as downright "selfish" after being tipped off by a concerned mum.

Jane Coulson, the owner of Play World in Gainsborough, told the BBC: "Someone deliberately bringing in something like chickenpox is very selfish

"If you want to have a chickenpox party, have it in your own home."

But Dr Sarah Jarvis, clinical director of Patient.Info, told The Sun that "chickenpox parties are never a good idea, full stop."

That's because the common childhood illness can "cause all sorts of serious complications", according to the GP.

"They are not that common, but it can lead to a really nasty bacterial infection, inflammation of the brain, pneumonia and it can occasionally be fatal."

Professor Franklin Joseph, consultant physician in general internal medicine and head of Dr Frank's clinic, added: "Deliberately exposing children to chickenpox might seem like a harmless way to 'get it over with,' but in reality, it's a risky gamble with their health. 

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"While most children recover from chickenpox without complications, the virus can cause severe illness, particularly in babies, pregnant women, and those with weakened immune systems. 

"You simply can't predict who will develop complications like pneumonia, skin infections, or even brain inflammation [known as encephalitis].

Risk of mpox being 'confused with chickenpox' after new killer strain detected in the UK - how to spot both

"A 'chickenpox party' might spread the virus faster, but it also increases the risk of serious consequences - something no parent would knowingly want."

It has been common practice in the past for children to be sent to play with friends sporting the tell-tale spots, in the hopes of the getting the common childhood ordeal over and done with.

Chickenpox is caused by the varicella zoster virus and is "very, very contagious", according to Dr Jarvis.

"It's not as infectious as, say, the common cold because you need to to touch [the chickenpox blisters] to get it," she noted.

But take into account how much children tend to touch or scratch at their spots.

If they then touch you, you may catch the virus or you could end up passing it on to someone in your household.

Chickenpox is known for its telltale itchy, spotty rash that blisters and scabs over.

But before these spots appear, the virus can also cause a high temperature, aches and pains, and loss of appetite.

Chickenpox symptom timeline

The main symptom of chickenpox is an itchy, spotty rash anywhere on the body.

Before or after the rash appears, you might also have:

A high temperature

Aches and pains, and generally feel unwell

Loss of appetite

Chickenpox happens in three stages, but new spots can appear while others are becoming blisters or forming a scab.

Stage 1: Spots appear

The spots can:

Be anywhere on the body, including inside the mouth and around the genitals, which can be painful

Spread or stay in a small area

Be red, pink, darker or the same colour as surrounding skin, depending on your skin tone

Be harder to see on brown and black skin

Stage 2: Spots become blisters

The spots fill with fluid and become blisters. The blisters are very itchy and may burst.

Stage 3: Blisters become scabs

The spots form a scab, some are flaky, while others leak fluid.

It usually gets better on its own after one to two weeks without needing to see a GP.

Source: NHS

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It can take one to three weeks for the spots to start appearing after you catch chickenpox - but the illness can be spread to other people from two days before the spots appear and until they have formed scabs.

Prof Joseph said: "For most healthy children, chickenpox is unpleasant but manageable.

"However, for some, it can be life-threatening."

It's not just toddlers at risk who are at risk of becoming very unwell from the illness.

"Babies, pregnant women, and anyone with a weakened immune system - such as people undergoing cancer treatment or living with chronic conditions - are at far greater risk of complications," Prof Joseph said.

Dr Jarvis said it was a "really bad idea" to potentially expose children whose immune systems aren't working well to chickenpox.

"Adults can also get unwell from it if they haven't had the infection before, especially if their immune system is compromised," the GP added.

Prof Joseph noted: "The varicella zoster virus can also lead to long-term issues like shingles later in life."

Shingles is a tingling, painful rash caused by the same virus as chickenpox.

The bug can stay in the body and be reactivated if someone's immune system is weakened by stress, certain health conditions or treatments like chemotherapy.

Proj Joseph advised: "Instead of actively spreading the virus, we should be focusing on preventing unnecessary suffering."

He added that "having multiple children exposed simultaneously can also potentially increase the pressure on already stretched NHS services if the children become ill at the same time and require hospital intervention".

If your little one gets unwell and breaks out in a rash, keep them them away from day care or school, Dr Jarvis stressed.

"You should definitely keep them away from other people, - particularly pregnant women or anyone who's older - until all the blisters have disappeared and scabbed over."

Ideally, you should keep them at home "one to two days before the rash appears" as they're infectious then too, but it many cases "you can't do anything about that", the GP added.

She advised parents to speak to pharmacist about how to tend to their tots.

But Dr Jarvis said that you shouldn't given your tot ibuprofen, as it may increase their chance of getting a serious skin reaction or bacterial infection.

Nor should you give them aspirin - nobody under 16 should have it - but other over-the-counter options like paracetamol can help ease your child's fever and antihistamines may be useful too.

Prof Joseph said: "The best thing parents can do is manage symptoms and prevent the virus from spreading.

"Keep your child comfortable by giving them plenty of fluids, using paracetamol, and applying soothing lotions like calamine to relieve itching. 

"Keeping their nails short can help prevent scratching, which reduces the risk of scarring and infection.

"Keep them home from school or nursery until all the spots have scabbed over - usually about five to seven days."

He urged: "If your child has a weakened immune system, or if you're pregnant and have been exposed to chickenpox, seek medical advice immediately.

"And if you're worried about severe symptoms - such as breathing difficulties, dehydration, or a very high fever - don't hesitate to call a doctor.

"It's always better to be safe than sorry when it comes to a virus like this."

Chickenpox vaccine

The chickenpox vaccine helps protect people from infection but it's only currently available on the NHS to people in close contact with someone who has a higher risk of getting seriously ill from chickenpox.

The chickenpox vaccine is recommended if you're healthy and all the following apply:

You're nine months old or over

You've not had chickenpox before

You're in regular or close contact with someone who's at risk of getting seriously ill if they get chickenpox, such as a child with leukaemia or an adult having chemotherapy

You should also have the chickenpox vaccine if you've not had chickenpox before and your work involves close contact with patients.

This includes:

Doctors and nurses

Ambulance staff

GP surgery and hospital receptionists

Hospital ward cleaners

Catering staff

Laboratory workers who are exposed to the chickenpox virus

It's possible that the chickenpox jab could be offered to to children as part of the UK's routine jabs programme, following recommendations by the Joint Committee on Vaccination and Immunisation.

A Surprising Infectious Disease Link To Gene Hackman's Death

The mystery surrounding the tragic death of actor Gene Hackman and his wife was solved this week when officials announced that his wife died of a rare infectious disease and Hackman of complications from Alzheimer's disease and heart disease. But did you know that his death may also be linked to an infectious disease?

What happened to Gene Hackman and his wife?

From media reports, the famous actor had been suffering from Alzheimer's. As is common in people with advanced dementia, he had withdrawn from public life and required intensive home support. On February 26, both he and his wife were found dead. An intensive, highly public investigation followed.

The conclusion of the investigation: Hackman's wife likely died on February 11, 2025, of an infection unique to the desert southwest, Hantavirus.

Hantavirus is similar to the well-known (and feared) Ebola virus. It is a viral hemorrhagic fever that first causes flu-like symptoms; it makes blood vessels leaky and leads to death from pneumonia and other organ failure. Unlike Ebola, hantavirus is primarily acquired from contact with the physical environment (specifically, contact with rodent feces or urine) and is not transmitted person-to-person.

The official report states that Hackman died of heart disease about seven days after his wife. I do not have any direct knowledge of this case, but this sounds to me more like a heart attack was the final mechanism of death. The underlying cause of his death was advanced dementia from Alzheimer's, which required full-time care. Once that care ceased, he died, with the final event being a heart attack.

Can Gene Hackman's Death Be Linked to an Infection?

Alzheimer's remains a critical area of research because we lack accurate diagnostic tests, effective monitoring tools, or highly effective treatments. The most important pathway to tests and treatments is understanding why people develop Alzheimer's.

Increasingly, researchers believe that infectious diseases may be a cause or contributor. Emerging research suggests that different types of infections lead to inflammation in the brain and or immune responses that lead to dementia.

Below, I describe two of the leading theories.

Source: NIH/National Institute on Aging

Neuroinflammation and infections

Infections by viruses (herpes simplex virus 1, varicella zoster virus) and by bacteria that cause gum disease have been linked to inflammation in the brain.

One hallmark of Alzheimer's is a fragment of proteins known as Amyloid-beta (Aβ). These fragments clump into plaques that damage neurons and blood vessels in the brain. The theory is that Aβ and another damaging protein called Tau are byproducts of the immune system fighting these infections. Alzheimer's may be an unintended consequence of the body's attempt to fight off viruses and bacteria.

Adding to this is the possibility that a genetic variant (the APOE ε4 allele) may make people more susceptible to herpes simplex virus-1 (the virus that causes cold sores), which may increase Alzheimer's risk.

Lifetime Impact of Infections

Another possibility is that repeated infections over a lifetime lead to cumulative brain damage, increasing the risk of AD or other forms of dementia.

In one study involving hundreds of thousands of people from Finland and the UK, researchers found that severe infections requiring hospital treatment were associated with a long-term increased risk of dementia, including vascular dementia and Alzheimer's.

Another study in Denmark analyzed data from 1.4 million people over 40 years to evaluate the association between recurrent severe infections and dementia. They found a clear dose-response relationship: the more episodes of severe infection you have in your lifetime, the higher your risk of developing dementia.

We do not know the exact reasons why this happens. Researchers hypothesize that infections trigger inflammatory cascades that can cross the blood-brain barrier, particularly when recurring frequently.

What does this mean for your health?

Prompt treatment of infections and certain vaccines may help protect against the development of Alzheimer's and other forms of dementia. In a future blog post, I'll discuss how this affects the decision to get the shingles vaccine.

There are many reasons to stay up-to-date on your vaccines, especially with measles resurging, and to seek prompt medical attention for symptoms of severe infection. And, as we learn more about the death of Hackman and his wife, keeping your brain healthy may be one additional reason.

Brain-eating Fungus Causes The Immune System To Attack Neurons

Infections often conjure images of bacteria or viruses, but certain fungi can also take their toll on us. They can hide in unsuspecting corners of the environment and interact with living organisms in ways that raise many questions.

One particular fungus, Beauveria bassiana, has captured attention because of its interactions with insects.

Its spores settle on an insect and then germinate and penetrate through the cuticle. The insect dies within days and forms the substrate for a white fungal mold that grows and flourishes.

Prof. Alicia Hidalgo, from the University of Birmingham, directed a recent investigation into infections in insects by this devastating fungus.

Immune responses to brain fungus

Fruit flies became the chosen subjects for this study because their immune system shares some features with that of more complex creatures.

Researchers often turn to these small insects when exploring disease processes in a simple model.

The researchers analyzed the effect of the fungus on the brains of flies and found that flies infected with B. Bassiana suffered a reduction in the number of brain cells.

They identified that the fly's own immune system was "tricked" by the invading fungus to start destroying brain cells.

In flies, Toll receptors are agents of the immune system. When infected with the fungus, the Toll-1 receptors in the flies triggered the release of antimicrobial peptides that attack and kill pathogens.

However, the fungus also provoked the Toll-1 receptors to produce another molecule, called Sarm, that suppresses the immune response and destroys brain cells instead.

"We have shown a process for how fungi have evolved to trick the immune system to get into the brain," said Prof. Hidalgo. Her findings suggest that a normal line of defense can accidentally turn against the very organ it's meant to protect.

Sarm's link to neurodegeneration

When the immune system tries to confront this fungus, the Sarm molecules step up their activity; they have the potential to sabotage defenses by encouraging cell damage in the brain.

"The key antagonist in the immune process is Sarm, a so-called master of destruction, that is causing cell death in the brain. The ability of B. Bassiana to trick the fruit fly immune system into activating the master of destruction Sarm and kill cells enables spores to beat the blood-brain barrier and start feeding on brain cells," commented Hidalgo.

The process, known as neurodegeneration, describes the gradual breakdown of nerve cells. If immune signals become confused, the result might be nerve destruction in the brain.

Experts note that this fungus, though hazardous to insects, is widely used for insect management in agriculture. It is developed into a type of pesticide and used to kills certain insects.

The findings offer a curious look at how a single microbe might manipulate host biology for its own benefit.

What does this fungus mean for humans?

"It is important to stress that B. Bassiana cannot affect humans," explained Dr. Deepanshu Singh, now a post-doc at the University of Manchester. The fungus targets insects, but it stays clear of mammals.

Still, other fungi are known to reach the human brain under certain conditions. These discoveries hint that parallel strategies might pop up in different species, especially when fungal organisms are trying to survive inside a host.

A broader perspective on fungal threats

Some scientists believe that future work could explore whether similar immune system misdirection happens in other animals.

Understanding how these pathogens find loopholes in the immune system may help researchers develop new interventions.

Fungal infections often get less attention than bacterial or viral illnesses, yet they can still pose serious threats.

The possibility that a fungus might slip into the human central nervous system and confuse its defenses encourages further research.

Implications for neurodegenerative diseases

The discovery that a fungal infection can manipulate immune responses to attack brain cells raises questions about similar mechanisms in humans.

Some neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease, involve immune system dysfunction and excessive inflammation in the brain.

If certain pathogens can trigger destructive immune pathways, this could offer new insights into how inflammation contributes to neurodegeneration.

Researchers may investigate whether similar immune evasion tactics occur in human infections, potentially linking fungal exposure to long-term neurological effects.

Possible next steps in fungal research

Scientists hope to identify molecules that can protect nerve cells when the immune system is tricked. Pinpointing the exact signals could spark novel medical approaches for people at risk of certain fungal infections.

Research also continues on ways to control fungal spread in agricultural settings without harming beneficial insects.

B. Bassiana remains a useful tool for pest management, though its tactics highlight the complexity of the microbe-host relationship.

The study is published in PLOS Biology.

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