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Bornholm Disease

Alternative Name : Epidemic pleurodynia,Sylvest’s disease , epidemic benign dry pleurisy,Bamble disease, the devil’s grip, devil’s grippe, epidemic myalgia, epidemic pleurodynia, epidemic transient diaphragmatic spasm or The Grasp of the Phantom

Definition:
Bornholm disease is a temporary illness that is a result of virus infection. The disease features fever and intense abdominal and chest pains with headache. The chest pain is typically worsened by breathing or coughing. The illness usually lasts from 3 to 14 days.

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The most common virus causing Bornholm disease is an enterovirus called Coxsackie B.

Group B coxsackieviruses are transmitted from person to person by fecal-oral contamination or direct mouth to mouth contact. Other people become infected with the virus if they touch contaminated items then put their fingers in their mouth before washing them properly. Contaminated items can include soiled diapers, shared toys and toilets.

Bornholm disease is also called epidemic myalgia and pleurodynia (because of inflammation of the lining tissue of the lungs).

Epidemic pleurodynia is contagious and occurs in clusters, meaning many people in an area get it around the same time. Up to 90% of epidemics occur in the summer and early fall. The illness most commonly strikes people younger than age 30, although older people also may be affected.

Coxsackie B virus is spread by contact and epidemics usually occur during warm weather in temperate regions and at any time in the tropics. As is typical with this virus family, it is shed in large amounts in the feces of infected persons. The disease can be spread by sharing drink containers, and has been contracted by laboratory personnel working with the virus

The disease is named after the Danish island where the first documented cases arose.

In 1872, Daae-Finsen reported an epidemic of “acute muscular rheumatism” occurring in a community called Bamble, giving rise to the name “Bamble disease” in Norway. Subsequent reports, published only in Norwegian, referred to the disease by this name. In 1933, Ejnar Sylvest gave a doctoral thesis describing a Danish outbreak of this disease on Bornholm Island entitled, “Bornholm disease-myalgia epidemica”, and this name has persisted

Symptoms:
The sudden onset of fever and pain occurs about four days after infection. Flu-like symptoms may be experienced during this incubation period.

There is pain in the chest or upper abdomen, usually on one side. It varies in intensity, but is often described as stabbing, or ‘grip-like’. The pain is spasmodic, lasting for 15 to 30 minutes at a time. Coughing, sneezing and sudden movements can make it worse.

The symptoms usually last about one to two days in children and about two to six days in adults. Sometimes, the pain and fever return after a day or two.

On rare occasions, there are several recurrences of pain and fever over a period of three weeks or more.

Complications are rare, but include inflammation of the testes (orchitis) or the heart (pericarditis, myocarditis), and meningitis.

Cause:
Inoculation of throat washings taken from people with Bornholm disease into the brains of newborn mice revealed that enteroviruses in the Coxsackie B virus group were likely to be the cause of Bornholm disease, and those findings were supported by subsequent studies of IgM antibody responses measured in serum from people with Bornholm disease. Other viruses in the enterovirus family, including echovirus and Coxsackie A virus, are infrequently associated with Bornholm disease.

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Group B coxsackieviruses are transmitted from person to person by fecal-oral contamination or direct mouth to mouth contact. Other people become infected with the virus if they touch contaminated items then put their fingers in their mouth before washing them properly. Contaminated items can include soiled diapers, shared toys and toilets.

Diagnosis:
Diagnosis is commonly simplified in an epidemic, although different causes of acute chest and abdominal pain must be excepted. Your doctor may push on muscles in your chest to notice if the pressure actuate a spasm of pain. Often, your doctor can examine the difficulty without any specific tests, particularly if there is an outbreak of the disease in your area. The infection from time to time disperse to cause inflammation in other organs, including the pleura (membrane surrounding the lungs), lungs, heart, liver, brain and testes.

Treatment :
The illness lasts about a week and is rarely fatal. Treatment includes the administration of nonsteroidal anti-inflammatory agents or the application of heat to the affected muscles. Relapses during the weeks following the initial episode are a characteristic feature of this disease.Painkillers and drugs can be used to reduce the fever.

The best treatment of Bornholm Disease is terminate bed rest, and fever and pain can be decreased by paracetamol for children or aspirin for adults. Recovery in uncomplicated cases is commonly finish within a week. Here is the list of several of the preclusion tips or tips for treating Bornholm Disease:

*People of any age may be involved although it frequently pretend people under the age of 30.
*Intravenous immune globulin may be utilised to treat newborns and those with a decreased immune system.

Prognosis:
Almost all generally healthy individuals recover completely from pleurodynia. However, about 5% of people develop acute viral meningitis as a complication of the coxsackievirus infection, and about 5% of adult males develop orchitis. Less common complications include hepatitis, pericarditis and myocarditis.

Prevention:
The viruses that cause epidemic pleurodynia can spread very easily among young children, who tend to put toys or fingers into their mouth. The disease is most likely to spread in day care centers. The best way to prevent infection is to wash hands thoroughly, especially before meals or after changing a diaper or using the bathroom. There is no vaccine to prevent pleurodynia.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://www.bbc.co.uk/health/physical_health/conditions/bornholmdisease1.shtml
http://www.intelihealth.com/IH/ihtPrint/WSIHW000/9339/24698.html?hide=t&k=basePrint
http://en.wikipedia.org/wiki/Bornholm_disease

http://www.associatedcontent.com/article/2914192/what_is_bornholm_disease.html

http://www.patient.co.uk/doctor/Coxsackie-Virus-Infection.htm

http://www.health-issues.org/rare-diseases/bornholm-disease.htm

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Second Time Dengu Attack Spells Danger

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Scientists now know why a second dengue infection is much more severe than the first.
………….
The long-kept secrets of the dengue virus — which affects between 50 and 100 million people every year — are tumbling out.

Scientists have long wondered why a re-infection (in the same or subsequent year) causes more complications, even becoming fatal, than when it strikes the first time. The puzzle has been finally solved — by two independent research teams. The knowledge gained by the scientists is expected to help design drugs and vaccines against dengue fever, which currently has no treatment.

Normally, viruses — which have very little genetic material of their own — co-opt the host’s genetic machinery to survive and replicate. More often than not, if the host has an efficient immune system, the invaders are destroyed. In most cases, the antibodies produced by the body stay for long, if not permanently, and fight off any subsequent attack by the same virus. But in the case of dengue, the second infection proves to be much more severe than the first.

Back in the 1970s, US virologist Scott Halstead hypothesised that the dengue virus may be receiving help from the very antibodies that are supposed to fight the infection. Halstead termed the phenomenon antibody-dependent enhancement (ADE) of infection. He got an inkling of this during his extensive clinical studies in Thailand in the 1960s.

For a good part of the ensuing four decades, Halstead’s assumption remained mere theory. But in February this year, Sujan Shresta, a Nepal-born virologist at the La Jolla Institute of Allergy and Immunology in California, came up with conclusive proof for Halstead’s hypothesis. “It’s a situation where antibodies can be bad for you — it’s counter to everything we know about the normal function of antibodies,” she says.

Dengue infection is transmitted by the Aedes aegypti mosquito. There are four known strains of the virus circulating in the world. Infection can cause diseases ranging from dengue fever, a flu-like illness, to the severest form — dengue haemorrhagic fever or dengue shock syndrome. The latter can cause the blood vessels to leak, leading to life-threatening shock. It is estimated that 2.5 billion people — that is, two-fifth of the world’s population — live in regions where dengue fever is rampant. While it is more common in South East Asia and South America, the incidence is rising in India too. Since 1996, the country had witnessed a number of dengue outbreaks and a few hundred Indians die of dengue-related complications every year.

Shresta’s team at La Jolla developed the first ever mouse model to study the disease. The scientists conducted experiments to prove that certain antibodies produced by the body against the virus indeed exacerbate the condition. The four strains of the virus circulate simultaneously, says Shresta. Infection with one provides lifelong immunity against that particular strain. In subsequent infections, where a different strain of the virus is involved, the antibodies do not recognise enough of the virus to neutralise it. “This starts a cascade of unusual molecular events — the ADE process — which leads to the antibodies contributing to, rather than fighting, the infection,” she explains.

Taking the research forward, a team of UK and Thai scientists identified specific antibodies involved in the ADE process. The study, reported early this month in the journal Science, showed that the culprits are antibodies against a particular viral protein called precursor membrane protein (prM). According to the researchers, if the antibodies are present in the body, the infection spreads faster with the antibodies against prM helping the virus infect more host cells. In fact, there is a several hundred-fold increase in the number of infected cells in the presence of the antibodies, they say.

“This is a significant piece of work. It shows the exact region for the enhancement — which is the prM, and not the E region of the virus, as we have been thinking so long,” says Shamala Devi Sekaran, a virologist at the University of Malaysia who has been studying the dengue virus for years.

“The study pinpoints the nature of the antibodies that are likely to cause the severest form of the disease in humans,” says Shresta. It will greatly help those trying to develop vaccines against dengue, she adds.

“Our research gives us some key information about what is not likely to work when trying to combat the virus. We hope our findings will bring scientists one step closer to creating an effective vaccine,” says Gavin Screaton, head of medicine, Imperial College London, and lead author of the study.

The biggest challenge is that the dengue vaccine will need to provide immunity against all the four strains of the virus at the same time. “If protection is incomplete, the vaccine can potentially protect against some viruses but leave the individual primed for a more severe outcome if he or she is infected with the others,” Screaton told Knowhow.

In addition to these developments, there have been two recent breakthroughs in controlling the dengue mosquito. Oxford University scientists developed sterile male Aedes aegypti mosquitoes which have undergone successful semi-field trials in Asia. And scientists at the University of Queensland developed a mutant strain of a bacterium called Wolbachia, which halves the adult life span of female Aedes aegypti mosquitoes in laboratory conditions.


Source: The Teleghraph ( Kolkata, India)

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New Clue to Fighting Dengue Fever

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The research, published in Science, also explains why those who recover from the virus have much worse symptoms if they catch it again.

Dengue fever is a viral infection spread by a mosquito bite. It is a major cause of illness worldwide, and cases are on the rise.

There is currently no licensed vaccine or drug treatment.

The researchers, based in the UK and Thailand, took blood samples from infected volunteers.

They found antibodies produced in response to the virus do not do a very effective job.

Rather than neutralising the virus, they actually help it infect more cells, springing into action when a person is infected a second time by a different strain of the virus.

Key information

This phenomenon accounts for why a second bout of dengue fever can be more severe and dangerous.

DENGUE FEVER
*Dengue fever is prevalent in sub-tropical and tropical regions including South East Asia and South America

*It is a major cause of illness worldwide, causing about 100 million episodes of feverish illness a year

*Symptoms include high fever, aching in the joints and vomiting

*Complications can rarely prove fatal

*There are four major strains of the virus

It also provides new insight into how to design a vaccine for dengue fever.

The authors of the Science paper say vaccines that steer clear of a key viral protein involved in the immune response should be the most effective.

Professor Gavin Screaton, head of the Department of Medicine at Imperial College London, led the study.

He said: “Our new research gives us some key information about what is and what is not likely to work when trying to combat the dengue virus.

“We hope that our findings will bring scientists one step closer to creating an effective vaccine.”

Professor Screaton said one of the major challenges was developing a vaccine for a virus that has four very different strains.

“The need for vaccines is enormous but the challenge is that in this case you need to hit four bugs all at once down a single needle,” he added.

Source: BBC NEWS: May 6. 2010

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Foe Turns Friend

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A-beta, a protein implicated in Alzheimer’s, may be the brain’s shield against germs.
………………...CLICK & SEE THE PICTURES
For years, a prevailing theory has been that one of the chief villains in Alzheimer’s disease has no real function other than as a waste product that the brain never properly disposed of.

The material, a protein called beta amyloid, or A-beta, piles up into tough plaques that destroy signals between nerves. When that happens, people lose their memory, their personality changes and they stop recognising friends and family.

But now researchers at Harvard suggest that the protein has a real and unexpected function — it may be part of the brain’s normal defences against invading bacteria and other microbes.

Other Alzheimer’s researchers say the findings, reported in the current issue of the journal PLoS One, are intriguing.

The new hypothesis got its start late one Friday evening in the summer of 2007 in a laboratory at Harvard Medical School. The lead researcher, Rudolph Tanzi, a neurology professor who is also director of the genetics and aging unit at Massachusetts General Hospital, said he had been looking at a list of genes that seemed to be associated with Alzheimer’s disease.

To his surprise, many looked just like genes associated with the so-called innate immune system, a set of proteins the body uses to fight infections. The system is particularly important in the brain, because antibodies cannot get through the blood-brain barrier, the membrane that protects the brain. When the brain is infected, it relies on the innate immune system to protect it.

That evening, Tanzi wandered into the office of a junior faculty member, Robert Moir, and mentioned what he had seen. As Tanzi recalled, Moir turned to him and said, “Yeah, well, look at this.”

He handed Tanzi a spreadsheet. It was a comparison of A-beta and a well-known protein of the innate immune system, LL-37. The likenesses were uncanny. Among other things, the two proteins had similar structures. And like A-beta, LL-37 tends to clump into hard little balls.

In rodents, the protein that corresponds to LL-37 protects against brain infections. People who make low levels of LL-37 are at increased risk of serious infections and have higher levels of atherosclerotic plaques, arterial growths that impede blood flow.

The scientists could hardly wait to see if A-beta, like LL-37, killed microbes. They mixed A-beta with microbes that LL-37 is known to kill — listeria, staphylococcus, pseudomonas. It killed eight out of 12. “We did the assays exactly as they have been done for years,” Tanzi said. “And A-beta was as potent or, in some cases, more potent than LL-37.”

Then the investigators exposed the yeast Candida albicans, a major cause of meningitis, to tissue from the hippocampal regions of brains from people who had died of Alzheimer’s and from people of the same age who did not have dementia when they died.

Brain samples from Alzheimer’s patients were 24 per cent more active in killing the bacteria. But if the samples were first treated with an antibody that blocked A-beta, they were no better than brain tissue from non-demented people in killing the yeast.

The innate immune system is also set in motion by traumatic brain injuries and strokes and by atherosclerosis that causes reduced blood flow to the brain, Tanzi noted.

And the system is spurred by inflammation. It’s known that patients with Alzheimer’s have inflamed brains, but it hasn’t been clear whether A-beta accumulation was a cause or an effect of the inflammation. Perhaps, Tanzi said, A-beta levels rise as a result of the innate immune system’s response to inflammation; it may be a way the brain responds to a perceived infection. But does that mean Alzheimer’s disease is caused by an overly exuberant brain response to an infection?

That’s one possible reason, along with responses to injuries and inflammation and the effects of genes that cause A-beta levels to be higher than normal, Tanzi said. However, some researchers say that all the pieces of the A-beta innate immune systems hypothesis are not in place.

Dr Norman Relkin, director of the memory disorders programme at New York-Presbyterian / Weill Cornell hospital, said that although the idea was “unquestionably fascinating”, the evidence for it was “a bit tenuous”.

As for the link with infections, Dr Steven DeKosky, an Alzheimer’s researcher at the Virginia School of Medicine, noted that scientists have long looked for evidence linking infections to Alzheimer’s and have come up mostly empty handed.

But if Tanzi is correct about A-beta being part of the innate immune system, that would raise questions about the search for treatments to eliminate the protein from the brain.

“It means you don’t want to hit A-beta with a sledgehammer,” Tanzi said.

But other scientists not connected with the discovery said they were impressed by the new findings. “It changes our thinking about Alzheimer’s disease,” said Dr Eliezer Masliah, who heads the experimental neuropathology laboratory at the University of California, San Diego.

Source : New York Times News Service

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New Remedies for Swine Flu

Honeybee venom and vitamin C may protect you against swine flu, suggest Indian researchers.

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Have no access to the H1N1 flu vaccine because of its being produced by a handful of global pharmaceutical biggies? Not to worry. Try honeybee venom or a good amount of vitamin C.

That’s the word from some Indian scientists. A caveat here. These ideas put forward by independent research groups are “hypotheses” rather than findings that have emerged from rigorous scientific experiments. But they stem from the basic premise that a nudge prepares the immune system better in the eventuality of a fatal viral attack.

A team of pharmacologists at Manipal University in Karnataka proposed the idea of using honeybee venom to shore up the human immune system in its fight against the swine flu virus. Their paper, which appears in the latest issue of the journal Medical Hypotheses, suggests honeybee venom therapy as a first-line strategy to quickly vaccinate the population in the event of a widespread H1N1 flu outbreak. It can provide passive as well as active immunisation against the infection, they argue.
……..-Nishi_tribal…honeybee stinging
“Many tribal communities use the sting of a honeybee as an antidote to colds and coughs,” says Rajeev Singla, lead author of the study. Singla, who teaches at the Shri Gopichand College of Pharmacy in Baghpet, Uttar Pradesh, says that bee venom’s anti inflammatory and immune-boosting properties are already well documented in modern science.

Even if the substance offers limited protection against swine flu, it is worth investigating as it is effective against several symptoms associated with the infection such as pneumonia and oedema, they say.

The second study, by researchers at the department of experimental medicine and biotechnology at the Post Graduate Institute of Medical Education and Research (PGI), Chandigarh, suggests that vitamin C can serve as a vaccine to control a H1N1 flu pandemic.

The study, scheduled to appear in the January 2010 issue of the journal Nutrition, builds upon past research to establish the efficacy of vitamin C in preventing common flu, an idea first proposed in the 1970s by Nobel Prize-winning American scientist Linus Pauling. Swine flu may be caused by a different influenza virus, but most of the symptoms associated with it are similar to those of the common cold.

The scientists explain that the viruses — there are nearly 100 of them — that cause flu enter the human body through the nasal route and attach themselves to a protein to get entry to the respiratory tract cells. Once there, the virus pushes its genetic material into the genome of the host cell. The virus thus takes over the host cell’s multiplication mechanism for its own proliferation.

But the PGI scientists think that it is possible to jeopardise the virus’s plan for replication, if adequate quantities of vitamin C are delivered to the cells in the respiratory tract.

The mixing of the flu viral genome with that of the human host cell will happen only when the latter is at a particular phase of the cell division cycle. But, Dibyajyoti Banerjee, lead author of the PGI study, says it possible to stop the infected cell from proceeding to that phase, if a high amount of vitamin C is present in the cell.“This restricts the viral genome integration in the human body,” Banerjee told KnowHow.

Delivering a high dose of vitamin C to the respiratory tract, however, is a challenge. It’s tough because no matter how big the dosage, very little of it reaches the respiratory tract, if delivered orally. That’s because of the digestion of the vitamin by the human digestive system.

To overcome this difficulty, the Chandigarh scientists propose a strategy of administering vitamin C through a combination of nasal and oral routes. “The combination of oral and inhalational delivery of vitamin C is important for attainment of high concentrations of it in the respiratory tract,” says Banerjee. The group is planning further studies to prove that this strategy will actually work, he adds.

Shahid Jameel, head of virology research at the International Centre for Genetic Engineering and Biotechnology, New Delhi, says it is possible to ward off many viral infections, including swine flu, by boosting general immunity. That’s because viruses depend entirely on the host for their multiplication.

As a result of co-evolution of the host and the virus, both have developed mechanisms to protect themselves.

“Just like we have immunity, viruses have ways to evade immunity. Eventually, this evolutionary tug of war leads to a virus that can infect, but not cause disease,” says Jameel.

That would be an ideal situation as the infection then cannot spread to others, he concludes.

You may click & see:->
*Bee venom therapy
*Apitoxin
*Stinger
*Hornet stings
*Characteristics of common wasps and bees
*Schmidt Sting Pain Index

Source: The Telegraph (Kolkata, India)

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