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Author Topic: 1918 Flu --> 'Side Effect' --> The Secret Present --> "The Forgotten Plague"  (Read 13431 times)
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« on: July 25, 2009, 08:06:49 AM »

1918 Flu  Side Effect -- The Secret Present

If we are witnessing a repeat of the 1918 Flu Outbreak, then this little nightmare of "The Sleeping Sickness" will follow in its wake. To give it its technical name "Encephalitis Lethargica"

Following the original pandemic in 1918, a nightmare of biblical proportions struck in the 1920's. A mysterious illness that left the victims in a state of paralysis and comma like state followed in the wake of the flu. It attacked the brain, leaving the victim like the living dead.



The 1918 Flu Pandemic did not 'just' kill more people than died during "The Great War", "The War to End All Wars", it had this devastating side effect.



How our modern society, bankrupt from a staged economic collapse, and with a controlled media would handle such a plague would be anyones guess. It is however possible that mass eugenics might be rolled out, and the patients left to die by the method "nil by mouth" or by being "put down". It is easy given a little thought to sell people the idea that it would be better to die than to be left in a comma.

Also it is worth considering that the modification of the 1918 Flu that the bio weapons people literally dug up from the Arctic, has been modified not to kill during the first round of the pandemic, but to decimate with this Sleeping Sickness. We simply will not know till around 2 or more years latter.



http://en.wikipedia.org/wiki/Encephalitis_lethargica
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« Reply #1 on: July 25, 2009, 08:09:16 AM »

Funny how only a short time ago the connection between the 1918 pandemic and "The Forgotten Plague" was written about in the press and even appeared on the odd documentary.

Now in the wake of the Swine Flu Epidemic, total and absolute silence on this connection.

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« Reply #2 on: July 25, 2009, 08:15:45 AM »

Health The forgotten plague - BBC

http://news.bbc.co.uk/1/hi/health/140297.stm

An epidemic of the mysterious illness that sent hundreds of thousands of people into a trance-like state in the 1920s could recur in the future, according to scientists.

 A programme on Encephalitis Lethargica, to be broadcast in the QED strand on Wednesday, looks into the disease and the theory that there could be a new outbreak in the future.

Encephalitis Lethargica leaves its victims mentally intact, but damages the area of the brain responsible for movement. Sufferers take on the image of living statues and can remain motionless and speechless for many years.

Sleepy Sickness, as it is also known, was thought by many doctors to be an illness from history, but occasional cases have been reported ever since the 1920s epidemic.

 Dr Stavia Blunt, from London's Charing Cross Hospital, said she has seen four patients with presumed Encephalitis Lethargica in the last five years.

She said some cases of the disease may be being misdiagnosed.

Deep sleep

 Medical historians say the first reported case of the disease was in Vienna during World War I. Within months, other cases were being reported across Europe and the rest of the world.

It affected people in bewildering ways. Some fell into a deep sleep - a bride was reported to have fallen asleep on the way to her wedding and never woke again.

 Others became violent, excitable or were driven mad by hallucinations. In 1928, the disease apparently disappeared.
A Hollywood film called Awakenings, starring Robin Williams, sparked recent interest in the illness. It told the story of Dr Oliver Sacks who tried to cure victims in a New York hospital in the 1960s.

 He managed to bring many of the 'frozen' patients out of their trance by giving them an experimental drug. But the effect was short lived.

Flu virus

 Efforts are now being made to isolate the cause of the disease. Professor John Oxford believes the pathogen may be an unusual strain of the 'flu virus - there was a worldwide influenza epidemic just before Encephalitis Lethargica started to appear. He said this is worrying.

"There will be another massive outbreak of influenza sometime in the near future," he said.

 "I think that gives an urgency to working out whether influenza is involved or not."


 Professor Oxford, who leads a team of virologists at the Royal London Hospital, is studying brain samples saved from the 1920s. He found them stored in his hospital's archive.

He is also examining the blood taken from recent victims. He hopes modern science can unlock the secrets of the disease.

"I certainly do not think the outbreak [in the 1920s] was a one-off. I wouldn't be surprised at all if there were succeeding outbreaks. And until we know what caused it, we can't plan things properly."

Unique story

 The QED programme tells the story of Philip Leather, who contracted the disease in the 1920s and still thinks he is a 13-year-old.

He is among the last survivors of the original outbreak, and his brain will be donated to medical science when he dies.
 The programme also hears the case of Rebecca Howells, 28, a modern victim of the disease. She spent more than one month in intensive care in a bizarre, restless coma.

 Doctors eventually gave Rebecca a massive dose of steroids and she made a full recovery.

One of the most remarkable features of the broadcast is the use of archive film, both from the 1920s and from the private film collection of Dr Oliver Sacks.

QED - The Forgotten Plague - is broadcast on BBC 1 on Wednesday, July 29, at 22:00 BST.
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« Reply #3 on: July 25, 2009, 08:36:09 AM »

"a bride was reported to have fallen asleep on the way to her wedding and never woke again. "

Don't all reply at once
 Grin
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« Reply #4 on: July 25, 2009, 08:52:07 AM »

It won't be forgotten for much longer if the virus which was recreated in a lab is released  Shocked 

Security fears as flu virus that killed 50 million is recreated
Thursday 6 October 2005
http://www.guardian.co.uk/society/2005/oct/06/health.medicineandhealth3

Scientists have recreated the 1918 Spanish flu virus, one of the deadliest ever to emerge, to the alarm of many researchers who fear it presents a serious security risk.

Undisclosed quantities of the virus are being held in a high-security government laboratory in Atlanta, Georgia, after a nine-year effort to rebuild the agent that swept the globe in record time and claimed the lives of an estimated 50 million people.

The genetic sequence is also being made available to scientists online, a move which some fear adds a further risk of the virus being created in other labs.

The recreation was carried out in an attempt to understand what made the 1918 outbreak so devastating. Reporting in the journal Science, a team lead by Dr Jeffery Taubenberger at the Armed Forces Institute of Pathology in Maryland shows that the recreated virus is extremely effective. When injected into mice, it quickly took hold and they started to lose weight rapidly, shedding 13% of their original weight in just two days. Within six days, all mice injected with the virus had died.

In a comparison experiment, similar mice were injected with a contemporary strain of flu, and although the mice lost weight initially, they recovered. Tests revealed that the Spanish flu virus multiplied so rapidly that after four days, mice contained 39,000 times more flu virus than those injected with the more common strain of flu.

The government and military researchers who reconstructed the virus say their work has already provided invaluable insight into its unique genetic make-up and helps explain its lethality. But other researchers warned yesterday the that virus could escape from the laboratory. "This will raise clear questions among some as to whether they have really created a biological weapon," said Professor Ronald Atlas at the centre for deterrence of biowarfare and bioterrorism at the University of Louisville in Kentucky.

Publication of the work and the filing of the virus's genetic make-up to an online database followed an emergency meeting last week by the US National Science Advisory Board for Biosecurity, which concluded that the benefits of publishing the work outweighed the risks. Many scientists remained sceptical. "Once the genetic sequence is publicly available, there's a theoretical risk that any molecular biologist with sufficient knowledge could recreate this virus," said Dr John Wood, a virologist at the National Institute for Biological Standards and Control in Potters Bar.
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« Reply #5 on: July 25, 2009, 09:01:25 AM »

Swine flu virus related to 1918 pandemic
Monday, 13 July 2009
http://www.independent.co.uk/life-style/health-and-families/health-news/swine-flu-virus-related-to-1918-pandemic-1744792.html

Swine flu penetrates deeper into the lungs and can inflict more damage than ordinary seasonal flu, scientists have found. The discovery could explain why the virus is able to cause severe illness in people with no underlying health problems.

Experts also believe swine flu is closely related to strains responsible for the 1918 pandemic which killed up to 40 million people worldwide.

Evidence suggests that people born after 1920 have little natural resistance to the virus.

US and Japanese researchers tested the ability of swine flu strains obtained from infected patients to cause disease in mice, ferrets, and macaque monkeys. They found that swine-origin influenza viruses (S-OIVs) were about five times more harmful than seasonal versions of the H1N1 flu strain.

Their effect on the lungs was reminiscent of H5N1 bird flu, which is almost always fatal when it infects humans. But in the case of swine flu, most victims recover. The viruses were also found to infect pigs without causing disease symptoms. This could be why there were no reports of flu outbreaks in pigs before humans started to get ill.

Close inspection showed that the new strains were similar to the 1918 pandemic viruses.

Antibodies collected from patients born before 1920 were able to recognise them, and would presumably offer some immunity. But there was little evidence individuals born after 1920 harboured antibodies that could target swine flu.

A report on the research appeared online today in the journal Nature.

The scientists, led by Dr Yoshihiro Kawaoka from the University of Wisconsin-Madison in the US, wrote: "Most human infections with swine-origin H1N1 influenza viruses (S-OIVs) seem to be mild; however, a substantial number of hospitalised individuals do not have underlying health issues, attesting to the pathogenic potential of S-OIVs..

"Our findings indicate that S-OIVs are more pathogenic in mammalian models than seasonal H1N1 influenza viruses."

The good news from the research was that Tamiflu and other antiviral drugs were effective against swine flu viruses.

However the scientists warned that sustained person-to-person transmission might lead to the emergence of more dangerous, drug resistant strains.

Commenting on the research, Professor Ian Jones, from the University of Reading, said: "This complete analysis of the current H1N1 is what we've been waiting for. It shows that the new virus is about five times more pathogenic than seasonal H1N1 but that, nonetheless, the major outcome to infection is recovery. For the few cases of severe infection the data will help in clinical management of hospitalised patients."

Professor Wendy Barclay, chair in influenza virology at Imperial college London, said: "By comparison with a seasonal human H1N1 virus, it is shown that the sw (swine) origin H1N1 infect cells deeper into the respiratory tract. It must be borne in mind that typical circulating human strains of H1N1 have been associated with rather mild illness in recent years, and that the sw origin H1N1 may be behaving in these animal models more like the type of H3N2 viruses that caused a pandemic in 1968."
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« Reply #6 on: July 25, 2009, 09:01:50 AM »

"a bride was reported to have fallen asleep on the way to her wedding and never woke again. "

Don't all reply at once
 Grin

 Must  have  been the prospect of marrying that pushed  her over the edge.

 Quote: The good news from the research was that Tamiflu and other antiviral drugs were effective against swine flu viruses.
 

Maybe a push to sell THAT
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« Reply #7 on: July 25, 2009, 09:03:46 AM »

What if the modification is to bio-engineer and 'improved' version to get an awesome kill ratio with this sleeping sickness ?

Not only will people not be able to resist, but vast amounts of people will be tied up caring for those who are sick, not exactly going to be able to "riot" or form a "militia" when your caring for sick relatives.

If it is a repeat of 1918 - and it looks like they engineered it, expect a Sleeping Sickness Plague to follow

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« Reply #8 on: July 25, 2009, 02:42:54 PM »

So while the "conspiracy theorists" are looking at a vaccine to do the damage, it is quiet likely that a second wave, a deadly wave of second plague in the form of sleeping sickness will sweep the world.

Some of you might recall "Awakenings" an Academy Award-nominated film 1990 starring Robin Williams and Robert De Niro. It was written by Dr Oliver Sacks, the neurologist.

Sacks worked at a chronic care facility in the sixties with a group of survivors of the 1920s sleeping sickness, encephalitis lethargica, who had been unable to move on their own for decades. These patients and his treatment of them were the basis of Sacks' book Awakenings.



You can read up on that Movie here
http://en.wikipedia.org/wiki/Awakenings

OR

Have a look on a video website for Trailers and clips.


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« Reply #9 on: July 25, 2009, 07:16:14 PM »

Who would go to a swine flu party eh? Would you want this virus (whether "dead" or not) injected into your veins - even if vaccines were not high tech bio-weapons..and maybe its the immune response that triggers sleeping sickness anyway..

Thanks for reminding about this, EvadingGrid, excellent thread.



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« Reply #10 on: July 25, 2009, 07:26:20 PM »

What if the modification is to bio-engineer and 'improved' version to get an awesome kill ratio with this sleeping sickness ?

Not only will people not be able to resist, but vast amounts of people will be tied up caring for those who are sick, not exactly going to be able to "riot" or form a "militia" when your caring for sick relatives.

If it is a repeat of 1918 - and it looks like they engineered it, expect a Sleeping Sickness Plague to follow

Interesting light that!  It will also be a logistical nightmare for the infrastructure if it will be as widespread as you state.  Zombified people.  That will be sucky.
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« Reply #11 on: July 25, 2009, 07:31:54 PM »

What is officially "crossing the line" now?

At what point do I quit my job, drop out of school, and run for cover?  

When 10,000 die?  The media would have me believe hundreds of thousands of ppl are sick right now, and millions will be sick by fall.  Even if I am able to refuse the coming mandatory vaccine, won't I just get sick when every jerkwad around me in society has taken the shot and has bird flu or w/e?

So, if I see 10,000 ppl in my city die from swine flu, what then?  It's prolly too late by then.

No matter how you slice it your f**ked.  So I try to just press onward, heading towards known oblivion, unable to stop from tumbling over because millions of dumbasses who don't get how the world works are pushing me from behind.

EDIT: My 600th post!



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« Reply #12 on: July 25, 2009, 07:40:45 PM »

Encephalitis Lethargica leaves its victims mentally intact, but damages the area of the brain responsible for movement. Sufferers take on the image of living statues and can remain motionless and speechless for many years.

What torture that would be!  Sounds like a plan for the evil NWO architects.
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« Reply #13 on: July 26, 2009, 07:50:36 AM »

Encephalitis Lethargica leaves its victims mentally intact, but damages the area of the brain responsible for movement. Sufferers take on the image of living statues and can remain motionless and speechless for many years.

What torture that would be!  Sounds like a plan for the evil NWO architects.

Exactly, so it would not take much persuasion to get people to act out Euthanasia.

The hospitals would not be able to cope, these people would be sent home, to be looked after by who ?
 
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« Reply #14 on: July 26, 2009, 08:16:11 AM »

Great thread EvadingGrid!  People consuming aspartame may also help accelerate this type plague too.   Angry
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« Reply #15 on: July 26, 2009, 09:35:59 AM »

Great thread EvadingGrid! people consuming aspartame may also help accelerate this type plague too.   Angry

Lets face it, we know they Bio Engineered this little baby in a Bio Weapons Laboratory.

Yet the kill rate is really low for a Engineered Pandemic.

So I'm thinking that it must have some other surprise engineered.

It has been suggested at great length that it is a Binary Weapon, with the second part being the Vaccine. Well that might well be the case, but that would be incredibly hard to pull off from a Science and Engineering perspective.

However, if they understand now why the original 1918 out break lead to the second wave plague of "Sleeping Sickness", then the genetic trait is already in the 1918 Flu.

So all they had to do was work out what factors that would enhance it.

Enhancing a Genetic Trait that is already present is much simpler than designing a binary vaccine weapon.from scratch. All you would need would be a very small team that could trial some educated guesses to discover how to "tune" the virus.

Balance that with designing a Binary Bio Weapon from scratch, how many people would you need for that stunt ? Money might not be the problem, but when a project requires not just teams but multiple laboratories and pushing the envelope of science to the extreme limits I begin to suspect the idea is not plausible. Why even start such a project with all the associated risks when you do not even have any reason to believe it will succeed ?
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« Reply #16 on: July 26, 2009, 11:03:28 AM »

The forgotten plague was most like geon burray syndrome which is a paralysing disorder caused by vaccines. It is the reason the government had to pay out over $4 billion dollars in damages after the first swine flu campaign.

Also, lets consider that the first virus was not isolated by scientists until 1922. Is it really 100% accurate to refer to the 1918 pandemic as a virus? Could have been a bacterial infection or a chemical warfare test.
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« Reply #17 on: July 26, 2009, 04:51:21 PM »

This video series (Sane posted on another thread) is excellent -history of the dust bowl, but goes back to the days of the flu pandemic in 1918. The point they made about people who contracted the flu was that they were more susceptible due to suffering from malnutrition - food shortages, etc., that weakened their bodies, and their ability to fight off the flu.

http://www.youtube.com/watch?v=eO-eVe2xJZs

Watching that reminded me of my grandfather, born in 1905 in Honolulu (he had a birth certificate by the way), and the story of his family of 12 kids ALL having the flu at the same time. They all survived - with home care by his mother and father - no vaccines, nothing scientific about it - more homespun remedies and their normal diet of fish, vegetables and taro (poi). A healthy diet.  The records of the flu in Hawaii bear this out..

http://1918.pandemicflu.gov/your_state/hawaii.htm

  • Hawaii’s experience of the influenza pandemic differed from that of the rest of the United States. In the summer of 1918, an early and less destructive wave of influenza arrived in Oahu. While a second and more lethal wave of influenza reached most communities on the mainland by early October, this second wave of influenza did not hit Hawaii until December.

    Workers on rural and isolated plantations suffered as influenza attacked all of the islands. c. 1910-1925. [Credit: The Library of Congress]  

    When the Hawaiian Territorial Medical Society met in November, members viewed the pandemic as a problem limited to the mainland. Papers read at this meeting focused on topics such as “Influenza with Special Emphasis on the Recent Epidemic on the Mainland.” There was no discussion of influenza as an issue in Hawaii itself.

    But by December, the Society’s medical officers were forced to reassess their views as a lethal wave of influenza now hit all of the islands. By the end of the year, the number of cases of contagious diseases reported to the Hawaiian Board of Health was 12,000 more than in the previous year with this increase being almost all due to influenza.

    While mortality and morbidity rates are often impossible to calculate, Hawaii does not appear to have suffered tremendously from the pandemic. In Honolulu, reports sent to the PHS indicate that thirty-two people had died in the city from influenza and sixteen of the city’s residents had died of pneumonia, a related complication, during January. On March 12, 1919, a letter from Chief Quarantine Officer to the Surgeon General stated “that for the week ended March 1st, there were 125 cases of influenza and 20 deaths in the City and County of Honolulu. Influenza was the cause of death in seven of the cases, while the remaining 13 were due to a complicating pneumonia.”

    Influenza remained a problem in the islands until the late spring when it began to slowly disappear.
-----------------------------------------

I don't think they had a lower death rate because the virus was weakened (Hawaiians were more susceptible to infections brought from the mainland, because they had less immunity due to distance and more isolated population in 1905).

I think it was the diet.

They ate healthy non-processed, fresh foods - fish, fruit, pork, beef, vegetables, rice and taro.
So healthy bodies can fight off disease better than weakened malnourished bodies... we can also add vitamins and minerals - basically use our own nutrition as a weapon against illness.



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« Reply #18 on: July 27, 2009, 09:10:04 AM »

The forgotten plague was most like geon burray syndrome which is a paralysing disorder caused by vaccines. It is the reason the government had to pay out over $4 billion dollars in damages after the first swine flu campaign.

Also, lets consider that the first virus was not isolated by scientists until 1922. Is it really 100% accurate to refer to the 1918 pandemic as a virus? Could have been a bacterial infection or a chemical warfare test.

Yes they went and dug up some frozen victims in the Acrtic ice, brought it back and reactivated it in the laboratory.

Folks it is accepted within the community that the present virus is based upon the 1918 Epidemic. What is not yet fully understood is to what "end"  it has been modified. Seems they have gone to a lot of trouble to resurrect the 1918 Virus, but they are not at present getting the kill ratio or pay off that they would 'enjoy'.

The thing is the original pandemic had an extra payload, the Sleeping Sickness. It seems reasonable to speculate that the new improved version of the 1918 virus has an enhanced Sleeping Sickness Ticking Time Bomb. This is not wild speculation, but based upon boring facts. Like it is way easier to enhance an already existing trait, than to do some sci-fi tin foil hat engineering.
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« Reply #19 on: July 27, 2009, 11:44:42 AM »

In this report , No relationship between 1918 virus and EL....

http://brain.oxfordjournals.org/cgi/content/full/127/1/21
Encephalitis lethargica syndrome: 20 new cases and evidence of basal ganglia autoimmunity
...
The recent discovery and identification of the 1918 influenza virus by Taubenberger and colleagues (Taubenberger et al., 1997) allowed this group the opportunity to examine archived EL brain specimens for 1918 influenza virus RNA. They failed to find influenza RNA in EL brains, and furthermore determined that the 1918 influenza virus was genetically incapable of neurotropic disease, and only capable of reproduction in the respiratory tree. The authors concluded that EL was unlikely to have been directly due to the 1918 influenza virus (McCall et al., 2001).
...
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« Reply #20 on: July 27, 2009, 12:03:43 PM »

In this report , No relationship between 1918 virus and EL....

http://brain.oxfordjournals.org/cgi/content/full/127/1/21
Encephalitis lethargica syndrome: 20 new cases and evidence of basal ganglia autoimmunity
...
The recent discovery and identification of the 1918 influenza virus by Taubenberger and colleagues (Taubenberger et al., 1997) allowed this group the opportunity to examine archived EL brain specimens for 1918 influenza virus RNA. They failed to find influenza RNA in EL brains, and furthermore determined that the 1918 influenza virus was genetically incapable of neurotropic disease, and only capable of reproduction in the respiratory tree. The authors concluded that EL was unlikely to have been directly due to the 1918 influenza virus (McCall et al., 2001).
...

Coincidence Theory  Grin

Actually they did find a correlation between those who came down with the sleeping sickness and those who had fallen foul of the flu pandemic, but that is just a coincidence. Just like people who have just been vaccinated with gardisill dropping dead, its all just coincidence  Roll Eyes

One thing I did note was that material linking the two events has disappeared, at least I could not find it very easily.
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« Reply #21 on: July 27, 2009, 12:21:13 PM »

I'm trying to find an article that linked it with the vaccinations that were given out back then.

http://www.whale.to/vaccines/shelton3.html
VACCINE AND SERUM EVILS BY HERBERT M. SHELTON
...
Within recent years other troubles have been definitely traced to vaccination. I have already quoted Dr. Osler’s statement that "at the height of vaccination convulsions may occur and be followed by hemiplegia." Paralysis is a more frequent result of vaccination than has heretofore been suspected. Dr. Osler says: "Cerebro-spinal meningitis has a curious predilection for soldiers." Captain Sheffield Neave, of England, says, "meningitis is a disease of soldiers and babies." During World War I there was a great mortality and invalidism among soldiers due to cerebro-spinal meningitis. Anti— vaccinationists declared it to he due to vaccination. This brought vigorous protests and loud denunciations from the devotees of pus and the smallpox goddess.
...
This means that the ordinary and regular course of mischief pursued by vaccination may easily result in the production of these diseases. The Lancet further says: "Though the path of infection cannot he traced, the authors would appear to have ample justification for concluding, in view of the close resemblance between the clinical histories, the uniformity of the pathological findings, and the absence of similar cases independent of vaccination that vaccination was a definite causal factor and no chance coincidence." (Italics mine).

In the year 1927 when Mr. Marky and Senator Love debated on vaccination, we exhibited on the platform, a little girl whose body was frightfully twisted, greatly emaciated and paralyzed as a result of vaccination. With the smooth sagacity of the suave politician and with resort to the ancient medical subterfuges of "secondary infection" and "intercurrent malady," Dr. Love attempted to make the audience believe the child’s troubles were due to something other than vaccination. But an "intercurrent affection" is mere bunk. It never existed outside the medical mind. The Lancet had formerly held to the same theory with regard to such cases as cited above. Referring in its issue of August 1, 1925, to the numerous cases on the continent, it declares: "Experiment and pathological research have shown that this form of the disease is not due to the virus of Jenners vaccine"…."There was latent infection" and "vaccination merely hatched it out."

"Latent infection" is another subterfuge that has long served the blundering medical profession when tuberculosis, syphilis and leprosy follow vaccination. But the end of this subterfuge is drawing near. The Lancet has unsaid what it declared in the quotation above. It declares: "Similar cases independent of vaccination were not observed at the same time nor any other time. The authors give cogent reasons against the assumption that the post-vaccinal cases described by them and by workers abroad are merely examples of poliomyelitis, (inflammation of the gray matter of the spinal cord) or encephalitis lethargic a (sleeping sickness), in which vaccination was an immaterial accident." It declares that encephalo-myelitis following vaccination always exhibits more extensive lesions than those of sleeping sickness and that "histologically, the inflammation in ordinary cases of poliomyelitis (infantile paralysis) differs conspicuously from that following vaccination."

In 1923, 1924 and 1925 great efforts were made in England to have everybody vaccinated. Thousands of vaccinations were performed. There occurred a great increase in the cases of Encephalitis-Lethargica. In 1924, there were 6,296 cases of this and similar affections reported in England and Wales, with a population of 38,746,000; or 162 cases per million of population. In Liverpool, with a population of 836,000 there were reported 257 such cases; or 306 cases per million of population.

Liverpool was fifty per cent better vaccinated than the average of England and Wales, and had almost 100% more Encephalitis. I presume this was due to an "intercurrent affection," or a "latent infection," or to a "secondary infection."


https://www.riskinstitute.org/peri/images/file/Lessons_from_1918_PartI.pdf
Lessons from the 1918 Spanish Flu - Part I of II
...
Widespread Illness will Occur (WHO 2006 c)
In 1918, half the world’s population fell sick to Spanish flu. The disease raged in Africa, Australia, Canada, Europe, New Zealand, the South Pacific, the United States— and even reached as far north as the arctic archipelago of Svalbard, 1000 kilometers north of the Norwegian mainland.

In addition to Spanish flu, another worldwide scourge raged unabated:
encephalitis lethargica--the disease depicted in the movie Awakenings (1990). During its reign of terror--from 1915 to its disappearance sometime between 1927 and 1930--the disease claimed or ravaged the lives of 5 million people worldwide (Duncan 2003). Regrettably, no causative agents were identified during the two pandemics; however, circumstantial evidence links Spanish flu and encephalitis lethargica or sleeping
sickness.

Both pandemics were globally distributed and closely related in time. Local, regional, and national epidemics of Spanish flu preceded ‘similar-sized’ outbreaks of encephalitis lethargica. Deaths were greatest in the 20 to 40 year age group for Spanish flu and in the 20 to 50 year age group for sleeping sickness. A large number of victims of encephalitis lethargica had had influenza in 1918. For example, in Western Samoa, Spanish flu killed 8,000 people, and 79 died of encephalitis lethargica between 1919 and 1922. A hundred miles away, American Samoa escaped flu through strict quarantine, and suffered only two cases of encephalitis lethargica. Past pandemics of encephalitis were recorded in close association with other influenza epidemics; for example, the great
influenza epidemic of 1889-90 preceded the notorious ‘nona’--a somnolent illness that was followed by Parkinsonism in almost all survivors.

Detractors of the theory would argue: the first cases of sleeping sickness preceded Spanish flu by several years; influenza was highly communicable, whereas encephalitis was non-communicable; not all cases of encephalitis lethargica had a history of earlier influenza infection; and not all influenza epidemics were associated with epidemic encephalitis (Duncan 2003). Moreover, new research suggests that encephalitis lethargica
may result from an autoimmune (an immune response against the body’s own tissues) infection, possibly post-streptococcal (Duncan 2006 c).


Today, H5N1 causes severe disease in animals and humans, with viral pneumonia and failure of many organs and the central nervous system (Liu et al., 2005; and WHO 2005 a). In 2004 a Vietnamese boy presented with severe diarrhea, followed by seizures, coma, and death. H5N1 was isolated from his cerebrospinal fluid and other specimens. The diagnosis, like his sister’s, was acute encephalitis. ‘These cases suggest that the spectrum of influenza H5N1 is wider than previously thought’ (de Jong et al., 2005). Recent research shows that the 1918 Spanish flu virus shares genetic similarities with today’s H5N1 (Taubenberger et al., 2005). Moreover, 1918 attacked multiple organs, including the central nervous system, of young healthy people, just as H5N1
appears to do today.

Perhaps experts, preparing for an influenza pandemic, should therefore examine the possibility of a wider spectrum of H5N1, and a longer medical legacy (Duncan 2006)
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TahoeBlue
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« Reply #22 on: July 27, 2009, 07:31:05 PM »

Wow, look what I found... (oh, and maybe some of the problems maybe reactions from the Tamiflu...)

http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5828a2.htm?s_cid=mm5828a2_e/?date=072309
Neurologic Complications Associated with Novel Influenza A (H1N1) Virus Infection in Children --- Dallas, Texas, May 2009

Neurologic complications, including seizures, encephalitis, encephalopathy, Reye syndrome, and other neurologic disorders, have been described previously in association with respiratory tract infection with seasonal influenza A or B viruses (1--2), but not with novel influenza A (H1N1) virus.

On May 28, 2009, the Dallas County Department of Health and Human Services (DCHHS) notified CDC of four children with neurologic complications associated with novel influenza A (H1N1) virus infection admitted to hospitals in Dallas County, Texas, during May 18--28. This report summarizes the clinical characteristics of those four cases.

Patients were aged 7--17 years and were admitted with signs of influenza-like illness (ILI) and seizures or altered mental status. Three of the four patients had abnormal electroencephalograms (EEGs). In all four patients, novel influenza A (H1N1) viral RNA was detected in nasopharyngeal specimens but not in cerebrospinal fluid (CSF). Antiviral therapy included oseltamivir (four patients) and rimantadine (three patients). All four patients recovered fully and had no neurologic sequelae at discharge. These findings indicate that, as with seasonal influenza, neurologic complications can occur after respiratory tract infection with novel influenza A (H1N1) virus. For children who have ILI accompanied by unexplained seizures or mental status changes, clinicians should consider acute seasonal influenza or novel influenza A (H1N1) virus infection in the differential diagnosis, send respiratory specimens for appropriate diagnostic testing, and promptly initiate empirical antiviral treatment, especially in hospitalized patients.

Case Identification

Since April 22, DCHHS has requested all hospitals in Dallas County to report details concerning patients admitted with novel influenza A (H1N1) virus infection. As of July 20, DCHHS had identified 405 persons with laboratory-confirmed novel influenza A (H1N1) virus infection in the greater Dallas area, including 44 hospitalized patients. No deaths had been reported. Of confirmed novel influenza A (H1N1) virus infections, 83% were in patients aged <18 years. Among these pediatric cases, 145 children, including 26 who were hospitalized, were identified through the Children's Medical Center of Dallas (CMCD) laboratory-based surveillance program. Medical records from admission and discharge for all hospitalized H1N1 patients are routinely screened by DCHHS epidemiology staff. Characteristics of hospitalized patients are compiled on an ongoing basis, with further investigation of cases noted to have unusual features and severe illness.

A patient with acute neurologic complications associated with novel influenza A (H1N1) virus infection was defined as having laboratory-confirmed novel influenza A (H1N1) virus infection of the respiratory tract associated with seizures, encephalopathy, or encephalitis within 5 days of ILI symptom onset, without evidence of an alternative etiology. Encephalopathy was defined as altered mental status lasting ≥24 hours. Encephalitis was defined as encephalopathy plus two or more of the following: fever ≥100.4°F (≥38.0°C), focal neurologic signs, CSF pleocytosis, EEG indicative of encephalitis, or abnormal neuroimaging indicative of infection or inflammation (1--2).

During April 22--July 20, seven possible cases of neurologic complications associated with novel A (H1N1) virus infection were identified. Three cases were excluded because the neurologic complications were determined to have alternative etiologies (e.g., hypocalcemia and apnea related to prematurity) or did not meet the case definition (e.g., altered mental status for <24 hours). Of the remaining four cases described in this report, one patient (patient A) was initially reported by a community hospital in Dallas on May 18. The three other cases were reported by CMCD to DCHHS during May 23--27. No additional cases had been reported in Dallas County through July 20.

Nasopharyngeal swab specimens collected from all three patients admitted to CMCD were tested for influenza A and B antigens by either Directigen EZ Flu A+B rapid enzyme immunoassay (EIA) (BD [Becton, Dickinson, and Company], Sparks, Maryland), QuickVue Influenza A+B test (EIA) (Quidel, San Diego, California), or D3 Ultra direct fluorescent assay (Diagnostic Hybrids, Athens, Ohio). All positive specimens were sent to DCHHS, and novel influenza A (H1N1) virus was identified by real-time reverse transcription--polymerase chain reaction (rRT-PCR) using CDC-approved primers and probe sets. All CSF samples were tested at CDC using rRT-PCR for influenza, enteroviruses, parechovirus, adenovirus, and human parainfluenza virus serotype 3. CSF for patients B and D were tested for additional viruses by a commercial laboratory (Viracor).*

Case Reports

Patient A. On May 17, a previously healthy black male aged 17 years visited a community hospital emergency department after 1 day of fever reaching 102.6°F (39.2°C), cough, headache, dizziness, and weakness. Influenza A was diagnosed by EIA, and the patient was discharged home with a prescription for oseltamivir. The patient was admitted the next day to another community hospital because of increased generalized weakness, disorientation to place, and markedly slow and intermittent responsiveness to questions. On physical examination, the patient was noted to be confused and unable to provide history of his own illness. He also was unable to lift his arms above his shoulders or stand. He had taken 1 dose of oseltamivir the morning of admission. A computed tomography (CT) head scan revealed pan-sinusitis, and CSF was normal (Table). The patient received ceftriaxone for 2 days, which was discontinued when CSF bacterial cultures indicated no growth. He received oseltamivir throughout his hospital admission. His mental status returned to normal on day three. He was discharged on day four with no apparent sequelae and completed a 5-day total course of oseltamivir.

Patient B. On May 23, a previously healthy Hispanic male aged 10 years was taken to a Dallas community hospital via emergency medical services after a 3-minute generalized tonic-clonic seizure and subsequent postictal mental state. The seizure occurred after 4 days of fever reaching 104.0°F (40.0°C), cough, decreased appetite, and fatigue. His family reported that the patient had contact with another child with ILI symptoms before the patient's illness onset. Upon initial evaluation in the emergency department, the patient was afebrile. A chest radiograph revealed a left lower lobe infiltrate, and a CT head scan was normal except for an incidentally noted single punctuate calcification in left frontal cortex. Influenza A was detected in a nasopharyngeal swab specimen by EIA. Three hours later, the patient had a second 3-minute generalized seizure. Intravenous (IV) lorazepam and ceftriaxone were administered, and the patient was transferred to a CMCD intensive-care unit.

On admission to CMCD, the patient was febrile, confused, and drowsy. He had difficulty answering questions and made frequent inappropriate attempts to get out of bed. CSF analysis was normal. He was administered IV fosphenytoin to prevent additional seizures, vancomycin and ceftriaxone for empirical treatment of bacterial pneumonia, supplemental oxygen via bilevel positive airway pressure for oxygen saturations <92%, and anticonvulsants. Over the ensuing 2 days, he had intermittent fevers reaching 102.0°F (38.9°C). On hospital day four, he had a prolonged partial complex seizure with focal onset (eye deviation to the right) and secondary generalization, lasting 30--40 minutes, which eventually was controlled by 4 doses of IV lorazepam and a bolus of IV fosphenytoin. Oseltamivir and rimantadine were initiated. Brain magnetic resonance imaging (MRI) with magnetic resonance angiography was normal, and an EEG was consistent with encephalopathy (Table). His mental status returned slowly to baseline by hospital day seven, when he was discharged without apparent sequelae to continue levetiracetam, amoxicillin, and clindamycin, and complete a 5-day course of oseltamivir.

Patient C. On May 26, a white male aged 7 years with a history of a simple febrile seizure 1 year previously was taken to a Dallas community hospital via emergency medical services after a seizure and 2 days of cough, nasal congestion, and fatigue. On the day of admission, he had been found at home on the floor, with tonic movements of his upper and lower extremities lasting at least 2 minutes. On admission to the community hospital, he was noted to have postictal drowsiness and a temperature of 100.8°F (38.2°C). A diagnosis of influenza A was made by EIA. Blood tests, CSF, and a CT head scan were normal (Table).

The patient was transferred the same day to CMCD, where he exhibited normal mental status and no fever or seizures. A brain MRI showed nonspecific white matter abnormalities not characteristic of infection or inflammation. Localized cerebral dysfunction was evident on EEG (Table). Oseltamivir and rimantadine were started on hospital day one, and the patient was discharged on hospital day three without any neurologic sequelae, to complete a 5-day course of both antivirals and to continue levetiracetam until reassessment by neurologists in 3 months.

Patient D. On May 27, a black male aged 11 years with a history of asthma was taken to CMCD because of 1 day of fever and vomiting. A household contact, his grandmother, had an upper respiratory infection 3 days before his illness. One day before admission, he had a fever of 102.0°F (38.9°C), fatigue, headache, abdominal pain, and vomiting, and was given bismuth subsalicylate twice and one 81 mg aspirin. At CMCD, he was febrile. Neurologic examination revealed ataxia. Soon after admission, the patient had a seizure consisting of episodic eye rolling and tongue thrusting. An EIA test for influenza A was positive, and oseltamivir, rimantadine, cefotaxime, and acyclovir were initiated.

During the first 2 hospital days, the patient was disoriented, had visual hallucinations, had difficulty responding to questions and following commands, had slow speech, and required supplemental oxygen via facemask for mild hypoxia and hypopnea attributed to decreased respiratory drive associated with encephalopathy. Chest radiograph was normal. An EEG was consistent with encephalopathy, and a CT head scan was normal (Table). The patient's mental status returned to normal by hospital day four. He completed a 5-day course of oseltamivir.

Reported by: AS Evans, MD, S Agadi, MD, JD Siegel, MD, Univ of Texas Southwestern Medical Center; WM Chung, MD, JT Carlo, MD, Dallas County Health and Human Svcs, Dallas, Texas. TM Uyeki, MD, J Sejvar, MD, S Lindstrom, PhD, D Erdman, DrPH, S Oberste, PhD, National Center for Immunization and Respiratory Diseases; SJ Olsen, PhD, Div of Emerging Infections and Surveillance Svcs, National Center for Preparedness, Detection, and Control of Infectious Diseases; F Dawood, MD, OW Morgan, PhD, EIS officers, CDC.

Editorial Note: Infection with seasonal influenza virus can be associated with neurologic complications (1--2), but the frequency with which these occur with novel influenza A (H1N1) virus infection is unknown. This is the first report describing patients with neurologic complications associated with novel influenza A (H1N1) virus infection. The severity of the neurologic disease in the four patients described in this report was less than the typical disease described in two studies of neurologic complications associated with seasonal influenza (1--2), which included reports of severe static encephalopathy and death. Only two of the four patients described in this report had seizures, and none died or had neurologic sequelae at discharge. Considering that clusters of influenza-associated encephalopathy in children have been reported during previous community outbreaks of seasonal influenza (1--2) and that children appear to be infected with novel influenza A (H1N1) virus more frequently than adults (3), additional neurologic complications in children are likely to be reported as the pandemic continues. Clinicians should consider influenza associated encephalopathy in the differential diagnosis of children with ILI and seizures or mental status changes, and remain aware of the potential for severe neurologic sequelae associated with seasonal or novel influenza A (H1N1) virus infection.

Neurologic complications in children associated with seasonal influenza have included acute cognitive and behavioral problems, focal neurologic deficits, and death from neurologic complications (4). Influenza-associated neurologic complications are estimated to account for up to 5% of cases of acute childhood encephalitis or encephalopathy (4) and were reported in 6% of influenza-associated deaths among children during one influenza season (2003--04) in the United States (5). The epidemiology of influenza-associated encephalopathy has been described extensively in Japan, where incidence has appeared to be higher than in other countries (1). In Japan, approximately 80% of influenza-associated encephalopathy cases occur in children aged <5 years (1,6), and neurologic signs typically develop within 1--2 days of influenza symptom onset (1,6). Manifestations have included seizures, altered consciousness, incoherence, irritability, and psychotic behaviors (1,6). Outcomes reported in one case-series from Japan ranged from complete resolution (in nearly 50% of cases), to mild (20%) or severe neurologic sequelae (10%), to death (20%) (6).

Neuroimaging results in influenza-associated encephalopathy might be normal, but in severe cases, abnormalities can include diffuse cerebral edema and bilateral thalamic lesions. EEG might show diffuse abnormalities (1,2,4). Only rarely is influenza virus detected in CSF, suggesting that neurologic manifestations might be an indirect effect of influenza respiratory tract infection (2,7).

For patients with respiratory illness and neurologic signs, diagnostic testing for possible etiologic pathogens associated with neurologic disease, including influenza viruses, is recommended (Cool. Health-care providers also should consider a diagnosis of Reye syndrome in patients with viral illness and altered mental status. Although one of the patients described in this report, patient D, received a salicylate-containing product and aspirin, no evidence of Reye syndrome was observed. Salicylates and salicylate-containing products should not be administered to children with influenza or other viral infections because of the increased risk for developing Reye syndrome (9).

Antiviral treatment should be initiated as soon as possible for any hospitalized patient with neurologic symptoms and suspected seasonal influenza or novel influenza A (H1N1) virus infection (2).† Although respiratory specimens should be obtained for appropriate diagnostic testing before administering antiviral agents, clinicians should not wait for the results before beginning treatment. Antiviral medications have been shown to decrease the risk for complications from influenza (10); however, the effectiveness of antiviral treatment to prevent influenza-associated encephalopathy sequelae is unknown. Clinicians also should send respiratory specimens for appropriate diagnostic testing. Although no vaccination against novel influenza A (H1N1) virus is available currently, CDC recommends that all children aged >6 months receive annual seasonal influenza vaccination to prevent illness and complications from infection with seasonal influenza virus strains.§

Acknowledgments
The findings in this report are based, in part, on contributions by E Brock, A Varghese, Children's Medical Center Dallas; L Miller, Charleton Methodist Hospital; C Rowe, Las Colinas Medical Center; J Stringer, E Bannister, PhD, J Rodriguez, S Hughes, K Baumgart, MPH, A Friedman, Dallas County Health and Human Svcs; and N Pascoe, Texas Dept of State Health Svcs.

References
Morishima T, Togashi T, Yokota S, et al. Encephalitis and encephalopathy associated with an influenza epidemic in Japan. Clin Infect Dis 2002;35:512--7.
Maricich SM, Neul JL, Lotze TE, et al. Neurologic complications associated with influenza A in children during the 2003--2004 influenza season in Houston, Texas. Pediatrics 2004;114:e626--33.
Dawood FS, Jain S, Finelli L, et al. Emergence of a novel swine-origin influenza A (H1N1) virus in humans. N Engl J Med 2009;360:2605--15.
Amin R, Ford-Jones E, Richardson SE, et al. Acute childhood encephalitis and encephalopathy associated with influenza: a prospective 11-year review. Pediatr Infect Dis J 2008;27:390--5.
Bhat N, Wright JG, Broder KR, et al. Influenza-associated deaths among children in the United States, 2003--2004. N Engl J Med 2005;353:2559--67.
Wada T, Morishima T, Okumura A, et al. Differences in clinical manifestations of influenza-associated encephalopathy by age. Microbiol Immunol 2009;53:83--8.
Ito Y, Ichiyama T, Kimura H, et al. Detection of influenza virus RNA by reverse transcription-PCR and proinflammatory cytokines in influenza-virus-associated encephalopathy. J Med Virol 1999;58:420--5.
Tunkel A, Glaser C, Bloch K, et al. Management of encephalitis: clinical practice guidelines of the Infectious Diseases Society of America. Clin Infect Dis 2008;47:303--27.
Belay ED, Bresee JS, Holman RC, Khan AS, Shahriari A, Schonberger LB. Reye's syndrome in the United States from 1981 through 1997. N Engl J Med 1999;340:1377--82.
Kaiser L, Wat C, Mills T, Mahoney P, Ward P, Hayden F. Impact of oseltamivir treatment on influenza-related lower respiratory tract complications and hospitalizations. Arch Intern Med 2003;163:1667--72.


Neurologic complication(s) diagnosed
 Encephalopathy
 Seizures, encephalopathy
 Seizures
 Encephalopathy
 
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trailhound
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« Reply #23 on: July 27, 2009, 07:57:57 PM »

Quote
Within recent years other troubles have been definitely traced to vaccination. I have already quoted Dr. Osler’s statement that "at the height of vaccination convulsions may occur and be followed by hemiplegia." Paralysis is a more frequent result of vaccination than has heretofore been suspected. Dr. Osler says: "Cerebro-spinal meningitis has a curious predilection for soldiers." Captain Sheffield Neave, of England, says, "meningitis is a disease of soldiers and babies." During World War I there was a great mortality and invalidism among soldiers due to cerebro-spinal meningitis. Anti— vaccinationists declared it to he due to vaccination. This brought vigorous protests and loud denunciations from the devotees of pus and the smallpox goddess.

   I feel like it might be in our best interests to consider the strong possibility the wolf is guarding the hen house. 

 Im trying to imagine facing quarantine (prison) for refusing vaccination Tongue  That would suck
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« Reply #24 on: October 11, 2011, 02:55:06 PM »

bump - A great thread
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