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Rise of the New Plagues Continues
Post by bigbunny on Jul 29, 2004, 6:48am
Encephalitis lethargica
By Dr Trisha Macnair
What is encephalitis lethargica?
Encephalitis lethargica is a mysterious disease that was the subject of the film Awakenings, starring Robin Williams and Robert De Niro. People with encephalitis lethargica may develop fever, headache, weakness and other symptoms, which can lead to a prolonged state of unconsciousness or to Parkinson's disease. But the cause remains a mystery.
Between about 1917 and 1928 a puzzling illness appeared and swept around the world. Doctors called it encephalitis lethargica, which simply meant 'inflammation of the brain that makes you tired'. Younger people, especially women, seemed to be more vulnerable but the disease affected people of all ages. Hundreds of thousands of people were struck down and many survivors were left to battle difficult symptoms for years. Some thought it was caused by a virus, some confused it with the epidemic of Spanish flu at that time while others blamed weapons used in World War I. But even now, more than 80 years later, scientists are uncertain what causes the condition.
Although the epidemic of encephalitis lethargica hasn't recurred, occasional cases had been reported for centuries beforehand and are still sometimes seen. Some experts suggest that it may be more common than we realise, but that many more minor cases go undiagnosed. Doctors in the south west of England are currently trying to pin down exactly how common it is. You can see details at: www.thesophiecamerontrust.org.uk/research.htm.
Over the years many other names have been given to the condition - or to diseases which appear to cause the same symptoms. These include von Economo's disease, Cruchet's disease, Akureyri disease (after a similar epidemic in Iceland in 1948), benign myalgic encephalomyelitis, or sleeping disease.
Symptoms show brain is affected
The symptoms of encephalitis lethargica can be very variable but the illness usually starts with a high fever, headache and often a sore throat. Double vision, disturbance of eye movements, weakness of the upper body, tremors and strange movements, neck stiffness, intense muscle pains, a slowing of physical and mental response, drowsiness and lethargy soon follow. Unusual brain and nerve symptoms may occur and the person's behaviour and personality may change too. Occasionally they become psychotic with extremely disturbed thinking. Sometimes the illness is mistaken for epilepsy, hysteria or even drug or alcohol abuse.
Long term effects can be severe
As the body shuts down, patients become increasingly sleepy and some may lose consciousness, slipping into a coma which can last months and years. This is why the disease is sometimes known as sleeping sickness. During the epidemic in the 1920s many died - but these days modern medicine can help to keep people alive.
However the disease leaves in its wake a variety of problems which can cause prolonged disability. Most people recovering from encephalitis lethargica develop a form of Parkinson's disease, with typical symptoms of slowness, tremor and abnormal muscle movements called dystonia. As with Parkinson's there may be very little facial movement so that although the person can hear, understand and is mentally okay, they don't appear to respond much to the world around them. These problems may develop as much as a year after recovery. There may also be problems with swallowing or with vision - and long term behavioural disorders. But some people do manage to make a full recovery.
Could this be an auto-immune disease?
Many people believe that a virus or other type of infection may somehow be to blame but there is not yet good evidence of any particular organism.
Some researchers have suggested that it might be an auto-immune disease, where the body's immune system is triggered by a throat infection (perhaps with a streptococcus bacteria) to attack the nervous system. Research shows that areas of the brain called the mid-brain and basal ganglia become inflamed during the illness. But while anti-brain antibodies can be detected, no viruses have been found. This suggests that the syndrome is not caused by a virus directly entering and attacking the brain - so could it be that the body's own immune cells are attacking the nerve cells here?
Treatment targets symptoms
While the cause of encephalitis lethargica remains unknown it is difficult to give specific treatment or prevent the disease. So there is no cure for the condition. Instead treatment is targeted at supporting the person through their illness, and dealing with the symptoms as they come up.
In the early stages, treatment on the intensive care unit may be necessary to keep the person breathing, fed and protected from other infections, especially if they are in a coma. Steroid drugs may help to reduce inflammation in the brain and reduce symptoms.
As the person slowly recovers, physiotherapy, nutritional support and speech therapy may all help speed them on the path back to normal. They may also need psychological support to deal with emotional and behavioural problems.
http://www.bbc.co.uk/health/conditions/encephalitis_lethargica.shtml
Re: Rise of the New Plagues Continues
Post by bigbunny on Jul 29, 2004, 6:49am
Mystery of the forgotten plague
Just a few months ago, a paper was published, with very little fanfare, in an obscure medical journal.
But the contents of the paper were astonishing. In it was a potential solution to what has been called the biggest medical mystery of all time.
Two young doctors had tracked down the probable cause of one of the most baffling epidemics of the 20th Century - a disease called Encephalitis Lethargica.
Encaphilitis Lethargica was a devastating illness that swept the world in the 1920's.
It attacked the brain, leaving victims like living statues, speechless and motionless.
During the outbreak, nearly a million died, and millions more were left frozen inside their useless bodies, in institutions.
Noone knew what had caused it, or how to treat it.
Reppearance
For virologist Professor John Oxford, the disease was not just a disease of the past. As an expert on the condition, he was convinced that it could reappear.
"I certainly do think that whatever caused it could strike again. And until we know what caused it we won't be able to prevent it happening again."
And in 1993, it seemed his fears were being realised.
Becky Howells was 23 years old, when she suddenly became very ill. She started shaking, becoming feverish, hallucinating.
Within hours she had become critically ill and was rushed to hospital. Doctors had no idea what was wrong.
They knew her brain was dangerously inflamed, but had no idea what was causing it.
Her doctor Stavia Blunt said: "I was shocked by her appearance, stunned. She had these very bizarre clawing movements of her arms. It was weird."
Her father Tom prepared himself for the worst.
"I said goodbye. I said goodbye at the resuscitation unit, because I didn't think I'd see her again," he said.
Astonishing conclusion
As doctors battled to save her life they were forced to an incredible conclusion.
Becky was suffering from Encephalitis Lethargica - a disease that had last appeared over 70 years before. And it was just as baffling now as it was then.
Professor Oxford was convinced that the solution lay in the past. He tracked down brain tissue samples from the original 1920 victims and tested them, looking for traces of a virus that could have been responsible for the outbreak all those years ago.
At the time, an unusually severe strain of influenza, Spanish flu, had swept the world, and it seemed possible that both epidemics were linked.
But despite exhaustive testing with the latest molecular probes, there was no evidence of any virus - flu or anything else.
Becky gradually recovered, but it was two years before she could restart her life.
More cases
And Becky was not an isolated case. Since then more and more patients have been discovered. All suffering from the same bizarre symptoms.
Patricia Vaughan, was an energetic, active woman when she was struck down with the mysterious illness four years ago.
Sadly, she did not make a full recovery and now needs full time care from her partner, Geoff Shillington.
"It's very hard, because no-one can help you and you're just sitting there watching somebody going downhill, and you can't do a thing about it," he said.
At Great Ormond Street Hospital, one young doctor, Dr Russell Dale was alarmed that the disease was more common than he had ever realised.
He started tracking down other similar cases. Word got round the medical community and colleagues began referring their own cases to him.
Gradually he build up a case load of over 20 patients - all with Encephalitis lethargica.
At this stage, the disease was still a complete mystery. Noone had any idea what might be causing it - or, more worryingly, how to treat it.
Analysis
Together with a colleague, Dr Andrew Church, the two doctors began analysing all their patients to see if they had anything in common.
We realised we must be onto something
Dr Andrew Church
The first clue was that many of the patients had had a sore throat before they were struck down with the illness.
So the two doctors started looking for evidence of bacterial infection - and particularly streptococcus bacteria which is a common cause of sore throats.
"It was amazing really and very exciting, when the first results came back," said Dr Church.
"We got first one, then two, then ten...then all the patients had the same result. So we realised we must be onto something."
They had discovered evidence of a rare form of streptococcus bacteria in all their patients.
The bacteria that can cause a simple sore throat had mutated into a much more severe form and triggered the attacks of encaphilitis lethargica.
Immune reaction
It seems that in some people the body has a massive immune reaction to the streptococcus bacteria and then turns on the body itself; attacking the brain and destroying it.
It was an astonishing discovery. But that was not the full story.
Dr Church as keen to see if there was any evidence to suggest that this might also have been the cause of the 1920 epidemic all those years ago.
Dr Dale went back to the original medical records of the time. And as he pored over the reports, he discovered two very telling pieces of evidence.
First, many of the original victims had also presented with sore throats, and secondly, in the detail was a reference to a particular bacteria - diplococcus. Diplococcus is a form of streptococcus bacteria.
It was astonishing. There in the medical records was a description of a bacterial infection very similar to the one causing the modern cases of Encephalitis Lethargica.
For Dr Dale and Dr Church it was a very exciting moment. Not only had they identified the cause of the modern cases, they may have finally cracked an 80-year-old medical mystery.
# Medical Mysteries: The Forgotten Plague was broadcast on BBC One on 28 July at 2235 BST.
Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/health/3930727.stm
Published: 2004/07/27 23:34:13 GMT
© BBC MMIV
Re: Rise of the New Plagues Continues
Post by bigbunny on Jul 29, 2004, 7:22am
Cancer Spreads Like Wildfire In Iraq
BAGHDAD, July 28 (IslamOnline.net & News Agencies) – Cancer and birth defects have been spreading like wildfire in Iraq since the1991 US-led Gulf War, prompting doctors to describe them as the Iraqi version of flu.
Depleted uranium (DU) used by the United States and its allies against Iraq has taken its toll on around120 , 000to140 , 000Iraqis, according to the latest estimates released by the Iraqi health ministry.
With Iraq becoming an almost radioactive toxic wasteland, the number of birth defects and cancer-infected Iraqis is on the rise day in and day out due to the lingering effects of the deadly nuclear substance, the London-based Al-Quds Press news agency reported Tuesday, July27 .
Dr Abdul Kazimi, director of Baghdad only nuclear medicine hospital, said 7500 Iraqis are being infected with cancer ever year.
The substance is also blamed for the so-called Gulf War Syndrome, the still-unexplained malady that has reportedly plagued hundreds of thousands of Gulf War veterans.
Press reports say about100 , 000tons of DU munitions had been used in the Desert Storm military operation, the first time such a weapon was used in a warfare.
On January16 ,1991 , the US launched its allied Desert Storm military operation to liberate Kuwait.
The unprecedented US-led aerial bombardment and DU armor-piercing shells forced the Iraqi troops to desperately retreat from Kuwait on February 27 .
Aggravated
Abdul Hamid Khalifa, an Iraqi specialist on carcinogens, said the crippling 13 -year-old US sanctions slapped on Iraq after the war have made matters worse.
"It is a disaster in the broad sense of the word that has slipped out of control," he said.
"Cases of cancer-infected Iraqis started emerging following the 1991 Gulf War with most of the cases concentrating in the south and women taking the brunt."
The specialist added that infantry troops were identified as receiving the highest exposures to DU radiation.
He further said that contaminated water, expired imported food stuff and devastated health infrastructure added insult to injury.
Khalifa stressed that environmental pollution is causing 70 percent of cancer cases and food 30 percent.
Farras Abd, an Iraqi citizen whose uncle is a DU victim, said prayers are his one and only option.
"The hospital is running out of medicine and can’t cope with the increasing number of cancer patients, who can’t afford traveling abroad for treatment," he noted.
Deadly Substance
According to the United Nations Environmental Program (UNEP), depleted uranium is a highly dense metal that is the byproduct of the process during which fissionable uranium used to manufacture nuclear bombs and reactor fuel is separated from natural uranium.
Uranium, a weakly radioactive element, occurs naturally in soil and water everywhere on Earth, but mainly in trace quantities.
A second, potentially more serious hazard is created when a DU round hits its target.
As much as 70 percent of the projectile can burn up on impact, creating a firestorm of ceramic DU oxide particles.
The residue of this firestorm is an extremely fine ceramic uranium dust that can spread by the wind, inhaled and absorbed into the human body and absorbed by plants and animals, becoming part of the food chain.
Once lodged in the soil, the munitions can pollute the environment and create up to a hundredfold increase in uranium levels in ground water, according to the UNEP.
DU is said to be radioactive for about 4 thousand years.
http://www.islamonline.net/English/News/2004-07/28/article02.shtml
Re: Rise of the New Plagues Continues
Post by bigbunny on Jul 29, 2004, 7:23am
Depleted Uranium Possible Cause for Dead Fish in Kuwait
KUWAIT CITY, Aug 29 (IslamOnline & News Agencies) - The cause of the death of nearly a thousand tons of fish found since mid-August is a riddle which Kuwaiti and international environmental experts are currently working diligently to solve, news agencies reported Wednesday.
According to the BBC's online service, an official investigation in Kuwait has been unable to determine the reasons behind the dead fish washing up on its shores.
Environment officials have suggested that a heat wave, which has sent temperatures soaring to more than 50 degrees Celsius ( 122degrees Fahrenheit) in the shade, might be to blame.
Water temperatures in the Gulf have reportedly risen as high as 36 degrees Celsius (roughly 95 degrees Fahrenheit).
The Kuwaiti government responded to the sudden influx of dead fish by imposing a ban on fishing in Kuwaiti waters and setting up a committee to examine the issue.
But, the committee has admitted that they have been unable to determine the cause of the phenomenon.
"A thousand tons of dead fish have been found [since mid-August]," the committee headed by health minister Mohamed Ahmed Al-Jarallah said in a statement carried by the official Kuna news agency, said BBC.
On Monday, Al Qabas newspaper quoted an environmental expert as citing depleted Uranium (DU) as one of the possible causes for the marine tragedy.
Other possibilities include toxic waste or radioactive sediment.
During the Gulf War in1991 , NATO forces used DU in weapons used against Iraq in Operation Desert Storm, said a report published by UAE daily, Al Bayan.
This was also the case during air strike operations, which continued for 38 days between January17 th and February23 rd of that year. The amount of DU used exceeded 900 tons.
According to a report issued in April 1995 by the Environmental Policy Institute, the DU resulted in the formation of nearly three tons of dust containing DU particles, said the paper.
According to the report, the dust spread throughout southern Iraq and possibly into the Kuwaiti and Saudi Arabian regions that have common borders with Iraq, posing a threat to a great portion of the Gulf region.
An IslamOnline correspondent in Kuwait said that environmental experts in the country said, on the condition of anonymity, that DU is the cause of the catastrophe and that the Kuwaiti government is keeping it under wraps while seeking the help of U.S and British environmental specialists.
Meanwhile, the Iranian news agency, IRNA, reported Wednesday that environmentalists have rejected speculation that the great numbers of dead fish found on Kuwaiti shores could have been washed ashore by marine pollution affecting the Iranian side.
Upon the arrival of the Iranian research ship "Qods" in Kuwaiti waters, Iranian Charge d'Affaires to Kuwait, Reza Ameri, said that no evidence of fish dying in Iranian waters has been found, reported IRNA.
He told reporters that, as earlier announced, the dead fish were all found only on Kuwaiti shores, adding that environmentalists are now looking into a local cause that to explain the phenomenon.
In Iraq Tuesday, a team of World Health Organization (WHO) experts began work investigating whether Iraqis are suffering from increased levels of cancer and birth defects as a result of DU used in the Gulf War, and U.N. sanctions.
The six-member team arrived in Baghdad Monday night to meet Health Ministry officials and view documents supporting Iraq's claims.
http://www.islamonline.net/English/News/2001-08/30/article5.shtml
Re: Rise of the New Plagues Continues
Post by bigbunny on Jul 29, 2004, 7:24am
U.N. Mulls Depleted Uranium Probes In Bosnia, Yugoslavia, Iraq
VIENNA, Jan 26 (News Agencies) - Two U.N. agencies are considering sending missions to probe the impact of depleted uranium (DU) munitions used in conflicts in the Balkans and Iraq, a statement said Thursday.
The International Atomic Energy Agency (IAEA) and the U.N. Environment Program (UNEP) "have agreed to consider ways and means to respond to requests for fact-finding missions to Bosnia-Hercegovina, the Federal Republic of Yugoslavia and Iraq," said the joint statement by the two U.N. agencies.
Pekka Haavisto, UNEP pointman on the uranium problem, met with U.N. officials in Sarajevo Thursday and is to visit Belgrade on Friday to discuss the possibilities of missions, it said.
A UNEP-led mission went to Kosovo last year to assess the impact of DU munitions. "UNEP will wait for the scientific findings of the report of the Kosovo mission, expected to be released in early March, before it embarks on new DU field assessments," said the statement.
Fears about possible links between depleted uranium (DU) munitions used in the Balkans and a rash of cancers among personnel who served in the region erupted last month, initially after a number of cases were uncovered in Italy.
http://islam-online.net/English/News/2001-01/27/article11.shtml
Re: Rise of the New Plagues Continues
Post by bigbunny on Jul 31, 2004, 10:00pm
Synthetic Prions Created In Laboratory
By Philip Cohen
NewScientist.com
7-30-4
By Philip Cohen NewScientist.com 7-30-4 Ý In a breakthrough that could offer new ways to combat mad cow disease and related human brain disorders like vCJD, the infectious prions which trigger these diseases may have been synthesised in a laboratory for the first time.
Researchers have been trying - unsuccessfully - to create mammalian prions in a test tube every since Stanley Prusiner, a biochemist at the University of California, San Francisco, first theorised in 1982 that prions were infectious particles composed entirely of protein.
Now Prusiner's team reports tantalising evidence that they have been able to build a mammalian prion from scratch. When these synthetic prions were injected into the brains of mice, they triggered a prion disease that could be passed to other animals.
"The implications are huge and open up many new ways to study prions and gain new insights about prion disease," says Giuseppe Legname, a senior scientist in Prusiner's lab and one of the lead authors of the study.
"This is an exciting and fascinating initial experiment," says Byron Caughey, a prion researcher at the Rocky Mountain Laboratories in Hamilton, Montana. "But we're on new ground here. There are details that need to be worked out before it's clear this is definitive proof."
Corrupted shape
According to Prusiner's protein-only prion theory, BSE and related diseases occur when a protein called PrP found in healthy brains assumes a corrupted "prion" shape. The prion can then perform an odd sort of replication by coaxing healthy copies of PrP to flip into the diseased shape.
Folding purified PrP into the prion form in a test tube has been the holy grail of prion science because it seemed like the only way to silence all doubt that protein - and not some contaminating brain virus, for example - were actually responsible for BSE. Furthermore, being able to study prions in isolation would give new insights into how PrP folds into a prion and how to prevent or reverse the process to treat prion diseases.
The protein-only theory received a boost in 2000 with the discovery of other proteins from yeast that seem to form prions in a test tube (New Scientist print edition, 5 August 2000). But despite exhaustive efforts by many labs, no one had managed to perform the same trick with ordinary PrP.
Instead, Legname says his team used a smaller fragment of PrP that was believed to form prions more easily. And rather than inject the synthetic prion into ordinary mice, the researchers used animals that were genetically modified to produce the same PrP fragment at a level 16 times higher than normal, making them more susceptible to prion infection.
The PrP fragment was produced in bacteria, purified and then encouraged to form prion containing fibres known as amyloid.
Rigid tails
Control mice that received a brain injection without the lab-made prions did not develop prion disease after 670 days. But animals that received the synthetic prions started showing the wobbly gait, ungroomed fur and rigid tails that are the clinical signs of rodent prion disease after 380 days.
Extracts from the brains of those diseased animals were injected into normal mice which started getting sick after, on average, only 154 days. That suggested the starting number of synthetic prions was low, but improved after one cycle of replication in a mouse brain, says Legname.
The data suggests that PrP did form a prion in the test tube. But Caughey points out an alternative, though he admits, less likely explanation: the prions weren't created in the test tubes, but in brains of mice overproducing the protein.
If that is true, those prions must have replicated so slowly they do not normally kill the mouse, but the additional injection of PrP accelerated their replication. To eliminate this possibility, it will be necessary to show that brain extracts from uninjected mice never trigger prion disease even when injected into a new animal.
Legname says those experiments are already under way. Prusiner's team is also busy testing many PrP folding conditions to find ways to make prion formation in the laboratory much more efficient.
Journal reference: Science (vol 305, p 673)
© Copyright Reed Business Information Ltd. http://www.newscientist.com/news/news.jsp?id=ns99996219
Re: Rise of the New Plagues Continues
Post by bigbunny on Jul 31, 2004, 10:05pm
Swollen chest may indicate anthrax attack
12:24 30 July 04
NewScientist.com news service
An anthrax bioterror attack could be spotted early by emergency room doctors if they look out for a specific set of unusual symptoms outlined by a new study.
Identifying someone who has inhaled anthrax can be extremely difficult as the symptoms are similar to common acute respiratory infections like pneumonia. But now Demetrios Kyriacou at Northwestern University in Chicago, US, and colleagues have pinpointed a distinct group of symptoms.
"We found certain clinical characteristic symptoms and laboratory findings will help discriminate between inhaled anthrax and other respiratory diseases," says Kyriacou, research director for the department of emergency medicine at Northwestern. He says the most important pointers are seen on X-ray images - a swollen chest and fluid in the chest cavity.
Other symptoms include nausea, vomiting and altered mental state, such as confusion. "If a physician sees something like this, you should think the patient may have inhaled anthrax" he told New Scientist. "Or if you see two or three patients at the same time with these symptoms, you may be witnessing the very early cases of a bioterror anthrax attack."
Historical cases
"The early detection of an outbreak and the rapid identification of infected individuals within an exposed population would allow for a fast and effective response," notes Jeremy Mogridge, who studies the anthrax toxin at the University of Toronto, Canada.
"The intentional release of only one kilogramme of Bacillus anthracis spores could lead to the deaths of over 100,000 people in a city of 10 million," Mogridge writes in a commentary accompanying Kyriacou's research letter in The Lancet.
As cases of inhaled anthrax – through terrorism or other wise – are rare, Kyriacou and his team trawled through medical literature to find 47 historical cases.
These included 11 cases from the 2001 anthrax attacks in the US, as well as cases dating back to 1880. The researchers compared the clinical symptoms to 376 control patients who had community-acquired pneumonia or influenza-like illness (ILI).
Swollen nodes
Certain findings from chest X-rays were much more common in patients who had inhaled anthrax. They were nearly 23 times more likely to show fluid in the chest cavity and a widening of the mid-chest tissue, called mediastinal widening, than patients with ILI.
The mediastina is the white area on an X-ray which represents tissues and vessels of the mid-chest above the heart, just behind the breastbone. This includes the gullet, windpipe and the major arteries.
Kyriacou says this symptom would be rare in an otherwise healthy person who had recently caught a respiratory infection. Inhaled anthrax causes the mid chest to enlarge as it prompts the lymph nodes in that area – which house some immune cells - to respond rapidly and swell.
The other symptoms, nausea, vomiting and altered mental state, were also much more likely to be seen with inhaled anthrax than ILI. The team has developed an algorithm to help doctors distinguish inhaled anthrax from common ILI, which it has submitted for publication.
Journal reference: The Lancet (vol 364, p 449)
Shaoni Bhattacharya
Re: Rise of the New Plagues Continues
Post by bigbunny on Jul 31, 2004, 10:07pm
Source: University Of California, San Francisco
Date: 2004-07-30
URL: http://www.sciencedaily.com/releases/2004/07/040729192250.htm
Prion Finding Offers Insight Into Spontaneous Protein Diseases
UCSF scientists are reporting what they say is compelling evidence that the infectious agent known as prion is composed solely of protein. Their findings promise to create new tools for early diagnosis of prions causing bovine spongiform encephalopathy, or “mad cow” disease, in cattle and Creutzfeldt-Jakob disease in people, they say. The researchers believe that their work may also help advance investigations of more common neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis.
The finding is reported in the July 30 issue of Science.
In the study, the researchers created a large fragment of the normal prion protein -- a harmless protein found in all mammals examined. They then folded this fragment into the abnormal shape that they suspected would give it the infectious properties of the prion. Next, they injected the folded protein fragment into the brains of mice genetically engineered to over express the same fragment, but with the shape of the normal prion protein. After a year, the mice developed prion disease and brain tissue from the inoculated mice was injected into wild-type mice that subsequently developed prion disease in about half a year.
“Our study demonstrates that misfolding a particular segment of the normal prion protein is sufficient to transform the protein into infectious prions,” says the lead author of the study, Giuseppe Legname, PhD, UCSF assistant adjunct professor of neurology in the laboratory of the senior author, Stanley B. Prusiner, MD, UCSF professor of neurology and director of the UCSF Institute for Neurodegenerative Diseases.
“A great deal of evidence indicates that prions are composed only of protein, but this is the first time that this has been directly shown in mammals. The challenge in the last few years has been to figure out exactly how to demonstrate that prions are made entirely of protein.”
Spontaneous prion diseases
The discovery that a small change in the condition of a cell can cause the development of a prion offers an explanation, says Prusiner, for the sporadic form of Creutzfeldt Jakob disease (CJD), which is responsible for 85 percent of cases of prion disease in humans (occurring in 1 or 2 people per million) and is believed to develop spontaneously. It also supports his belief, he says, that sporadic forms of prion disease are caused by prion strains that are different from the one causing bovine spongiform encephalopathy (BSE) in cattle in Britain. He says he thinks that sporadic BSE will be found in one to five cattle per million and predicts such numbers will be found with increased testing for BSE.
“The finding represents a renaissance in prion biology,” says Prusiner. “For the first time, we can create prions in the test tube, which will change the way scientists do experiments in the field. We now have a tool for exploring the mechanism by which a protein can spontaneously fold into a shape that causes disease.”
More broadly, he says, the advance may lead to similar changes in the way studies are conducted for other neurodegenerative diseases that involve protein misprocessing, including Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis. Each disease involves a particular protein that undergoes some form of misprocessing, in terms of a shape change, metabolism or degradation, or proteolysis. At this point, it is not clear which of these forms of misprocessing occurs in each disease, says Prusiner. However, as in prion diseases, the misprocessing involves a profound conformational change that most often occurs spontaneously.
“The insights that scientists have made into the spontaneous misprocessing of prion proteins have already aided progress in studies of other neurodegenerative diseases,” says Prusiner. “But we hope that our new findings with synthetic prions will help scientists investigating other neurodegenerative diseases to move one step further in understanding how misprocessing is spontaneously initiated, and how it progresses.”
The production of synthetic prions is the latest milestone in the 30-year effort by UCSF scientists to move in on the biochemical composition of the elusive agent, which causes a variety of similar rare, fatal, brain-destroying diseases, including sporadic CJD and variant CJD, in humans, BSE, or “mad cow” disease, in cattle, scrapie in sheep, and like illnesses in deer, elk and mink. Prion’s fatal dance
The researchers have long maintained that a prion does not contain nucleic acid, the genetic material of life (DNA or RNA). Viruses, which have a nucleic acid core, replicate by high jacking the machinery of a cell and using it to synthesize more nucleic acid. In contrast, prions are an aberrant form of a normal protein (thus composed of amino acids) that form when a particular segment of normal prion protein in the brain’s nerve cells, or neurons, loses its corkscrew-shape structure (known as an alpha helix) and flattens into so-called beta sheets. They suspect that individual normal prion proteins (PrPC) occasionally misform in all people and relevant animals, but are routinely “cleared,” or removed, from brain cells. However, in rare cases, they suspect, the abnormal protein, or prion (PrPSc), is not cleared.
Once conversion occurs, they hypothesize, the prion moves on to other normal prion proteins, pinning and flattening their spirals, initiating a process that occurs repeatedly, akin to a deadly Virginia reel in the brain. The accumulation and aggregation of the flattened beta sheets leads to structural damage of the nerve cells, causing cell degradation that generally leads to death in less than a year. Prions can arise spontaneously, result from an inherited mutation in prion protein gene or develop through infection from an exogenous source.
When the protein-only theory was postulated by Prusiner, in 1982, it was met with skepticism. In subsequent years, the UCSF scientists and numerous other groups have reported substantial evidence to support the hypothesis, reflected in the fact that Prusiner was awarded the Lasker Prize, in 1994, and the Nobel Prize in Physiology or Medicine, in 1997, for the discovery “of prions - a new biological principal of infection,“ which he named prion (PREE-on), for proteinacious infectious protein. Still, despite the wealth of scientific studies producing evidence to support the theory, a direct, straightforward test the prion theory has eluded researchers until now.
Re: Rise of the New Plagues Continues
Post by bigbunny on Jul 31, 2004, 10:07pm
The goal has been to create a bonafide prion in the lab, which would be proven to be such by its ability to infect animals and cause a fatal illness. The challenge, says Prusiner, has been the inability to determine the details of the prion’s three-dimensional structure at the atomic level. “If we knew this,” he says, “we could have designed a physical assay that would tell us we are now making PrPSc in the test tube.”
The new study represents the latest tactic by Prusiner and his colleagues to get around this block: working from the belief that beta-sheet-rich structures harbor prion infectivity, but without knowing which segments are responsible, the team set out to create a synthetic agent made up of a subset of beta-sheet-rich structures that assemble into amyloid fibers, which they hypothesized might contain some prion infectivity.
The research
Following the strategy used to establish that a virus or bacterium is the cause of a particular infectious disease, UCSF scientists reported 20 years ago that prions purified from brains of rodents that were clumped into amyloid fibrils triggered disease when injected into the brains of healthy animals, and produced mad cow-like brain pathology.
Because prions are unprecedented, UCSF scientists wanted to go one step further and produce synthetic prions. The scientists chose to produce a fragment of the normal PrP in E. coli since bacteria are known not to carry prions. The fragment was chosen because it corresponds in length to the truncated PrP that assembles infectious amyloid fibrils when purified from infected brains.
After purifying the PrP fragment from E. coli, they altered its conformation so that it might become an infectious prion. They did this by taking the segment of the protein that they know has the capacity to form amyloid, and placing it in a shaking device to promote amyloid formation. They tracked the process with thioflavin T, a dye that fluoresces in the presence of amyloid.
After 40 hours, amyloid was detected. To accelerate the reaction time, the team then took some of these amyloid fibrils, and used them as a “seed” for the production of nascent amyloid fibrils in a second shaking tube. This time amyloid fibrils were detected after 10 hours. These were called “seeded” amyloid fibrils.
Then, to determine if the PrP fragment was infectious, the amyloid fibrils, either unseeded or seeded, were inoculated into transgenic mice making the normal version of the same PrP fragment. Importantly, the mice express truncated PrP at 16 times the level that PrP is normally made in wild-type mice. The over expression of the PrP fragment in these mice shortens the incubation times, which already approach the lifespan of mice. Prusiner and his colleagues also thought that if the truncated PrP expressed in the transgenic mice corresponded precisely to the PrP fragment produced in bacteria, this would provide the most sensitive system for detecting newly formed prions.
Notably, amyloid is a structure that, depending on the protein it contains, has been implicated in a number of brain diseases including Alzheimer’s and Parkinson’s diseases.
After about 300 days, with none of the transgenic mice sick, the researchers were ready to declare the study a failure. But then, at 380 days, one of the mice showed symptoms of a prion-like disease. Eventually, all of the inoculated mice showed neurologic disease, the last one 660 days after injection.
Prusiner and his colleagues then inoculated more transgenic as well as wild-type mice with brain extract prepared from one of the sick mice. The prions in the brain extract caused disease in about 150 days in the wild-type mice and in about 90 days in transgenic mice expressing full-length PrP.
In each case, on the primary passage, the scientists detected four hallmarks of prion disease – (1) clinical signs of neurologic dysfunction (ataxia, or loss of motor coordination, and rigidity), (2) neuropathologic changes in the brain (vacuolation, deposits of PrPSc and astrocytic gliosis), (3) resistance of PrPSc to breakdown by protease and (4) most importantly, serial transmission of prion infectivity to wild-type and other transgenic mice.
While the results strongly indicate that the subset of beta-sheet-rich structure represented by amyloid harbors prion infectivity, the scientists report that they have preliminary evidence that other beta-sheet-rich structures may also harbor prion infectivity. And they are interested in producing prion preparations that have much higher levels of prion infectivity than the two reported.
“Our findings gives us the opportunity to start exploring prions on a new level,” says Legname.
Co-authors of the study were Ilia V. Baskakov, PhD, who, at the time the study was started was a postdoctoral fellow in the UCSF Institute for Neurodegenerative Diseases (IND), and is now at University of Maryland in Baltimore; Hoang-Oanh B. Nguyen, a staff research assistant in the UCSF/IND; Detlev Riesner, professor of biochemistry at the Institut fur Physikalische Biologie, Heinrich-Heine Universitat, Dussedldorf, Germany; Fred E. Cohen, PhD, UCSF adjunct professor of pharmacology, and Stephen J. DeArmond, PhD, UCSF professor of pathology and neuropathology.
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 1, 2004, 11:12am
Can Non-Stick Make You Sick?
EPA Studying Whether Teflon Poses Health Risks
By Brian Ross, Rhonda Schwartz and Maddy Sauer
ABCNEWS.com
Nov. 14— For Bucky Bailey's parents, the 22-year-old's wedding day in August of this year was one they feared might never come, given how their son started life. Bucky was born in January of 1981 with only one nostril and a deformed right eye.
"The doctors told us not to get attached to him because he probably wouldn't make it through the night," Sue Bailey, Bucky's mother, told 20/20. "They didn't know what to say. … I mean, they had never seen a baby like this before. … I cried so many tears I couldn't cry another tear."
Today, two decades later, scarred from more than 30 surgeries, Bucky is coming forward and telling 20/20 he wants to know who or what is responsible for a life that has not been easy.
"I've never, ever felt normal. You can't feel normal when you walk outside and every single person looks at you. And it's not that look of 'he's famous' or 'he's rich,' " Bucky said. "It's that look of 'he's different.' You can see it in their eyes."
Chemicals Widely Detected in Blood
The Bailey family and others lay the blame at the place where Sue worked when she became pregnant with Bucky — the huge DuPont plant in Parkersburg, W.Va., where workers mix the chemicals for Teflon, the famed non-stick substance used on pots and pans.
Teflon, a product advertised as making life easy, is also used in a different form to keep stains off carpets and clothing. DuPont calls these products the housewives' best friend.
Teflon and the chemicals used in its production have grown into a $2 billion-a-year industry. This includes ammonium perfluorooctanoate, known as C-8, which has been linked to cancer, organ damage and other health effects in tests on laboratory animals.
The same chemical, C-8, was found not only in the blood of Sue Bailey when she became pregnant but, it turns out, is in the blood of virtually every American, in much smaller but still detectable levels. This discovery make this a story that reaches far beyond what happened in one small town in West Virginia.
"In retrospect, this may seem like one of the biggest, if not the biggest, mistakes the chemical industry has ever made," said Jane Houlihan, vice president for research at the Environmental Working Group, an activist organization.
"And how could they not be in our blood?" Houlihan said. "They're in such a huge range of consumer products. We're talking about Teflon, Stainmaster, Gore-tex, Silverstone. So if you buy clothing that's coated with Teflon or something else that protects it from dirt and stains, those chemicals can absorb directly through the skin."
Houlihan and her colleague, Kris Thayer, senior scientist at EWG, have been poring over 20 years of confidential DuPont papers and other industry documents on Teflon.
Highest C-8 Levels Found in Children
According to the Environmental Protection Agency, some of the highest C-8 levels were found in some of the children tested. Even DuPont says that it cannot rule out that Teflon-connected products, such as Stainmaster carpet treatment, give off the chemical, although at blood levels the company says are far too small to be a problem.
"We are confident when we say that the facts, the scientific facts, demonstrate that the material is perfectly safe to use," Uma Chowdhry, Dupont's vice president of research and development, told 20/20. Chowdhry is the DuPont executive chosen to defend Teflon, and she claims that the substance is completely safe, despite the fact that the key chemical, C-8, is in everyone's blood.
"We do not believe there are any adverse health effects," she said. "There are lots of chemicals that are present in our blood."
Now the unexpected discovery of the almost universal contamination of Americans' blood from C-8, combined with worrisome laboratory studies, has led to a high priority investigation by the EPA of the chemical's risks.
"It's a potential threat," said Houlihan. "And the EPA's moving fast in studying this. Human blood levels are too close to the levels that harm lab animals. That's why they're moving too fast."
The ‘Teflon Flu’
There is another more immediate health problem from Teflon, according to the Environmental Working Group. Cooking with Teflon can make a person sick with a temporary flu if a non-stick pan gets overheated.
"It feels like the flu," said Houlihan, "headaches, chills, backache, temperature between 100 and 104 degrees."
DuPont says that fumes are released from the pan when it is overheated, which they say occurs at temperatures that are not reached during normal cooking.
As the Environmental Working Group showed 20/20 in a kitchen demonstration, however, a pan can reach that temperature in just a few minutes.
"At 554 degrees Fahrenheit," said Houlihan, "studies show ultrafine particles start coming off the pan. These are tiny little particles that can embed deeply into the lungs."
The hotter the pan gets, the more chemicals are released. "At 680, toxic gases can begin to come off of heated Teflon," Houlihan said.
It turns out, DuPont has known about the "Teflon flu" for years.
"You get some fumes, yes," said Chowdhry, "and you get a flu-like symptom, which is reversible." Chowdhry said the flu is temporary and lasts at most for a couple of days. She also added that a warning about the flu, while not on the pans themselves, is on the DuPont Web site.
In the demonstration for 20/20, a piece of bacon was just getting crisp when the Teflon pan went beyond the initial warning point of 500 degrees.
"I've never cooked bacon," said Chowdhry. "I can't comment."
The Environmental Working Group has tried without success to get the government to order that warning labels be put on non-stick pans.
Bird Owners Beware
One consumer warning DuPont does issue about Teflon fumes involves not humans, but birds. The fumes from overheated Teflon pans can be lethal to them.
Shelby Greenman told 20/20 that her pet cockatoo keeled over in its cage down the hall from the kitchen after all the water boiled out of a Teflon pan.
"I didn't smell anything, I didn't see any smoke," she said. "As soon as they inhale it, it's over. There's nothing they can do to help them."
Bird owner groups say thousands of birds have been killed by Teflon fumes. DuPont says this occurs because birds have small and sensitive lungs.
"People should not have birds in an unventilated kitchen," said Chowdhry.
Long-Term Effects?
The greatest concern about C-8 is that it may cause possible long-term harm to a generation that has grown up using Teflon products. Scientists say that if there are any long-term effects, the first place they'd look for them would be in the people who have had the greatest exposure to the chemicals — the people who work, live and drink the water near the Teflon plant in West Virginia.
"With neighbors like DuPont, you don't need no enemies," said Earl Tennant, a local resident.
Now a lawsuit brought by local residents, including the family of Bucky Bailey, accuses DuPont of trying to cover up what the company knew about Teflon's risks.
"We have alleged in the lawsuit that DuPont has been well aware of these problems for many years," said Cincinnati attorney Robert A. Bilott, who filed the case.
Perhaps most telling is an internal DuPont document, only now made public, that shows the company knew that of eight women working on the Teflon line in 1981, two had children with birth defects — not just Sue Bailey, but a second mother whom 20/20 was able to locate.
Click here to see the company document on birth defects.
The other mother, Karen Robinson, gave birth to a son who also had a defect involving his eye. "DuPont should be held accountable for their actions in keeping all this secret from the public," Robinson told 20/20.
Now a grade school principal, Robinson said she only recently found out that she had an extremely high level of the Teflon chemical C-8 in her blood. She fears that her second child, a daughter, has also been affected.
"I gave birth to a daughter. Two years ago we discovered that she has a birth defect that affects her kidneys. One kidney did not grow. One kidney grew to three times its normal size," she said.
DuPont denies that it was trying to cover up what happened to the children of Karen Robinson and Sue Bailey. It says the reason that the company did not disclose the birth defect study to the government for 22 years was because there was nothing to connect the defects with the chemical C-8. DuPont continues to insist that Teflon and the chemicals used in it are safe for its workers to handle.
Chowdhry said that in the general population incidences of birth defects are "not uncommon."
"We have had scientists pore over the data. In the realm of scientific fact, this is not considered a statistically significant sample," she said. "All the other children were normal. And since then we have not seen a preponderance of birth defects."
Chowdhry acknowledged that DuPont has not done a subsequent study to examine birth defects among its workers.
More studies of Teflon chemicals are now happening, but Bucky and others wonder why it has taken so long. What happened to Bucky Bailey has become part of the federal government's high priority review of whether Teflon and its chemicals are safe.
"I have to think about if I want to have children or not. And I cannot put them through what I went through," Bucky said.
Pending its review, the EPA says it is not now advising consumers to stop using Teflon products. The results of the agency's review of the safety of C-8 and of Teflon-related products that may release it are expected in coming months.
http://abcnews.go.com/sections/2020/Living/Teflon_investigation_031114.html
For Web resources on the Teflon health debate:
http://abcnews.go.com/sections/2020/Living/Teflon_Internet_resources_031114.html
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 4, 2004, 6:11am
Dietary neurotoxin linked to Alzheimer's
22:00 02 August 04
Neurotoxins from blue-green algae present in certain foods or water can accumulate in proteins and might cause brain diseases like Alzheimer’s after many years, suggests a new study.
The latest research explains how a devastating neurodegenerative disease common on the remote Pacific island of Guam can still strike people down decades after they have left the island.
The disease, called amyotrophic lateral sclerosis/Parkinsonism dementia complex (ALS/PDC), has symptoms resembling those of both Parkinson’s and Alzheimer's disease. The brain damage it causes is similar to that found in Alzheimer’s patients.
The latest theory is that the islanders’ taste for flying foxes is to blame. A neurotoxin called BMAA found in the fruit of the cycads on which the flying foxes feed, is thought to become concentrated in the flying foxes' flesh. BMAA, in turn, is made by a blue-green alga, or cyanobacterium, that lives in the roots of the cycads (New Scientist print edition, 10 January).
But this theory does not explain everything. Many islanders who leave Guam develop ALS/PDC decades later. BMAA is a water-soluble chemical, which means the body should soon get rid of it. So how BMAA caused brain damage so long after exposure had puzzled scientists.
Now a team led by Paul Cox, director of the National Tropical Botanic Garden in Hawaii, has shown that that BMAA is sometimes incorporated into proteins in place of normal amino acids. BMAA’s structure was already known to resemble that of the amino acids that make up the proteins in our body.
Levels of this protein-bound form of BMAA in the cycad flour eaten by islanders, in the flesh of flying foxes and in the brains of ALS/PDC victims, are typically around a hundred times higher than that of the free form, the team found.
Protein tangles
This BMAA would slowly be released as proteins are broken down, Cox suggests. So for years after eating contaminated food, people’s brains would be exposed to low levels of the neurotoxin. What is more, the abnormal proteins containing BMAA could also damage the brain in several ways, for instance by binding together to form the protein tangles characteristic of both ALS/PDC and Alzheimer’s.
The study also raises intriguing new questions. As controls, about 20 brain samples from Canada were also tested for BMAA alongside the eight samples from Guam. As expected, no BMAA was found in the brain of the 13 Canadians who had not died from neurological diseases. But protein-bound BMAA was found in the brains of eight Canadian victims of Alzheimer’s disease.
Cox stresses that the study does not prove that BMAA plays a role in Alzheimer's or other brain diseases. “The sample size that we have studied is too small," he says.
Liver cancer
And it still has not been proven conclusively that BMAA is the cause of ALS/PDC on Guam, Cox adds. However, its presence in the brain could be a sign that people have been exposed to other, as-yet-unknown cyanobacterial toxins.
The idea is plausible, says cyanobacteria expert Hans Paerl of the University of North Carolina in Chapel Hill, US. Cyanobacteria are common in freshwaters and seas worldwide, and thrive in polluted, nutrient-rich waters. “Their influence is expanding as we nutrify the environment,” he says.
For example, in China there is growing evidence that cyanobacterial contamination of drinking water is to blame for the high rates of liver cancer in some regions, says Paerl. “We are just starting to put the pieces of the puzzle together.”
Journal reference: Proceedings of the National Academies of Sciences (DOI: 10.1073/pnas.0404926101)
Michael Le Page
http://www.newscientist.com/news/news.jsp?id=ns99996229
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 4, 2004, 6:54am
Schizophrenia Linked To Flu, Study Shows
Associated Press
8-3-4
CHICAGO -- A new study adds more evidence to a body of research that suggests the children of some women who get the flu while pregnant are at higher risk of developing schizophrenia.
The latest study examined the women's blood samples, which indicated that those who had the flu during the first half of pregnancy were three times more likely than non-infected women to have children who developed schizophrenia later in life, the researchers said.
They emphasized that the overall risks are still quite small. Only about 1 per cent of the U.S. population has schizophrenia and the results suggest that about 97 per cent of babies born to women who had the flu while pregnant will not develop schizophrenia.
Lead author Dr. Alan Brown theorized that the damage occurs only in a small number of genetically susceptible fetuses since most pregnant women with the flu end up with healthy children. He said more research is needed to confirm the link.
However, Dr. Robert Yolken, a Johns Hopkins University scientist who has long studied the role viruses may play in mental illness, said the latest findings along with previous evidence make it ìpretty clear that influenza infection during pregnancy is a risk factor, probably one of several risk factorsî for schizophrenia.
Dr. Yolken said the added knowledge might lead to interventions to help keep pregnant women healthy. Already, women who will be more than three months pregnant during the flu season are urged to get the flu shot.
Virtually all previous studies had relied on recollections from mothers of schizophrenics about flu exposure during pregnancy, or on evidence that mothers had been pregnant during flu outbreaks, Brown said.
By contrast, Dr. Brown and his colleagues were able to analyze blood samples taken decades earlier from pregnant women participating in a separate study. In the women's blood serum, the researchers measured levels of antibodies to strains of flu viruses that had been prevalent during 1959 through 1966, when the women were pregnant.
The study, which appears in August's Archives of General Psychiatry, is ìthus far the most robust evidenceî of the flu-schizophrenia connection, said Dr. Brown, a psychiatrist at New York Psychiatric Institute and Columbia University.
Compared with women who hadn't been infected, women with flu antibodies during the first half of pregnancy had a threefold risk of having children who developed schizophrenia. An even bigger, sevenfold risk occurred during the first trimester, a critical period for fetal development, though those results were less statistically certain because there were fewer first-trimester blood samples, Dr. Brown said.
The study involved 189 women ó 64 of whom had children who developed schizophrenia and 125 whose children did not.
The disease, among the most severe mental illnesses, typically involves delusions, hallucinations and disordered thinking. Schizophrenia usually first appears in adolescence or early adulthood.
It is thought to be caused by a combination of genetic and environmental factors, including obstetric complications during pregnancy; Dr. Brown said his research suggests that up to about 14 per cent of cases may be linked with prenatal exposure to influenza.
Other research has suggested infections other than flu might be involved, including measles and genital herpes during pregnancy, which may adversely affect the developing fetal brain.
Dr. Brown said he suspects that in the case of influenza, antibodies or proteins called cytokines produced by the mother's immune system in response to the infection pass through the placenta into the fetus and disrupt brain development.
http://www.theglobeandmail.com/servlet/story/RTGA
M.20040802.wskitz0802/BNStory/specialScienceandHealth/
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 4, 2004, 6:58am
AIDS Reduces African Life Expectancy To 33
By Elizabeth Davies
The Independent - UK
8-4-4
The Aids pandemic is ravaging countries in sub-Saharan Africa, drastically reducing life expectancy in some parts to less than 33 years, a new UN report said yesterday.
The devastating impact of the crisis can be seen most clearly in seven African countries, including Malawi and Mozambique, where babies born in 2002 are not expected to live past 40 years because of the prevalence of HIV. Children in Zambia, where 17 per cent of the population are infected with the virus, are predicted to live just 32 years. The seven countries have, between them, seen an average drop in life expectancy of 13.5 years since 1990, the UN human development report said.
"In all these countries, Aids is reversing the hard-won development gains of recent decades," said Elizabeth Lwanga, the deputy director of the United Nations Development Programme (UNDP) for Africa. "We need an unprecedented response to this crisis, which is taking a devastating toll on our communities."
With almost a quarter of its population infected with the virus, Zimbabwe has been the country most dramatically affected. Life expectancy there has plummeted from 57 years in 1990 to 34 in 2002.
In Swaziland, where one in three people between the ages of 15 and 49 are Aids sufferers, life expectancy has dropped by almost 20 years, and in Botswana, where the disease affects 37 per cent of the population, people can expect to live 16 years less now than in 1970.
Sub-Saharan Africa is home to just over 10 per cent of the world's population - and to almost two thirds of all people living with HIV. In 2003, an estimated three million people in the area became infected for the first time, while 2.2 million died. As a result, many of the countries are considerably poorer than they were a decade ago; 13 of them are virtually the first countries in the UNDP report's history to have suffered a reversal in living standards.
The UNDP administrator, Mark Malloch Brown, said that the virus caused such destruction because it affected all aspects of life. Those who fell victim to the disease left behind them countries struggling to cope with the loss of such a large proportion of the workforce.
"The Aids crisis cripples states at all levels, because the disease attacks people in their most productive years," said Mr Malloch Brown. "It tears apart the foundation of everything, from public administration and health care to family structures."
Mohga Kamal-Smith, a health policy adviser for Oxfam, pointed to the failure of the international community as one of the main reasons for the devastation. "As the epidemic spread, the donor contributions from richer countries went down," she said. "Hardly any of the governments have achieved the 0.7 per cent GDP contribution that they committed to."
The UNDP's annual report shows the drop in contributions from the highest-ranked countries in the list, particularly from Norway and the US.
The lead author of the report, Sakiko Fukada-Parr, acknowledged that the most afflicted countries face enormous problems but said she believed that solutions may be found.
"Aids is currently presenting a very basic problem in human development," she said. "But other countries, like Senegal and Brazil, have achieved partial success in fighting the disease, due to easily accessible medicine and all elements of the countries getting involved."
© 2004 Independent Digital (UK) Ltd http://news.independent.co.uk/world/africa/story.jsp?story=541516
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 4, 2004, 7:08am
Mad Cows Found In UK Born After Feed Ban
By Justin Huggler
United Press International
8-4-4
Mad cow disease has been detected in two English cows born years after protective safeguards were put in place, authorities announced Tuesday.
The cases raise questions about whether the safeguards, which banned the inclusion of infectious animal parts in cattle feed, were strictly followed. The U.S. government has relied on similar safeguards to protect U.S. herds and consumers.
In addition to posing a threat to herds, mad cow disease is also a concern to humans because people can contract a fatal brain disease called variant Creutzfeldt-Jakob disease from consuming infected beef products.
One of the infected cows was born in Devon in December 1999, 40 months after the feed ban was put in place in 1996 to prevent the spread of the deadly disease, the Department for Environment, Food and Rural Affairs said. The other case was born in Shropshire in February 1998, 19 months after the ban took effect.
The infected cows were slaughtered in June and July, but it was not confirmed they were infected until Monday.
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 8, 2004, 3:17am
Fears of vCJD timebomb revived
10:48 06 August 04
NewScientist.com news service
A “significant number” of people in the UK may be harbouring vCJD with no clinical symptoms, reveals the study of a new case. The work suggests the epidemic of the human form of mad cow disease may be far from over.
The second case of vCJD linked to a blood transfusion was announced by the UK department of health on 22 July. But investigations have now revealed that this person, who had no clinical symptoms and died from other causes, is the first case of vCJD to be found in the largest genetic subgroup of the population.
The discovery has major implications for the ultimate extent of the vCJD epidemic, as about 50 per cent of the UK population falls into this group.
“What this finding now indicates is that the largest genetic subgroup is susceptible to this infection,” warns James Ironside, director of the UK’s National CJD Surveillance Unit in Edinburgh, UK, and one of the study team. “From one case you can’t extrapolate too far but it seems that many of them are likely to be infected.”
This is because exposure to vCJD by eating infected beef was “likely to be widespread” in the late 1980s and early 1990s, he says. The 142 deaths seen in the UK so far have affected people in a smaller subgroup, who may have a shorter incubation time.
Person-to-person
The case is also ominous because it is the second believed to be acquired through a person-to-person blood transfusion. Furthermore, the donor had not developed any symptoms of vCJD at the time of donation, showing such people can still transmit the disease.
The first transfusion case was identified in December 2003 in the UK. The patient died from vCJD seven years after receiving a blood transfusion from a donor who also later died of the disease.
“I don’t want to be alarmist about this – but this really is an important case,” Ironside told New Scientist. “Firstly, it means this genotype is susceptible; secondly, it clearly means vCJD is being harboured; and thirdly, the illness was almost certainly acquired as a result of a blood transfusion.”
He says the “secondary transmission” via blood transfusion also raises the issue of transmission via surgical instruments. No known cases of vCJD have been transmitted this way, but Ironside notes: “Unfortunately, with this disease, if the worst can happen it apparently does.”
Common combination
In the latest case, the patient died from a non-neurological disorder five years after receiving blood from a donor who subsequently developed and died from vCJD. The patient was the one of 17 identified as having received blood from infected donors.
An autopsy revealed that the patient had the mutated prion proteins responsible for vCJD in the spleen, despite showing no symptoms of the devastating disease. These rogue proteins were not found in the brain, spinal cord, or tonsils.
Crucially, the patient is the first to have the commonest combination of genes for the normal prion protein. All vCJD deaths to date have occurred in people who have two identical genes – one each from their mother and father. But there is another version of the gene and the latest patient was “heterozygous”, i.e. they had one of each type.
Ironside says that because the number of vCJD cases peaked in 2000, “there was a view that may be this was the beginning of the end”. But the new case shows that heterozygous people may just be incubating the disease for longer.
That view is supported by studies of other similar diseases, like kuru in Papua New Guinea, which show that heterozygous people can incubate the diseases for a long time. “Incubation periods over several decades are not uncommon,” says Ironside.
Tonsil and appendix
Azra Ghani, an epidemiologist at Imperial College London, UK, who has been modelling the course of the vCJD epidemic agrees the discovery is of major importance. She estimates that if heterozygous people are similarly susceptible to those who are not, there might be a doubling of projected deaths.
Her group currently estimates 50 to 60 more cases in the UK by 2080, based on the numbers of real cases. However, she cautions that initial data from a survey of tonsil and appendix tissue suggests there may be 3800 more cases.
She also told New Scientist that the potential for blood transfusion to spread vCJD holds “greater uncertainty” as there are many unanswered questions: “How infectious is blood? What sort of dose would you need?”
Unquantifiable risk
The UK’s Department of Health stepped up its precautionary measures for blood transfusion in December 2003 and again after the second case was announced in July.
John Reid, the secretary of state for health, stressed the “small but unquantifiable risk” at that time. "People should continue to have a blood transfusion when it is really necessary. Any slight risk associated with receiving blood must be balanced against the significant risk of not receiving it,” he said.
Ironside stresses the urgent need for a blood test to detect vCJD. If many people are incubating the disease, he warns, “we have no means of detecting them preclinically”.
“We should take some comfort from that fact that we have not seen a huge mass of epidemics in humans,” he says. “But the idea that vCJD’s going away now cannot be considered to be the case.”
Journal reference: The Lancet (vol 364, p 527)
Shaoni Bhattacharya
http://www.newscientist.com/news/news.jsp?id=ns99996249
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 8, 2004, 4:17am
Lyme disease still No. 1 vector-borne illness
The number of cases of the tick-borne disease are increasing as people and animals continue on a collision course.
By Susan J. Landers, AMNews staff. Aug. 9, 2004.
Washington -- Scientists tracking ticks bearing pathogens employ many of the same techniques used by the crack team of Las Vegas crime scene investigators on the popular television series "CSI," with one important difference.
"Rather than determining whether a drop of blood found at the scene of the crime belongs to suspect A, B or C, we are looking to see if the DNA we extracted from a tick belongs to human pathogen A, B or C," said Richard Dryden, PhD, professor of biology at Washington and Jefferson College in Pennsylvania.
The pathogens he pursues are those that cause Lyme disease, babesiosis and human granulocytic ehrlichiosis, or HGE.
Lyme disease may have been bumped from the headlines by West Nile virus during the past few years, but it is still the most prevalent vector-borne disease in the United States.
The Centers for Disease Control and Prevention found there was a 40% increase in the incidence of Lyme disease, from 17,000 cases in 2001 to 23,763 cases 2002. Preliminary figures for 2003 -- totals have not yet been tallied -- forecast rates at a similar level.
Although the disease rarely causes death, the illness, especially if untreated, can be serious, resulting in facial palsy, meningitis or carditis.
Those bitten by an infected tick may also develop neurologic or joint abnormalities.
Dr. Dryden is beginning a four-year study funded by the CDC to help pinpoint areas in the Eastern United States where ticks are most heavily concentrated. The plan is for localities to take action to get rid of these "hot spots" and inform residents about their risk of contracting a tick-borne disease, said Dr. Dryden.
While all states except Hawaii, Montana and Oklahoma have reported cases of Lyme disease, the disease is most common in Northeast, mid-Atlantic and upper North Central states.
Ninety-five percent of cases were from Connecticut, Delaware, Maine, Maryland, Massachusetts, Minnesota, New Hampshire, New Jersey, New York, Pennsylvania, Rhode Island and Wisconsin.
While there are annual variations in the tick population, there has likely been a real increase in the number of cases, said Paul Mead, MD, a CDC medical epidemiologist.
Greater awareness of the disease and recognition of its characteristic bull's eye rash plus increased development of wooded areas inhabited by the deer and mice that are host to the ticks likely account for the boost in reported cases, said Michael Zimring, MD, director of the Center for Wilderness and Travel Medicine at Mercy Medical Center in Baltimore.
Covering up is key
Prevention is still the name of the game in efforts to control Lyme disease. "People have to wear long sleeves, slacks tucked into socks, light-colored clothes and an application of insect spray containing DEET," said Dr. Zimring. "And once you get out of the woods, take a shower and do tick checks with partners. It could be a lot of fun."
If ticks haven't settled in for longer than 24 hours, or some say 36 hours, it is less likely a person has contracted Lyme disease, said Dr. Zimring.
Dr. Dryden takes pride in the fact that neither he nor any of his tick-collecting team has contracted a tick-borne illness.
The team dresses entirely in white, looking more like house painters than tick hunters, to allow easy tick spotting. Every 15 minutes they check each other for the tiny arthropods.
"In addition, we have duct tape around the cuffs of our long-sleeved shirts and around our socks into which our pants are tucked," Dr. Dryden reported.
One of the ironies is that there are relatively few ticks in and around Washington and Jefferson College's south-central Pennsylvania location, so Dr. Dryden and his team have to travel to reach potential hot spots in their quest for the bacterium Borrelia burgdorferi, which causes Lyme disease.
He is also on the lookout for the hemoprotozoan parasites of the genus Babesia that causes babesiosis. The number of cases of that disease is in the hundreds rather than the thousands, but the disease can be deadly.
HGE, the third disease on Dr. Dryden's list, is a bacterial disease that was first described in 1994. Its symptoms are the same as those of babesiosis -- the seemingly common "flu-like symptoms."
http://www.ama-assn.org/amednews/2004/08/09/hlsc0809.htm
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 8, 2004, 4:19am
Bush-Meat Trade Breeds New HIV
By Amitabh Avasthi
NewScientist.com
8-5-4
NEW YORK -- The HIV virus has jumped from primates to people on at least seven separate occasions in recent history, not twice as is commonly thought.
And people in Cameroon are showing up with symptoms of HIV, but are testing negative for both the virus and its primate equivalent SIV, the virus from which HIV is thought to have evolved. That suggests that new strains of an HIV-like virus are circulating in wild animals and infecting people who eat them, sparking fears that such strains could fuel an already disastrous global HIV pandemic.
The warnings come from experts who gathered this week for the annual meeting of the Society for Conservation Biology at Columbia University, New York. They say that deforestation and the trade in bush meat are creating the ideal conditions for new diseases to emerge, as people have ever closer contact with exotic animals that harbour novel pathogens.
The conference reports follow the discovery earlier in 2004 that simian foamy virus, another disease that infects monkeys, has been found in bush-meat hunters and three different species of primates. As yet, it has not caused ill-effects, but it could mutate into something more insidious.
"Basically, this is a virus looking for a disease," says William Karesh, director of the World Conservation Society's field veterinary programme.
Small game
Despite those concerns, we still do not have a clear idea of how many wild animals are killed and eaten, David Wilkie, co-chair of the Bushmeat Crisis Task Force (BCTF), told the conference. He has carried out the first-ever survey of daily bush-meat consumption by rural communities in Gabon.
Over two years, he documented a flourishing, but previously unrecognised, informal trade in bush meat, where rural communities hunted and ate small game, having already caught most available primates. He thinks official studies of bush meat sold in markets account for only 40 per cent of the total bush meat eaten in the country.
"In the Congo basin alone, between one and five million metric tonnes of bush meat was consumed last year," says Heather Eves, head of the BCTF, a non-governmental organisation that monitors the trade.
And the dangers of eating such animals are real. The BCTF points out that SIV infection has now been reported in 26 different species of African nonhuman primates, many of which are hunted and sold as food.
Wake-up call
The bush-meat trade is not the only way new diseases could jump into humans. The trade in wildlife, both for agriculture and as pets, is a major global business estimated to be worth billions of dollars. In 2002 alone, for instance, over 38,000 mammals, 365,000 birds, two million reptiles, 49 million amphibians, and 216 million fish were imported into the US.
In 2003, monkeypox jumped from pet prairie dogs to their human masters. That "was just a gentle wake-up call," says Tonie Rocke, an epidemiologist with the US Geological Survey. Previously the disease had only been known to infect humans after bush-meat hunters ate red colobus monkeys.
The trade in exotic farmed meat also appears to have sparked an unusual outbreak of a common human parasite called Trichinella. In 2004, a farmed crocodile in Papua New Guinea was discovered with Trichinella, which was only thought to infect mammals, after being fed wild pig meat (Emerging Infectious Diseases, vol 10, p 1507).
In 1999, another farmed crocodile in Zimbabwe was similarly infected. "There is a strong chance that infected crocodiles may be in other countries, and could infect humans who eat them," says Edoardo Pozio, a parasitologist at Rome's institute of public health. People in Papua New Guinea who eat crocodile meat have already been found to have the parasite, which can cause fever, rashes, and respiratory and neurological problems in humans.
Rocke says there are few safeguards to prevent the spread of diseases through the wildlife trade, and is calling for stricter import and quarantine restrictions.
http://www.newscientist.com/news/news.jsp?id=ns99996239
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 8, 2004, 4:20am
Drug-Resistant Bacteria
Deaths On The Rise
'Hospitals Need To Be Prepared For Larger Outbreaks
Caused By This Organism And More Severe Disease'
By Sheryl Ubelacker
Canadian Press
8-5-4
TORONTO -- A bacterial agent commonly found in health-care settings has been blamed for the deaths of 100 patients in the last 18 months in a single Quebec hospital, says an infectious disease expert at the facility, who is calling for government action to forestall more outbreaks across the country.
Dr. Jacques Pepin says cases of Clostridium difficile at University Hospital in Sherbrooke have been steadily increasing. And the incidence among those most vulnerable to the disease - patients aged 65 and older - jumped 10-fold between 1991 and the end of 2003.
The infection has been blamed for killing 54 patients in 2003 and another 46 in the first six months of this year at the 683-bed hospital, said Dr. Pepin, lead author of a study in the Canadian Medical Association Journal.
Using patient records, the University of Sherbrooke researchers compiled cases of C. difficile and deaths from the infection over the last 14 years. They found the proportion of patients who died within 30 days of diagnosis soared to almost 14 per cent in 2001 from less than 5 per cent in 1991.
"A lot of these patients were quite elderly people and for some of them, they obviously died for other reasons," Dr. Pepin said Wednesday from Sherbrooke, explaining that many were being treated for other serious illnesses. "But ... in my opinion, the vast majority of these patients died directly of this infection."
Outbreaks of C. difficile have killed almost 90 patients at several hospitals in both Montreal and Calgary. And more recently, a patient died of the disease in a hospital in Newmarket, just north of Toronto. In June, Quebec's chief medical officer ordered hospitals to record all cases of the infection so the province can determine if the disease is actually on the rise.
C. difficile is a garden-variety bacterium in hospitals and usually poses no threat to healthy people. But it can become dangerous for hospital patients treated with antibiotics for other illnesses, such as pneumonia, because the drugs kill off so-called good bacteria in the intestinal tract, allowing C. difficile to flourish.
It then begins secreting a toxin, said Dr. Pepin. "And it is this toxin which starts producing the symptoms."
The most obvious symptom is diarrhea, which can be so severe that some patients lose too much fluid in their bodies and go into shock caused by plummeting blood pressure and then die, he said.
Dr. Pepin theorizes that the C. difficile mini-epidemics may be related to a greater number of older patients occupying hospital beds because of an aging population and the possibility that more virulent strains of the bacterium have developed, which produce more toxins.
"It used to be considered just something annoying. You'd get four or five loose stools a day ... and it wouldn't be that bad," said Dr. Pepin. "But what we've been seeing for the last couple of years is much more severe diarrhea. So if you have 15 or 20 bowel movements a day," the chance of it spreading from patient to patient is much greater.
As well, cuts in health-care dollars have meant many Canadian hospitals have not been renovated, making it more difficult to ensure sanitary conditions, he said, noting that in some Quebec hospitals, there can be 40 patients on a ward sharing one or two bathrooms.
"The result is that in some of these old buildings, the sanitary conditions are intolerable. I mean, it's indecent."
Dr. Pepin, noting that treating a single patient with C. difficile costs about $10,000, said funding is needed from the province to improve hospital infrastructure so the infection can be better controlled. But he also believes Ottawa must take a role as it did in helping to combat the SARS outbreaks last year that killed 44 Canadians - far fewer than have died from C. difficile.
"I think what would be needed at the federal level would be some research to look at better treatments and better infection-control measures," he said. "There is certainly a possibility that it might spread outside of Quebec. The potential for transmission is there."
While it is not mandatory to report cases of C. difficile to government agencies, Health Canada is helping to fund a study to determine how pervasive the disease has become in Canada.
Dr. Andrew Simor, head of microbiology at Sunnybrook and Women's College Health Sciences Centre, said the Toronto hospital is among about 20 or 25 across the country that will be taking part in the study beginning this fall.
A surveillance of C. difficile in 20 Canadian hospitals was done in 1997, said Dr. Simor, an infectious disease specialist. "But in view of the recent reports from Quebec and Montreal, as well as from other parts of the world, of increasing Clostridium difficile infection rates and also what appears to be an increasing severity of the disease, we thought it would be very important to repeat our previous study to see if there has been a change and what parts of the country are involved."
Besides the possibility of a more virulent strain, overuse of antibiotics in general and the two used specifically to treat C. difficile - metronidazole and vancomycin - may have contributed to strains that are also becoming drug-resistant, doctors say.
Until researchers can produce more effective treatments or a vaccine against the C. difficile toxin, the best strategy for controlling the disease in hospitals is strict infection-control measures - washing hands, using gloves and gowns, and maintaining sanitation - coupled with appropriate use of antibiotics, Dr. Simor said.
"I think all hospitals across the country need to be prepared for larger outbreaks caused by this organism and more severe disease," he said. "One thing we've learned about the spread of infectious disease is that none of us live in a protected, isolated environment.
"So a problem that appears in another country in the world or in a certain part of Canada, it's likely to be on our own doorstep sooner or later."
http://www.theglobeandmail.com/servlet/story/
RTGAM.20040804.winfec20804/BNStory/National/
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 13, 2004, 12:25pm
Rise In Dementia Deaths Linked To Environment
By Celia Hall
Medical Editor
The Telegraph - UK
8-13-4
The number of deaths related to dementia and other mental disorders has soared in 20 years, with serious implications for health services, patients and their families, a researcher said yesterday.
Deaths are occurring in younger age groups, said Colin Pritchard, of Southampton University medical school's mental health group, in the journal Public Health.
For example, deaths from dementia in men aged 55 to 64 increased by 29 per cent in England and Wales between 1979 and 1997.
Dementia deaths overall in England and Wales in the 45 to 74 age group rose from 1,116 in men in 1979 to 3,290 in 1997 and from 2,204 to 6,100 in women.
Prof Pritchard analysed deaths in several developed countries in two categories: mental disorder deaths, which includes illnesses such as dementia and Alzheimer's; and neurological disease deaths, including conditions such as motor neurone disease.
In the second category, the increases over the period were more marked in people aged 65 to 74. For men and women respectively, the increases in England and Wales were 14 per cent and 18 per cent.
Similar rises in both categories can be seen in across Europe, North America, Australia and Japan. They cannot simply be accounted for by people living longer.
Prof Pritchard said yesterday: "The first reason for these changes has to be environmental. There is no other logical reason for the increases in these diseases in people still in their sixties.
"One study in California, for example, has found a correlation between the use of pesticides and an increase in Parkinson's disease.
"On the human side, I am very concerned. There is nothing more harrowing for a person or their family when their humanity is eroded, which happens with these mental diseases that can leave the person as a husk of who they have been.
"This causes distress and anguish for the individual and for their family. We are going to need increasing numbers of care beds and there will be great pressure on the community services."
© Copyright of Telegraph Group Limited 2004.
http://www.telegraph.co.uk/news/main.jhtml?xml=/news/2
004/08/13/ndemen13.xml&sSheet=/news/2004/08/13/ixhome.html
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 14, 2004, 12:09am
vCJD continues to baffle scientists; teenagers disproportionately susceptible
That young people tend to eat more beef products is not enough to explain the strikingly high proportion of new-variant Creutzfeldt-Jacob disease cases among children and adolescents. An article published this week in BMC Infectious Diseases, shows that young people must also be more susceptible to vCJD infection because of their age.
New detailed estimates of the UK population's dietary exposure to bovine material according to age have recently become available. Pierre-Yves Boëlle and his colleagues from Assistance Publique Hôpitaux de Paris and Université Joseph Fourier, Grenoble plugged this information into a mathematical model that predicts the age distribution of vCJD cases.
"We found that exposure alone could not explain the young age of vCJD cases as seen in the UK," said Boëlle. "An additional effect of age-dependent susceptibility was required to fully account for the age of the vCJD cases."
If the researchers considered exposure to beef products as the only risk factor, the predicted age distribution did not fit well with the actual age distribution of the 137 reported cases. This model predicted that 48% of those with vCJD are over 40, whereas in reality only 10% of people affected by the disease fall into this age group.
The predicted distribution of cases was much closer to the actual age distribution if the researchers considered both exposure and an age-dependent susceptibility to the disease as risk factors. The susceptibility to vCJD was predicted to increase during childhood, peak during adolescence and decrease sharply afterwards.
With this model, 12% of cases were estimated to be in people over 40, and the predicted ages of people with the disease showed good agreement with the actual distribution of cases.
The researchers suggest that, "one possible explanation for the difference in susceptibility could be that the permeability of the intestinal barrier changes with age, as the number of Peyer's patches decrease." However, they stress that further research is needed, as this is a very unusual characteristic of an infectious disease.
###
This press release is based on the following article:
Epidemiological evidence of a higher susceptibility to vCJD in the young
PY Boëlle, JY Cesbron and AJ Valleron
BMC Infectious Diseases, 2004. 4:26
To be published Tuesday 10 August, 2004
Upon publication, this article will be available free of charge according to BMC Infectious Diseases' Open Access policy at http://www.biomedcentral.com/1471-2334/4/26
Please quote the journal in any stories you write, and link to the article if you are writing for the web.
###
For further information about this research, please contact Dr Pierre-Yves Boëlle by email at boelle@u444.jussieu.fr or by phone on: 33-149-283-226
Alternatively, or for more information about the journal or Open Access publishing, contact Gemma Bradley by email at press@biomedcentral.com or by phone on 44-207-631-9931
http://www.eurekalert.org/pub_releases/2004-08/bc-vct080904.php
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 14, 2004, 11:20am
Texas Man Dies From Flesh-Eating Bacteria
Aug 14, 8:42 AM (ET)
HOUSTON (AP) - A man has died from flesh-eating bacteria that entered his body through a minor cut on his leg.
Dr. Kenneth Dean Creamer, 52, died late Thursday in a Victoria hospital where he had been treated since July 17, two days after he was exposed to the saltwater bacteria vibrio vulnificus.
Creamer, a Houston dentist, apparently hurt himself July 15 when he slipped on a dock during a fishing trip. Within days, both Creamer's legs had to be amputated and he went into a coma, a hospital spokeswoman told the Houston Chronicle for its Saturday editions.
Creamer is the seventh vibrio-related death in Texas this year, according to the Texas Department of Health. The federal Centers for Disease Control said a typical year brings 16 vibrio-related deaths in the Gulf Coast states.
Health experts said the bacteria is common in the Gulf and most prevalent in coastal and bay waters in warmer months. The bacteria can be ingested in contaminated seafood or absorbed through skin wounds.
http://apnews.excite.com/article/20040814/D84F0HI00.html
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 15, 2004, 3:02am
Date: 11 Aug 2004 From: ProMED-mail
Source: ABC Local website [edited] http://abclocal.go.com/wabc/news/print_wabc_081104_rabies.html
By N.J. Burkett
Health officials on Long Island say they have their 1st known case of rabies in decades.
It was discovered in Brookville after a raccoon, killed by a dog, tested positive. And now as a precaution a family of 4 and the dog are undergoing a series of rabies vaccinations.
While rabies is common in other parts of the New York metropolitan area, here on Long Island it is practically unheard of. That's why county health officials are so concerned, and why worried residents jammed the health department's help lines with hundreds of calls on Wednesday.
County health officials are laying dozens of traps to determine if the outbreak is isolated, or widespread.
The health commissioner says the signs of rabies in an animal like a raccoon are unmistakable. Abby Greenberg, Nassau Co. Health Commissioner: "Circling, staggering, drooling, similar to seeing someone drunk."
Melissa Berman, neighbor: "They told us they're going to be setting up traps, all along the block, around the block, and around our houses. So, I had to keep my dog inside."
Long Island exterminator Shawn Love has been trapping raccoons for more than 20 years. He's convinced that if there's one rabid raccoon, there's bound to be more.
Shawn Love, Raccoon Exterminator: "A male raccoon travels almost 10 miles in a day. So I think they might find some more."
No one can remember a human case of rabies anywhere on Long Island. Now the county health commissioner is urging people to be extremely careful.
-- ProMED-mail promed@promedmail.org
[Hopefully the dog's rabies vaccine is up-to-date. Rabies is preventable by a vaccine in domestic animals. It is wise to vaccinate your pet even if you believe it will always remain indoors. It is a cheap precaution against a deadly disease for the pet owners as well as the pet.
When there is a possibility of exposure, it is standard procedure to provide pre-exposure rabies vaccine to the people and revaccinate the dog. However, it is important to note that raccoon distemper can be difficult to distinguish from rabies based on clinical signs alone.
Although other parts of New York have rabies, Long Island has mysteriously avoided the disease for years. That is no longer the case. - Mod.TG]
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 17, 2004, 5:58am
HPV May Cause
Prostate Cancer
By Celia Hall
Medical Editor
The Telegraph - UK
8-16-4
The virus responsible for cervical cancer in women is being investigated as a cause of the rising number of cases of prostate cancer in men.
Human papilloma virus (HPV), a sexually transmitted infection which causes more than 90 per cent of cervical cancers, is caught by men and women equally but there has been little research into HPV in men.
Tim Oliver, professor of medical oncology at Barts and The London School of Medicine and Dentistry, who is studying the possible link, said: "There is an almost religious conviction that HPV causes cervical cancer in women and it is clear that men and women are exposed to the virus equally. Yet there has not been much interest in HPV infection in men."
He also believes that increased levels of unprotected sex which began with the introduction of the Pill in the 1960s may account, in part, for the rise in prostate cancers 20 years later.
Prof Oliver's research, sponsored by the prostate cancer charity Orchid, has already revealed evidence of HPV in archive samples of prostate cancer tissue from the 1950s. Now he is planning a further trial which will look for HPV in prostate tissue taken at recent post mortem examinations.
The picture is complex because both HPV and prostate cancer are common. But Prof Oliver says evidence is emerging that infections of the prostate in young men may cause damage that predisposes them to cancer in later life.
"If this is the case and HPV is implicated, then the long-term goal would be the development of a male HPV vaccine programme in the future, which you would need to give to teenage boys," he said.
Dr Richard Sullivan, the head of clinical trials at Cancer Research UK, said the causes of prostate cancer needed to be understood in order to develop preventive methods.
There are more than 24,700 new cases of prostate cancer diagnosed in the UK every year, with the disease killing 10,000 men annually.
http://www.telegraph.co.uk/news/main.jhtml;sessionid=3RFTD
GNZG2XDVQFIQMGSM54AV
CBQWJVC?xml=/news/2004/08/16/nhpv16.xml&sSheet=
/news/2004/08/16/ixhome.html&secure
Refresh=true&_requestid=129880
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 17, 2004, 6:01am
An interesting view of the role of Prions:
Prions speed evolution
Helen Pearson
Sloppy proteins may help organisms adapt.
Prions, the twisted proteins usually linked to disease, could help organisms adapt to tough situations by subtly altering the proteins manufactured by a cell1. The discovery backs the idea that proteins as well as DNA are vital in driving evolution.
Prions are proteins that twist into one of two shapes. In mammals, one type of prion seems to be harmless in one form but is infectious in the other. It is thought to underlie mad cow disease and its human equivalent, variant Creutzfeldt-Jakob disease (vCJD).
But scientists studying yeast (Saccharomyces cerevisiae) have found that, in some cases, infectious prions may have an important role. In a colony of yeast cells, some cells carry the 'normal' type of the protein, whereas others harbour the infectious form, which accumulates into clumps and is passed from one cell to another.
Four years ago, Susan Lindquist and Heather True of the Whitehead Institute in Cambridge, Massachusetts, showed that this yeast prion can change the way that cells behave. In their infectious form, the prions sometimes helped the yeast to adapt, changing their rates of survival when they were grown in various nutrients or temperatures.
Now Lindquist and her colleagues have worked out how the prions do this. In its non-infectious form, the protein normally helps to read and convert the DNA code into other proteins. But in its infectious form, the prion stops working. This means that many proteins are manufactured slightly sloppily.
Evolutionary short-cut
The team believes that prions may therefore offer a speedy way for yeast to evolve, because those cells with the infectious prion churn out a whole range of slightly altered proteins. Normally this is bad news for the yeast, but when the cells find themselves in a tough spot, one or two of them may grow better in the new conditions as a result, and so help the colony to survive.
This mechanism may be important for helping yeast stay alive over the short term, says True. It gives the cells time to pick up the permanent genetic changes they need to survive, which are then passed on to subsequent generations.
The finding runs against the general assumption in evolution that when organisms adapt to a change in their environment, they do so by acquiring random mutations in their DNA.
"I think the whole concept is very important," says molecular biologist Michael Snyder at Yale University in New Haven, Connecticut. Other proteins in different organisms could do a similar thing, Snyder suggests, by subtly altering the shape or amount of proteins made. "We don't know how extensive this is," he says.
http://www.nature.com/news/2004/040816/full/040816-1.html
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 18, 2004, 10:41am
AIDS cluster raises concerns about resurgence
By Tina Susman
Staff Correspondent
August 18, 2004
Charlotte, N.C. -- It was a scientific discovery that no scientist wanted to make, an outbreak one likened to a looming genocide of young, black men.
In November 2002, North Carolina health officials began a new form of blood testing designed to catch HIV infection far sooner than standard screening, which often doesn't detect the virus for two or three months after it enters the body. They quickly found five HIV cases in people with infections so fresh they had tested negative in conventional screenings.
Surprisingly, two were black college students from the same small town, yet they didn't know each other.
"That got us to thinking there might be a problem," said Dr. Peter Leone, an AIDS researcher with the state Department of Health.
He and others began reviewing known HIV cases in North Carolina college men dating back to 2000. They were alarmed at what they found. In 2000, the number infected with HIV was six. In 2001, it was 19. By 2002 the number was 29. By the end of 2003, it had jumped to 84, and 73 of them -- 88 percent -- were black.
Interviews with the students uncovered a total of 119 HIV cases once their sexual contacts were added in, and indicated a network of sexual activity spanning two dozen colleges in six states and the District of Columbia.
"There has never been a description of a cluster of HIV cases among college students like this, ever," said Leone, who called the trend a "potential genocidal issue" affecting young black men.
"It's not a good foretelling of where HIV is moving," he said. "This is the next wave."
The numbers are indicative of the racial disparity involving the spread of AIDS in the United States, where blacks comprise 12 percent of the population but accounted for 54 percent of new HIV cases in 2002, according to the Centers for Disease Control and Prevention.
When new cases are concentrated in such a young population, as in North Carolina's college students, researchers say the numbers are particularly ominous because of the potential threat to the best and the brightest of America's young black men.
No single state's problem
"In Africa it has really wiped out a generation of educated young people," said Dr. David Jolly, an assistant professor in the Department of Health Education at North Carolina Central University in Raleigh, one of 11 Historically Black Colleges and Universities -- a consortium of colleges founded to educate African-Americans -- in the state. Jolly is also director of the counseling center at NCCU. "I don't know if that's where we're headed here, but I do think that this is not a North Carolina phenomenon. If it's happening here, it's probably happening in other states as well."
Researchers, educators and students are trying to determine what led to the spike and how to stop it, an effort that is forcing them to confront issues such as homosexuality and bisexuality that are often ignored or hushed up in the black community. In addition, it is highlighting some of the shortfalls of AIDS education programs, which blacks say for too long have presented the disease as one of older gay, white men.
"I ask people, 'How do you get AIDS,' and they say, 'Oh, by being gay,'" said DeMishea Charleston, 20, a student at Johnson C. Smith University in Charlotte, N.C., who teaches fellow students about HIV and AIDS. She is among 32 so-called peer educators at the school, which is in the system of historically black colleges.
Complexity of coming out
And few black college men feel comfortable admitting to being gay or bisexual, particularly in the conservative South, where Charleston said the church plays a prominent role in most African-Americans' lives.
"In the black community, you just don't come out and say things like that, things that you know the church is down on, that you know are going to be detrimental to your position in the community," said Charleston, herself deeply religious. In addition, counselors say coming out is more difficult for black men in a society where they already are marginalized for the color of their skin.
"I would surmise that if you were black, white, yellow, brown, purple, or pink with red dots, if you are in fact not sure of your orientation that's not something you're going to rush out and announce to the world, but particularly if you happen to be a minority kid," said Phyllis Gray of the state Health Department, who has been working to enhance HIV education among blacks.
In fact, 67 of the 73 infected black men told researchers they had sex with other men, but they did not consider themselves gay and did not think they were at risk of contracting HIV. Twenty-seven of those men said they also had sex with women, raising fears that the spike in HIV-positive black college men will spread to young black women.
Not everyone's convinced
The denial of one's homosexuality or bisexuality contributes to the spread of HIV in a number of ways. Those in denial are less likely to prepare themselves for a sexual encounter with another man by carrying condoms when they go to clubs or parties where gay men congregate, Leone said. If they have wives or girlfriends, they are less likely to use condoms for fear of arousing their female partner's suspicions. Additionally, if they consider AIDS a gay disease but don't call themselves gay, they convince themselves that they are immune to it regardless of how they behave. Teaching AIDS prevention is also hampered when men are in denial.
"If they did identify themselves as gay and if they belonged to organizations for gay men, you could do HIV education for them through those organizations," said Jolly. "But if they don't associate with gay organizations, it's harder to reach them."
Schools like Johnson C. Smith and North Carolina Central have beefed up their peer education programs in the wake of the findings. Among other things, they are increasing the number of student educators and counselors and planning free HIV testing for students. In addition, incoming freshmen who start classes Aug. 23 are being given hour-long classes dubbed HIV 101 that provide instruction in putting on condoms, and that debunk misconceptions about AIDS: that it can be spread by kissing, that you can tell by looking at someone if they are HIV-positive, that AIDS is no longer a lethal disease thanks to new drugs.
In North Carolina, where policy in public schools is to teach abstinence-only in place of sex education, student educators say such courses are crucial. "They don't really know what HIV is or how it's transmitted," said Elisha Washington, 20, a peer educator at Johnson C. Smith, who recalls explaining to one freshmen class how rapidly the virus could spread. "Their reaction was 'no way, that can't happen.'"
One of the most effective ways to reach students is by having HIV-infected students speak to them, something difficult to do given the stigma of not only being a gay black man, but a gay black man with HIV.
"Why would any reasonably rational, thinking individual want to come out and talk about something they are going through when society doesn't foster an environment that would encourage him to do so?" said Jonathan Perry, 27, a Johnson C. Smith senior who nevertheless disclosed in 2001 that he is gay and HIV-positive.
Perry said he was prompted to come out during a school discussion on AIDS, because rumors had spread that he had the disease. Perry wanted to make clear even though he carried the virus, he was not dying of AIDS.
While Perry said he has not been shunned by fellow students, he acknowledges that his own mother has been reluctant to accept him as either gay or HIV-positive. In addition, he and others acknowledge that so far, no other gay, HIV-positive college students in the state have joined him in going public.
At schools in the HBCU network, where women students far outnumber men, the HIV statistics have complicated male-female relationships. With so many of the infected men describing themselves as straight even while having sex with other men -- a practice known as being on the down low -- female students admit to a new wariness.
"You don't know if they're gay or straight," said Washingon. Carleston described herself as far more reluctant to date, and often skeptical and stand-offish when approached by male students.
One positive outcome of the frightening findings has been to open up discussion about HIV, AIDS, and sexual practices among young blacks, counselors and researchers say. North Carolina remains the only state to have studied AIDS among college students, though, raising concerns that the trend is spreading unchecked elsewhere.
http://www.newsday.com/news/nationworld/....y-top-headlines
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 19, 2004, 8:15am
Proof Mad Cow Prions Stick To, Remain In Certain Soils
University of Wisconsin-Madison
8-18-4
Dirt may help scientists answer a question that has baffled them for decades: How does chronic wasting disease (CWD) in deer and elk spread from animal to animal?
By turning to the land, University of Wisconsin-Madison researchers show that prions - infectious proteins considered to be at the root of the disease - literally stick to some soil types, suggesting that the landscape may serve as an environmental reservoir for the disease.
The findings will be discussed during a poster presentation on Wednesday, Sept. 10, in New York City at the 226th national meeting of the American Chemical Society.
Extraordinarily resistant to a range of environmental conditions and decontamination measures, prions are abnormally folded proteins that can make an animal,s brain as holey as a sponge. They,ve been implicated as the cause of diseases such as mad cow and scrapie in sheep.
Once infected, deer and elk, for example, experience a number of neurological and behavioral problems - staggering, shaking and excessive salivation, thirst and urination - until they waste away, many times dying in fields or woods. The disease is always fatal, and, to date, there is no cure.
Even though chronic wasting disease was first detected in free-ranging deer and elk in Colorado and Wyoming during the mid-1980s, it received a charge in scientific and public interest in February 2002, when the first evidence of the disease in Wisconsin appeared.
"The route by which CWD is transmitted from animal to animal is not understood," says Joel Pedersen, an environmental chemist and lead investigator on the soil study. "Strong circumstantial evidence suggests an environmental reservoir exists." Reports show, for instance, that healthy elk placed in pens where animals infected with CWD had once lived developed the fatal disease.
With funding from a recently awarded five-year, $2.4 million grant from the Department of Defense,s National Prion Research Program, Pedersen and his colleagues are examining the ability of the infectious agent to associate with or be absorbed by certain soil particles.
"Soil is a candidate [as an environmental reservoir] because grazing animals ingest it both inadvertently, as part of feeding, and on purpose, as part of certain deer behaviors," explains Pedersen.
To begin to understand how the disease stays in the environment, Pedersen and his colleagues turned to sand and clay - common components found in soils. Because of differences in surface area and mineral composition, Pedersen says sand and clay represent different ends of the spectrum in the ability to absorb proteins.
From the study,s results, the capacity of sand and clay to take up abnormally folded proteins, says the lead researcher, "differs dramatically."
Pedersen and his colleagues determined this by taking samples of sand and clay and adding infectious prions taken from hamsters, as well as a water-based solution representing one found naturally in soils. After removing the water and doing further analysis, they noticed that many of the prions in the sand mixture remained in the water solution, whereas those in the clay mixture stuck to the particles, surface.
"Almost all the prions in the clay mixture associated with the clay, not the water," says Pedersen, adding that this finding suggests that the movement of prions through the landscape depends on the soil environment.
Understanding how the infectious agent moves - or, in the case of soils with high clay concentrations, stays put - could lead to new information on disease transmission or techniques for managing CWD. For instance, Pedersen says, "If we decide to bury infected carcasses, a clay liner underneath the landfill may be a good idea."
But while clay soils may work to contain infection, they may also help spread it. Whereas prions in sandy soils either may wash away or travel deeper into the ground, says Pedersen, those in clay soils may remain near the surface. "Because the material may be more available for ingestion by animals," he explains, "the rate of infection may be greater."
Analyzing the absorption capacity of sand and clay is just the first step, says Pedersen. In addition to quantifying the ability of prions to bind to these two soil components, they,ll consider other soil materials, additional soil minerals and organic matter. Also under way are studies to determine the degree to which prions in different soil types remain infectious.
"What we,ll be getting at is if prions are more likely to persist in some environments," says Pedersen, adding that results from all these studies will help natural resource managers and other experts perform risk assessments for the spread of CWD and similar diseases across the landscape. "Understanding the role of soil in the spread of CWD is critical in designing and implementing effective disease strategies."
http://www.innovations-report.de/html/berich
te/biowissenschaften_chemie/bericht-21264.html
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 19, 2004, 8:15am
Can Mad Cow/CWD Prions Get Into The Water? - Yes
From Patricia Doyle, PhD
dr_p_doyle@hotmail.com
8-18-4
Hi Jeff, Here is some data on an extremely important aspect of prion transmission: contaminated water.
Patty
Note - As we know, the Brits killed and buried millions of cattle... and some of them had mad cow. As these bodies decompose, prions will enter the groundwater. But, even more amazing, is the use of cow bones in some UK municipal water filters! -ed
Researchers To Study Fate Of Prions In Wastewater
5-27-4
With funding from the U.S. Environmental Protection Agency, a group of UW-Madison researchers will investigate what happens if infectious prion proteins - considered the cause of chronic wasting disease and mad cow disease - enter wastewater treatment plants.
Joining UW-Madison scientists Judd Aiken and Joel Pedersen currently investigating the fate of prion proteins in soil and landfills, Katherine (Trina) McMahon and Craig Benson, both faculty members in civil and environmental engineering, will examine the ability of these infectious proteins to withstand the processes used to treat wastewater.
At most treatment plants, microorganisms decompose biodegradable material in the sewage and, in theory, should also disintegrate infectious proteins, says McMahon. But as she points out, prion proteins generally are very resistant to degradation.
"Prion proteins can be viewed as an environmental contaminant," says McMahon, adding that it currently is not known how long these proteins can remain intact and infectious in the environment.
"Prions have not been detected in wastewater entering treatment plants, but we can imagine several scenarios in which we may need to be concerned about the presence of prions in wastewater," she says.
During this one-year project, which is supported with a grant of nearly $100,000, McMahon and her co-investigators will focus on several questions, including what percentage of these proteins would be degraded during treatment and what percentage would be released back into the environment in treated water. If prions are released, the researchers will determine if the proteins remain infectious.
McMahon says answers to these questions will be of particular interest to the engineers of treatment plants receiving water from slaughterhouses or rendering facilities, as well as septic tank owners who dress deer and potentially wash infected tissue down the drain.
"The EPA," adds McMahon, "would like to know what the fate of prions would be in wastewater treatment plants to determine if they need to ensure that prions are excluded from waste streams entering these facilities."
http://www.sciencedaily.com/releases/2004/05/040526064629.htm
More Madness Over Cow bones In English Water Filters
By Dirk Beveridge
The Associated Press
After stirring up a ruckus with vegetarians by filtering water through charcoaled cattle bones, an English utility said Tuesday it's looking for less controversial ways to keep the supply clean. Yorkshire Water PLC said it would "continue to consult closely" with the vegetarians, while assuring the handful of affected rural customers that their water is safe.
"There is a whole vast array of treatment processes that are available," Yorkshire Water spokesman Richard Sears said. "All are not suitable for every water treatment plant."
Before the Vegetarian Society started complaining, the charcoal cow filters seemed perfect for remote areas of the Yorkshire moors, where water is frequently discolored by peaty minerals after a heavy rainfall. Yorkshire Water's filters are made from the brittle bones of sacred Indian cattle that live to an old age because of religious custom. Yorkshire Water has always said none of the infamous British "mad cows" were ever carbonized into the charcoal.
The utility said Tuesday that no good alternatives had immediately been found for the 11 small filtration plants that use the cow bones, but that it's still investigating -- without making any promises.
"We've got through the first hurdle," enthused Chris Dessent, a spokesman at the Vegetarian Society. "Yorkshire Water is admitting there is a problem."
The dispute gained new momentum in December when Yorkshire Water complained to advertising regulators about a one-time newspaper advertisement taken out by the vegetarian group showing a dead cow by a water well.
"In some parts of the world, dead cows can end up in the drinking water," the headline read. "In some parts of Yorkshire, they're put there."The message continued: "If you're a vegetarian, or wish to avoid meat, you'd think you'd be safe with a glass of ordinary tap water. Not in North Yorkshire."
Just 2,868 of Yorkshire Water's 4.5 million customers are affected. But it was an emotive appeal in a land where 6 percent of the 58 million residents are believed to be vegetarian and animal rights are a significant political issue.
The Advertising Standards Authority planned to issue a ruling Wednesday siding with Yorkshire Water on two out of three counts.The ruling, which carries no sanctions, finds the ad "offensive and distressing because of the gratuitous use of the headline and the photograph," and also "unfairly denigratory to Yorkshire Water.
"Despite that, the ad was not "misleading and irresponsible," as Yorkshire Water had contended, the ruling says. After the charcoaled cows made news last summer, Yorkshire Water had said it could not cater to the "individual dietary needs or individual religious, ethical or medical needs" of all customers.
(First published 4-8-98)
EPA Concern Over CJD Prions Entering The Water Supply
By Todd Hartman
Rocky Mountain News - Denver
The EPA is scrutinizing laboratory practices at the Colorado Division of Wildlife, worried that the infectious agents believed to cause chronic wasting disease could wash into public sewers and underground septic tanks.
Water regulators with the Environmental Protection Agency could require wildlife officials to alter plumbing at division laboratories in Fort Collins, Craig and elsewhere to ensure that the persistent protein - called a prion - doesn't accumulate in water supplies.
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 19, 2004, 8:15am
"The concern is that there's so little known about the prions, that we think we ought to be taking a relatively protective, conservative approach to things," said Steve Tuber, director of water programs for EPA's regional office in Denver. "We're just being careful." For the moment, the agencies are exchanging proposals on how to handle the matter. At the root of the problem: How to ensure tiny bits of tissue, or other possibly contaminated fluids or animal hair, don't make it through floor drains when laboratory areas are washed down.
The EPA hasn't been a visible player in the CWD problem - a fatal brain malady in deer and elk - until now.
The federal agency's timing could make things tough for the Division of Wildlife, as it gears up for a fall hunting season in which state workers are prepared to conduct up to 50,000 analyses on deer and elk heads to test for the presence of the disease.
"At this point, we're still in operation (for testing). We intend to be - we hope to be - all the way through hunting season," said John Smeltzer, a division supervisor. "If we need to modify our processes, we will do so."
With archery season under way for nearly a week and some rifle hunting allowed on private lands, about 100 heads - most of them elk - have been submitted to the state for CWD testing, said Division of Wildlife spokesman Todd Malmsbury.
Neither agency could say what the ultimate solution will be. The EPA has recommended a number of possibilities, including the use of absorbent paper on lab benches to soak up blood or other fluids. The division has pledged to come back with some ideas of its own, Tuber said.
Prions pose the same problem as some toxic and radioactive contaminants: They appear to have a long life and survive in the environment for at least a few years. Researchers have found that animals placed in long-empty pens once home to infected animals can acquire the disease, presumably because the prions remain viable in the soil.
In addition, prions are hard to destroy, resistant to extreme heat - up to 1,100 degrees - sunlight and many disinfectants. Agencies responsible for containing the spread of CWD have often incinerated deer and elk carcasses at very high temperature to ensure destruction of the prion.
There are no known cases of a human developing CWD. Nevertheless, scientists urge people to avoid eating meat from infected animals. A related ailment, mad cow disease, which strikes cattle, has made the leap into humans, killing more than 120 people overseas.
Tuber emphasized that the Division of Wildlife isn't disposing contaminated animal tissue "in any intentional way," but that the EPA is concerned with residue left behind. "They are taking precautions; we've asked them to take additional ones," Tuber said.
Of most immediate concern is a special EPA permit needed for a Fort Collins laboratory where parts of the brain, tonsils and lymph nodes are removed from deer and elk heads. When the lab is washed down, the rinse water flows to an underground septic tank. Under the law, the lab is considered an industrial discharger and is operating under temporary permission. But the EPA wants more steps taken before issuing a permit.
It will be several more weeks, after more detailed talks between EPA and Division of Wildlife scientists, before the agency will decide whether to grant a permit, Tuber said.
He said the EPA wanted to avoid interfering in the division's testing program.
"We want to give them an opportunity to keep that protection in place, and at the same time be protective of groundwater," Tuber said.
Also of concern is the division's laboratory in Craig, where rinse water is sent to a public wastewater treatment plant. The solution there could involve pre-treatment of some kind before the discharge can be released into the sewers, Tuber said.
Smeltzer said the division will work with the EPA, but believes it takes significant precautions already. He notes that very small amounts of tissue are handled in the labs - the brain samples extracted are about the size of two grains of rice, he said - and that workers frequently spray down work areas with a disinfectant known to be effective in neutralizing prions.
Tuber said the EPA also needs to look at processing plants, where deer and elk are carcasses are prepared. "It's something that we're just starting to get to," he said. (First published 9-6-2)
Patricia A. Doyle, PhD
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 19, 2004, 8:16am
An interesting proposition:
CWD/BSE - Escaped Bioweapons
From Patricia Doyle, PhD
dr_p_doyle@hotmail.com
8-19-4
I believe that Chronic Wasting Disease originated in the 1960s when the US military/UK Burroughs Wellcome took sheep TSE and were able to infect deer, thus causing the species jump. More than likely, the experiments in the UK entailed the use of cattle - taking sheep TSE and infecting cattle...ergo: BSE, Mad Cow in bovines and CWD in deer and elk.
At that time, researchers did not realize the ticking time bomb they had created with prion disease...because they thought it was a 'slow-virus.' As an agra-bioweapon, a slow virus would be extremely valuable. In other words, a slow virus would allow more time for more animals to be infected. In essence, they believed entire herds could be destroyed.
I think the UK and the US both had Japan's Unit 271 notes, boxcars full of them, and the research on Kuru probably intrigued the bioweaponeers. Of course, at the time when CWD originated in 1967, we were in the Cold War and wanted a thorough weapon to kill off Soviet livestock.
The UK, our ally, also desired a good weapon. Scrapie was virulent, quickly contracted and spread from sheep to sheep and necessitated complete herd euthanization. If one could cause cattle or other animals to contract scrapie, livestock damage would be thorough. Such agraterrorism, when developed by the US, was, of course, called 'defense.'
Little did the weaponeers know that they spawned a massive, deadly epidemic in the US, known as CWD, and in the UK as BSE/Mad Cow. I still haven't been able to find the time-line or time frame for UK bovine experimentation. It's very highly classified. I was surprised I found any information at all about the US experiments in Colorado. Amazingly, I did, and we posted it.
Speaking about bioweapons...the latest are tweaked viruses: West Nile-like Virus from the US to Japan, also WNV in Portugal and the UK.
If the cases occur in the US to Japan, etc, I expect the virus is NY 99 West Nile-LIKE Virus...it is NOT the same critter as the classic WNV from Europe and the Mideast.
Patty
Japan: Suspected 1st Human Case of West Nile Virus May Be Travel-related
Source: Kyodo News Online Fri 6 Aug 2004 [edited]
An Okinawan woman recently back from a trip to the United States is suspected of having contracted either West Nile virus or Japanese encephalitis virus, health ministry officials said Thu 5 Aug 2004. The National Institute of Infectious Diseases in Tokyo will investigate the cause of the disease, examining samples of the woman's blood and spinal fluid. The results of the investigation are expected to be released on Mon 9 Aug 2004 or later. If the woman, who is 42, tests positive for the West Nile virus, it will be Japan's 1st case of the disease.
Preliminary tests have detected [virus nucleic acid sequences] suspected to be those of West Nile virus or Japanese encephalitis virus. Establishing whether the virus is West Nile virus or Japanese encephalitis virus will take several more days. Both types of virus are carried by mosquitoes and have similar genetic make-up The symptoms of the diseases are also similar.
The woman was taken to hospital in Okinawa after suffering fever, headache, vomiting and drowsiness during her return flight from the United States on 31 Jul 2004, according to officials of the Tuberculosis and Infectious Diseases Control Division of the Health, Labor and Welfare Ministry. The woman traveled with her husband and son to California, Arizona, Washington, New York, Boston and Pennsylvania beginning on 17 Jun 2004. The woman has since left the hospital and is recovering, and her husband and son are healthy, the officials said.
The Ministry called for calm in Japan, even in the event that the case is confirmed to involve West Nile virus infection, saying West Nile virus does not transmit from person to person. Alarmed by a widespread outbreak of the virus in the United States and Canada, the Ministry decided last month to extend the period of banning blood donations from those returning to Japan from abroad as part of stepped-up efforts to contain West Nile virus, for which there is no vaccine.
About 80 percent of those who contract the virus develop no symptoms. Those who do develop symptoms, which include fever and headache, begin to experience them about 2 weeks after being infected. Serious cases, mainly in elderly people, include such symptoms of encephalitis as paralysis and impaired consciousness. During 2003, nearly 10 000 people suffered the disease worldwide and about 260 of them died.
http://home.kyodo.co.jp/all/display.jsp?an=20040806066
-- From Akira Goto Assistant Medical Director Daido Life Insurance Company dolphin@mail.ne.jp
[ProMED-mail thanks Narufumi Suganuma of Fukui Medical University School of Medicine and an anonymous Japanese correspondent for submitting similar reports of the same suspected case of imported West Nile virus fever. Confirmation of the diagnosis is awaited. West Nile virus and Japanese encephalitis virus (unlikely to have been contracted in the USA) are closely related viruses belonging to the Japanese encephalitis virus group of mosquito-borne flaviviruses. These viruses can be discriminated only by careful RT-PCR or serological tests. - Mod.CP]
Patricia A. Doyle, PhD
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 19, 2004, 8:22am
Source And Identification Of Prions
By Shadow
8-19-4
In the 1960s, Thomas Brock,a University of Wisconsin/Madison professor, was taking samples of thermophilic (heat tolerant) bacteria in Yellowstone National Park geyser pools when he discovered a stable, highly heat-resistant thermophile he named T. Aquaticus.
This organism survived in the near boiling temperatures at the mouth of the geysers, and exhibited unique enzymatic properties that were later determined to be invaluable to several industries. These included use in laboratory procedures such as Polymerase Chain Reaction (PCR). Another use was in the sucrose/fructose industry, as an enzyme to convert corn and grains to fructose, allowing the development of a multibillion dollar sweetener industry for many foods-such as carbonated soft drinks. Many industries also developed around this highly economical source of sucrose/fructose.
Thermophiles have several distinct characteristics that should be noted here. They are an ancient class of protein called Archaea, which are thought to be one of the first lifeforms on this planet. They are found in undersea thermal vents , in high temperature petroleum bearing rock strata, and possibly in the myriad of bacteria that make decomposition of organic life occur in nature post mortem. These are very stable protein strands, that are able to fold themselves up into impenetrably dense nodules, which then apparently secrete a metallic shell or casing (this may be part of the metabolic process of the protein, or a protective reaction to environmental conditions). Various thermophiles are able to bind copper, iron, and gold. The rapid enzymatic process exhibited by thermophiles seems to be connected to the presence of these metals, and accumulations of these trace metals in living tissue would be strongly indicative of the presence of these thermophilic proteins.
In the manufacturing process for sucrose/fructose, corn is steeped in a solution containing a concentration of thermophilic bacteria, which through their rapid and high temperature enzymatic reactions allow the efficient separation of corn into corn syrup-in this case, sucrose and fructose.
This product is then refined and used in commercial food applications. The residual material (corn mash, hulls, and such-these would contain enormous concentrations of these thermophiles) are also sold as commercial feed for cattle, poultry, and swine.
The group of apparently prion-related neural diseases such as CWD, CJD, Alzheimer's Disease, or Parkinson's disease seem to be related to the release of these thermophiles into the food chain. As it is widely known that these products are used as domestic animal and game feeds (deer bait, etc.) and since rodents and wild animals would have access to these feeds, the possible connection to the current epidemic of CWD observed in North America may also possibly be linked to this same source.
The excess iron or metals found in the brain tissue of Alzheimer's, Parkinson's and Huntington's disease patients may indicate high concentrations of these thermophiles in the neural tissue of these patients.
Since it has been determined by the scientific community that the prion proteins bind metals (in particular, copper and iron), and since the characteristics of extremophiles and prions are identical in very many aspects-enough to be considered identical.
There is very likely a connection between the dissemination of prions in the environment and their introduction into the food chain via the sucrose /fructose extraction industrial residue that is sold as commercial animal feeds, as well as a connection to the North American CWD epidemic.
Shadow
ConspiracyNewsNet.com
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 19, 2004, 8:23am
Unknown Prion Disease Killing Seattle Woman
"... neurosurgeons used some of the same instruments to operate on 12 other patients."
By Tracy Vedder
KOMO-TV Seattle
8-19-4
SEATTLE - Doctors at Harborview Medical Center are some of the best in the country, but now they are stumped. They've got a patient with a mystery disease.
The illness is not mad cow disease, even though it looks like it. And doctors are turning to scientists at the Centers for Disease Control for help.
Doctors know the woman who arrived at Harborview in July has some sort of fatal, brain-wasting disease. But they don't know exactly what it is. And that's critically important for other brain surgery patients who might have been exposed.
Harborview neurosurgeons took a brain biopsy -- a small piece of brain tissue -- from the woman in July. They hoped she had some type of treatable vascular disease and needed the biopsy for a diagnosis.
"Is this a bacterial disease? Is this vasculitis?" says Chief of Neurosurgery Dr. Rich Ellenbogen. "That's what we were looking for."
The initial test results were horrific. "The patient that we're talking about has an invariably fatal disease," says the head of Harborview's Neuro Pathology, Dr. Tom Montine.
Doctors don't know the exact disease, but they know it's in a family of always fatal diseases similar to mad cow and Creutzfeldt-Jakob.
Dr. Montine describes what happens, "the brain just starts to disappear, it literally just degenerates away."
The head of the Creutzfeldt-Jakob Foundation, Florence Kranitz, has seen people die from this disease. "It is dehumanizing, it is probably the most awful disease on the face of the earth."
What's even worse? Before Harborview got the results from the biopsy, neurosurgeons used some of the same instruments to operate on 12 other patients. And prions, believed to cause these diseases, are not killed by common sterilization.
"If you've ever seen anyone struggling with this disease or die of this disease," says Kranitz, "then you want to make sure that not even one person is exposed to it if it's preventable."
Harborview says it does twice the standard sterilization, using heat for twice as long and automatic washers. The standard method of sterilization if a hospital knows there is a risk of prions, is to soak the instruments in caustic solution of lye in addition to the other techniques.
That's what Harborview did once it confirmed the possibility that prions were present, but after surgery on 12 other patients.
Top experts in the country agree the risk of transmission at Harborview from one patient to another is very, very low. Harborview's Chief of Neurosurgery agrees, "I think the answer to that is miniscule, it is approaching zero."
Harborview has no plans at this time to notify those 12 brain surgery patients, because they're waiting for definitive word from the CDC as to the exact disease. That could be months away.
http://www.komotv.com/news/printstory.asp?id=32675
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 20, 2004, 4:46pm
Deadly Bird Flu Found In Pigs For First Time
8-20-4
BEIJING (AFP) -- China said it had made the first ever discovery of a deadly strain of bird flu in pigs, a development that could have ominous implications for efforts to restrict the disease's spread to humans.
Scientists detected the lethal H5N1 virus in pigs tested in 2003 and again in others this year, China National Avian Influenza Reference Laboratory director Chen Hualan told a conference.
United Nations health and agricultural officials said they had not been informed about the find by the Chinese government and were immediately seeking confirmation.
"A very important point is that in 2003 and 2004 we started finding this virus in pigs in different areas in China," Chen said in a presentation at the International Symposium on the Prevention and Control of SARS and Avian Flu.
"This is a rather dangerous signal in terms of public health."
The highly respected scientist later told journalists the H5N1 virus was discovered in pigs in southeast China's Fujian province in 2003 and in "another place" in 2004, but only in one farm.
"It is not just the first time it has been found in China but in the world," Chen said.
H5N1 is the most deadly strain of the bird flu virus and has killed 27 people across Asia this year.
The UN's World Health Organization (WHO) and Food and Agriculture Organization (FAO) said Chen's remarks were the first they had heard of the new development.
"I think it's something we've long warned can happen. I don't think we're shocked, but we need more details," said WHO spokesman Roy Wadia.
"If it's confirmed, it's a new chapter that's been written in the bird flu story."
Scientists have warned that if pigs are infected, the virus could mutate to a more lethal form that could spread more easily to humans because pigs are a "mixing vessel" in which viruses swap genes.
Until now H5N1 had been found only in poultry and while it was suspected to be carried by swine no cases in pigs had been officially reported, FAO officials said.
Thailand, Vietnam and China have all recently reported new cases of bird flu in poultry following outbreaks of the H5N1 virus earlier this year that led to the culling of millions of birds, devastating poultry industries.
Malaysia reported an outbreak earlier this week and was scrambling to contain it.
Chen Friday refused to provide more details. It was unclear whether she had been authorized to release the information or inadvertently revealed it.
"We probably should not talk about this anymore.... Don't report it. Once it's reported, it will make a lot of people really scared," she said.
Julie Hall, WHO's Beijing-based coordinator for communicable disease surveillance and response, urged China and other countries to be on alert and "think the worst case scenario".
"If the bird flu virus were to change significantly and be able to jump more easily from animals to humans, we would obviously be in a situation where we need to strengthen systems even further," Hall said.
Chen declined to say how China responded to the outbreak of H5N1 in pigs and whether any had been culled. She said no human infections had been detected.
The Ministry of Agriculture did not immediately comment.
The delayed announcement raised concerns China still may not be as forthcoming as it should be, despite promising to keep international health agencies well-informed after being criticized for covering up a SARS outbreak last year.
The FAO said it wanted to find out from Chen's lab -- the chief facility in China for bird flu -- whether the pigs were actually infected with the disease or whether they may have just been contaminated by material from birds in the same farm.
"If we found it in the nostril, a superficial part of the body, it would not be as significant. If we found it in an organ, say the lungs, (especially in a sick pig) that would be significant," said Juan Lubroth, senior officer for animal health in the FAO's infectious disease centre in Rome.
H5N1 is believed to have been found first in geese in southern China. The exact source and way it is transmitted to humans is still not known. No human vaccine is available.
http://story.news.yahoo.com/news?tmpl=story &u=/afp/20040820/hl_afp/health_flu_china_pigs
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 21, 2004, 11:14pm
Another aspect of the alleged global warming to be considered:
HK heat 'risks bacteria growth'
By Chris Hogg
BBC correspondent in Hong Kong
Environmentalists warn that densely built cities like Hong Kong could become breeding grounds for bacteria and viruses as temperatures rise.
Research from the city says global warming and rapid urbanisation will raise the temperature in the territory by 3.5 degrees over the next 100 years.
Scientists from Hong Kong Observatory suggest the annual number of hot days will double by the end of the century.
They say the forest of buildings in Hong Kong magnifies the heat effect.
Last week Hong Kong sweltered under a thick cloud of smog, caused by stagnant conditions and high temperatures.
Now comes a suggestion that global warming is set to make things far worse and the temperature will increase almost three times faster than it did over the past century.
Harvest concern
In the future, if the humidity and heat get worse, it will create favourable conditions for diseases to grow and spread.
Earlier this year, there was a warning that rising sea levels in the territory could cause flooding in years to come during typhoon surges, when the wind whips up huge waves.
Mainland China, Hong Kong's main food supplier, is expected to experience an even faster increase in temperature.
Environmentalists claim that harvest will suffer as a result, with the yields dropping by one tenth for each one-degree rise in temperature.
People should conserve power, they say.
The more they use their air conditioners, for example, the power they use will cause more carbon dioxide to be released into the atmosphere, adding to the "greenhouse effect" and heating up the city as a result.
Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/asia-pacific/3585536.stm
Published: 2004/08/21 10:21:30 GMT
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 24, 2004, 6:42am
At least 25 hippos die of mysterious disease in Uganda
http://www.terradaily.com/2004/040822103933.vbf3jbcs.html
KAMPALA (AFP) Aug 22, 2004
At least 25 hippopotami have died of a mysterious disease in Uganda's sprawling Queen Elizabeth National Park, authorities said Sunday.
"We have sent experts to get samples from the carcasses and live ones to investigate the cause of these strange deaths," the Uganda Wildlife Authority's executive director Arthur Mugisha told AFP by telephone.
He said the team includes veterinary doctors and officials from the agriculture ministry, adding that an EU-supported disease control programme was already on the ground to study the suspected soil-borne disease.
Mugisha said the deaths began late last month, when game officials found five dead hippos one day and three the next, which he said "was out of the ordinary."
He said the sampling would take nearly a week, followed by several days of diagnosis and analysis in the capital Kampala.
More than 10,000 flamingos died in a park in northern Tanzania in June and July, also from an unknown disease.
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 27, 2004, 8:14am
Which is the plague - polio or the WHO:
Africa 'faces new polio threat'
Africa could be on the verge of a major polio outbreak, the World Health Organization has warned.
Mali and Guinea have reported their first cases of the disease in five years. Three cases have also been reported in the Darfur region of Sudan.
The WHO had previously predicted that polio could be eradicated by the end of this year.
These latest cases are being blamed on problems vaccinating people in parts of Nigeria last year.
Islamic clerics in Kano state condemned immunisation campaigns as an American plot to make Muslim women infertile.
Unable to vaccinate in the region, the WHO tried to prevent polio spreading further by protecting people in neighbouring countries.
This is an extremely important development
Bruce Aylward,
Global Polio Eradication Initiative
However, Guinea and Mali were outside the ring of countries targeted by WHO and the United Nations Children's fund (UNICEF) in an immunisation campaign launched in February.
Ten African countries, which had previously eradicated the virus, have now reported new cases.
'Big implications'
Bruce Aylward, co-ordinator of the Global Polio Eradication Initiative, said the latest cases suggested efforts to contain the virus were not working.
"This is an extremely important development," he said. "Earlier this year, we had conducted a synchronised campaign in a group of countries around Nigeria and Niger.
"What we are seeing is the virus actually breaking beyond that into a second tier of countries - so very big implications."
The WHO is worried that a major polio outbreak could be around the corner. The high season for polio transmission begins in September.
Officials have drawn up plans to mount three vaccination campaigns in 22 African countries, over the next 12 months.
It's aimed at halting the present outbreak, and banishing polio from the continent forever.
But as yet there aren't enough funds to carry it out - US$50m is needed by the end of this year alone. There are also questions over whether people will accept the vaccination teams.
Kano leaders recently changed their stance and a four-day campaign took place. However, it is estimated that only 60% of children were brought forward, which is not enough to stem the virus.
Polio is a highly infectious disease caused by a virus, which invades the nervous system. It can cause total paralysis in a matter of hours.
The disease can strike at any age but mainly affects children under three years of age.
Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/health/3594694.stm
Published: 2004/08/24 13:33:53 GMT
© BBC MMIV
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 27, 2004, 8:37am
Bird Flu Spreading Faster Than Thought, WHO Warns
The Globe and Mail
8-23-4
BEIJING (AP) -- China denied assertions Monday that a deadly strain of bird flu that killed 27 people in Asia has been discovered in the country's pigs, as the World Health Organization warned the disease will take several years to contain.
A new outbreak of the virulent H5N1 strain of avian influenza in Malaysia and flare-ups in Thailand and Vietnam indicate that the disease may be entrenched in parts of Asia.
In addition, researchers in northeastern China said last week that they had found H5N1 in pigs ñ intensifying fears that the virus could mutate into a version that could lead to human-to-human infections.
China's Agricultural Ministry, however, said on its website Monday that the government has tested 1.1 million pigs and poultry and that the results ìshow that we do not have the H5N1 bird flu virus in pigs.î
Neither the Chinese lab nor the ministry explained what kind of tests were carried out on the pigs, which are genetically similar to humans.
Earlier this year, nasal swabs from pigs in Vietnam tested positive for bird flu, but more-conclusive blood tests later showed they were not infected.
The ministry said it had informed the WHO of the results.
The WHO office in Beijing had no immediate comment, but Shigeru Omi, the UN agency's director for the Western Pacific, said earlier Monday that the Chinese researchers' statements need to be examined carefully.
Mr. Omi told reporters in Penang, Malaysia, that the disease will keep popping up because it ìis circulating more widely than we expected among poultry.î
Containing it will take ìseveral years, at least,î said Mr. Omi, who was attending an anti-tobacco meeting overshadowed by bird flu.
He also urged the creation of a communicable-diseases surveillance system in Asia to respond quickly to diseases ñ such as SARS or H5N1 ñ that originate with animals.
Meanwhile, Malaysian Health Minister Chua Soi Lek said that a doctor and her three children had tested negative for avian flu. Three other patients with flu symptoms were discharged Sunday after they showed no sign of avian flu, Mr. Chua said.
"I must emphasize that until now that only chickens have avian flu, no humans are infected," he said.
Bird flu ravaged poultry flocks throughout Asia earlier this year and killed 27 people in Vietnam and Thailand. More than 100 million birds across 10 Asian countries died of the disease or were slaughtered.
In February, 17 million birds in the Fraser Valley in British Columbia were slaughtered in efforts to stamp out the disease.
© Copyright 2004 Bell Globemedia Publishing Inc. All Rights Reserved.
http://www.theglobeandmail.com/servlet/story/RTGA
M.20040823.wavian0823/BNStory/International/
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 27, 2004, 9:01am
Think Twice Before You Place That Call
By William Thomas
Investigative Journalist
8-24-4
Though intended for renovations, Chris Anderson would like all visitors to deposit their cellular phones in the cement mixer by his front door. This sounds excessive - until you step into Anderson s orchard, where the pegged needle of a shrieking electromagnetic radiation (EMR) meter placed beside a connected cell phone still shows significant exposure 100 feet away.
Much to the chagrin of this certified EMR-mitigation specialist, every day some 300 million cell phone users are reaching out and touching someone you love. Yourself, and anyone else within range of the microwaves emitted by your phone.
Mesmerized by magical gadgets, we have yet to count the costs of miniature radio transmitters that are transforming Marconi s invention into new possibilities for portable personal pollution. As entire nations reach for pocket communicators, the explosively emergent $40 billion a year mobile phone industry is poised to deliver a Wireless Revolution that over the next five years is expected to double the one billion people connected by telephone lines over the past century.
Silicon sensors are already calling to each other. Soon, countless communicating microchips embedded in everything from bumpers to brooms will be sending streams of encoded electrical energy through glass, steel, concrete, bone and flesh.
Exquisitely sensitive to subtle electromagnetic harmonies, human brains and bodies as intricate as galaxies depend on tiny electrical impulses to conduct complex life-processes -including the ability to read, recall and respond to these words. Acting as antennas, our anatomies just as easily tune into spurious signals from radio and microwave transmissions. Blake Levitt, author of Electromagnetic Fields, says that when it comes to cell phones, a worse frequency could not have been chosen for the human anatomy.
As cell phones conquer consumer minds and markets, researcher Carol Anne Patton notes that the brain reaches peak absorption in the UHF bands, right where cellular telecommunications operate. British military scientists have discovered that cell phone transmissions disrupt the brain sites for memory and learning, causing forgetfulness and sudden confusion. Other studies show that electromagnetic signals from cellular phones reduce the ability to concentrate, calculate and coordinate complicated activities such as driving a car. Startled by $4 billion a year in extra claims among cell phone-wielding drivers, North American insurers did a double-take that found simply juggling cell phones is not causing a 600% increase in accidents.'
Hands-free mobile speaker-phones cause even more crashes because they typically emit 10 times more brainwave interference than handheld units.
For all drivers dialing out, University of Toronto investigators report that the heightened probability of cracking up your car persists for up to 15-minutes after completing a call. That s comparable to the risk of crashing while driving dead drunk exclaims Dr. Chris Runball, chairman of the B.C. Medical Association s emergency medical services committee. Reeling from dial-a-collision costs, the government of British Columbia may join England, Spain, Israel, Switzerland and Brazil in banning the use of cell phones by drivers.
In New Zealand, cell phone towers are prohibited on school property because of possible health effects, but Health Canada regulations ignore the hidden hazards of cell-wrenching cell phones, which send pulsed signals through the skull in a process one expert likens to jackhammers on the brain.
One of a handful of licensed electricians who understand electromagnetic fields well enough to eliminate them from household wiring, McGinnis has been testing EMFs and collaborating with fellow testers and researchers for nearly a decade. In Victoria, where he has helped residents defeat six cell phone towers, there was dancing in the streets after Microcell Connexions withdrew its application to erect a microwave transmission tower against the Wishart Elementary School fence in the spring of 1998.
The cell phone's second-hand microwave and radio-frequency (RF) pollution pose invisible but significant risks to bystanders - particularly children riding in cars that transmit amplified cell phone signals through their steel structure. Reporting the conclusions of a 12-person British study team, scientist Sir William Stewart told London s Financial Times that children may be more vulnerable because of their developing nervous system, the greater absorption of energy in the tissues of the head and a longer lifetime of exposure.
Roger Coghill became a long-standing advocate for health warnings to be affixed to mobile phones after this biologist found that cell phone transmissions damage the ability of white blood cells to ward off infectious disease by disrupting the immune system s electromagnetic communications.
Dr. Neil Cherry has measured accelerated aging, increased cell death and cancers caused by radio frequency microwaves from cell phones and their relay towers. With the brain s electro-chemical communications repeatedly zapped by lightning-like cell phone pulses, this Ph.D. biophysicist warns that headaches, fatigue, lethargy, nausea, dizziness, depression, arteriosclerosis and even Alzheimer s can result from frequent or prolonged calls.
There is also a higher incidence of cardiac problems, Cherry comments, in terms of the timing function in hearts. You get more heart attacks and more heart disease, it has now been shown in many studies.
The biophysicist from Lincoln University in Christ Church, New Zealand has also found that cell phones can murderously modify moods. In brains and bodies seriously derailed by tiny imbalances in trace minerals and hormones, depression, suicide, anger, rage and violence can result when calcium and serotonin levels are disrupted by cell phone transmissions.
In 1995, mobile phone sales in North America exceeded the birth rate. Hired by the Cellular Telecommunications Industry Association to condone cell phones, public health scientist George Carlo found that tumors on the outside of the brain are more than doubled among cell phone callers - particularly on the right side of the head where cell phones are usually held. Carlo told ABC s 20/20 that cell phone causes genetic damage that leads to cancer.
Warning of the potential for a global health disaster, ABC recommended prudent avoidance of cell phones after finding that every cell phone they lab-tested exceeded the Federal Communication Commission s standards for EMF absorption rates. EMF researcher Dave Ashton cautioned 20/20 viewers that because cell phones constantly search for the nearest repeating tower, long-term damage comes from cell phones in the stand-by mode. cell phone shields and headsets cannot adequately address these problems, Ashton added.
Dr. Carlo later told London s Express newspaper that cell phones cause genetic damage following a dose-response curve. That is, the more a person uses a cell phone, the more cellular destruction and health risks they incur. Cell phone-confused cells can go crazy, Carlo cautioned. Experiments on captive animals show that this cumulative DNA damage is passed on to succeeding generations.
Addicted as we are to a culture of convenience, we forget how inconvenient it is to contract cancer. An Adelaide Hospital study confirmed Carlo s conclusions after finding B-cell lymphomas doubled in mice within 18 months of one-hour daily exposure to power densities experienced by a cell phone user. -B-cell lymphomas are implicated in 85% of all cancers.
Ready Or Not
As magazine-size cellular relay antennas hidden in church steeples and rooflines keep popping up just about everywhere, more and more communities are declaring their airspace a No Fry Zone. But in Canada, where cell phone towers come under federal jurisdiction, municipalities are only advisers to a process in which no permits are required to erect transmitter towers deemed necessary for national security.
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 27, 2004, 9:01am
Many more lives are involuntarily imperiled by non-emergency calls. Pat Irwin was working in a Colwood health food store when she noticed a truck unloading metal framework. The next morning, a new cell phone tower was ready to add its emissions to another BC Tel tower already operating down the street. There had been no announcement, no public hearings - just a quiet notification to the municipality that a tower was going up, literally overnight.
The intruder radiated for a month when Irwin felt her immunity dropping. She wondered if other changes in her energy and menstrual cycle were not from the moon or something that I ate.
Irwin also seemed more irritable after her central nervous switchboard began receiving round-the-clock cell phone calls. With cellular relay towers in Kansas and Oklahoma being shut down because they interfered with passing aircraft, Irwin sensed how the same transmissions plucked her own electrical circuitry, inflicting a chronic edginess that twangs human nerves. Sleep disorders, she learned, are common among people exposed to high levels of electromagnetic pollution.
After several other women in the same business centre reported similar symptoms, Irwin quit her job. I saw it as something that was there to stay and I d be daily exposed to it over a long period of time, she told Alive. All this stuff is what were playing with on a daily basis.
There is nothing safe about the new 1.9 gigahertz broadcasting frequency. Much like a boxer taking repeated blows to the head, rapidly pulsing cell phones signal permanent brain damage. A study by Dr. Peter Franch found unequivocally that cells are permanently damaged by cellular phone frequencies. This cellular damage, Franch noted, is maximized at low dosage - and inherited unchanged, from generation to generation.
Katharina Gustavss, a certified Building Biology consultant with 25 years experience, explains that CDMA s 217 Hz spikes are very close to the frequencies of human cell membranes. Gustavss accompanied a Microcell technician to the Colwood microwave relay tower Irwin and others had complained about. When he waved a spectrum analyzer, Gustavss checked the display and saw pretty scary energy spikes.
"What's that?", she asked the tech. I've never seen that before, he told her. It turned out that this cell phone tower tester only set his meter to an averaging mode. Switching to real time froze the readings at scary maximum output levels.
How dangerous are cell phones? The risk is extremely high, declares Dr. Cherry. There are 66 epidemiological studies showing that electromagnetic radiation across the spectrum increase brain tumors in human populations."
Cherry says that because cancer takes a decade to develop, it will be another 10 years before mobiles manifest a big bonanza in brain tumors. But he adds, we re already seeing acute effects that are noticed within minutes of using a cell phone.
After two minutes conversation, a cell phone s digitized impulses disable the safety barrier that isolates the brain from destructive proteins and poisons in the blood. Professor Leif Salford, the neurologist who carried out the research for this finding, informed the Daily Mail: It seems that molecules such as proteins and toxins can pass out of the blood, while the phone is switched on, and enter the brain. We need to bear in mind diseases such as MS and Alzheimer s which are linked to proteins being found in the brain.
Dancing With The Telecomonster
If you must pack a cell phone, treat it like a loaded pistol. Keep it turned off. Don t carry it near ovaries, testicles, or the heart. For partial protection, buy an antenna shield. Limit calls to one-minute, six to 10 minutes a month. Never fire off a cell phone with children anywhere in sight.
When it comes to cells, consciousness and cell phones, every call is collect. How can convenience count more than cancer? What is gained by being in constant contact with disembodied voices, while being out of touch with the friends and neighbours immediately around us? Are we comfortable having our location continually traced by monitoring authorities?
Unless we start voting with our wallets, consumer complacency could prove as species-limiting as corporate cynicism. Microwave frequencies are the same as those used in radar and your microwave oven, says Florida cell phone tower opponent Joe Chwick. You wouldn't think of sticking your head in the oven, but there is no hesitation to putting the cell phone to your ear
Having somehow survived three-million years of evolution without them, many contemporary hominids claim they cannot live without them. But -can exquisitely sensitive electromagnetic beings live with cell phones -and the towers their signals ride in on? Like polyethylene food and water containers, plastic cookers and coffee-makers, microwave ovens and petroleum powered vehicles, cell phones could be one of those brilliantly beguiling inventions we have to let go. Would hanging up on such an intrusive and hazardous addiction be so terrible?
On Jan. 1, 2001 I cancelled my cell phone service
Originally published in Alive magazine
NOTES
For a fee, an electrical engineer has about five different types of meters, including very effective gaussmeters, to measure these fields. The most expensive meters have the most accurate measurements. These can cost thousands of dollars, so it is best to hire an engineer who has them already.
We returned our new laptop*, as the field with 18" of the screen was horrendous. The fields from satellites/cell phones and satellites/computers have been causing documented brain tumors for 20 years.
Laptops fields can be measured; there's a significant difference between models.
Don't ever stick your face within 10 inches of the screen for longer than a couple minutes, the field does start to substantially diminish about 20 inches from the screen on some models - for others, the field is a thick, heavy, and three feet deep of detrimental EMF, so that would drape your head and chest in the field.
http://www.emraa.org.au/rf/icnirpguideline.htm#top
http://www.buergerwelle.de/bodyscience.html
All of the articles on this site are good to skim through
http://www.igwl.de/pdf/MOBILFUN/KLAGENG.PDF
http://omega.twoday.net/stories/230816/
The aptness of Russia for a launch of "World Without Waves"
We and many scientists believe digital phones are far more dangerous than analog phones because the signals are pulsed at much higher mirowave frequencies and laboratory studies have shown that pulsed radiation is more damaging to biological tissue than steady state radiation (Analog). as found with the Dr. Henry Lai reports of DNA single and double strand breaks, at lower then most cell phone power levels, using the RF frequencies of newer digital cell phones. The Lai Studies results were or are repeatable as done in DNA.
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 29, 2004, 8:07am
'Rare' gut disease rates soaring
A gut disorder, thought to affect a small number of patients, is becoming much more common, US researchers warn.
Rates of the disease rose so much in recent years that they now rival better- known gut problems such as Crohn's disease.
But because eosinophilic oesophagitis is relatively unheard of, patients can wait years for a diagnosis.
The Cincinnati Hospital scientists' concerns are published in New England Journal of Medicine.
On the up
Lead author Dr Marc Rothenberg said: "There is so little information about the disease that patients often suffer for a number of years before a diagnosis is made."
His team looked for evidence of EE in tissue samples taken from patients at the Cincinnati Children's Hospital coming in with gullet problems.
The condition may have been there for some time but we have not been looking for it.
Dr Alan Ireland, consultant gastroenterologist at the Royal Sussex Hospital
Over a period of about 12 years they found 315 patients with evidence of EE in their tissue samples.
Only 2.8% of these were found before 2000, which the researchers said suggested the disease had become more common in the later years.
Rates of EE have not been reported in other regions so it is hard to estimate what the national rate might be, they said.
But if the rates are the same as this elsewhere, the annual occurrence would be one in every 10,000 children.
Poorly recognised
This would put it on the same level as the well-recognised gut problem Crohn's disease.
"Despite this, there is a current paucity of information about EE and many practitioners have not recognised its prevalence," they said.
EE causes similar symptoms to reflux disease - vomiting and difficulty with swallowing food - but does not respond to the same treatments.
Scientists do not know what causes this disease of the gullet or oesophagus.
They believe it might be related to some type of allergy because it is characterised by severely elevated levels of eosinophils which are a type of white blood cell involved in inflammation and allergic responses.
Dr Rothenberg and colleagues found EE appeared to run in families suggesting there might be some genetic trend that could be studied.
Dr Alan Ireland, consultant gastroenterologist at the Royal Sussex Hospital, said others had started to report this disease too.
He said this might be a true increase in the disease or simply down to more reporting.
"The condition may have been there for some time but we have not been looking for it," he said, but agreed it was an under-recognised condition in the UK.
Treatable
Mr Steve Attwood, consultant surgeon at North Tyneside General Hospital who has carried out research on EE in adults, said: "I'm sure it's more common than people identify."
He said patients with this condition often had to "go round the houses" seeing different doctors and having different examinations that don't reveal the problem.
"The patient is still suffering and they are treated as if there is something wrong with their mind rather than their body. It can be very frustrating for the patients."
He said anyone with problems with their swallowing who has been thoroughly investigated but has had normal test results should ask their doctor if a sample of their gullet lining has been taken to check for EE.
He emphasised that the condition was not life threatening and was treatable with drugs.
Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/health/3598924.stm
Published: 2004/08/29 02:39:23 GMT
© BBC MMIV
Re: Rise of the New Plagues Continues
Post by bigbunny on Aug 31, 2004, 8:38am
1000s Of Brits To Be Warned Of Possible vCJD Infection
By Liam McDougall
Health Correspondent
The Sunday Herald
8-29-4
Thousands of people who received blood products prior to 1999 are to be warned they may be incubating variant Creutzfeldt-Jakob Disease (vCJD), the human form of mad cow disease.
Health chiefs are to take the unprecedented step of writing to all those patients who received the blood from donors who subsequently died from the brain-wasting disease.
The move, ordered by the department of health in England, is the strongest sign yet that ministers are preparing for a new epidemic of the disease spread through blood.
Until now, they have always maintained that infection through a transfusion is a "theoretical risk".
The letters are to be sent out to patients, including hundreds of Scots, at the end of September after the Health Protection Agency carried out a risk assessment on UK patients who received blood or plasma products, prior to all plasma being sourced from the US in 1999.
It is understood the letters will urge each patient to contact a specialist. The vCJD risk assessment, first announced by Westminster Health Secretary John Reid in December last year, was ordered at the time as a precautionary measure after a patient who had received a trans fusion from someone with vCJD also died of the disease.
Although the donor showed no signs of the condition when they gave blood in 1996, they developed the disease in 1999 and subsequently died from vCJD. The recipient of the blood died in the autumn of 2003 and at a post-mortem vCJD was found in their brain.
On December 17 last year Reid told the Commons that the case was "not a proven causal connection" but that "the possibility of this being transfusion-related cannot be discounted". It was the first report in the world to warn of the possible transmission of vCJD from person to person via blood.
In March he banned blood donations from anyone who had received a transfusion since 1980 to prevent vCJD being spread.
The department of health last night refused to reveal the outcome of the risk assessment, but it is understood that behind-the-scenes talks have been ongoing with senior health officials and groups such as the Haemophilia Society about the potential outcome of the exercise.
Other categories of patients, such as those with leukaemia, burns victims and pregnant women, can all be treated with blood products. But those most exposed are likely to be haemophilacs who use the products to help their blood to clot.
The latest figures from the National CJD Surveillance Unit in Edinburgh show the number of deaths in the UK definitely or probably caused by vCJD now stands at 147. However, news of the department of health move has fuelled fears of a new epidemic of vCJD, the human form of BSE, from blood.
Bruce Norval, a haemophiliac from Fortrose, near Inverness, said: "It's very possible that we will have a secondary epidemic via blood from the initial victims who contracted vCJD by eating infected beef."
Scientists have estimated that almost 4000 people could be harbouring vCJD, based on studies of appendix samples.
A Department of Health spokeswoman said: "We have asked the HPA to lead on preparations for notifying patients who have received plasma products, and we have been working with the agency, clinicians' representatives and patient groups."
© newsquest (sunday herald) limited
Re: Rise of the New Plagues Continues
Post by bigbunny on Sept 3, 2004, 11:46am
Mystery Disease Killing
Chickens In Indonesia
Washington Times
8-31-4
YOGYAKARTA, Indonesia (UPI) -- Indonesian poultry farmers, following a bird flu outbreak, are facing another mysterious disease that has killed thousands of chickens in the past few days.
Apart from the deaths, which have caused heavy losses, farmers in Yogyakarta's Sleman region say the problem has been aggravated by the fact that the surviving chickens are not breeding, the Straits Times reported Tuesday.
And the disease is spreading rapidly.
Sick chickens first salivate and show symptoms of diarrhea, then die within hours, farmers said.
The head of the poultry division of the Sleman agriculture agency, Suwadi Azis, said his office had not received any reports from poultry farmers on the disease outbreak. But he said the symptoms indicated the outbreak could be Newcastle Disease.
"If that is the disease, we already have the vaccine to prevent its further spread," he said.
Copyright 2004 United Press International http://washingtontimes.com/upi-breaking/20040831-015915-7762r.htm
Re: Rise of the New Plagues Continues
Post by bigbunny on Sept 3, 2004, 11:46am
Cats may carry the bird flu virus
The bird flu virus that can kill humans has the potential to be spread by cats, scientists have found.
It had been thought that domestic cats were resistant to diseases caused by influenza A viruses - one of which, H5N1, is responsible for avian flu.
The disease killed at least 20 people in Asia earlier this year, and forced farmers to cull almost 200m birds.
The research, by Erasmus Medical Center, Rotterdam, is published in the journal Science.
If any virus is going to cause a great human pandemic in the near future, then it is likely to be H5N1
Professor John Oxford
The researchers warn that their findings may mean that cats are a potential source of infection for humans.
It also underlines the ability of the virus to evolve to infect new species.
H5N1 cannot currently pass from person to person, but scientists fear that if the virus does acquire this ability, it could pose a serious threat to millions.
The Dutch team focused on cats after some anecdotal reports emerged during the recent outbreak linking the disease to the animals.
They investigated whether the virus could make cats sick when it was introduced into the airways, or when the cats ate infected chickens.
The six cats developed severe lung disease and passed the disease onto two additional cats kept in close quarters.
The authors also tested the effect of another type of influenza virus, H3N2, that most commonly causes flu in humans.
Cats exposed in the same way to this virus did not develop disease.
Writing in Science, the researchers say: "The implications are that, during H5N1 virus outbreaks, domestic cats are at risk of disease or death from H5N1 virus infection, either due to feeding on infected poultry or wild birds, or due to contact with infected cats.
"Second, the role of cats in the spread of H5N1 virus between poultry farms, and from poultry to humans needs to be re-assessed.
"Third, cats may form an opportunity for this avian virus to adapt to mammals, thereby increasing the risk of a human influenza pandemic."
Professor John Oxford, an expert in virology at Queen Mary College, London, told BBC News Online the study was "very significant and slightly alarming".
He said there was little evidence at present that cats could be infected with other forms of human flu virus, and so the possibility that H5N1 could mix with a human virus inside a cat and produce a deadly new strain was probably slim.
However, he agreed that it was possible that cats could be responsible for avian flu spreading from farm to farm - a phenomenon which has baffled scientists.
Professor Oxford said there was also work to suggest that pigs could be infected with H5N1, and, unlike cats, they could also harbour human versions of the virus.
"H5N1 is getting more and more worrisome," he said.
"If any virus is going to cause a great human pandemic in the near future, then it is likely to be H5N1."
Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/health/3620532.stm
Published: 2004/09/02 23:00:11 GMT
© BBC MMIV
Re: Rise of the New Plagues Continues
Post by bigbunny on Sept 3, 2004, 12:14pm
New Virus Suspected In Two Crib Death Cases
By Marilynn Marchione
AP Medical Writer
9-1-4
MILWAUKEE -- A virus recently discovered in Japan is suspected in two "crib deaths" in Wisconsin, raising new questions about how many of these mysterious tragedies might be caused by germs.
The cases mark the first time the virus has been identified in the United States. Whether it killed the babies is not clear, but both were sick before they died and had signs of disease in their lungs.
Sudden infant death syndrome ó also called "crib death" for the devastating way it is usually discovered ó is a catch-all term for unexplained deaths in children less than a year old. About 2,200 occur each year in the United States, mostly involving babies between 2 and 4 months old.
Brain or breathing abnormalities, genetic mutations and birth defects are possible causes. The risk rises if babies live with smokers, are put to sleep on their stomachs, or are bundled in too many clothes or covers.
Infections also have long been implicated. However, many SIDS victims are not tested for viruses that might be the culprit.
The Wisconsin cases should prompt research into whether SIDS is often caused by the newly discovered type of virus, said Dr. Mark Pallansch, who identified it at the federal Centers for Disease Control and Prevention after a Milwaukee virologist detected it.
"That is the question to be asked," he said. "At this stage we just have very little information about the involvement of these viruses in human disease."
Separately, a study in Thursday's New England Journal of Medicine suggests that a protein long linked to stillbirths and some birth defects may play a role in SIDS. Researchers from England and Scotland found that pregnant women who had high amounts of it in their blood were nearly three times more likely to have a baby die of SIDS than were women with lower amounts.
In recent years, pilot projects in several states have found a surprising number of infections in SIDS victims. It has also long been known that many victims have high amounts of immune system cells and substances, indicating they were fighting germs. SIDS is also more common in winter, when viruses thrive indoors.
Germs that cause mild illness in adults can be fatal to infants. Sometimes they kill indirectly, by magnifying other dangers, said Dr. Marian Willinger, who oversees SIDS research for the National Institute of Child Health and Human Development. If parents pile blankets on a sick child, it becomes harder for the baby to breathe and regulate its body temperature, she said.
Officials are trying to figure how the newly recognized virus, human parechovirus-3, or HPEV-3, fits in. Japanese scientists reported its discovery earlier this year after studying a 1-year-old girl who developed a high fever, diarrhea and temporary paralysis in 1999.
The virus' origin is a mystery. How the Wisconsin babies got it is another.
The first was a 4-week-old Appleton girl who died last September, after she and her family had colds. Her mother is a travel agent, but she worked from home in the two previous months and had no face-to-face contact with clients who went to Asia.
The second case occurred two weeks later, 30 miles away, in a 4-month-old Fond du Lac girl who also had cold symptoms. Her father had recently been to China and Australia, but her family had no known contact with the other victim's family.
"Other than the virus itself, we do not have a linkage," said Wisconsin's state epidemiologist, Dr. Jeffrey Davis.
The virus was detected in Wisconsin through a study that Milwaukee County Medical Examiner Dr. Jeffrey Jentzen launched in 1987 with Gerald Sedmak, the Milwaukee Health Department virologist who discovered the new germ in the two dead babies.
So far, they have found viruses in a third of the 1,200 cases studied, though most are not believed to have caused death. Still, that is a surprisingly high rate, said Dr. Kurt Nolte, who started a similar project in New Mexico.
"All of these viruses are potentially fatal. That's why people protect their newborns when they bring them home. You don't pass your brand-new baby around to 45 people," Nolte said.
In a Chicago study in the 1990s, Dr. Fern Hauck, a University of Virginia SIDS researcher, found infections in 10 percent of SIDS victims. She is now helping the CDC revise forms for reporting sudden and unexpected infant deaths.
"The goal is to really have everyone in the country who deals with infant deaths to extensively review everything in the background to make sure no stone is left unturned to find the diagnosis," Hauck said.
Davis agreed: "Not everything reported as SIDS is SIDS. Every one of these situations deserves an answer as to why it occurred."
SIDS deaths declined 50 percent after the federal government's Back to Sleep campaign in 1994, which urged parents to put babies to sleep on their backs.
SIDS is more common in babies of parents who are young or uneducated, and among blacks and American Indians.
http://story.news.yahoo.com/news?tmpl=story
&u=/ap/20040901/ap_on_he_me/sids_virus
Re: Rise of the New Plagues Continues
Post by bigbunny on Sept 11, 2004, 6:49am
ADHD parents 'are also affected'
By Paul Rincon
BBC News Online science staff, at the BA festival
Parents of children with attention deficit hyperactive disorder (ADHD) often show signs of the condition themselves, research has suggested.
University of Wales at Bangor scientists said this made dealing with their child's condition more difficult.
But they told the British Association Festival of Science in Exeter that sharing these symptoms did not put the child at any greater risk.
Nor did it mean ADHD adults necessarily had poor parenting skills, they argued.
Children with ADHD have extreme difficulty sitting still, learning or concentrating; and looking after these children can be exhausting for parents.
Those parts of the brain that are under-active are those that we use for stopping ourselves, for holding ourselves back
Professor Eric Taylor, Institute of Psychiatry
Dr David Daley, from Bangor's School of Psychology who led the research, said: "Parenting a child with ADHD when you have symptoms yourself must be the most difficult thing to do."
However, he said his study of over 250 parents and children indicated there might be some positive aspects to sharing ADHD traits between parent and child.
The research confirms that in families with shared symptoms, ADHD parents are more likely to engage in negative and undesirable parenting practices, and have a negative emotional relationship with their child.
But this group of parents is also more likely to engage in affectionate and constructive parenting when dealing with their child.
This includes the parent expanding on a child's play idea, without criticism, and spending more time playing together, all of which are positive parenting traits.
'Less developed'
The conference also heard further evidence of the genetic basis for the condition.
Professor Eric Taylor of the Institute of Psychiatry said the disorder had a genetic component of around 80%, but that ADHD was not caused by one gene, but by the cumulative effect of several, which had small effects.
He said scans showed real differences in the brains of children with the condition.
Magnetic Resonance Imaging (MRI) scans found they tended to have smaller right frontal lobes, a small vermis (a feature of the brain region known as the cerebellum) and some regions of the basal ganglia are also smaller.
Professor Taylor said: "Those parts of the brain that are under-active are those that we use for stopping ourselves, for holding ourselves back."
He said only a third of children with the severe form of the disorder were receiving medication.
Researchers from the institute followed children from the age of seven who displayed hyperactive behaviour but had not been diagnosed with a disorder.
They then followed them until they were aged 17.
It was found that those children had a four-fold increase in the likelihood of developing a mental disorder.
About 250,000 in children in Britain are believed to have ADHD. Some 80,000 have the more severe form of the disorder.
Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/health/3640346.stm
Published: 2004/09/09 12:10:09 GMT
© BBC MMIV
Re: Rise of the New Plagues Continues
Post by bigbunny on Sept 17, 2004, 7:14pm
Dutch bird flu infected hundreds of people
Updated 17:04 15 September 04
NewScientist.com news service
Dutch scientists have found that more than twice as many people as thought may have been infected during a bird flu outbreak in Dutch chickens in 2003.
The flu is not the same as the one now breaking out again in East Asia, but it shows once again that these viruses are capable of unpleasant surprises.
The 2003 outbreak, which led to the culling of 31 million birds on more than a thousand farms, was of a flu virus called H7N7, after the type of surface proteins it carries. The bird flu that spread across East Asia earlier in 2004, and has broken out again over the past two months, is called H5N1.
H7N7 had not been previously known to cause serious infections in people. But during the Dutch outbreak, 86 people who were in contact with sick birds got either a mild eye infection, or typical flu symptoms. One vet died of pneumonia caused by H7N7.
More worrying, three more sick people had not been directly in contact with chickens, but only with people who had been working with sick birds, showing the virus is capable of limited human-to-human spread.
Viral antibodies
Since then, Marion Koopmans and colleagues at the Dutch National Institute for Public Health and the Environment (RIVM), have been testing people who had contact with either sick chickens, or chicken workers, but had no suspicious symptoms. At a meeting this week in the Netherlands, they reported that of 419 people who worked with sick chickens, 212, more than half, had antibodies to the virus. Most of them had no symptoms at all, Arnold Bosman of the RIVM told New Scientist.
The researchers also confirmed that H7N7 can spread between people. Of 62 people who had contact with chicken workers, but not chickens, 33 had antibodies to H7N7. The work is due to be published in a few weeks.
Most of the antibodies were caused by an actual infection, not just exposure to large amounts of viral proteins, says Bosman, because taking antiviral drugs, as chicken workers were asked to do, seems to have kept people from developing antibodies to H7N7 - although some people on the drugs did anyway.
Dangerous hybrid
This means H7N7 can infect people more readily than was thought, and without causing symptoms. The fear is that H7N7 might infect someone who is also carrying human flu, allowing a dangerous hybrid to emerge.
That is an even greater fear in Thailand and Vietnam, where a handful of people have contracted H5N1 bird flu since the virus broke out again in poultry in August.
H5N1 is a much nastier virus, killing 29 of the 40 confirmed human cases in Thailand and Vietnam. But, so far, it seems incapable of human-to-human spread.
However, H5N1 can spread undetected in poultry that have been vaccinated against it, posing a constant risk of surprise infection, and possibly undergoing dangerous adaptive changes.
Citing the risk to human health, Thailand decided on Wednesday not to vaccinate poultry against H5N1, unlike China and Indonesia, despite the risk of outbreaks and intense pressure to vaccinate from the cock-fighting industry.
Debora MacKenzie
http://www.newscientist.com/news/news.jsp?id=ns99996407
Re: Rise of the New Plagues Continues
Post by bigbunny on Sept 17, 2004, 7:54pm
Singapore warns of deadly illness
Authorities in Singapore have expressed concern about the rising death toll from the tropical disease melioidosis.
Twenty-three of the 57 people diagnosed with the soil-born disease from January to July died, health officials said.
This pointed to a mortality rate of 47% - three times as much as with the deadly respiratory infection Sars.
The high death toll led officials to investigate whether Singapore may have been targeted by a biological warfare attack - but this was ruled out.
Melioidosis is listed by the US government as a potential bacteriological weapon.
No vaccine
The disease is most common in South-East Asia and northern Australia.
It is caused by bacteria that enter the body when contaminated dust is inhaled or when bruised skin comes into contact with contaminated soil.
The infection can spread from the skin through the blood to the heart, brain, liver, kidneys, joints, and eyes.
There is no vaccine for melioidosis. It can be treated with antibiotics if detected early.
Singapore has an annual average of 67 cases and 12 deaths from the disease.
The authorities have given no reason for this year's rise.
During the Sars outbreak in Asia from late 2002 to mid-2003, Singapore recorded 33 deaths from the viral respiratory infection.
Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/asia-pacific/3667834.stm
Published: 2004/09/17 23:06:08 GMT
© BBC MMIV
Re: Rise of the New Plagues Continues
Post by bigbunny on Sept 17, 2004, 8:01pm
'Clear' bacteria link to Crohn's
The clearest evidence yet that Crohn's disease is caused by a type of bacteria blamed for a similar animal disorder has been published by US researchers.
Mycobacterium avium subspecies paratuberculosis (Map) was found for the first time in the blood of people with the disorder.
Half of the 28 people with Crohn's tested positive for Map.
Dr Saleh Naser, from the University of Central Florida, who led the research, said a large-scale study was needed.
Crohn's disease affects 100,000 Britons and can cause a variety of symptoms from a lack of appetite to chronic diarrhoea and abdominal pain.
The cause of the disease is not yet known but the Map bacterium, which causes Johne's disease, a similar intestinal disorder, in cattle, sheep and goats, was first linked to Crohn's 20 years ago.
Dr Naser's team took blood samples from 52 people - 28 with Crohn's, nine with ulcerative colitis, another inflammatory bowel disease (IBD), and 15 people without a IBD.
Blood
The live bacterium was found in the blood of 14 patients with Crohn's but in none of the people without the disorder.
It is the first time the bacterium has been found in the blood as other studies have focused on human tissue.
Two people with ulcerative colitis were also reported to have Map present but the study said this could have been because they had Crohn's.
Traces of Map DNA were found in some of the people with ulcerative colitis and three without an IBD.
The study suggested this was because Map is common in the environment with exposure most likely to happen through the food and water supply.
The findings now need to be replicated in other laboratories. Whatever one's view, Map cannot continue to be ignored in Crohn's disease
Professor Warwick Selby, of the Royal Prince Alfred Hospital in Australia
However, it is thought these people would not have developed Crohn's as people with the disorder have to be genetically susceptible first.
In the past, scientists have claimed Crohn's is passed to humans through milk.
Dr Naser said: "The fact that some people had Map DNA in their blood is worrying. It suggests the bacterium is not just opportunistic.
"It is present more than we think. We know cattle and sheep have this bacteria so it is possible animals may be spreading the disease and pasteurisation is not doing the job it should be."
'Significant'
He said the fact that half the people with Crohn's had Map was a "significant number" and future studies should result in a higher proportion.
"We only took a small blood sample, if we are right, Map will be present in a greater proportion of people with Crohn's.
"What we now need is more work to prove this theory."
Writing in the Lancet, Professor Warwick Selby, of the Gastroenterology and Liver Centre at the Royal Prince Alfred Hospital in Australia, agreed more research was needed.
"This report may still fall short of proving that Map is one of the causes of Crohn's disease but as with similar studies it raises many important questions.
"The findings now need to be replicated in other laboratories. Whatever one's view, Map cannot continue to be ignored in Crohn's disease."
Dr Martin Sarner, the honorary secretary of Core, formerly the Digestive Disorders Foundation, said if it could be proved Map caused Crohn's it would represent a huge breakthrough for patients.
"It would help in the treatment of the disease. It is terribly debilitating for people.
"At the moment people are with given medication, which just keeps the inflammation at bay or they have surgery which can involve cutting away tissue.
"And the problem they face is that it can just keep coming back."
Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/health/3663336.stm
Published: 2004/09/16 23:48:34 GMT
© BBC MMIV
Re: Rise of the New Plagues Continues
Post by bigbunny on Sept 21, 2004, 8:48am
Danger seen in plan to resurrect deadly '18 influenza virus
http://www.dailystar.com/dailystar/news/39554.php
SEATTLE - University of Washington scientists plan to infect monkeys with a killer flu virus grown from cells exhumed from victims of the 1918 epidemic.
They hope the insight they gain will unravel the mystery of why millions of people worldwide died from the virulent flu strain, and lead to development of better vaccines and drugs that may save lives in the future.
"This was the most deadly infectious disease in the history of mankind, killing at least 40 million people," said Dr. Michael Katze, a UW microbiologist and principal investigator for the local arm of the project. "To this day, nobody understands why the virus was so deadly."
Most experts believe another killer flu pandemic is overdue, Katze said, so it's critical to gain information about the disease.
The UW received part of a $12.7 million grant, funded largely from Congress' $1.7 billion biodefense appropriation to the National Institutes of Health, to collaborate on the 1918 flu study with Mount Sinai School of Medicine in New York and the Armed Forces Institute of Pathology in Washington, D.C.
Caution urged
A skeptic of resurrecting and enlivening the 1918 flu virus, however, said it is critical to first make sure we are adequately protected against creating a "man-made" pandemic.
"This project could create a new bug that infects someone in the lab who then walks out at the end of the day and, literally, kills tens of millions of people," said Ed Hammond, director of a biotechnology and bioweapons watchdog organization called the Sunshine Project, based in Austin, Texas.
Although Hammond said he could accept the noble intentions of the UW scientists, he noted that there are no national laboratory standards for dealing with this particular virus. The lack of regulatory protection, he said, stems from the fact that influenza is generally regarded as a fairly routine disease.
"But this organism, the 1918 virus, is something else," Hammond said. "It's very dangerous and easily spread."
Protection called essential
He contended that the 1918 virus deserves one of the highest levels of laboratory containment systems, known as Biosafety Level 3 Ag - so-called because the criteria were set by the U.S. Department of Agriculture. The only greater level of protection (in which lab workers don self-contained "moon suits" inside a pressurized, air-locked, multi-layered lab) is Biosafety Level 4.
The first step in this project will be to spend about $300,000 of the grant to beef up the biosafety levels of protection at the Seattle facility, said Dr. William Morton, director of the regional primate research center at the UW.
"We do need to have an elevated level of containment," Morton said. The lab facilities, which are primarily used today for HIV research involving primates, are built to Biosafety Level 2.
But Morton said it's not clear that the 1918 flu study will require all the Biosafety Level 3 Ag protections. He said the current plan is to create an "enhanced" level 3 lab on one floor of the primate center, located in a non-descript research building in Belltown.
Morton said the precise design for converting the lab would depend upon recommendations from the NIH.
Re: Rise of the New Plagues Continues
Post by bigbunny on Sept 21, 2004, 9:45am
HIV/AIDS Fuels Tuberculosis Crisis - UN
By Anthony Mitchell
Associated Press Writer
9-20-4
ADDIS ABABA, Ethiopia -- The spread of HIV/AIDS is fueling a massive tuberculosis crisis that could see one billion people infected in the next 20 years, the U.N. warned Monday.
A staggering 35 million people could also die of TB in that time if its growth continues unchecked, the World Health Organization said at the start of a two-day conference in the Ethiopian capital, Addis Ababa.
The conference is seeking to promote joint treatment of the two leading killer diseases in the world. AIDS kills 8,000 people worldwide a day while another 5,000 die from TB.
TB is the most common infection among - and the leading killer of - people living with HIV/AIDS.
TB infects an estimated 8.7 million people a year and kills 2 million a year. It is spread by airborne bacteria that settle into the lungs and cause long-term infection. Many people who are infected do not become ill themselves but can spread it.
Of the estimated 25 million Africans now living with HIV, about eight million also harbor the bacillus that causes TB.
Each year, 5-10 percent of these eight million co-infected people develop active TB and up to four million will develop the disease at some point in their lives, the WHO said.
The "deadly interaction" of TB and HIV threatens to evolve into a global public health crisis and called for urgent action to stop the co-epidemic, said Mario Raviglione, head of the WHO fight against TB. The danger is compounded by the appearance of drug-resistant TB strains.
Earlier Monday, a senior US health official called on Ethiopia's political leaders to go for public tests for HIV in a bid to help end the stigma affecting those living with the virus.
Julie Gerberding, director of the US Center for Disease Control, was speaking during a three-day visit highlighting projects funded under U.S. President George W. Bush's US$15 billion initiative to combat HIV/AIDS.
"Having a visible political leader getting an HIV test helps, there is no question about it," Gerberding said. "I would encourage all leaders to have an HIV test as I have done."
Copyright © 2004 The Associated Press. All rights reserved. The information contained in the AP News report may not be published, broadcast, rewritten or redistributed without the prior written authority of The Associated Press.
http://story.news.yahoo.com/news?tmpl=story&cid=541&ncid=54
1&e=1&u=/ap/20040920/ap_on_he_me/africa_tb_crisis
Re: Rise of the New Plagues Continues
Post by bigbunny on Sept 24, 2004, 8:27pm
Lack of vaccine raises fears of flu pandemic
10:37 23 September 04
Exclusive from New Scientist Print Edition. Subscribe and get 4 free issues.
Fears that bird flu could mix with human flu to create a highly infectious, deadly new strain heightened last week after Thailand reported that human flu is circulating in areas where there have been renewed bird flu outbreaks in poultry. The country does not have enough human flu vaccine to protect all workers against simultaneous infection by both viruses.
The H5N1 bird flu that rampaged across east Asia in 2003 is making a comeback, with outbreaks in poultry in Thailand, Vietnam and also Malaysia, which had not had any outbreaks until recently. In Thailand and Vietnam, H5N1 has killed at least four people in recent months, but so far there are no reports of it spreading from human to human.
The big fear is that the H5N1 virus could turn into a strain capable of causing a human pandemic, either by mutating or by picking up genes from human flu viruses. The latter can happen if people are infected by both viruses at the same time; to prevent this, the World Health Organization says people most at risk of co-infection should be given flu drugs or vaccinated against human flu.
The Thai health ministry announced last week that it will vaccinate poultry workers in affected areas, after human flu cases in two districts where there have been recent outbreaks of H5N1 in poultry. Klaus Stöhr, head of influenza at the WHO, says everyone who keeps backyard poultry in areas where there has been a recent H5N1 outbreak could be at risk.
Donated vaccine
But vaccinating all such people in Thailand and Vietnam would take more than half this season’s total production of vaccine. And Thailand has only 100,000 doses of donated flu vaccine. “We do not have sufficient vaccine to prevent co-circulation,” says Prasert Thongcharoen of Mahidol University in Bangkok, a member of the WHO’s expert committee on viral diseases.
The reason is that the flu season is starting in the northern hemisphere, and all the vaccine manufactured so far is going to rich countries there. “There is no excess,” says Stöhr. “There is no vaccine available for Vietnam.”
What vaccine is available in Thailand will go to places with ongoing H5N1 outbreaks. But this will prevent co-infection only if outbreaks are detected promptly and reported. The most recent human deaths from H5N1 in Thailand and Vietnam occurred before the poultry outbreaks that caused them had been reported.
An alternative way to reduce co-infection would be vaccinating poultry against H5N1. But Thailand ruled this out last week, partly because of evidence that imperfect vaccines encourage more virulent strains to evolve (New Scientist print edition, 27 March 2004).
Stöhr says surveillance must be stepped up so that if a deadly strain does emerge, it is detected as early as possible to give vaccine makers a head start. “We’ll have that much more vaccine for each day earlier that we know it is coming.”
Debora MacKenzie
http://www.newscientist.com/news/news.jsp?id=ns99996427
Re: Rise of the New Plagues Continues
Post by bigbunny on Sept 26, 2004, 8:37am
World's First Human-To-Human Bird Flu Transmission
ABC Asia Pacific TV -Radio Australia
9-26-4
The world's first human-to-human transmission of a lethal strain of bird flu is suspected to have taken place in Thailand
The alarm has been raised by the World Health Organisation, as Peter Lloyd reports from Bangkok.
Suspicion of human to human transmission centers on the case of a 26 year old woman who traveled from Bangkok to northern Thailand to visit her daughter in hospital and then attend her funeral. A week after returning to the capital the woman also died from what is believed to have been bird flu. It was only then that her child's fatal illness fell under suspicion of being the deadly strain of avian influenza.
The WHO Thai representative Kumara Rai says there is no evidence of the mother having had any contact with fowl, instead suspecting she caught the deadly virus from close physical contact with her daughter. Her sister is now in hospital with severe pneumonia. Lab test results are expected as soon as Monday but the Geneva headquarters of W.H.O has been asked to send experts to Thailand to help in the investigation.
http://abcasiapacific.com/news/stories/asiapacific_stories_1207134.htm
Thailand Full Alert - Bird Flu Transmitted Among Humans
ChinaView.cn
9-26-4
BANGKOK (Xinhuanet) -- The Thai government has taken human safety as priority in face of possible bird flu transmission among people, the Thai Prime Minister Thaksin Shinawatra said on Saturday.
The Agriculture Ministry and the Public Health Ministry have been ordered to closely work together to reduce the risk of people being infected with the fowl epidemic, while eagerly waiting for the result of lab test as whether the virus had been transmitted between human, the prime minister said in his weekly radio-broadcast speech.
Three deaths with symptoms of pneumonia, including a pair of mother and daughter and a boy, have been listed as suspected casesof bird flu infection and the result will come out in three days.
The 11-year-old girls, who died on September 12, had record of contacting with birds when she was alive, and her 26-year-old mother became sick and showed symptoms of infection after visitingher at the hospital in northeastern province of Kamphaengphet.
The mother passed away on Monday, which rang alarm among experts and doctors who were afraid of possible transmission of the avian influenza virus among people.
The deceased girl's aunt, who has never touched infected poultry,has also reported flu-like symptoms.
"Neither the mother of the dead girl or her aunt have risk behaviors which can lead to infection except they were close to a patient with bird flu-like symptoms," Dr Charal Trinvudhipong, acting health permanent secretary, was quoted by Saturday's Bangkok Post as saying.
"Health authorities are awaiting the outcome of lab test results,especially from the aunt to show if bird flu has mutated and changed into a form that can pass between humans," he said.
Since the avian influenza rebounded in the kingdom in July, only an 18-year-old man has died last month in central Thailand, pushing the kingdom's bird flu casualty to 9.
In the first wave of bird flu outbreak at the beginning of thisyear, eight people in Thailand were killed by the epidemic.
Another 19 people have died in Vietnam, bringing the Asian death toll to 28.
Besides, there have been 128 patients in Thailand under observation for possible infection of the disease since early July.
Now, 114 of the cases have been cleared and the rest are still waiting for the test result.
Re: Rise of the New Plagues Continues
Post by bigbunny on Sept 30, 2004, 11:43am
Virulent Form of Hepatitis E In Iraq's Drinking Water
From Patricia Doyle, PhD
dr_p_doyle@hotmail.com
9-29-4
Hello Jeff - The health situation, or should I say lack of health, in Iraq is critical. People are developing cancers as well as birth defects of newborns due to depleted uranium. The weapons and the military hardware containing depleated uranium are a danger, not only to Iraqis, but also to people in the US. Depleated Uranium products used in Iraq are made here in the US. People live near the factories and DU products are trucked and railed across the US. Polution from the factors can seep into water tables and pollute the air.
Iraq has no safe water in the entire country. Sewage treatment plants are not on line and the water contains viruses and bacteria. Part of the problem is the fact that Iraq still does not have uninterrupted electricity. With all of the billions of dollars going to rebuild Iraq, and with all of the PR we hear from the Bush administration about a post war Iraq, we have a nation that presents major health risks for people.
International Herald Tribune online
By James Glanz
NY Times
9-24-4
A virulent form of hepatitis that is especially lethal for pregnant women
has broken out in 2 of Iraq's most troubled districts, Iraqi Health Ministry officials said in interviews here this week, and they warned that a collapse of water and sewage systems in the country is probably at the root of the illnesses.
The disease, called hepatitis E, is caused by a virus that is often spread by sewage-contaminated drinking water. The officials said that their limited ability to test for the virus had already been overwhelmed by the hepatitis outbreaks, suggesting that only a fraction of the actual cases have been diagnosed. But in Sadr City, a Baghdad slum that for months has been convulsed by gun battles between a local militia and American troops, as many as 155 cases have turned up.
The 2nd outbreak is in Mahmudiya, a town 56 km (35 miles) south of Baghdad that is known as much for its kidnappings and drive-by shootings as for its poverty, where 60 suspected cases have been seen. At least 9 pregnant women are believed to have been infected, and one has died. There have been 5 reported deaths overall. "We are saying that the real number is greatly more than this, because the area is greatly underreported," said Dr. Atta-alla Mekhlif al-Salmani, head of the viral hepatitis section at the Health Ministry's Center for Disease Control.
The World Health Organization is rushing hepatitis E testing kits, water purification tablets, informational brochures and other materials to Iraq to help with the outbreaks, said Dr Naeema al-Gasseer, the health agency representative for Iraq and a UN health official, who is now based in Amman, Jordan.
But viral hepatitis comes in numerous forms, and another ominous set of statistics suggests that the quality of water supplies around the country has deteriorated since the American-led invasion last year, Salmani said. In 2003, there were 70 per cent more cases of hepatitis of all types reported across Iraq than in the year before, he said. During the first 6 months of 2004, there were as many cases as in all of 2002.
In yet another indication of the deteriorating safety of both water and food in Iraq, the number of reported cases of typhoid fever is up sharply this year, said Dr Nima S Abid, the ministry's director general of public health and primary health. Hospitals across the country are also full of children with severe forms of diarrhea, Abid said.
The immediate reason for the outbreaks in Sadr City and Mahmudiya appear to be easy to pin down, Abid said. The lack of infrastructure induces families to tap into water mains with improvised hoses, he said, citing his own visits to the communities. They then use small electric pumps to bring water into their homes. But in these same communities, sewage either seeps from damaged pipes into the ground or runs freely in the streets. So, through cracks and holes in people's hoses, sewage is sucked in too, becoming mixed with the drinking water and spreading the virus. "The problem is that there is a leakage in the sewer system of Sadr," said an assistant to the director general for water in the Baghdad municipality. "Our treatment plant produces water with WHO specifications," said the assistant, who asked to be identified only as Khalid, "and our test records are very good." The assistant said that there had been a major water project under way for Sadr City, but that the dangerous security situation had made it impossible to proceed.
George A Robertson, PhD
Vice President Science & Technology
PDA
An International Association for Pharmaceutical and Biopharmaceutical
Science and Technology
3 Bethesda Metro Center, Suite 1500
Bethesda, MD 20814 USA
<robertson@pda.org>
[The viruses responsible for hepatitis A and hepatitis E are structurally similar, but phylogenetically distinct, enteric viruses transmitted by similar routes. An effective vaccine is available for control of hepatitis A virus infection, but there is no vaccine for control of hepatitis E. Although both viruses are relatively heat resistant, boiling of drinking water would provide a first line of defence against the spread of infection. - Mod.CP]
Patricia A. Doyle, PhD
Re: Rise of the New Plagues Continues
Post by bigbunny on Oct 1, 2004, 8:56am
Saturday, September 18, 2004
1918 killer flu virus to be tested in UW lab
Study needed to head off next epidemic, scientists say
By TOM PAULSON
SEATTLE POST-INTELLIGENCER REPORTER
University of Washington scientists plan to infect monkeys with a killer flu virus grown from tissue exhumed from victims of the 1918 epidemic.
They hope the insight they gain will unravel the mystery of why tens of millions of people worldwide died from the virulent flu strain and lead to development of better vaccines and drugs that may save lives in the future.
"This was the most deadly infectious disease in the history of mankind, killing at least 40 million people," said Dr. Michael Katze, a UW microbiologist and principal investigator for the local arm of the project.
"To this day, nobody understands why the virus was so deadly."
Most experts believe another killer flu pandemic is overdue, Katze said, so it's critical to gain information about the disease.
The UW received part of a $12.7 million grant, funded largely from Congress' $1.7 billion biodefense appropriation to the National Institutes of Health, to collaborate on the 1918 flu study with Mount Sinai School of Medicine in New York and the Armed Forces Institute of Pathology in Washington, D.C.
A skeptic of resurrecting and enlivening the 1918 flu virus, however, said it is critical to first make sure we are adequately protected against creating a "man-made" pandemic.
"This project could create a new bug that infects someone in the lab who then walks out at the end of the day and, literally, kills tens of millions of people," said Ed Hammond, director of a biotechnology and bioweapons watchdog organization called the Sunshine Project, based in Austin, Texas.
Although Hammond said he could accept the noble intentions of the UW scientists, he noted that there are no national laboratory standards for dealing with this particular virus.
The lack of regulatory protection, he said, stems from the fact that influenza is generally regarded as a fairly routine disease.
"But this organism, the 1918 virus, is something else," Hammond said. "It's very dangerous and easily spread."
He contended that the 1918 virus deserves one of the highest levels of laboratory containment systems, known as Biosafety Level 3 Ag -- so-called because the criteria were set by the U.S. Department of Agriculture.
The only greater level of protection (in which lab workers don self-contained "moon suits" inside a pressurized, air-locked, multilayered lab) is Biosafety Level 4.
The first step in this project will be to spend about $300,000 of the grant to beef up the biosafety levels of protection at the Seattle facility, said Dr. William Morton, director of the regional primate research center at the UW.
"We do need to have an elevated level of containment," Morton said.
The lab facilities, which are primarily used today for HIV research involving primates, are built to Biosafety Level 2.
But Morton said it's not clear that the 1918 flu study will require all the Biosafety Level 3 Ag protections.
He said the plan is to create an "enhanced" level 3 lab on one floor of the primate center, located in a non-descript research building in Belltown.
The difference between a routine Biosafety Level 3 lab and the Biosafety Level 3 Ag lab is significant. Only the latter has an air-lock entry, a system for decontaminating wastewater and various other filters or devices aimed at minimizing the spread of infectious disease.
Morton said the precise design for converting the lab would depend upon recommendations from the NIH.
Karen Van Dusen, UW director of environmental health and safety, said Hammond is correct that there are no agreed-upon laboratory standards for dealing with the 1918 flu virus.
"Our situation here is very similar to the early days of the AIDS epidemic, figuring out how to safely deal with HIV," Van Dusen said.
This is because the 1918 virus had disappeared after the outbreak.
Viral DNA was recovered a few years ago from the exhumed bodies of those killed in the pandemic. Most of the DNA came from those who had died in northern latitudes where the permanently frozen ground had preserved viral DNA.
Scientists at the Armed Forces Institute of Pathology and at Mount Sinai led some of the expeditions to dig up the 1918 victims and genetically reconstitute the virus.
"We intend to be very cautious," Van Dusen said. "No matter what standard comes out, we intend to meet or exceed it" -- unless the recommendation is Biosafety Level 4. "If they're going to require a Biosafety Level 4, we won't do this," she said.
Katze has already been working with non-infectious, genetic fragments of the 1918 flu virus. He and his colleagues have shown that the macaque monkeys develop infections similar to that of humans and should provide excellent animal models for trying to decipher this killer bug's mode of operation.
Katze's team will seek to learn more about the nature of the 1918 flu by inserting key genes from the killer flu into a common flu strain. The flu virus has only eight genes, said Katze, so they hope to rapidly target which genes are most responsible for virulence. The monkeys will be euthanized weeks after being infected, the UW scientists said, to allow for tissue, cellular and genetic testing.
P-I reporter Tom Paulson can be reached at 206-448-8318 or tompaulson@seattlepi.com
http://seattlepi.nwsource.com/health/191418_flu18.html
Re: Rise of the New Plagues Continues
Post by bigbunny on Oct 1, 2004, 8:57am
More 'Evidence' That AIDS Is A Man-Made Disease
From Dr. Alan Cantwell, MD
alancantwell@sbcglobal.net
10-1-4
More "evidence" that AIDS is a man-made disease.......although this "conclusion/speculation" carefully avoided by the authors in this Journal of Medical Primatology.
If the epidemic didn't come from monkeys...........then it certainly could have come from "the hand of man" -- unless one wants to postulate an extraterrestrial origin.
The "missing link" is that HIV was deliberately seeded into the American gay and the African black population via government and WHO-sponsored vaccine programs in the late 1970s. Also there is no "link" between the outbreak of AIDS in American gays and the outbreak in Africa.
It's about time we stopped blaming primates......particularly when tens of thousands have been locked up for decades in laboratories and biowarfare labs -- and who have been subjected to all kinds of experimental torture and virus exchange experiments. What scientific absurdity and chutzpah to blame primates for the current decimation of black Africa from AIDS!! And such a travesty to think that most doctors still believe this nonsense.
Please forward this article on to interested others. Hopefully more people will wake up to this obvious selective genocide program.
Alan
PS: For more information --- Go to www.google.com and type-in "man-made AIDS" -- there are 134,000 citations!!!!!!
Begin forwarded message:
From: BiGoldberg@xxxxx
Date: September 30, 2004 11:33:20 AM PDT
To: BiGoldberg@xxxxx
Subject: No evidence that AIDS can be contracted from monkey/chimp & 10/04 JMP
In the 10/04 Journal of Medical Primatology article titled "AIDS as a zoonosis? Confusion over the origin of the virus and the origin of the epidemics," Preston Marx et al. conclude:
"These arguments indicate that viral cross-species transmission is in itself not the only requirement for the generation of epidemics, and that the ancestry of HIV should not be confused with the origins of AIDS. Other factors must be required for HIV adaptation and epidemic spread of SIV in the new human host. Therefore, AIDS is not a zoonosis, but a human infectious disease of zoonotic origin."
"With the advent of AIDS, avian flu, Ebola and SARS, the question of what launches new epidemics and pandemics is extremely important. The somewhat shocking answer is that we actually know nothing about the factors that launch animal viruses into epidemics or pandemics. Equally important is the question as to why most animal viruses fail to reach a sustained human-to-human transmission. These are critically important questions that are being bypassed. When we think zoonosis, we should think of diseases like rabies. There is no evidence that a person can contract AIDS from a monkey or chimpanzee. There is still a missing link."
--------------------------------------
Marx PA, Apetrei C, Drucker E. AIDS as a zoonosis? Confusion over the origin of the virus and the origin of the epidemics. J Med Primatol 2004 Oct;33:220-226.
Division of Microbiology and Immunology, Tulane National Primate Research Center, 18703 Three Rivers Road, Covington, LA 70433, USA. Tel: (985) 871 6518; fax: (985) 871 6248; e-mail: pmarxj@tulane.edu
Abstract: Based on findings demonstrating the simian ancestry of HIV, AIDS has been reported to be a zoonosis. However, this theory has never been proved and must seriously be questioned. Several arguments show that HIV-AIDS is not a zoonosis. (i) If AIDS were a zoonosis, there must be evidence of AIDS being directly acquired from an animal species, as is rabies, a disease that is directly acquired from animals. (ii) Despite long-term and frequent human exposure to SIV-infected monkeys in Africa, only 11 cross-species transmission events are known, and only four of these have resulted in significant human-to-human transmission, generating HIV-1 groups M and O and HIV-2 groups A and B. The closest relatives of SIVcpz (HIV-1 group N) and of SIVsm (HIV-2 groups C-H) are extremely rare, with only six HIV-1 group N-infected patients and only single individuals known to be infected by HIV-2 groups C-H. SIV, while capable of cross-species transmission, is thus poorly adapted for disease and epidemic spread. If AIDS were a zoonosis that is capable of significant human-to-human spread, there would be a plethora of founder subtypes and groups. (iii) Human exposure to SIV is thousands of years old, but AIDS emerged only in the 20th century. If AIDS were a zoonosis that spread into the human population, it would have spread to the West during slave trade. (iv) Experimental transmission of SIVs to different species of monkeys is often well controlled by the new host, showing that the virus and not the disease is transmitted. Therefore, we conclude that cross-species transmission of SIV does not in itself constitute the basis for a zoonosis. Transmission per se is not the major requirement for the generation of the AIDS epidemic. All HIVs do derive from simian species, but AIDS does not qualify as a zoonosis and this explanation cannot in itself account for the origin of AIDS epidemic. It is important to distinguish AIDS from true zoonoses (e.g. rabies) because research is needed to understand the processes by which animal viruses cause sustained human-to-human transmission, epidemics and even pandemics. Much is known about emerging viruses, but almost nothing is known about emerging viral diseases.
Introduction
The emergence of AIDS in the late 1970s in the USA was the first sign of one of the deadliest pandemics in human history. In relatively short time, AIDS became a leading cause of mortality in the world and a cause of serious economic and social problems in of Central and southern Africa. The prevalence of Human Immunodeficiency Virus (HIV) increased rapidly, reaching apocalyptic levels of 30% by the end of the 20th century in southern regions of Africa [61]. Significant economic consequences have resulted from the reduction in life expectancy in some African nations [61]. In addition, the number of orphans in regions most affected by HIV has increased dramatically. A second wave of the epidemic reached Asia, where billions of people are at risk, with tens of millions already infected in India and China [61]. AIDS, therefore, is a major health problem in need of rapid and equitable medical and political solutions. The development of effective antiretroviral drugs (ARV) has partially controlled the problem in developed countries [45]. However, in developing countries, ARV is not yet available in spite of efforts by UNAIDS and other non-governmental organizations to provide drugs at least to patients in the late stages of infection [http://www.who.int/3by5/en/]. An effective prevention strategy for controlling mother-to-child HIV transmission was implemented in some African countries and has showed promising results [6,34]. The increased transmission of resistant viruses reported in Western countries is a major concern [60] and the magnitude of this problem may further increase with the advent of ARVs in those regions where treatments are administered without monitoring the virus infection. Effective vaccines are an ideal solution to control in AIDS worldwide, but vaccine development has been too slow to meet the need. Moreover, although moderate optimism was generated by recent reports showing control of SIVmac replication in macaques [1,49,51,53], the mechanism of immune protection in rhesus macaques and their relevance to HIV-AIDS is not known [21].
Re: Rise of the New Plagues Continues
Post by bigbunny on Oct 1, 2004, 9:00am
In this context, debates on the origin of HIV have generated a dispute concerning the fundamental character of AIDS. Based on results showing the simian origin of HIV [14,17,28], AIDS was treated as a zoonosis [31]. This hypothesis was based on data showing cross-species transmission of SIV [14,27]. Supporting data for SIV as the origin of HIV are (i) similarities in viral genome organization; (ii) close phylogenetic relationships between SIV and HIV; (iii) SIV prevalence in the natural host; (iv) geographic coincidence and (v) plausible routes of transmission. Both the SIVsm/HIV-2 and SIVcpz/HIV-1 groups fulfill these criteria [13,17,28]. However, although the simian source of HIV is acknowledged, the emergence of the AIDS epidemic is not understood. Moreover, the idea that AIDS is a zoonosis has never been proved and must be seriously questioned.
Results and Discussion
Why is this question important? Is this simply a semantic argument? It is important to distinguish AIDS from true zoonoses (e.g. rabies) because research is needed to understand the processes by which animal viruses cause epidemics and even pandemics. Although much is known about the origin of HIV, nothing is known about the mechanism of AIDS emergence. This field of AIDS research does not end with the discovery of the source of HIV. We must eventually understand the adaptive process(es) in the new host that will (or perhaps more importantly will not) launch an emerging disease. We know much about emerging viruses, but almost nothing about emerging viral diseases.
A strong rationale for studying the character of AIDS is the social implications that have serious consequences for the ecology of non-human primates. An incorrect assumption concerning the risk of acquiring AIDS from simian bush meat may result in deliberate killing of monkeys to prevent the spread of AIDS, a disastrous consequence for endangered non-human primates (NHPs) that is likely to have little effect on the AIDS epidemic.
An illustration of the confusion caused by misinterpretations of data on the origin of AIDS, the disease, is reaction of the non-scientific press in reports showing that chimpanzees were the source of HIV-1, the virus. 'Chimpanzee meat blamed for AIDS epidemic'[23] was the headline in a frontpage article in the New York Times. The first paragraph of the article stated that 'Chimpanzees slaughtered for food in west central Africa was the original source of AIDS'. Another was from the Daily telegraph which stated that: 'AIDS started by humans eating chimps'. The fact that the original scientific paper suggested that route of human infection with SIVcpz was exposure to blood during hunting and butchering and not the ingestion of meat [28] is incidental to the bigger issue that research only identifies the source of the virus and not the mechanism by which AIDS emerged. The corrected headline would have been, 'Chimpanzees slaughtered for food in west central Africa was the original source of HIV'. The results indicate that humans have been exposed to SIV-infected bush meat for thousands of years, but AIDS only emerged in the 20th century. If AIDS were a simple zoonosis with potential to become a health threat in humans as reported [31], it would have appeared earlier in Africa and would have emerged in the West during the era of slave trade when millions of Africans were brought to North and South America [33].
Definitions - what are zoonoses?
The definition of a zoonosis is 'a disease of animals that may be transmitted to man under natural conditions (e.g. brucellosis, rabies)' [24] or 'a disease communicated from one kind of animal to another or to a human being; usually restricted to diseases transmitted naturally to man from animals' (Medical Dictionary Online, http://cancerweb.ncl.ac.uk/cgi-bin/omd). Interestingly, in the Dictionary of Virology it is emphasized that the term zoonosis is frequently misused: 'a zoonosis is a disease or an infection naturally transmitted between vertebrate animals and humans. However, the term has been frequently misunderstood' [40]. The emphasis is on a zoonosis being a naturally acquired disease from an animal source. There is no evidence for AIDS being acquired directly from an animal source.
Stedman's Medical Dictionary [56] provides more details. Zooanthroponosis -- a zoonosis normally maintained by humans, but can be transmitted to other vertebrates (e.g. ameobiasis to dogs, tuberculosis); Amphixenosis -- a zoonosis maintained in nature by humans and lower animals (e.g. staphylococcoses). Amphixenosis would be the correct term for AIDS if it were a disease maintained in nature by animal to animal transmission and humans to human transmission. But the argument is more than semantics.
Arguments against AIDS as a zoonosis
The following facts do not support AIDS as a zoonosis.
1. In spite of the large number of exposures to SIV-infected monkeys in Central and West Africa [41,48], extensive molecular epidemiologic studies have documented only 11 cross-species transmission events during the last 50 years. Only four of these cross-over events resulted in epidemic strains. They are HIV-1 group M, the major group of viruses of the pandemic, group O, which is responsible for perhaps 5% of cases in Cameroon [4] and groups A and B of HIV-2, which are the epidemic forms of HIV-2 [19,27]. Figure 1 shows some of the closest relatives of SIVcpz (HIV-1 group N) and of SIVsm (HIV-2 groups C-G) (Fig. 2). These viruses are extremely rare in humans, with only six HIV-1 group N-infected patients known [3,8] and only single individuals infected by HIV-2 groups C-H (Fig. 1)[13,20,27,62]. These findings indicate that cross-species transmission of SIV is not in itself sufficient for spread into new human populations to generate an epidemic.
Re: Rise of the New Plagues Continues
Post by bigbunny on Oct 1, 2004, 9:00am
The concept that viruses transmitted across species are usually weak pathogens unsuited for initiating large-scale epidemics is not unique to SIV. Direct transmission of avian influenza virus has relatively lower epidemic potential compared with recombinant influenza viruses originating from the pig 'mixing vessels'. Only 18 cases of H5N1 influenza infection were recorded in Hong Kong [16]. These cases were severe, with a mortality rate of more than 30%. However, no evidence of human-to-human transmission of H5N1 virus was found [37]. Moreover, serological screening of poultry workers directly exposed to the avian virus has shown that about 10% were seropositive, and that the infection was asymptomatic or mildly symptomatic, with no secondary cases reported [9]. These findings suggest a need for adaptation of animal-origin viruses before they are capable of human-to-human transmission.
2. Experimental cross-species transmissions of SIVs in different species of monkeys have shown that in many cases the virus is relatively non-pathogenic and cleared by the new host [54,57, C. Apetrei, unpublished]. Moreover, some of the HIV-2 groups show low pathogenic potential in the human host [13,27]. Although baboons were reported to develop AIDS following infection with HIV-2 [5] it was clearly shown that serial passage of the virus in baboons will result in an increased pathogenicity [39]. We recently had the opportunity to characterize the outcome of cross-species transmission of SIVsm in three black mangabeys [2]. Although AIDS was observed in one animal, the SIVsm infection was cleared in the remaining two. These findings lead to the conclusion that cross-species transmission of a lentivirus is not the only requirement for the selection of a pathogenic virus in the new host and that studies have to be conducted to characterize the mechanisms of virus adaptation to the new host.
3. The SIVs infections in their natural host are generally asymptomatic in spite of high viral loads over long periods of time [10,12,22,29,43,50]. Immunodeficiency is extremely rare in African non-human primate hosts [2,38,46,55,58] and generally occurs after long incubation periods that exceed the normal life span of non-human primate species [46]. This finding reinforces the assumption that a change in the pathological potential of the virus is needed for SIV to become pathogenic in a new primate host [39]. In zoonotic diseases such as rabies or West Nile encephalitis, the animal source is also susceptible to the disease [11,52].
4. Finally, in Central Africa, humans have been exposed for centuries to SIVs and the epidemic only emerged in the second half of the last century, which suggests the intervention of some factor(s) favoring the emergence of HIV. These factors could be deforestation, increase of urbanization and travel in the 20th century [15]. In addition, it has been postulated that the main factor behind the emergence of HIV in human population may have been an increase in injections, unsterile needles and syringes as well as unsafe transfusion practices. This factor may have significantly promoted viral adaptation through serial passages [25,42] or favor adaptation by other mechanisms such as recombination.
And what if AIDS was a zoonosis?
If AIDS was a zoonosis, then human exposure to SIV would result in AIDS in the SIV-infected individual. Are there any data to support this assumption? During the study of SIV infections in macaques, cases of human laboratory workers becoming infected with SIV were reported. SIVsm had been accidentally transmitted to humans in laboratories in the US but in one case the infection was cleared [35] whereas in the second case (a human infection with SIVsmB670), a persistent non-symptomatic infection had been observed [36]. Macaques inoculated with SIVhu failed to develop productive infection due to the occurrence of deletions in different genomic regions [59]. This suggest that (i) SIVsm directly transmitted to humans is of low pathogenicity and (ii) that the cross-transmitted SIVsm must undergo adaptation into the new human host in order to replicate efficiently to generate immune suppression and to initiate an epidemic.
Most of the SIVs found thus far have not been grown in vitro and are only known from sequences. However. it has been repeatedly reported that most SIVs will replicate in human peripheral blood mononuclear cells (PBMCs) [18,31,48,47]. This is an overstatement. For example, only four SIVs of 13 reported in Cercopithecus monkeys have been isolated and only one of them (SIVlhoest) is known to grow on human PBMCs. Remaining viruses (SIVsun, SIVsyk and SIVtal) have a very restrictive host-related tropism [7,26,30,32,44].
These arguments indicate that viral cross-species transmission is in itself not the only requirement for the generation of epidemics, and that the ancestry of HIV should not be confused with the origins of AIDS. Other factors must be required for HIV adaptation and epidemic spread of SIV in the new human host. Therefore, AIDS is not a zoonosis [42], but a human infectious disease of zoonotic origin.
Conclusion
With the advent of AIDS, avian flu, Ebola and SARS, the question of what launches new epidemics and pandemics is extremely important. The somewhat shocking answer is that we actually know nothing about the factors that launch animal viruses into epidemics or pandemics. Equally important is the question as to why most animal viruses fail to reach a sustained human-to-human transmission. These are critically important questions that are being bypassed. When we think zoonosis, we should think of diseases like rabies. There is no evidence that a person can contract AIDS from a monkey or chimpanzee. There is still a missing link.
Re: Rise of the New Plagues Continues
Post by bigbunny on Oct 3, 2004, 11:48pm
Dementia - a symptom with many causes from Alzheimers to poisonings
A symptom with many causes: Alzheimer’s, arteriosclerosis, Parkinson’s, CJD, AIDS, poisonings etc Dementia is not a diagnosis – it is a symptom of some underlying dysfunction. Dementia is not an inevitable consequence of ageing – it always has a cause.
The early signs of dementia are brain fog, poor short term memory, poor concentration, difficulty learning and so on. If these symptoms are tackled early then progression to dementia may be halted.
The causes of dementia are as follows:
Poor blood supply See arteriosclerosis – risk factors for and prevention of
Prion disorders We are just finding out how little we know about a new range of brain disorders caused by prions. Prions are proteins which are not DNA, are normally present in the brain, can replicated themselves but can be normally broken down by the body. However if they are twisted they become resistant to breakdown by the body. When this happens in the brain, there is a build up of this useless material which destroys nerve cells and the brain degenerates. The best known example is CJD, but there is evidence to suggest that Alzheimer’s disease is also a prion disorder as is Parkinson’s disease and motor neurone disease.
What is not known is how prions are made or passed on. I have been greatly interested in the BSE issue, particularly the Purdey theory. Purdey believes that prions can be created “de novo” by the action of toxins in the brain particularly heavy metals and organophosphate pesticides. Once these prions have been created they become infectious in their own right.
On the basis of the Purdey ideas, I believe the following: BSE – this is initiated in the brain of the cow by the cumulative action of toxins such as organophosphate pesticides and manganese. These toxins are made more toxic where there is a copper deficiency. CJD – this may be acquired in the same way – ie the cumulative action of toxins such as organophosphate pesticides and manganese. Since prions once created become infectious in their own right, it is also possible that it is acquired when material from cows is injected into humans (many vaccinations were made from cows – not something the vegetarians were told). I think it is unlikely that CJD is acquired though eating beef. Alzheimer’s – poisoning by aluminium and possibly other heavy metals or chemicals Parkinson’s – poisoning by pesticides (high incidence of Parkinson’s in agriculture and horticultural workers) and manganese (manganese miners get PD) and probably other toxins (some drugs cause PD). Motor neurone disease – poisoning by plant toxins (cicad) and other substances as yet unknown.
Hormonal disturbances Myxoedema madness (underactive thyroid) is a much forgotten diagnosis. This is often overlooked in Down’s sydrome where the mental retardation is put down to the Down’s and no thought given to other possible diagnoses.
Poisonings Alcohol – a relatively small amount disturbs short term memory Pesticides – the farmers with “sheep dip flu” develop a sub-cortical dementia. Drugs – especially psychoactive drugs like major tranquillisers (Largactil) Heavy metals – lead, cadmium, aluminium, etc
Anatomical problems Brain tumours Hydrocephalus Blood clots (sub-dural haematoma) These are all possible causes of dementia. Any patient with a progressive dementia should have a brain scan.
Psychological and psychiatric conditions Severe on-going, unremitting depression can lead to a dementia.
Alzheimer’s disease Only too often I see patients who have gone demented and have been diagnosed as having Alzheimer’s without having been properly investigated to exclude other causes. If I had a patient with dementia I would want to go through: MRI brain scan All the causes of brain fog, poor memory, difficulty thinking clearly Tests for hypothyroidism Trial of B12 injections (dementia can occur well before levels become sub-normal – all results below 600 should be treated by injections) Hair analysis for heavy metals
Possible causes of Alzheimer’s The link between Alzheimer’s and aluminium was discovered at a renal unit in Leeds where 10% of the patients developed “dialysis dementia”. It was discovered that the water used for dialysis was not distilled water but tap water. Alum is used to clear tap water (otherwise the water was brown from the peat). Aluminium in the alum therefore passed freely into these patients causing dialysis dementia.
Aluminium should be avoided. The main sources are: Deodorants – nearly all are aluminium based and pasted on under the arms in sweaty areas where they can easily be absorbed. Antacids (acid blockers - it amazes me that these are allowed to contain aluminium!) Aluminium pots and pans, cooking foil Aluminium cans for drinks Cigarette smoke Aluminium is made more toxic where there is a zinc deficiency. Zinc deficiency is very common.
http://www.drmyhill.co.uk/article.cfm?id=175
Re: Rise of the New Plagues Continues
Post by bigbunny on Oct 8, 2004, 7:22am
Virulent 1918 flu genes resurrected
18:00 06 October 04
NewScientist.com news service
Deadly genes from the human influenza virus which caused the 1918 pandemic have been resurrected by scientists in an attempt to understand what made the strain so virulent.
The “Spanish flu” - which may have killed as many as 50 million people in the great pandemic - owed its deadliness largely to one of its surface proteins, say the researchers.
They have tested reconstructed viruses equipped with the protein and warn that it might one day return. If it does, anyone born after 1918 will have virtually no immunity.
Yoshihiro Kawaoka of the University of Wisconsin in Madison, US, and colleagues have reconstructed five of the eight genes of the 1918 virus, from fragments in victims buried in permafrost, and from clinical samples.
They reconstructed the two surface proteins - haemagglutinin (H) and neuraminidase (N) - from the 1918 flu strain, and substituted them for the H and N of current flu strains from mice and humans.
Mouse-killers
Previous experiments elsewhere found that equipping viruses that already caused flu symptoms in mice with the 1918 H resulted in a flu hybrid which made mice sick, even though the H from a human virus should not have been able to do this.
Kawaoka’s team went one step further by putting the 1918 H into human flu viruses that do not normally affect mice. This turned the viruses into mouse-killers.
The 1918 H even made a virus that normally kills mice even more lethal. In every case, the 1918 hybrid replicated more, invaded the deeper tissues of the mouse lungs, and caused nastier lesions. Similar experiments with the N protein from the 1918 flu human strain showed no such effect.
Experiments with the more virulent strains were conducted at the highest possible level of containment, at Canada’s National Microbiology Laboratory in Winnipeg.
Immune response
The key to the 1918 strain’s deadliness seems to be the effect of its H protein on molecules that are part of the host’s immune response, called pro-inflammatory cytokines. The severity of many viral diseases results from over-induction of this immune response (New Scientist print edition, 6 September, 2003).
Kawaoka’s team found that hybrid viruses carrying 1918 H induced cytokines that activated a class of white blood cells called macrophages. It also attracted white blood cells called neutrophils into the alveoli, or air sacs, of the lungs. There, instead of just fighting infected cells, they caused runaway damage to lung tissue.
The team warns that viruses equipped with a similar H could still be circulating among wild birds. And there may be little protection if it ever invades humans again. Kawaoka’s team found that, while people who experienced the 1918 flu have antibodies that neutralise the reconstructed 1918 H, people immune to currently-circulating flu viruses - even of the same family as the 1918 strain - have almost no protection.
Meanwhile, the shut-down of a vaccine plant in Liverpool, UK, belonging to Chiron Vaccines, which manufactures the flu vaccine, may result in vaccine supply problems in the US and the UK. The plant, closed amid fears that production had become contaminated, makes half of the flu vaccine for the US market.
Journal reference: Nature (vol 431, p 703)
Debora MacKenzie
http://www.newscientist.com/news/news.jsp?id=ns99996502
Re: Rise of the New Plagues Continues
Post by bigbunny on Oct 8, 2004, 7:56am
Pollutants 'in children's blood'
Environmental campaigners are warning potentially dangerous chemicals are present in children's blood.
A study of seven UK families by the World Wildlife Fund and the Co-operative Bank found children were worse affected than their grandparents.
The WWF says the chemicals, such as Organochlorine pesticides, should be phased out to protect children.
But some scientists say the fact a chemical is present does not necessarily mean it is dangerous.
The world is composed of 'chemicals' and that many of the most hazardous are natural
Medical Research Council's Institute for Environment and Health spokesman
Researchers carried out blood tests on 33 people aged from nine to 88, to see if any of 104 man-made chemicals were present.
Of the chemicals analysed, 80 were detected. Children were found to have 75 chemicals in their blood, 75 were found in parents and 56 in grandmothers.
Eighty-two percent of the people tested had at least one perfluorinated chemical in their blood.
DEHP - which is present in many plastics - was found in over three-quarters of the volunteers, including children.
It has been suggested the chemical could disrupt hormone levels.
Chemicals, such as PCBs and DDE - a breakdown product of the banned insecticide DDT - were found in everyone, despite being banned in the UK at least a decade before the children were born, but on average the older generations had higher concentrations.
Some of the children were also found to have higher concentrations of newer chemicals, such as brominated flame-retardants - used in everyday products such as furniture and TVs, and perfluorinated chemicals - used in the manufacture of non-stick pans, than older generations.
'Opportunity'
The researchers say their findings suggest all British children are likely to be contaminated with hazardous chemicals.
Justin Woolford, WWF Chemicals and Health Campaign Director, said: "These results are extremely worrying because of the unknown long-term health effects of the majority of industrial chemicals people are exposed to.
"The contamination of three generations of UK families, including children as young as nine, with hazardous man-made chemicals clearly illustrates that industry and government have failed to control these chemicals."
The WWF says proposed EU chemicals legislation, known as Reach, currently being considered by member states for consideration, provides a "once in a generation opportunity" to bring in controls for these substances.
But a spokesman for the Medical Research Council's Institute for Environment and Health in Leicester told BBC News Online: "The world is composed of 'chemicals' and many of the most hazardous are natural."
He added that the presence of 'older' chemicals such as DDT in all age groups was not surprising as they were "ubiquitous throughout the globe and very persistent" - which was why they were banned.
He said: "At first sight it is rather worrying that 'new' chemicals such as the brominated flame retardants are occurring at higher levels in the children.
"But we would need to see the rest of the data to assess the actual difference in levels and whether this is statistically and biologically significant."
Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/health/3723934.stm
Published: 2004/10/07 23:19:38 GMT
Re: Rise of the New Plagues Continues
Post by bigbunny on Oct 8, 2004, 7:57am
Teflon's sticky situation
By Chris Summers
BBC News Online
It's on saucepans, clothing, even buildings, but now Teflon - the famed non-stick chemical - is at the centre of a slippery controversy about cancer and birth defects.
Since its invention in the 1930s, amateur and professional cooks alike will acknowledge their debt of gratitude to Teflon. Over the years, the non-stick coating on pots and pans has helped turn out countless perfect fried eggs and cheese soufflés.
But for how much longer? Environmentalists have called for the withdrawal of a chemical which is a key ingredient in the manufacture of Teflon because of growing health fears.
Perfluorooctanoic Acid, PFOA for short, is a synthetic chemical used in the manufacture of advanced plastics including Teflon.
Today, all new man-made chemicals must undergo rigorous testing to be marketed in Europe. But PFOA is one of 100,000 or so chemicals which avoided the test because they were invented before 1981.
Teflon was invented in the 1930s by DuPont, the US firm which uses it today to make non-stick cookware, and also markets it as a coating for clothes and carpets.
The company recently agreed to an out-of-court settlement to a class action lawsuit brought by around 50,000 residents who lived near its West Virginia plant.
The residents, who lived along the Ohio river south of Parkersburg, West Virginia, claimed the company had contaminated local water supplies with PFOA, which they alleged was linked to birth defects and other health hazards.
Among the plaintiffs was Bucky Bailey, who was born with a single nostril and a deformed face. His mother fell pregnant with him while working at DuPont's Parkersburg plant.
DuPont eventually agreed to pay $50m in cash to the plaintiffs, plus $22m in legal costs. The company also agreed to spend $10m on special water treatment facilities to filter out PFOA.
But, crucially, DuPont did not accept liability and maintained PFOA did not pose any danger to the public.
Water tests
"We want to make very clear that settling this lawsuit in no way implies any admission of liability on DuPont's part," says DuPont lawyer Stacey J Mobley.
DuPont have some brilliant scientists.. I don't believe they couldn't find an alternative
Dr Tim Kropp
At the same time, DuPont is facing another multi-million dollar lawsuit from the US environmental watchdog for allegedly failing to disclose the results of secret water tests in 1984.
It faces being fined $27,000 for every day since 1984.
Now, environmental campaigners on both sides of the Atlantic want to ban the controversial chemical.
"PFOA accumulates in the body and in the environment and studies on animals suggest a link to birth defects. We are very concerned about it," says Karine Pellaumail, from Friends of the Earth.
Dr Tim Kropp, a toxicologist working for environmental activists in the US says tests carried out by the US firm 3M suggested high doses of PFOA led to various forms of cancer in rats.
"DuPont have some brilliant scientists and I don't believe that they couldn't find an alternative if they put their minds to it," says Dr Kropp.
'Respond with compassion'
But DuPont disagrees. "There is no evidence that PFOA is harmful," says its director of media relations, Clifton Webb. "We are very confident that there are no health effects associated with the public's exposure to PFOA at the levels we have seen."
FACTS ABOUT TEFLON
Invented in US in 1930s
1946, first marketed by DuPont as Teflon
Has the lowest coefficient of friction of any solid material known to man
Found on pots, pans, overcoats, bullets and pine lining
However, he accepts that, in high enough doses, PFOA could be carcinogenic to animals.
As for those who had suffered birth defects, such as Bucky Bailey, he says the firm would "respond with compassion and concern, but they are not related to exposure to PFOA".
According to 3M's tests, PFOA was present in five parts per billion in the bloodstream, says Mr Webb.
Workers exposed to it were likely to have a level "thousands of times higher", he concedes, but there was no evidence it was doing them harm.
As for substitutes, the company has identified around 100 possible alternatives to PFOA - which is used as a processing aid in Teflon - but none could produce the sufficient "quantity or quality" required. Cost, he says, is not an issue.
Last year the American Environmental Protection Agency (EPA) launched an investigation into the chemical's effects, a study that's being watched by the British government.
It acknowledges "considerable scientific uncertainties" on the issue but says there is no reason anyone should stop using Teflon products.
But the EPA is expected to submit a more comprehensive risk analysis next month.
Last year the British government called for a related chemical, perfluorooctane sulphonate (PFOS), to be withdrawn. It followed 3M's decision to abolish the chemical from its well-known Scotchgard products after health concerns were raised.
"PFOA is related to it but nowhere near as much research has been done into it and we are awaiting the outcome of the EPA's research," says a spokesman for Defra.
Others are seeking a more restrained response. Professor Scott Mabury, head of environmental chemistry at the University of Toronto, says a ban on PFOA would be "Draconian" and the answer was to go back to the factory and make sure residual levels of the polluting chemicals were removed in the production process.
"It's an engineering problem," he says. "It's not impossible."
Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/uk_news/magazine/3697324.stm
Published: 2004/10/07 09:21:24 GMT
Re: Rise of the New Plagues Continues
Post by bigbunny on Oct 8, 2004, 8:17am
Scientists Crack Secret Of
1918 Flu Virulence
Patricia A. Doyle, PhD
10-8-4
INFLUENZA A VIRUS, VIRULENCE, 1918 PANDEMIC STRAIN
Date: Thu 7 Oct 2004
From: ProMED-mail
Source: New York Times, Thu 7 Oct 2004 [edited]
http://www.nytimes.com/2004/10/07/science/07virus.html
Critical Gene A Suspect In Lethal Epidemic
By Nicholas Wade
10-8-4
By recreating the influenza virus that killed up to 50 million people in 1918-19, researchers may have identified the gene that turned it into one of the most lethal in human history. The gene, one of 8 in the virus, seems to have an unexpected capacity for sending the body's immune system into overdrive, causing inflammation, hemorrhage and death, the scientists report today in the journal Nature. The research team, led by Dr Yoshihiro Kawaoka of the University of Wisconsin, has been trying to determine just why the 1918 virus was so lethal and how defenses could be devised if a similar virus appeared in the future. Although the virus has long since perished, Dr Kawaoka and his colleagues were able to recreate it because the composition of its genes had been reconstructed from the preserved tissue of victims. The genes have been reconstituted over the last few years by Dr. Jeffery K Taubenberger and colleagues at the Armed Forces Institute of Pathology in Washington.
Drs Kawaoka, Taubenberger, and others have been reinserting the 1918-type genes into ordinary influenza viruses to see whether they can pinpoint which of the genes made the virus so lethal and how it did so. In the latest of these experiments, which Dr Kawaoka reports today, a gene called the haemagglutinin or HA gene seems to be largely responsible for the dire effects of Spanish flu, as the 1918 epidemic is also known. Recreating such a dangerous organism is not an experiment to be undertaken lightly. Dr Kawaoka's approach required replacing the HA and another gene in a mild influenza virus with the Spanish flu versions and infecting mice with the novel agent. Because of the obvious hazards, he at first conducted the work in the most secure type of biological laboratory, designated Biosafety Level 4, one of which was available at the National Microbiological Laboratory in Winnipeg, Canada. He said that after satisfying himself that the souped-up virus was susceptible to an antiviral agent known as Tamiflu, he transferred the research to a Biosafety Level 3 laboratory at the University of Wisconsin.
Dr R Timothy Mulcahy, chairman of the university's biosecurity task force, said that the chances of escape from the Biosafety Level 3 facility were minimal and that Dr Kawaoka had been "extremely prudent" in starting out at the higher level. "If there were an escape there would be treatments," Dr Mulcahy said. He noted that another group of researchers had already worked with similar engineered influenza viruses in a Level 3 facility owned by the Department of Agriculture in Athens, Ga.
The HA gene studied by Dr Kawaoka's team is well-known to flu experts because it changes from year to year. Since the protein made by the gene is the one singled out for attack by the immune system, the body's defenses are caught off guard each year as flu virus arrives with a novel version of the protein to which the body has no prior immunity. The HA protein's role is to latch onto the surface of human cells and then help the virus merge into the cell's outer membrane. Researchers recently worked out the exact 3-dimensional structure of the Spanish flu version of the HA protein, but could see no other function that it was designed to serve. The same is true of the other Spanish flu genes recovered by Dr. Taubenberger. In the current state of knowledge, the genes betray no clear hint of what made [the virus] so lethal.
That makes it necessary to conduct experiments like Dr Kawaoka's, in which researchers physically reconstruct the virus and try to understand how it works. What he has now found is that the Spanish flu version of the HA gene, in addition to its break-in and enter roles, seems able to trigger the release of cytokines, the signaling agents with which the immune system gears itself up for massive attack against an infectious agent. Uncontrolled overdrive can make the immune system kill the body in order to save it, through excessive inflammation. The virus carrying the Spanish flu version of the HA gene produced high levels of cytokines in mice, Dr Kawaoka says, and this is probably what led to the inflammation and lung damage that killed them.
Dr Adolfo Garcia-Sastre, a flu expert at the Mount Sinai School of Medicine who has constructed a similar virus, said the HA gene might be causing extra virulence simply by helping the virus replicate better, not because of any special effect on cytokine production. But either way, the finding helped focus attention on the gene's role, he said. Survivors of the 1918 epidemic have high levels of antibody to the engineered virus, Dr Kawaoka reports, but people infected recently with a similar class of influenza virus do not.
"Thus, a large section of the population would be susceptible to an outbreak of a 1918-like influenza virus," he and his colleagues conclude.
-- ProMED-mail
promed@promedmail.org
The reference for the paper cited above is as follows: Darwyn Kobasa, et al. Enhanced virulence of influenza A viruses with the haemagglutinin of the 1918 pandemic virus. Nature 2004; 431: 703-7 (7 Oct http://www.nature.com/cgitaf/DynaPage.taf?file=/
nature/journal/v431/n7009/abs/nature02951_fs.html . The 19 authors are from the Department of Pathobiological Sciences, University of Wisconsin, Madison, Wisconsin, the Special Pathogens Program, National Microbiology Laboratory, Health Canada and Department of Medical Microbiology, University of Manitoba, Winnipeg, Manitoba, Canada, and 7 research institutions in Japan.
The introduction to the paper states that: "The 'Spanish' influenza pandemic of 1918-19 was the most devastating outbreak of infectious disease in recorded history. At least 20 million people died from their illness, which was characterized by an unusually severe and rapid clinical course. The complete sequencing of several genes of the 1918 influenza virus has made it possible to study the functions of the proteins encoded by these genes in viruses generated by reverse genetics, a technique that permits the generation of infectious viruses entirely from cloned complementary DNA.
Thus, to identify properties of the 1918 pandemic influenza A strain that might be related to its extraordinary virulence, viruses were produced containing the viral haemagglutinin (HA) and neuraminidase (NA) genes of the 1918 strain. The HA of this strain supports the pathogenicity of a mouse-adapted virus in this animal. Here we demonstrate that the HA of the 1918 virus confers enhanced pathogenicity in mice to recent human viruses that are otherwise non-pathogenic in this host. Moreover, these highly virulent recombinant viruses expressing the 1918 viral HA could infect the entire lung and induce high levels of macrophage-derived chemokines and cytokines, which resulted in infiltration of inflammatory cells and severe haemorrhage, hallmarks of the illness produced during the original pandemic."
This is a significant piece of research, suggesting that the virulence of the 1918 pandemic influenza virus may have been a property of its HA gene. However, it does not identify the specific feature of this HA molecule that promotes the enhanced inflammatory response (in mice). - Mod.CP
Patricia A. Doyle, PhD
Re: Rise of the New Plagues Continues
Post by bigbunny on Oct 8, 2004, 8:17am
More Madness - US Officials
Try To Salvage
Tainted Flu Shots
Patricia A. Doyle, PhD
10-8-4
Hello Jeff - This is just amazing! US officials are trying to salvage some of the tainted Chiron flu shots for use on the public which will comprise mainly the elderly and infirm...and when (not if) people taking the tainted shots get ill and die, their death certificates will probably read cause of death as influenza and not bad vaccine.
I believe the interest in getting the vaccine to market is purely monetary. Taking contaminated vaccine is far more risky then getting influenza.
Anyone who gets a flu shot this Fall has NO WAY of knowing where the vaccine was manufactured or if it is from the tainted vaccine. This sounds like Russian Roulette. It doubtful that the patient would be told the truth. I really don't see doctors or health clinics waring patients that the shot they are getting might be contaminated. It is simply a toss of the dice. A mighty big gamble.
Patricia Doyle
http://www.wnbc.com/health/3790466/detail.html
U.S. Officials Try To Salvage Flu Shots From Tainted Supply
Anxious Patients Stand In Long Lines For Shots
10-7-4
With flu shot clinics being canceled nationwide, U.S. health officials are trying to salvage some vaccine held up in a British factory.
They met with British regulators in London on Thursday to discuss Britain's move to temporarily shut down Chiron Corp., the supplier of half the American flu vaccine supply.
Britain defended the move, which stunned U.S. health officials this week. They say the vaccine was tainted with a bacteria.
American health officials wanted to examine test results. They also will visit the Chiron factory where the vaccine is being held to see if any can be salvaged.
Back in the United States, phones have been ringing off the hook in doctors' offices with patients eager to get the vaccine.
Flu shot clinics that have gone on despite the shortage have seen huge lines. In Potomac, Md., a flu shot clinic at a grocery store had such a large turnout that police had to be called to direct traffic.
U.S. health officials are scrambling to find out which cities and states will have the worst vaccine shortages.
The Centers for Disease Control and Prevention says it'll be weeks before that can happen. Most of the doses have gone to private distributors, not state health departments.
The government says it will urge those distributors to ration the vaccine out to those most in need -- the youngest, oldest and sickest.
"We don't get most of the high-risk people anyway. In a sense, the added focus will bring more of those people out and get them to medical care. A silver lining in a cloud," said Dr. Michael Elkort, of Newton-Wellesley Hospital in Massachusetts.
"At risk" patients include: children between 6 months and 23 months old; adults 65 years and older; anyone with underlying chronic medical conditions; some pregnant women; and health-care workers and child-care providers.
"We're concerned there's not enough in the country to give to the children," said Lorretta Chow, mother of a 2-year-old.
However, experts say that Chiron didn't make any of vaccines designed for young children, so the supplies of that vaccine won't be affected by the shortage.
Previous Stories:
October 6, 2004: Officials, Doctors Worry About Flu Vaccine Shortage
October 6, 2004: Facing Flu Vaccine Shortage, Officials Urge Rationing
Distributed by Internet Broadcasting Systems, Inc. The Associated Press contributed to this report. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.
Patricia A. Doyle, PhD
Re: Rise of the New Plagues Continues
Post by bigbunny on Oct 9, 2004, 10:25am
Source: University Of Toronto
Date: 2004-10-04
URL: http://www.sciencedaily.com/releases/2004/10/041004192941.htm
Offspring At Risk From Maternal Occupational Exposure To Solvents
TORONTO -- Researchers at The Hospital for Sick Children (Sick Kids) and the University of Toronto (U of T) have linked maternal exposure to organic solvents in the workplace with poorer performance on measures of neurocognitive function, language, and behaviour in offspring. This research is reported in the October 2004 issue of the journal Archives of Pediatrics and Adolescent Medicine.
There are many types of organic solvents, but they all share chemical properties that make them easily inhaled and they can easily penetrate skin. Work environments where solvents are used include manufacturing and industry jobs involving painting and plastic adhesives, nail salons, dry-cleaning operations, and medical laboratories.
"Reducing exposure to organic solvents during pregnancy is warranted until a more refined risk assessment is possible," said Dr. Gideon Koren, the study's principal investigator, director of Sick Kids' Motherisk Program, a senior scientist in the Sick Kids Research Institute, and a professor of Paediatrics, Pharmacology, Pharmacy and Medicine and Medical Genetics at U of T. "We need to look at dose and exposure to specific solvents, as well the time during pregnancy of exposure."
The study looked at 32 women who were exposed to organic solvents in the workplace for at least eight weeks of pregnancy, starting in the first trimester, along with their children, who were between the ages of three and nine years (at the time of testing). The exposed women reported a high level of protective equipment use at work. These women were matched with non-exposed women in a control group, and their children.
"We found that the children of the exposed women had significantly lower verbal cognitive functioning than the non-exposed children in the control group. We also saw greater inattention and hyperactivity in the exposed children," said Dr. Maru Barrera, a co-author of the study, a psychologist and associate scientist at Sick Kids, and an associate professor of Population Health Sciences and Human Development and Applied Psychology at U of T.
Other members of the research team included Dr. Dionne Laslo-Baker, the study's lead author, Dafna Knittel-Keren, Dr. Eran Kozer, Dr. Jacob Wolpin, Dr. Sohail Khattak, Dr. Richard Hackman, and Dr. Joanne Rovet, all from Sick Kids.
The study was supported by Physician Services Inc. and Sick Kids Foundation. Dr. Laslo-Baker received a doctoral research award from the Canadian Institutes of Health Research (CIHR). Dr. Koren holds a CIHR Senior Investigator Award and is the holder of the Research Leadership in Better Pharmacology During Pregnancy and Lactation and The Ivey Chair in Molecular Toxicology at the University of Western Ontario.
The Hospital for Sick Children, affiliated with the University of Toronto, is Canada's most research-intensive hospital and the largest centre dedicated to improving children's health in the country. Its mission is to provide the best in family-centred, compassionate care, to lead in scientific and clinical advancement, and to prepare the next generation of leaders in child health.
Pregnant women exposed to organic solvents in the workplace can call Sick Kids' Motherisk Program at 416-813-6780 for further information.
This story has been adapted from a news release issued by University Of Toronto.
Re: Rise of the New Plagues Continues
Post by bigbunny on Oct 11, 2004, 9:08am
More Insanity - 1918 Flu
Research In BSL
3 NOT BSL 4
From Patricia Doyle, PhD
Hello, Jeff - I was releived to read the following concerns of other scientists regarding working with the letal 1918 flu hybrid using BSL 3 instead of BSL 4.
In my opinion finding and working with the two genes expressing lethality should mandate the pathogen as a bioweapon and clearly should be worked on using BSL 4.
I shutter to think what accidental release of this new 1918 flu strain would mean in terms of lives lost. ....or, theft of the pathogen by persons unknown!
Patricia Doyle
INFLUENZA A VIRUS, VIRULENCE, 1918 PANDEMIC STRAIN (02)
A ProMED-mail post
ProMED-mail is a program of the
International Society for Infectious Diseases
http://www.isid.org
Date: Fri 8 Oct 2004
From: Karl M Johnson
A comment on appropriate level of containment...
Professor Kawaoka's team is to be congratulated for successful recreation of the 1918 influenza virus with it apparent increased virulence for mice. But if that virulence transfers to humans, I am deeply concerned about his decision to take the agent from BSL-4 [biosafety level 4] containment to BSL-3 [biosafety level 3] after finding that level of pathogenicity. We have already experienced 3 breaks in technique and containment of the SARS coronavirus this year. Escape of this influenza strain could lead to a repeat of history that would be completely preventable if that virus were "put back in its box".
Personally, I would never permit work with this agent under conditions lower than BSL-4. The University of Wisconsin and appropriate federal agencies should convene an emergency meeting to sort this out, ensuring that Dr Kawaoka has ongoing access to BSL-4 containment so that he can continue this undeniably important work.
--
Karl M Johnson
<KarlMJohnson@aol.com>
[Dr Johnson expresses valid concerns about the disease security aspects of Dr Kawaoka's research, particularly in view of the finding of the enhanced pathogenicity of the construct containing the 1918 HA subunit. His call for a reassessment of the situation should be heeded. - Mod.CP]
Patricia A. Doyle, PhD
Re: Rise of the New Plagues Continues
Post by bigbunny on Oct 11, 2004, 9:09am
More Concerns On Lethal
1918 Flu In BSL 3 Labs
From Patricia Doyle, PhD
dr_p_doyle@hotmail.com.com
10-10-4
Hello Jeff - I have included below some comments regarding the lack of safety by researchers who have reconstructed the 1918 pandemic strain of Influenza. The research team had been using BSL 4 but, has now dropped down to BSL 3.
The comments below are by scientists who have serious reservations about the BSL now used for the LETHAL flu virus research. SARS escaped the research lab by infecting researchers working on the virus.
The comments below also include worries about bioterrorists. The new letal 1918/contemporary hybrid is a ticking time bomb. In this modern age of technology, we were unable to safely provide contemporary flu vaccine. Can you imagine the chaos should this new reconstructed letal 1918 flu virus escape the lab?
According to Dr. Kawaoka, "we have tamiflu, therefore BSL 3 should be sufficient for the new hybrid 1918 flu."
Amazing. Seems like they just don't care about the public safety anymore.
Patricia Doyle
INFLUENZA A VIRUS, VIRULENCE, 1918 PANDEMIC STRAIN (03)
A ProMED-mail post
ProMED-mail is a program of the
International Society for Infectious Diseases
http://www.isid.org
Date: Fri 8 Oct 2004
From: Myron Pulier
Further comment on the disease security issue -
In the press report cited in the ProMED-mail post archived as "Influenza A virus, virulence, 1918 pandemic strain 20041007.2754", Dr Kawaoka seems to indicate that the possibility of treatment of other influenza type A strains with "Tamiflu" (oseltamivir) makes biosafety level 3 containment sufficiently prudent for his new 1918 pandemic-like one.
However, shortening duration of symptoms once they appear and preventing development of clinical illness by initiating treatment shortly after exposure does not necessarily amount to maintaining sufficient control of person-to-person spread to prevent another pandemic, should the virus infect someone. Even in clinical research, few drugs are 100 per cent effective; and in actual clinical use, effectiveness is less than efficacy, so that some patients may not respond well to treatment. Prophylaxis against illness is not the same as prevention of infection and leaves open the potential for transmission by an asymptomatic carrier.
Furthermore, oseltamivir has not been tested clinically against any comparably virulent strain, and potential of the virus for rapid extension throughout the lungs might overwhelm the protection offered by the drug, however unlikely that may seem at present. Presumably Dr Kawaoka has determined through experiment that his particular strain happens not to be one that is resistant to oseltamivir at pharmacologic concentrations, and hopefully there will be no opportunity for his viruses to pick up or develop alleles that confer resistance.
Nonetheless, with stakes so high, it may pay to return the reconstructed virus to a level 4 facility... and to take special steps to secure that facility against bioterrorists.
----
Myron L Pulier, MD
Clin Assoc Prof Psychiatry
UMDNJ-NJ Medical School
pulierml@umdnj.edu
Archive Number 20041008.2757
Published Date 08-OCT-2004
Subject PRO Influenza A virus, virulence, 1918 pandemic strain (02)
Date: Fri 8 Oct 2004
From: Karl M Johnson
A comment on appropriate level of containment -
Professor Kawaoka's team is to be congratulated for successful recreation of the 1918 influenza virus with it apparent increased virulence for mice. But if that virulence transfers to humans, I am deeply concerned about his decision to take the agent from BSL-4 [biosafety level 4] containment to BSL-3 [biosafety level 3] after finding that level of pathogenicity. We have already experienced 3 breaks in technique and containment of the SARS coronavirus this year. Escape of this influenza strain could lead to a repeat of history that would be completely preventable if that virus were "put back in its box".
Personally, I would never permit work with this agent under conditions lower than BSL-4. The University of Wisconsin and appropriate federal agencies should convene an emergency meeting to sort this out, ensuring that Dr Kawaoka has ongoing access to BSL-4 containment so that he can continue this undeniably important work.
[Dr Johnson expresses valid concerns about the disease security aspects of Dr Kawaoka's research, particularly in view of the finding of the enhanced pathogenicity of the construct containing the 1918 HA subunit. His call for a reassessment of the situation should be heeded. - Mod.CP]
Patricia A. Doyle, PhD
Re: Rise of the New Plagues Continues
Post by bigbunny on Oct 17, 2004, 10:54am
It is postulated that one cause of mental illness is infectious diseases such as Lyme Disease. Please note that this letter is from a 1998 journal before the CTs really became a problem:
Infectious Diseases and Mental Illness:
Is There a Link?
To the Editor: The report by Hatalski et al. (1) on Borna virus as a probable human pathogen provides yet another example of an infectious agent being tentatively associated with neuropsychiatric disorders. Earlier this year, researchers at Rockefeller University and the National Institute of Mental Health suggested that after streptococcal infection, some children may be at increased
risk for obsessive-compulsive disorders and Tourette syndrome (2). The human B-cell antigen D8/17, believed to be a marker for increased susceptibility to oststreptococcal rheumatic heart disease, has been tentatively linked to this increased risk for psychiatric illness in children.
Other reports of patients with complicated Lyme borreliosis, including some whose infections have progressed to encephalopathies, describe persistent verbal and memory deficits among these patients (3). In a few Lyme disease patients, the only overt symptoms of disease at the time of initial diagnosis and treatment were classified as mental confusion (4). Two newly emergent
infectious diseases in the United States, leptospirosis and neurocysticercosis, have been found among inner city residents and poor immigrants, respectively. Occasionally leptospirosis has been associated with a variety of postinfectious psychiatric symptoms, including depression,
dementia, and psychosis (5). Neurocysticercosis, a tropical parasitic infection, is increasingly associated with emergency room admissions for seizures and epilepsy (6). Still other infectious diseases are being examined for links with cognitive symptoms and emotional disorders.
The primary cause of many common psychiatric disorders, including depression, manic depression, anxiety, and schizophrenia, remains a mystery. The World Health Organization estimates that 1.5 billion people worldwide
suffer from a neuropsychiatric disorder. Of the 10 leading causes of disability in 1990, four were psychiatric disorders: unipolar depression, manic depression, schizophrenia, and obsessive-compulsive disorders (7). The National Institute of Mental Health recently estimated that as many as 20% of young Americans ages 7 to 14—
approximately 10 million children—have mental health problems severe enough to compromise their ability to function (8). Infectious agents mayplay a role in some of these diseases to some unknown degree. A better understanding of the role of infection may speed treatment and prevention efforts and reduce the degree of disability and stigma associated with mental illness.
Vaccines and antimicrobial agents might enhance current therapeutic options for mental illnesses. Even if infectious diseases were a primary factor in only 1% of neuropsychiatric illnesses, some 10 million persons might benefit from antimicrobial therapies. Identifying those
susceptible to neuropsychiatric illnesses (because of environmental factors or genetic predisposition) may also permit vaccination or antimicrobial prophylaxis and a subsequent lowering of disease incidence.
Physicians and federal agencies addressing the problems of emerging infectious diseases should examine the possibility of infection as a cause of mental illness. Better communication among infectious disease and mental health experts, as well as additional training, will be
needed to shed light on the growing phenomenon of infectious diseases manifesting themselves as neuropsychiatric disorders.
Edward McSweegan
National Institute of Allergy and Infectious
Diseases, Bethesda, Maryland, USA
References
1. Hatalski CG, Lewis AJ, Lipkin WI. Borna disease. Emerg Infect Dis 1997;3:129-35.
2. Swedo SE, Leonard HL, Mittleman BB, Allen AJ, Rapoport JL, Dow SP, et al. Identification of children with pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections by a marker associated with rheumatic fever. Am J Psychiatry 1997;154:110-2.
3. Benke T, Gasse T, Hittmair-Delazer M, Schmutzhard E. Lyme encephalopathy: long-term neuropsychological deficits years after acute neuroborreliosis. Acta Neurol Scand 1995;91:353-7.
4. Fallon BA, Nields JA. Lyme disease: a neuropsychiatric illness. Am J Psychiatry 1994;151:1571-83.
5. Mumford C, Dudley N, Terry H. Leptospirosis presenting as a flaccid paraplegia. Postgrad Med J 1990;66:218-20.
6. Garcia H, Tsang V, Gonzalez A, Gilman R. Cysticercosis in the U.S. and Peru. Presented at the 6th Annual National Institutes of Health International Centers for Tropical Disease Research Meeting; 1997 May 5-7; Bethesda, Maryland.
7. World Health Organization. The global burden of disease [cited 1998 Jan 5]; [2 screens]. Available from URL: http://www.who.ch/programmes/mnh/msamain.htm
8. Children’s mental health research severely neglected, says National Institute of Mental Health Director. Washington Fax [serial online] 1997 Apr 8 [cited 1998 Jan 5]. Available from URL: http://www.washington-fax.com
http://www.cdc.gov/ncidod/EID/vol4no1/adobe/vol4no1.pdf
Re: Rise of the New Plagues Continues
Post by bigbunny on Oct 17, 2004, 11:44am
Lyme Disease is a curiosity. It is said to be borne by Ticks and apparently requires a mechanism whereby the host is burrowed into disease carrying-agent. Remarkably we have seen in recent times the photos of "tendrils" or polymer fibres in the air and we have seen the presence of these fibres in the wounds of the afflicted.
It strikes me that many of pathogens comprising the "New Plagues" can be distributed via these polymer fibres given the observed behaviour of these fibres when in contact with humans.
If this proposition has any merit then the analyses which rely upon the traditional means of disease transmission must be clearly wrong.
As to whether this is an intended consequence of the CTs one cannot say unless and until the reason for the use of these polymer fibres is finally discerned.
Re: Rise of the New Plagues Continues
Post by bigbunny on Oct 19, 2004, 7:05am
This behaviour of bacteria may explain why certain new plagues are appearing:
Bacteria are genetically modified by lightning
10:12 19 October 04
http://www.newscientist.com/news/news.jsp?id=ns99996525
Lightning is nature’s own genetic engineer. By opening up pores in soil bacteria it allows them to pick up any stray DNA present, report Timothy Vogel, Pascal Simonet and their colleagues at the University of Lyon in France.
This hitherto unknown phenomenon might help explain why gene swapping is so common among bacteria.
Mild electric shocks are routinely used to genetically engineer bacteria in the lab, so Vogel and Simonet wondered whether lightning could have the same effect. Although it would kill bacteria near the point of contact, those further away would get a milder shock.
The researchers persuaded physicist colleagues to blast bacteria with artificial lightning. So far they have shown that two strains of the soil bacterium Pseudomonas - as well as a lab strain of E. coli - take up “bait” DNA when zapped by lightning.
The researchers suspect the phenomenon is widespread, speeding up the rate at which bacteria evolve. Genetic studies show bacteria frequently pick up foreign genes, usually from other bacteria, but natural DNA uptake rates are too sluggish to explain the observed diversity.
Lightning might also have speeded up the evolution of the first bacteria, Vogel says.
Journal reference: Applied and Environmental Microbiology (DOI: 10.1128/AEM.70.10.6342-6346.2004)
Andy Coghlan
Re: Rise of the New Plagues Continues
Post by bigbunny on Oct 24, 2004, 9:49am
It's Official: TV Linked to Attention Deficit
by Jean Lotus
A study from the American Academy of Pediatrics shows that watching videos as a toddler may lead to Attention Deficit Hyperactivity Disorder (ADHD, also called ADD in UK) in later life.
TV watching "rewires" an infant’s brain, says Dr. Dimitri A. Christakis lead researcher and director of the Child Health Institute at Children’s Hospital and Regional Medical Center, Seattle, Wash. The damage shows up at age 7 when children have difficulty paying attention in school.
"In contrast to the way real life unfolds and is experienced by young children, the pace of TV is greatly sped up." says Christakis. His research appears in the April 2004 issue of Pediatrics. Quick scene shifts of video images become "normal," to a baby "when in fact, it’s decidedly not normal or natural." Christakis says. Exposing a baby’s developing brain to videos may overstimulate it, causing permanent changes in developing neural pathways.
"Also in question is whether the insistent noise of television in the home may interfere with the development of ‘inner speech’ by which a child learns to think through problems and plans and restrain impulsive responding," wrote Jane Healy, psychologist and child brain expert in the magazine’s commentary.
Babies brains grow rapidly
Even a child playing with its own fingers has the neural patterning that comes from bending, flexing, stretching and grasping. Scientists tell us that the brain develops in completely unique ways between birth and three years. As a kiddie viddie baby sits "mesmerized", neural paths are not being created. This is crucial brain development that stops by age three.
"You don’t want to think that something as innocent as half-an-hour’s peace and quiet could reduce your kid’s chances later in life," says Claire Eaton, 27-year-old mother from Lewisham, Australia.
Setting up baby for failure in school
Are parents who use infant videos such as "Baby Einstein" and "Teletubbies" putting their child at risk for a lifetime of Special Ed classes, school "behavioral therapy" and Ritalin?
In the study of more than 2,000 children, Christakis found that for every hour watched at age one and age three, the children had almost a ten percent higher chance of developing attention problems that could be diagnosed as ADHD by age 7. A toddler watching three hours of infant television daily had nearly a 30 percent higher chance of having attention problems in school.
Infant videos: They wouldn’t sell them if they were dangerous --Would they?
An explosion of kidvids for the bouncy chair set has hit the market. These include Baby Einstein, Baby Mozart, So Smart etc. TV shows, such as Teletubbies, aim at 18-month-old toddlers. These videos are peddled as "educational tools" to "give your baby a head start." The truth is, they are a video-tether that keeps baby out from underfoot.
"Max is learning German right now from a video"
Parents take away crucial life experiences from their child every time they pop in Baby Einstein. But they do love how it takes the baby out of their hair for awhile Listen to what parents say in testimonials about infant videos:
"I love spending time with my boy but let's face it, there are times when you just have to have 10 minutes or so to yourself so that you can wash the dishes or do laundry; that's when you pop this video in. It's 25 minutes of entertainment that holds the attention of even very young children. ," (son 10 months) Chris Hudson from San Antonio, TX.
There are times I rewind it and play it again and again until I get the dishes done and order restored. My son is captivated (and hopefully learning something). Mom I n Connecticut
The only thing I wish is that the videos were longer than 30min. Melissa Perruzi, Clinton Mississippi
(From Baby Eisntein reviews on Amazon.com).
Big problem for little people
Twenty-six percent of US children younger than age two have TV in their bedrooms - often watched from the crib, and 36 percent of families leave the TV on almost all of the time, even when no one is watching, according to a 2000 Kaiser Family Foundation study.
Don’t put your child at risk!
The good news is, infants and toddlers don’t need television to distract them. Humans raised children for 50,000 years before television sets and you can do it too. Your children can learn to entertain themselves or play with your supervision.
"When one-year olds are playing with a toy, they can explore it, poke at it, drop it," says Yale University Television Researcher Dorothy Singer. "They’re learning about space, about sound, and they’re developing sense of competence. Watching a TV show just doesn’t provide the same sensory experience."
Leaving a child alone with the TV is never a good idea.
"Would you entrust you toddler into the care of a baby sitter, even for a few minutes, who cannot hear or see your child?" writes Nancy Hall of Yale University’s Bush Center in Child Development and Social Policy. "Would you leave your child in an environment that encourages passivity, limits creativity and results in increased aggressive behavior? Many 1-year-olds are spending time regularly with just such a baby sitter: the television set."
What is Attention Deficit Hyperactivity Disorder?
ADHD affects 12 percent of US school children and has increased dramatically over the past 50 years. Studies show ADHD increased with the introduction of children’s television in the 1950s and then spiked higher in the mid 1980s when VCRs and home video became commonplace. Although the condition is known to be genetic, scientists have noted its rapid spread throughout every social class of children, and guessed that there could be an environmental cause. TV watching is a cause, this study shows.
How much TV should I let my baby watch?
No child under age two should watch television at all, the Academy of American Pediatrics advised in 1998. Doctors blame TV for increasing aggression and obesity in children, now they add ADHD risk to early TV use.
http://www.whitedot.org/issue/iss_story.asp?slug=ADHD%20Toddlers
Re: Rise of the New Plagues Continues
Post by bigbunny on Oct 27, 2004, 6:51pm
Glowing insect bug 'harms humans'
A new disease has been identified caused by a luminous bug that has evolved in insects, scientists say.
There have been about a dozen cases of the bug - Photorhabdus asymbiotica - in the US and Australia, which causes pustulant sores to appear on the body.
In insects, the disease leaves the bodies glowing, the University of Bath and London School of Hygiene and Tropical Medicine scientists said.
They are now warning more insect bugs may mutate to threaten humans.
The team believe the sores caused Photorhabdus asymbiotica may also glow but this has not been proved so far as victims have been treated before tests could be done.
Insects are numerous and reside in close proximity to man, yet they have been generally ignored as a potential source of microbes that could be harmful for man
Dr Nick Waterfield, of the University of Bath
The scientists have also said it could be more common than has been reported as it may have been diagnosed as something else.
The findings, revealed in the latest edition of the Nature Reviews Microbiology website, are part of a wider research project looking at the emergence of diseases.
While the infection can be easily treated and is not considered dangerous, the team said bacteria in insects could soon mutate to throw up potentially deadly diseases.
DNA studies have suggested the bubonic plague, which killed millions of people in the 14th and 17th centuries, emerged from insects as does anthrax.
Malaria, a disease closely associated with insects, is only carried by mosquitos, it is not an insect-based disease as the plague was thought to be.
Similarities between human and insect immune systems mean that many of the bacteria that causes insect diseases have a head start in mutating to attack humans.
Dr Nick Waterfield, from the University of Bath, said: "Most scientists are looking at diseases of farm animals as the biggest threat to humans.
"Insects are numerous and reside in close proximity to man, yet they have been generally ignored as a potential source of microbes that could be harmful for man.
"As well as passing microbes directly into our bloodstream when they bite us, insects can also act as a reservoir to `cook up' future human diseases.
"Understanding the mechanism that the bacteria use to change their disease-causing ability is important if we are to successfully treat emerging infectious diseases before they get out of control and become epidemics."
He also said the situation was being complicated by climate change, which has meant insects can survive and breed in more places.
Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/health/3951889.stm
Published: 2004/10/25 14:15:13 GMT
Re: Rise of the New Plagues Continues
Post by bigbunny on Oct 27, 2004, 6:52pm
Aids warning over bushmeat trade
A study of African hunters has shown that a virus similar to HIV has passed from apes to humans from bushmeat of the kind that is being sold illegally in the UK.
A leading scientist has told the File On 4 programme that the virus was probably passed on to tribesmen via body fluids when the animals were slaughtered and butchered.
Assistant Professor Nathan Wolfe, who tested more than 1,000 hunters for Johns Hopkins University, found a retrovirus from the same family as HIV in a number of them.
This is most likely the mechanism by which HIV emerged into the human population
Nathan Wolfe, Johns Hopkins University
"This is the area of the world where HIV came from, and this is most likely the mechanism by which HIV emerged into the human population," he said.
Although the full public health implications are still unknown, the fear is that the new virus could result in a new disease which would have global impact.
UK imports
The File On 4 team accompanied environmental health officers to spot inspections at London shops where they found illegal bushmeat from West and Central Africa.
About 5 million tonnes of bushmeat, which originates from animals such as antelopes, snakes, gorillas and elephants, is eaten in these regions of Africa every year.
It is estimated that 12,000 tonnes of all manner of illegal meat is smuggled into the UK annually, a significant proportion of which is thought likely to be bushmeat.
There may also be serious implications for the health of British domestic livestock as the foot and mouth outbreak was linked to illegal meat imports in 2001.
Under cover
Posing as rich white loggers and accompanied by an undercover worker from the Last Great Ape project, File On 4 journalists travelled to Cameroon where pygmy hunters offered to kill gorillas, seen as the best meat.
All they wanted in return was the ammunition and the meat of the gorilla to eat.
The journalists were offered the skull, palms, and legs of the gorilla free of charge as long as they could provide the bullets to shoot it.
One pygmy said they had lost count of the number of gorillas they had killed.
Abject poverty forces such hunters to kill any animal, no matter how rare or unfit for human consumption, and transport it out of the country through black markets.
It is not known whether anybody has become sick from the virus.
File on 4 is broadcast on Radio 4 on Tuesday 26 October at 2000 BST and repeated at 1700 BST on Sunday 31 October.
Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/programmes/file_on_4/3954963.stm
Published: 2004/10/26 13:27:14 GMT
Re: Rise of the New Plagues Continues
Post by bigbunny on Oct 29, 2004, 8:24pm
TB poses major threat to millions
Tuberculosis will continue to kill millions in developing countries unless radical action is taken, an aid organisation has warned.
TB can be easily treated, but Medecins San Frontieres says inadequate attempts to control the disease mean it is now spiralling out of control.
MSF says drug-resistant strains, coupled with HIV pose a major threat.
The charity is calling for massive investment in developing new diagnostic tests and drugs.
TB kills people in the thousands without us being able to detect or treat them properly, or in time.
Dr Jean-Herve Bradol
New TB drugs and diagnostic tests are being developed by initiatives such as the Global TB Alliance and FIND (Foundation for Innovative New Diagnostics).
However, MSF says action is also required to ensure all people with TB are guaranteed access to care.
Frustration
Dr Jean-Herve Bradol, president of MSF France, said: "Tuberculosis is one of our biggest frustrations as medical professionals.
"In the countries MSF works in, TB kills people in the thousands without us being able to detect or treat them properly, or in time."
Dr Francine Mattys, TB advisor of the MSF Campaign for Access to Essential Medicines, said radical action was required to tackle the problem.
She said: "Massive investment in developing new diagnostic tests and drugs is needed now, so that we can effectively diagnose and treat all those with TB in the shortest possible time."
Inadequate test
Most TB programmes in developing countries rely on sputum microscopy for detection of TB.
Developed in 1882, this method only detects the bacilli that cause the disease in about 50% of all people with TB.
Its performance is even poorer in children and people infected with HIV.
Treatment of TB is long and relies on medicines that were invented 40-60 years ago.
Dr Ilse Ramboer, a physician from MSF's TB programme in Guinea Gonakry, said: "In Guinea, and many other developing countries, we regularly see people who have already been treated for TB but return a year or two later with new TB-like symptoms."
"These people could be re-infection cases. But they could also be on their way to developing multidrug-resistant TB - there is no way of telling because most resource-poor settings have no access to drug sensitivity testing."
Experts fear that the combination of multidrug-resistant TB and HIV/Aids could have a devastating impact in Africa.
MSF treats roughly 20,000 TB patients every year in over 30 projects around the world.
The issue will be discussed at the Union World Conference on Lung Health in Paris later this week.
Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/health/3954721.stm
Published: 2004/10/26 11:15:50 GMT
Re: Rise of the New Plagues Continues
Post by bigbunny on Oct 29, 2004, 9:06pm
Newborn mice given Prozac grow up depressed
17:00 26 October 04
Mice treated with the antidepressant Prozac early in life grow into adults with emotional problems, a new report concludes.
Whether the drug has the same effect on people is unknown. But the result will add to the growing debate over what risks Prozac (fluoxetine) and similar SSRI drugs (selective serotonin reuptake inhibitors) pose for young children and unborn babies.
"If they really need these drugs, people should take them. They can be life savers," says Jay Gingrich, a psychiatrist at Columbia University in New York City, US, who led the research. "But it is a little bit alarming to find they might carry risks that aren't apparent until later in life."
Researchers began injecting mice with fluoxetine four days after birth until they were 21 days old. Nine weeks after their last injection, the adult animals were given a series of behavioural tests designed to assess their level of anxiety and depression.
The team found that rodents who received drug as newborns were more intimidated by new surroundings and moved more slowly to avoid painful shocks compared to controls. "They are more inhibited in novel situations," says Gingrich. "Extrapolating to people, we'd say the mice are showing symptoms of anxiety and depression or emotional problems."
Suicidal thoughts
"It's fascinating," says Tim Oberlander, a developmental paediatrician at the University of British Columbia in Vancouver, Canada. "It suggests these chemicals can cause crucial changes in the developing brain."
SSRIs work by increasing the level of the neurotransmitter serotonin in the brain and can be extremely effective in treating depression. They have been widely prescribed and make huge amounts of money for the drug companies that sell them.
But the drugs have become the focus of some controversy. Recently, for example, GlaxoSmithKline was accused of withholding data from clinical trials, the results of which suggested that depressed children taking their SSRI drug Paxil (paroxetine) had more suicidal thoughts than placebo controls.
The use of SSRIs by pregnant women has been considered safe. For example, studies have shown that these women give birth to babies of normal weights, with unimpaired cognitive and language skills. But more recent research has suggested these medications may cause subtle neurological changes in the developing fetus.
Two years ago, for example, Oberlander and his colleagues reported that babies exposed to SSRIs in the womb were less sensitive to pain. And earlier in 2004, other researchers reported that SSRI-exposed infants had altered sleep patterns and a higher incidence of tremors. But it is not clear if these effects disappear soon after birth.
Difficult decisions
Gingrich's work suggests that even transient treatment with Prozac - and potentially other SSRIs - can have lasting, paradoxical changes. Even though the drug can treat depression in adult mice, it seems to trigger symptoms of depression in mice exposed to it as newborns.
"It suggests that the immature nervous system responds very differently than a mature one to the same drug," he says.
Even with this new evidence, pregnant women with depression still face a difficult decision over whether or not to take SSRIs, says Gingrich. Being depressed carries its own risks to babies since it can lead to poor care-giving and self-harm.
"It's important to assess for each patient whether there are non-pharmacological ways of addressing these emotional problems, while we try to get a handle on what the risks really are," he says.
Journal reference: Science (vol 306, p 879)
http://www.newscientist.com/news/news.jsp?id=ns99996579
Re: Rise of the New Plagues Continues
Post by bigbunny on Oct 30, 2004, 8:15am
While the "news" is relatively old it is nice to have the truth confirmed:
Power Lines Double Risk Of Cancer In Children
By Charles Arthur
Technology Editor
The Independent - UK
10-30-4
Living near a high-voltage power line roughly doubles the risk of childhood cancers such as leukaemia, scientists say.
Dr Gerald Draper of the Oxford-based Childhood Cancer Research Group said a recent study he led looked at 35,000 cases of childhood leukaemia and other cancers between 1962 and 1995, and results suggest a slightly higher chance of children living within 100 metres of a high-tension overhead cable developing the disease.
But he angrily denied claims that the work had been suppressed by himself or the Department of Health, which commissioned the study. He also emphasised that the link to childhood cancers was weak.
An independent group, the Trentham Environmental Action Campaign, estimated the power-line effect would cause between two and six of the 500-odd cases of child leukaemia reported each year in Britain. On average, one in 2,000 children under 15 develops leukaemia, and there are 1,500 childhood cancers each year. Some international studies have shown children exposed to the highest electromagnetic fields (EMF) in the home - as it often is in houses below power lines - are twice as likely to suffer leukaemia as children exposed to low EMF.
About 0.5 per cent of the UK population live in houses above that level, says the National Radiological Protection Board, which advises the Government on hazards from radiation.
Maureen Asbury, president of the Trentham campaign, said: "The Government should act now. We aren't prepared to wait 10 years while they dither. First, ministers should legislate against building houses near power lines. Then they should set up a project to remove the lines that traverse homes. We know it can't be done immediately, but it needs to be started."
But Dr Draper dismissed claims made on Sky News that he or the Department of Health had tried to keep the findings secret. "We hope to submit our paper, which is now complete, to a journal in about a fortnight for publication," he said. "But it is untrue to say the DoH is suppressing this work: it has been among those pressing me to get it published.
"Second, even if it wanted to suppress them, my contract allows me to publish what I want."
Sky News had claimed the results of the study were kept under wraps for three years, after being presented in 2001. Dr Draper said he had had no results to discuss in 2001. "About 18 months ago, I ran a private workshop with other scientists to talk about my preliminary findings, which were fuzzy; I did not understand them fully myself and wanted to see if there were other explanations."
He rechecked the calculations to produce the final report. The study does not find the biological mechanism by which power lines might increase the risk of cancers.
© 2004 Independent Digital (UK) Ltd http://news.independent.co.uk/uk/health_medical/story.jsp?story=577526
Re: Rise of the New Plagues Continues
Post by bigbunny on Oct 31, 2004, 10:03am
And now for something really scary:
Viral Hemorrhagic Fevers
What are viral hemorrhagic fevers?
Viral hemorrhagic fevers (VHFs) refer to a group of illnesses that are caused by several distinct families of viruses. In general, the term "viral hemorrhagic fever" is used to describe a severe multisystem syndrome (multisystem in that multiple organ systems in the body are affected). Characteristically, the overall vascular system is damaged, and the body's ability to regulate itself is impaired. These symptoms are often accompanied by hemorrhage (bleeding); however, the bleeding is itself rarely life-threatening. While some types of hemorrhagic fever viruses can cause relatively mild illnesses, many of these viruses cause severe, life-threatening disease.
The Special Pathogens Branch (SPB) primarily works with hemorrhagic fever viruses that are classified as biosafety level four (BSL-4) pathogens. A list of these viruses appears in the SPB disease information index. The Division of Vector-Borne Infectious Diseases, also in the National Center for Infectious Diseases, works with the non-BSL-4 viruses that cause two other hemorrhagic fevers, dengue hemorrhagic fever and yellow fever.
How are hemorrhagic fever viruses grouped? Go to top of page
VHFs are caused by viruses of four distinct families: arenaviruses, filoviruses, bunyaviruses, and flaviviruses. Each of these families share a number of features:
* They are all RNA viruses, and all are covered, or enveloped, in a fatty (lipid) coating.
* Their survival is dependent on an animal or insect host, called the natural reservoir.
* The viruses are geographically restricted to the areas where their host species live.
* Humans are not the natural reservoir for any of these viruses. Humans are infected when they come into contact with infected hosts. However, with some viruses, after the accidental transmission from the host, humans can transmit the virus to one another.
* Human cases or outbreaks of hemorrhagic fevers caused by these viruses occur sporadically and irregularly. The occurrence of outbreaks cannot be easily predicted.
* With a few noteworthy exceptions, there is no cure or established drug treatment for VHFs.
In rare cases, other viral and bacterial infections can cause a hemorrhagic fever; scrub typhus is a good example.
What carries viruses that cause viral hemorrhagic fevers? Go to top of page
Viruses associated with most VHFs are zoonotic. This means that these viruses naturally reside in an animal reservoir host or arthropod vector. They are totally dependent on their hosts for replication and overall survival. For the most part, rodents and arthropods are the main reservoirs for viruses causing VHFs. The multimammate rat, cotton rat, deer mouse, house mouse, and other field rodents are examples of reservoir hosts. Arthropod ticks and mosquitoes serve as vectors for some of the illnesses. However, the hosts of some viruses remain unknown -- Ebola and Marburg viruses are well-known examples.
Where are cases of viral hemorrhagic fever found? Go to top of page
Taken together, the viruses that cause VHFs are distributed over much of the globe. However, because each virus is associated with one or more particular host species, the virus and the disease it causes are usually seen only where the host species live(s). Some hosts, such as the rodent species carrying several of the New World arenaviruses, live in geographically restricted areas. Therefore, the risk of getting VHFs caused by these viruses is restricted to those areas. Other hosts range over continents, such as the rodents that carry viruses which cause various forms of hantavirus pulmonary syndrome (HPS) in North and South America, or the different set of rodents that carry viruses which cause hemorrhagic fever with renal syndrome (HFRS) in Europe and Asia. A few hosts are distributed nearly worldwide, such as the common rat. It can carry Seoul virus, a cause of HFRS; therefore, humans can get HFRS anywhere where the common rat is found.
Re: Rise of the New Plagues Continues
Post by bigbunny on Oct 31, 2004, 10:03am
While people usually become infected only in areas where the host lives, occasionally people become infected by a host that has been exported from its native habitat. For example, the first outbreaks of Marburg hemorrhagic fever, in Marburg and Frankfurt, Germany, and in Yugoslavia, occurred when laboratory workers handled imported monkeys infected with Marburg virus. Occasionally, a person becomes infected in an area where the virus occurs naturally and then travels elsewhere. If the virus is a type that can be transmitted further by person-to-person contact, the traveler could infect other people. For instance, in 1996, a medical professional treating patients with Ebola hemorrhagic fever (Ebola HF) in Gabon unknowingly became infected. When he later traveled to South Africa and was treated for Ebola HF in a hospital, the virus was transmitted to a nurse. She became ill and died. Because more and more people travel each year, outbreaks of these diseases are becoming an increasing threat in places where they rarely, if ever, have been seen before.
How are hemorrhagic fever viruses transmitted? Go to top of page
Viruses causing hemorrhagic fever are initially transmitted to humans when the activities of infected reservoir hosts or vectors and humans overlap. The viruses carried in rodent reservoirs are transmitted when humans have contact with urine, fecal matter, saliva, or other body excretions from infected rodents. The viruses associated with arthropod vectors are spread most often when the vector mosquito or tick bites a human, or when a human crushes a tick. However, some of these vectors may spread virus to animals, livestock, for example. Humans then become infected when they care for or slaughter the animals.
Some viruses that cause hemorrhagic fever can spread from one person to another, once an initial person has become infected. Ebola, Marburg, Lassa and Crimean-Congo hemorrhagic fever viruses are examples. This type of secondary transmission of the virus can occur directly, through close contact with infected people or their body fluids. It can also occur indirectly, through contact with objects contaminated with infected body fluids. For example, contaminated syringes and needles have played an important role in spreading infection in outbreaks of Ebola hemorrhagic fever and Lassa fever.
What are the symptoms of viral hemorrhagic fever illnesses? Go to top of page
Specific signs and symptoms vary by the type of VHF, but initial signs and symptoms often include marked fever, fatigue, dizziness, muscle aches, loss of strength, and exhaustion. Patients with severe cases of VHF often show signs of bleeding under the skin, in internal organs, or from body orifices like the mouth, eyes, or ears. However, although they may bleed from many sites around the body, patients rarely die because of blood loss. Severely ill patient cases may also show shock, nervous system malfunction, coma, delirium, and seizures. Some types of VHF are associated with renal (kidney) failure.
How are patients with viral hemorrhagic fever treated? Go to top of page
Patients receive supportive therapy, but generally speaking, there is no other treatment or established cure for VHFs. Ribavirin, an anti-viral drug, has been effective in treating some individuals with Lassa fever or HFRS. Treatment with convalescent-phase plasma has been used with success in some patients with Argentine hemorrhagic fever.
How can cases of viral hemorrhagic fever be prevented and controlled? Go to top of page
With the exception of yellow fever and Argentine hemorrhagic fever, for which vaccines have been developed, no vaccines exist that can protect against these diseases. Therefore, prevention efforts must concentrate on avoiding contact with host species. If prevention methods fail and a case of VHF does occur, efforts should focus on preventing further transmission from person to person, if the virus can be transmitted in this way.Because many of the hosts that carry hemorrhagic fever viruses are rodents, disease prevention efforts include
* controlling rodent populations;
* discouraging rodents from entering or living in homes or workplaces;
* encouraging safe cleanup of rodent nests and droppings.
For hemorrhagic fever viruses spread by arthropod vectors, prevention efforts often focus on community-wide insect and arthropod control. In addition, people are encouraged to use insect repellant, proper clothing, bednets, window screens, and other insect barriers to avoid being bitten.
For those hemorrhagic fever viruses that can be transmitted from one person to another, avoiding close physical contact with infected people and their body fluids is the most important way of controlling the spread of disease. Barrier nursing or infection control techniques include isolating infected individuals and wearing protective clothing. Other infection control recommendations include proper use, disinfection, and disposal of instruments and equipment used in treating or caring for patients with VHF, such as needles and thermometers.
http://www.cdc.gov/ncidod/dvrd/spb/mnpages/dispages/vhf.htm
Re: Rise of the New Plagues Continues
Post by bigbunny on Nov 7, 2004, 8:15am
C. difficile superbug likely to spread beyond Quebec: microbiologist
Last Updated Fri, 22 Oct 2004 09:47:54 EDT
TORONTO - Quebec's epidemic of C. difficile shows all hospitals need to be vigilant about hygiene to prevent the dangerous strain from spreading across Canada, public health experts said Thursday.
Researchers found 7,000 people have been infected with C. difficile in Montreal since 2003, an infection rate that is four times higher than the preceding year.
Clostridium difficile can cause severe diarrhea and death from dehydration.
"We need to take it very seriously," said Dr. Allison McGeer, an infectious disease specialist at Toronto's Mount Sinai Hospital. "[C. difficile] is an increasing problem in the United Kingdom and the United States. We've had a number of big outbreaks in Canada."
Aside from Montreal, hospitals in Calgary and Ottawa have experienced periodic outbreaks.
So far, evidence suggests the more virulent strain is confined to Quebec. The province is seeing four times the number of infections as the national average.
Tracking C. difficile across Canada
The bacteria may not stay in Quebec, according to Dr. Andrew Simor, a microbiologist at Sunnybrook and Women's College Health Sciences Centre in Toronto. He is a leading a national study on the extent of the C. difficile problem.
"Some of the patients transferred to us from Quebec or from the United States may well bring this organism with them and introduce to Ontario or to other parts of the country," said Simor.
The strain that is killing patients in Quebec has also caused outbreaks in hospitals in at least six states.
Infectious disease experts said conditions at hospitals in Quebec probably helped to escalate the epidemic. At many older hospitals, three or four patients stay in the same room and share the same bathroom.
The problem is that microscopic spores from feces can survive on surfaces for months. The bacterial spores are very difficult to clean off or kill.
Others said the main factor is health-care workers who fail to wash their hands. People in Quebec are worried about sending family members to affected hospitals, and some are angry the public wasn't told sooner about the problem.
"In this particular outbreak, patients could have done things to protect themselves had they known," said Dr. Ken Flegel, a specialist in internal medicine at Royal Victoria Hospital. "Visitors could have done things to help patients be protected."
http://www.cbc.ca/story/science/national/2004/10/21/c_difficile041021.html
Re: Rise of the New Plagues Continues
Post by bigbunny on Nov 12, 2004, 2:11am
"Superflu" a Threat as Ducks Emerge as Stealth Carriers
Bijal P. Trivedi
for National Geographic News
November 8, 2004
The bird flu that has killed millions of poultry in east Asia may be tougher and more dangerous to humans than previously suspected.
The avian influenza virus in question is the highly pathogenic (illness causing) A virus subtype H5N1. On some poultry farms it has killed 100 percent of infected birds.
Research from St. Jude Children's Research Hospital in Memphis, Tennessee, revealed that domestic ducks infected with H5N1 shed large quantities of virus in feces as well as through the respiratory tract. The 2004 strain of H5N1 survives longer in the outside environment than those from earlier outbreaks. But most disturbing is the fact that ducks carrying the virus do not die or show any symptoms of disease.
![[image]](http://news.nationalgeographic.com/news/2004/11/images/041108_bird_flu.jpg "[image]")
Ducks at a commune in Beijing, China, are fattened prior to sale to area restaurants. Domestic ducks infected with bird flu shed large quantities of virus in feces as well as through the respiratory tract.
The World Health Organization (WHO) released these results prior to publication of the St. Jude report because of their significance for public health.
"H5N1 is now circulating widely in Asia. It is becoming increasingly pathogenic and we are discovering it can infect more and more types of mammals," said Klaus Stöhr, who leads the Global Influenza Programme at the World Health Organization in Geneva, Switzerland.
In its most recent incarnation the virus has killed humans. To date there have been 44 confirmed human cases of H5N1 flu in Thailand and Vietnam. Of these, 32 people died—a fatality rate of 75 percent. Survivors suffer from severe pneumonia.
"We believe we are closer than ever to the next pandemic [widespread outbreak]," Stöhr said. Statistically, pandemics tend to occur every 10 to 27 years. It has been 36 years since the last one struck, and Stöhr thinks the next is long overdue.
At present H5N1 cannot spread easily from person to person. There has been only one recorded instance of probable human-to-human transmission, although this cannot be confirmed experimentally, because scientists lack the appropriate biological specimens.
Superflu
Experts fear that the H5N1 virus could acquire genes from human influenza viruses that will transform it into a "superflu," allowing rapid spread among people. The more people H5N1 infects, the greater the chance these human and bird viruses will intermingle and produce a pandemic strain.
Scientists classify influenza viruses based on the hemagglutinin (H) and neuraminidase (N) proteins that cover the surface of every influenza virus.
There are 15 forms of H proteins that have been identified on influenza Type A viruses; all 15 viruses are found in birds. But only H1, H2, and H3 viruses circulate widely in humans.
Viruses of the H5 and H7 subtype are the "bad guys of the flu world," said Richard Webby, a virologist at St. Jude Children's Research Hospital. "We don't want H5 or H7 viruses in humans." These viruses have the capacity to become highly pathogenic and cause a much more pervasive disease than the influenza viruses currently circulating in the human population.
Until 1997 scientists believed that it was impossible for birds to directly infect humans with H5N1. But an outbreak in Hong Kong in 1997 that killed six of 18 people infected with the virus proved the contrary.
Though H1, H2, and H3 influenza viruses now circulate within the human population every flu season, each one triggered a pandemic upon its debut.
Three Pandemics
New viruses, to which the people have never been exposed, cause pandemics because humans lack immunity—which only results from exposure. This situation occurred three times in the last century. In 1918 an H1N1 virus triggered the notorious Spanish flu pandemic that killed at least 20 million worldwide, 500,000 in the U.S. alone. In 1957 and 1958 another new influenza virus, H2N2, dubbed the Asian flu, killed 70,000 Americans. In 1968 and 1969 the Hong Kong flu, H3N2, killed 34,000 in the U.S.
H5N1 is becoming more lethal and may be better suited to infect mammalian hosts. Studies in mice published earlier this year show that H5N1 is evolving rapidly. The H5N1 virus isolated from ducks in mainland China in 2002 was more deadly than that from 1999.
One approach to preventing a pandemic has been to eliminate the virus from its animal reservoir by killing millions of chickens. But this is economically devastating to countries like Thailand, which is the fourth largest producer and exporter of chickens. Almost a hundred million chickens have died or been culled since the 2004 outbreak.
In many places ducks and chickens mingle freely on family farms. They wander in and out of the home, and children are frequently the ones who tend the animals. Although no transmission of H5N1 from duck to human has been reported so far, this now merits consideration in light of human cases that cannot be tied to poultry outbreaks.
"How do you identify infected ducks? What cautionary measures do you recommend if you can't tell if ducks are sick or not?" Stöhr said. "This is going to complicate our strategy in controlling this virus."
Virus Gets Tougher
Outbreaks of H5N1 in poultry have been reported in Laos, Cambodia, Vietnam, Thailand, Indonesia, Malaysia, and China. And new results from St. Jude suggest that the virus is getting tougher. The 2004 H5N1 can survive at 37 degrees Celsius (98 degrees Fahrenheit) for six days, compared with just two days for the H5N1 virus from the 1997 outbreak.
"We can't eradicate this virus any time soon," said Tim Uyeki, a medical epidemiologist in the influenza branch of the Centers for Disease Control and Prevention in Atlanta, Georgia. "Even if infected poultry are culled, the virus persists in the feces and soil under certain environmental conditions. Unless you could disinfect the entire areas with H5N1 contamination, the virus could continue to spread to healthy poultry."
"As H5N1 continues to circulate in poultry and evolve, the virus will become an increasing public health threat. It's a ticking time bomb," Uyeki said.
Robert Cook, chief veterinarian at the Bronx-based Wildlife Conservation Society in New York, believes that a global surveillance program would be a vital early warning system for spotting new potential pandemics. Such a system should bring together disease data from wildlife, livestock, and humans.
The WHO will hold an informal meeting in Geneva on November 11 for vaccine makers and representatives from government and regulatory agencies to discuss a pandemic vaccine project.
There is currently no approved human vaccine for H5N1. One potential vaccine was "very effective in ferrets," said Webby, who co-developed and tested it at St. Jude. Webby's vaccine is scheduled for clinical trials that will gauge safety and efficacy.
All pandemic viruses in the last century arose quickly and traveled around the world in less than a year. It takes about eight months of R&D before vaccine production can begin. "We now have a window of opportunity to get this done," Stöhr said.
Bijal P. Trivedi is a freelance science and health journalist based in Washington, D.C.
http://news.nationalgeographic.com/news/2004/11/1108_041108_avian_flu.html
Re: Rise of the New Plagues Continues
Post by bigbunny on Nov 16, 2004, 3:36pm
Computer use link to eye disease
Heavy computer use could be linked to glaucoma, especially among those who are short-sighted, fear researchers.
Glaucoma is caused by increased fluid pressure within the eye compressing the nerves at the back, which can lead to blindness if not treated.
The findings, published in the Journal of Epidemiology and Community Health, are based on 10,000 Japanese workers.
The authors and experts recommend more research, particularly because being short-sighted is a known glaucoma risk.
Eye strain
Dr Masayuki Tatemichi, from Toho University School of Medicine, and his colleagues tested the sight of workers in four different Japanese companies, employing over 5,000 people each.
The employees were asked to complete questionnaires about their computer use, both at home and at work, and any history of eye disease.
The researchers then divided the employees according to how much they used a computer, labelling them light, medium or heavy users.
It will be important to follow this study with further research.
David Wright chief executive of the International Glaucoma Association
Computer use was categorised in four blocks of five years, ranging from less than five years to more than 20 years, as well as four blocks of the average amount of time spent at the screen per session, ranging from less than one hour to more than eight hours at a time.
Those classified as heavy users tended to be men and younger.
Overall, 522 (5.1%) of the employees were found to have visual field abnormalities.
Workers who were classified as heavy computer users were more likely to be long-sighted (hypermetropia) or short-sighted (myopia).
Around a third (165) of these workers had suspected glaucoma.
Upon further analysis, heavy computer use, suspected glaucoma and short-sightedness appeared to be interlinked.
The authors do not know why this might be, but believe it could be that short-sighted people are more susceptible to computer use-related eye strain.
Glaucoma is the most important cause of irreversible blindness worldwide, affecting more than 500,000 people in the UK alone.
Compounded by the fact that more and more people are using computers, the researchers said: "In the next decade, therefore, it might be important for public health professionals to show more concern about myopia and visual field abnormalities in heavy computer users."
More research
But they said their findings needed confirming because the study included mainly men and the refractive errors (which indicate how short- or long-sighted someone is) were not measured officially.
Nick Astbury, president of the Royal College of Ophthalmologists, pointed out that Japanese populations have a high prevalence of myopia anyway and that short-sightedness is a known risk factor for glaucoma.
"I doubt whether staring at computers makes any difference," he said.
David Wright, chief executive of the International Glaucoma Association, said: "There may be a risk in heavy use of computer equipment.
"It would be wise for anyone involved in such heavy usage to ensure that they receive regular comprehensive eye examinations in order to detect the earliest possible signs of the development of glaucoma when treatment is most effective."
He said three eye tests should be carried out to check for glaucoma: ophthalmoscopy (a visual examination of the optic disc), tonometry (a measurement of pressure in the eye) and perimetry (which checks for visual field anomalies).
"It will be important to follow this study with further research in other ethnic populations in order to establish the complete validity of this initial indication of a potential problem and also to address the ethnic risk factors should the evidence add to the Japanese report," he said.
Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/health/4008185.stm
Published: 2004/11/16 02:21:35 GMT
Re: Rise of the New Plagues Continues
Post by bigbunny on Nov 16, 2004, 3:37pm
Brain inflammation link to autism
Scientists have produced compelling evidence that autism may in some cases be linked to inflammation of the brain.
They found certain immune system components that promote inflammation are consistently activated in people with autism.
Autistic children have difficulties in social interaction, may show repetitive behaviours and may have unusual attachments to objects or routines.
The Johns Hopkins University research is published in Annals of Neurology.
These findings reinforce the theory that immune activation in the brain is involved in autism.
Dr Carlos Pardo-Villamizar
Autism is a disorder of the developing brain that appears in early childhood. It is estimated to afflict between two and five of every 1,000 children and is four times more likely to strike boys than girls.
The condition has a strong genetic component. For instance, in identical twins, where one twin has autism, both are usually affected.
However, the number of children with autism appears to be increasing more than expected for a genetic disorder.
This suggests too that genetic abnormalities require the influence of other factors to cause the disorder.
Birth complications, toxins, diet, and viruses and other pathogens have been suggested, though there is no strong evidence for any of these.
In recent years, there have been scientific hints of immune system irregularities in children with autism, but not all studies have confirmed this.
The Johns Hopkins team sought a more definitive answer by looking not at the immune system overall, but at immune components inside the relatively sealed environment of the nervous system.
They examined brain tissue from 11 people with autism, aged five to 44 years, who had died of accidents or injuries.
Key chemicals
Compared with normal control brains, the brains of the people with autism were found to contain abnormal patterns of immune system proteins called cytokines and chemokines consistent with inflammation.
Researcher Dr Carlos Pardo-Villamizar said: "These findings reinforce the theory that immune activation in the brain is involved in autism, although it is not yet clear whether it is destructive or beneficial, or both, to the developing brain."
Similarly, samples of cerebrospinal fluid obtained from six children with autism were also found to contain elevated levels of cytokines.
The researchers say it might eventually be possible to develop a diagnostic test for autism based on looking for signs of inflammation - and that treating this inflammation might reduce the symptoms of autism.
However, Dr Andrew Zimmerman, a paediatric neurologist at the Kennedy-Krieger Institute in Baltimore who also worked on the study, said it was possible that inflammation was produced as a result of the brain trying to combat some other process damaging to brain cells.
A spokesperson for the National Autistic Society said other scientists had also examined the possible connection between the immune system and autism.
One study has linked the condition to the disease encephalitis, while another found raised levels of nitric oxide in the plasma of children with autism.
This chemical plays a role in the immune response, and which is known to affect neurodevelopmental processes.
Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/health/4004075.stm
Published: 2004/11/15 00:02:56 GMT
Re: Rise of the New Plagues Continues
Post by bigbunny on Nov 16, 2004, 3:51pm
Archive Number 20041113.3071
Published Date 13-NOV-2004
Subject PRO/EDR> Iodine poisoning - Russia
http://www.promedmail.org/pls/askus/f?p=2400:1001:17696905213587496990::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,27205
Iodine poisoning - Russia
***********************
A ProMED-mail post <http://www.promedmail.org>
ProMED-mail is a program of the International Society for Infectious Diseases
<http://www.isid.org>
Date: 12 Nov 2004
From: David Jarrett <JARRETT@afrri.usuhs.mil>
Source: Moscow Times, 9 Nov 2004 [edited]
<http://www.themoscowtimes.com/>
Reactor shutdown sparks panic
-------------------------------
A minor incident at the Balakovskaya nuclear power plant created widespread panic in Saratov and nearby regions, with people clearing iodine off drugstore shelves and several being rushed to the hospital with symptoms of iodine poisoning.
Reactor No. 2 at the Balakovskaya nuclear power plant, located outside the city of Balakov in the Saratov region, some 900 km southeast of Moscow, shut down on Thursday [11 Nov 2004] after a pipe burst, but, there was no radiation leak, the Federal Nuclear Power Agency said in a statement on Friday [12 Nov 2004].
However, the incident, which was 1st reported on Friday [12 Nov 2004] morning, sparked a panic, after Saratov radio stations reported the news, along with advice to residents about how to protect themselves from radiation, Gazeta.ru reported. Greenpeace activists then hit the streets in regional cities and towns to distribute leaflets explaining how to protect oneself from a radiation leak.
Some local residents said they saw a white cloud above the plant and did not believe the authorities' assurances, suspecting a cover-up like the one that followed the 1986 explosion at the Chernobyl nuclear power plant, Russian media reported.
"I tell you that there will not be a 2nd Chernobyl. It is not those times anymore when you hide information," Igor Maly, head of the local branch of
the Emergency Situations Ministry, said on NTV television.
Sergei Kiriyenko, President Vladimir Putin's envoy to the Volga Federal District, made a quick visit late Friday [12 Nov 2004] to Saratov to try to calm fears. But, rumors spread quickly throughout the day that authorities were trying to hush up the danger and were informally advising schools to let children go home early. Some kindergartens rushed to seal their windows.
Adding to the speculation was the unusual appearance of several generals, and about a dozen government vehicles with black military license plates, Kommersant reported on Saturday [13 Nov 2004]. The officials were there as part of a regularly planned Emergency Situations Ministry exercise.
Worried Saratov residents cleared drugstore shelves of iodine, and more expensive iodine-based medicines such as sea kale and vitamins, RIA-Novosti and the Regnum news agency reported. Some vendors at outdoor markets started selling iodine to panicked customers at 10 rubles [USD 0.35] a drop, the Newsinfo.ru website said. At least 7 people checked into Saratov hospitals with symptoms of iodine poisoning. "The whole city lost their heads," Anna Vinogradova, head of Saratov's department of environmental protection, told Kommersant. "All the telephone lines were busy. People were telling each other to drink vodka, take iodine, and -- no matter what
-- not to use public drinking water."
Reports of panic also poured in from the neighboring Tambov, Penza, Ulyanovsk, and Nizhny Novgorod regions, as well as Astrakhan and Rostov, even though the 2 regions do not border Saratov.
The nuclear power plant's reactor was restarted early Saturday [13 Nov 2004] and was running normally, Interfax reported.
Russia has 10 nuclear power plants with a total of 30 nuclear reactors, which are regularly shut down for repairs or due to minor accidents.
[Byline: Simon Saradzhyan]
David Jarrett MD, FACEP
COL MC USA
Director, Armed Forces Radiobiology Research Institute
<JARRETT@afrri.usuhs.mil>
[Excessive intake (ingestion) of various forms of iodine -- including tincture of iodine, Lugol's solution, Pima syrup, amiodarone (Cordarone), radiographic contrast, potassium iodide (SSKI), iodinated glycerol (organidin), and others -- produce several clinical signs.
Clinical signs include pain in the mouth and throat, a metallic taste in the mouth, fever, thirst, shock, cessation of urine production, vomiting, diarrhea, and abdominal pain. Additionally, there may be delirium, stupor, and seizures.
Gastric lavage with activated charcoal therapy may be the best means of therapy, as well as supportive care. Survival depends upon the amount ingested and time to treatment. Death is possible, and esophageal stricture is a possible complication. - Mod.TG]
Re: Rise of the New Plagues Continues
Post by bigbunny on Nov 16, 2004, 4:07pm
City deaths rise with ozone levels
21:00 16 November 04
Short-term increases in ozone pollution lead to higher death rates in cities, according to the largest ozone mortality study ever carried out. The study could be an important influence on future policy decisions regarding ozone standards.
Ground-level ozone - unlike protective ozone at higher atmospheric altitudes - is produced mostly by human activity and has doubled since 1900. The gas forms when sunlight interacts with emissions from cars and power plants - such as nitrogen dioxide - and is generated in greater quantities when air temperatures are high.
Previous studies have shown that ozone causes inflammation of the lungs and increases both hospital admissions and asthma attacks. But these studies have produced inconsistent results when assessing the pollutant's effect on the risk of death.
This may be because the studies used a variety of analytical methods and a limited range of locations, say Michelle Bell, an environmental health scientist at Yale University in New Haven, Connecticut, US, and her colleagues.
Respiratory problems
Bell's team analysed death records for 95 US cities - representing about 40% of the population - over 14 years. They found that a person is 0.52% more likely to die on a given day when ozone levels during the previous week rose by 10 parts per billion. That figure is slightly higher - 0.64% - when the researchers looked only at deaths due to cardiovascular and respiratory problems.
"If ozone levels were decreased by 10 ppb, about 4000 lives would be saved in the US each year," Bell told New Scientist.
And the benefit could actually be even greater. "This underestimates the total impact of ozone on mortality because it [does not capture] the impact associated with a lifetime exposure to high ozone levels," says Bell.
The results may have implications for public policy, as the US Environmental Protection Agency - which partially funded the study - is currently reviewing its standards for maximum daily ozone levels.
Lowering limits
Studies showing ozone's negative health effects forced the permitted US levels down in 1997 from 120 ppb for the highest hour in any given day to 80 ppb over an eight-hour period.
They may well be lowered again. The current study showed that when ozone rose by 10 ppb, even if still peaking below the current upper limit, the risk of death still increased by 0.15% the following day.
"Ozone is clearly a problem, particularly for those that spend a lot of time outdoors, for those exercising, for asthmatics, and maybe others," says Bart Ostro, chief of the air pollution epidemiology unit at the California Office of Environmental Health Hazard Assessment in Oakland, US. "Moving to ever-cleaner cars and controlling some of the large stationary sources of nitrogen dioxide, such as power plants, are important steps."
Bell agrees: "There are a lot of things we can do on an individual basis, such as taking the bus to work or carpooling. We can also look at the exposure to ozone - if high ozone levels are anticipated, people can stay indoors or not exercise outdoors."
Journal reference: Journal of the American Medical Association (vol 292, p 2372)
Maggie McKee
http://www.newscientist.com/news/news.jsp?id=ns99996685
Re: Rise of the New Plagues Continues
Post by bigbunny on Nov 21, 2004, 5:12pm
17 November 2004
An Apple A Day Keeps Alzheimer's Away
Researchers at Cornell University say the antioxidant quercetin found in apples and some other fruits and vegetables appears to protect brain cells against oxidative stress, a tissue-damaging process associated with Alzheimer's and other neurodegenerative disorders. The new study - appearing in the Journal of Agricultural and Food Chemistry - adds strength to the theory that the risk of developing Alzheimer's and similar diseases may be reduced by increasing one's intake of antioxidant-rich foods.
"On the basis of serving size, fresh apples have some of the highest levels of quercetin when compared to other fruits and vegetables and may be among the best food choices for fighting Alzheimer's," says study leader C.Y. Lee. "People should eat more apples, especially fresh ones." He cautions that protection against Alzheimer's using any food product is currently theoretical and adds that genetics and environment are also believed to play a role in the disease. Lee also points out that results so far are limited to cell studies and that more advanced research, particularly in animals, is still needed to confirm the findings.
For the current study, the researchers exposed groups of isolated rat brain cells to varying concentrations of either quercetin or vitamin C. The cells were then exposed to hydrogen peroxide to simulate the type of oxidative cell damage that is believed to occur with Alzheimer's. Brain cells that were treated with quercetin had significantly less damage to both cellular proteins and DNA than the cells treated with vitamin C and the cells that were not exposed to antioxidants. This demonstrates quercetin's stronger protective effect against neurotoxicity, according to the researchers. Quercetin's mechanism of action is still something of a mystery, but some suspect it might work by blocking the action of highly-active chemicals called free radicals, an excess of which are thought to damage brain cells as well as other cell types over time.
Lee said that even though quercetin was relatively stable during cooking, fresh apples are better sources of quercetin than cooked or processed apple products because the compound is mainly concentrated in the skin of apples. In general, red apples tend to have more of the antioxidant than green or yellow ones, although any apple variety is a good source of quercetin, he adds. For those who don't like apples or may have difficulty eating the whole fruit, there are some promising alternatives. Other foods containing high levels of quercetin include onions, which have some of the highest levels of quercetin among vegetables, as well as berries, particularly blueberries and cranberries.
http://www.scienceagogo.com/news/20041017040431data_trunc_sys.shtml
Re: Rise of the New Plagues Continues
Post by bigbunny on Nov 21, 2004, 5:44pm
Once in the population how do you get rid of it:
Source: Infectious Diseases Society Of America
Date: 2004-11-19
URL: http://www.sciencedaily.com/releases/2004/11/041119015015.htm
Were Zoo Workers Infected With Cancer-causing Animal Virus?
Evidence of exposure to a monkey virus possibly related to cancer has been found in the blood of North American zoo workers, according to a study in the December 15 issue of The Journal of Infectious Diseases, now available online. The virus, a polyomavirus known as simian virus 40 (SV40), has long been a subject of public health concern, in part because it has been shown to cause cancer in laboratory animals, and some investigators have reported SV40 DNA in human tumors.
The authors, Eric A. Engels and coworkers at the National Cancer Institute, National Institutes of Health, Rockville, MD, the Centers for Disease Control and Prevention, Atlanta, GA, and The Johns Hopkins University School of Medicine, Baltimore, MD, studied 254 zoo workers, 109 of whom handled primates extensively and the remainder not at all. An antibody assay showed that SV40 reactivity was more common among primate workers (23 percent) than among the other workers (10 percent). These low rates, which suggested absence of ongoing SV40 replication, contrasted with assay results showing 85 percent and 56 percent reactivity, respectively, for two other polyomaviruses, BK and JC, which are highly prevalent in humans and establish lifelong infection.
When the investigators used particles of SV40, BK, and JC to evaluate whether SV40-positive reactions were specific or represented cross-reacting antibody responses, only 14 of 29 subjects demonstrated specific reactivity. Engels and coworkers commented that this suggested that much of their SV40-positive results were probably due to BK or JC virus cross-reactivity.
The investigators cautioned that there is as yet no definitive evidence that SV40 can persistently infect humans, and that the health consequences of SV40 exposure, including the risk of cancer, are still unknown. Nevertheless, they concluded that their study "suggests that individuals who work closely with nonhuman primates are occupationally exposed to SV40," and that further studies of the issues involved are needed.
In an accompanying editorial, Keerti Shah of The Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD, commented that, "although humans in contact with primates may become infected with SV40, currently available evidence does not suggest that SV40 circulates independently in the community or that it contributes to the development of any human cancer." Because of uncertainties in the evidence, however, he recommended further studies, including closer study of those exposed to primates, "that investigate the 'full signature' of SV40 infection" like genomic sequences, transcripts, antibodies, T cell response, and so on.
###
Founded in 1904, The Journal of Infectious Diseases (JID) is the premier publication in the Western Hemisphere for original research on the pathogenesis, diagnosis, and treatment of infectious diseases; on the microbes that cause them; and on disorders of host immune mechanisms. Articles in JID include research results from microbiology, immunology, epidemiology, and related disciplines. It is published under the auspices of the Infectious Diseases Society of America (IDSA), a professional society based in Alexandria, Va., representing nearly 8,000 physicians and scientists who specialize in infectious diseases. (For more information, visit www.idsociety.org.) Nested within the IDSA, the HIV Medicine Association (HIVMA) is the professional home for more than 2,600 physicians, scientists and other health care professionals dedicated to the field of HIV/AIDS. HIVMA promotes quality in HIV care and advocates policies that ensure a comprehensive and humane response to the AIDS pandemic informed by science and social justice. (For more information, visit http://www.hivma.org.)
Re: Rise of the New Plagues Continues
Post by bigbunny on Nov 21, 2004, 6:19pm
US Study Links More Than 200 Diseases To Pollution
By Geoffrey Lean
Environment Editor
The Independent - UK
11-17-4
Pollution has been linked to about 200 different diseases, ranging from cerebral palsy to testicular atrophy, as well as more than 37 kinds of cancer, startling US research shows.
The study, which the authors say probably underestimates the full toll of the contamination, will focus attention on the need for information on the tens of thousands of chemicals routinely released into the environment.
But Britain has weakened the proposed European Union regulations to provide safety information on the substances at the behest of the US government.
The research, by doctors at what was then the University of California and at the Boston Medical Center, was restricted to listing only effects that had been found by several different studies and which are often well known.
More than 120 diseases have been definitively linked to pollution, and in another 33 evidence of a link is judged to be "good". For the rest the evidence is "limited".
Nine different pollutants have been "verified" to cause asthma - including four from car exhausts, the subject of an Independent on Sunday campaign - the study shows. Testicular atrophy is caused by oestrogen, increasingly found in British rivers that supply drinking water. Mercury poisoning can cause cerebral palsy, while more than 50 pollutants - ranging from dioxins to PCBs - have been shown to cause cancer.
Other effects include: kidney disease, heart disease, hypertension, diabetes, dermatitis bronchitis, hyperactivity, deafness, sperm damage and Alzheimer's and Parkinson's diseases.
One of the authors, Dr Ted Schletter of the Boston Medical Center, said yesterday: "The human body is in constant conversation with this chemical milieu and some substances have turned out to be important contributors to disease." He said pollution often acted in concert with genetic predispositions to developing particular illnesses.
Dr J Peterson Myers, chief executive of the Virginia-based Environmental Health Sciences, said because science continued to find new effects of pollution, the number of diseases linked to it was "very much higher".
At the last count - more than 20 years ago - more than 100,000 chemicals were in use in Europe. Few have been properly tested.
Blood tests in the UK, the rest of Europe and the US indicate that most people carry potentially hazardous chemicals in their bodies.
The European Commission has been trying to introduce a new directive requiring industry to provide safety information on the 30,000 most common chemicals, but this measure has been watered down because of pressure from the Bush administration.
A leaked cable signed by Colin Powell, the US Secretary of State, complains that the measures "would be significantly more burdensome to industry and government" and would "impact" on US exports to Europe. Tony Blair, President Jacques Chirac of France and Chancellor Gerhard Schrder of Germany wrote a joint letter to the Commission and succeeded in weakeningthe measure.
© 2004 Independent Digital (UK) Ltd http://news.independent.co.uk/uk/environment/story.jsp?story=582743
Re: Rise of the New Plagues Continues
Post by bigbunny on Nov 21, 2004, 6:23pm
Flu Pandemic Near, Experts Fear
By Helen Branswell
Canadian Press
11-19-4
TORONTO - The global community of influenza experts is a small circle. These days, it's an exhausted, alarmed one as well.
Many influenza authorities are suffering sleepless nights, eyes trained on Asia where they fear a viral monster is readying itself to unleash a perfect storm of flu on the world.
Should that happen, what will follow will be a public health disaster that will make SARS seem like child's play, they believe.
Between a quarter and a third of the world's population will fall ill, according to new World Health Organization estimates, and 1 per cent of the sick will die.
Do the math and the numbers defy credulity; between 16 million and 21 million people would die in a matter of mere months. In Canada, 80,000 to 106,000 people would be expected to succumb.
Armed with that math, think of the consequences. Panic. Crippled health-care systems. Economic disruption on a global scale. Grounded airlines. Distribution networks that will grind to a halt. Social instability.
Or, "three years of a given hell," as a leading U.S. epidemiologist, Michael Osterholm, puts it: "I can't think of any other risk, terrorism or Mother Nature included, that could potentially pose any greater risk to society than this."
Until recently, official guesstimates of the expected death toll of a new pandemic have been modest. Using mathematical models devised by the U.S. Centers for Disease Control, Canada's public health agency estimates between 11,000 to 58,000 here people might die.
The CDC models point to between two million and seven million deaths worldwide.
Many question those figures and say they're far too rosy. And many believe the WHO's new numbers are overly optimistic as well.
Dr. Osterholm is one of them. He's done age-adjusted calculations based on the experience of the 1918 Spanish flu, the worst pandemic in known history.
Laying 1918 fatality rates over the world's current population, Dr. Osterholm suggests between 36 million and 177 million people would die if a pandemic of similar severity hit again. (The top figure is based on half the world's population becoming infected.)
But public discussion of numbers like those makes many in the flu world nervous, fearing the figures are so impossibly large they take on the mantle of science fiction.
"None of these models can 100 per cent predict what's going to be happening. And it would be wrong in my view to always play the worst case scenario," cautions Dr. Klaus Stohr, head of the WHO's global influenza program.
"Irrespective of what type of model we are talking about, the figures are certainly not comforting," he continues. "None of these estimates would suggest that we should let down our efforts in pandemic preparedness."
But Dr. Osterholm and others around the globe are extremely concerned those efforts are moving at a snail's pace. They fear governments and vaccine companies are dismissing the potential disaster as too hypothetical, too apocryphal.
"This to me is akin to living in Iowa ... and seeing the tornado 35 miles away coming. And it's coming. And it's coming. And it's coming. And it keeps coming," says Dr. Osterholm, who is a special adviser to U.S. Health Secretary Tommy Thompson and associate director of Homeland Security's National Center for Food Protection and Defence.
"You just see it. And we're largely ignoring it."
The "it" Dr. Osterholm refers to is a nasty strain of influenza A known as H5N1, so named because of the hemagglutinin (H) and neuraminidase (N) proteins on the virus's outer shell. Though flu is notoriously unpredictable, H5N1 is currently considered the leading candidate to spark the next pandemic.
With 500 years of history to guide them, experts say flu pandemics are inevitable.
The highly unstable RNA viruses are constantly recombining (mutating) and reassorting (swapping genes with each other). The result: new forms of flu are always finding ways to slip past the immune system's sentries to pick the lock of the human respiratory tract.
When an entirely new version appears, one to which no one has any immunity, a pandemic occurs. And with 36 years having elapsed since the last pandemic, experts warn another could come at any time.
The thought of an H5N1 pandemic chills the hearts of those who've been following the virus's evolution since it was first known to have infected humans, in Hong Kong in 1997.
Dr. Keiji Fukuda of the CDC's flu branch investigated the Hong Kong outbreak and others since. He sighs softly when asked whether the prospect of an H5N1 pandemic robs him of sleep.
"More nights than I like," admits Dr. Fukuda, head of epidemiology for the branch.
Dr. Fukada chooses his words with care. He often describes H5N1 developments as "spooky," the closest he gets to hyperbole.
"When a pandemic will occur and what the agent might be is completely unknowable," he says.
"Nonetheless I think that all of us are definitely working under an increased sense of urgency because of all of the events that have gone on in Asia....
"We know that we're not adequately prepared. And to that extent we are pushing things pretty urgently."
Since the beginning of the year H5N1 has killed millions of chickens and forced the culling of tens of millions more in at least nine Southeast Asian countries.
It has defied long-standing flu dogma by directly infecting and killing mammals previously thought to be immune to an avian virus, house cats, leopards and tigers among them.
It's also killed 32 of the 42 people -- mainly children and young adults -- known to have caught it in Vietnam and Thailand. There is much suspicion in the flu world that other deaths elsewhere have gone unreported.
Efforts to eradicate the virus from chicken stocks have so far failed. Some believe the virus has become endemic in a region where dense human populations live cheek by jowl with animals that can be a mixing bowl for virus reassortment.
Factor in the inadequacy of the international vaccine system, which under current regulatory rules could only produce enough pandemic vaccine for a fraction of the world's people, add the lack of surge capacity in hospitals the world over and the picture looks bleak, says Dr. Osterholm, who is also director of the Center for Infectious Disease Research and Policy at the University of Minnesota.
"You keep adding all these things up and you see -- we are talking about a perfect storm."
Re: Rise of the New Plagues Continues
Post by bigbunny on Nov 21, 2004, 6:23pm
More worrisome still is the fact that H5N1 is currently behaving much like the dreaded Spanish flu, which had the astonishing capacity to swiftly kill people in the prime of life.
Flu generally kills the old and the very young; it weakens their systems, making them prey to secondary infections like pneumonias which they can't fight.
But the Spanish flu was different. It's believed that virus sparked what's called a cytokine storm -- a cascading hyper-reaction of the immune system so severe that attacking the invader actually killed the host.
"Everything that we're seeing in the virus-host interaction in Southeast Asia says cytokine storm," Dr. Osterholm says.
If H5N1 becomes a pandemic strain and retains that fearsome feature, in addition to the very young and the very old -- flu's normal targets -- young, healthy people with robust immune systems would be at great risk.
Some influenza pandemics of the 20th century:
Spanish Flu - Caused by an H1N1 virus. Emerged in the spring of 1918, subsided by 1920. Estimated to have killed 30,000 to 50,000 Canadians and at least 50 million people around the globe, though a lack of good figures from the developing world means the actual death toll might have been double that.
Asian Flu - Hit in 1957-58. Caused by an H2N2 virus. Estimated to have killed one million to four million in the developed world.
Hong Kong Flu - Caused by an H3N2 virus, it hit in 1968-69. Estimated to have killed from one million to four million people in the developed world.
Glossary of terms related to influenza pandemics:
Influenza - A disease of the respiratory tract caused by a large family of ever-evolving RNA viruses. Influenza viruses live in the guts of wild aquatic birds, causing no illness. But they create disease in a wide variety of mammals, including humans, seals, horses, pigs, and ferrets.
Influenza epidemic - The outbreaks of illness seen regularly, mainly during winter months in the northern hemisphere.
Influenza pandemic - A global influenza outbreak caused by a strain that hasn't circulated before in humans. Pandemics lead to widespread illness around the globe, high numbers of hospitalizations and deaths.
Recombination - One of the two ways a pandemic strain can develop. A novel strain from nature mutates to the point where it can easily infect humans and spread among them.
Reassortment - The second way a pandemic strain can arise. A strain from nature that can't easily infect humans encounters a strain that can, generally in a pig. The two viruses swap genetic material, giving the novel strain the ability to jump easily into humans.
Hemagglutinin - The H in a flu virus's name, a surface protein that allows the virus to attach to and infect cells in the respiratory tract, where the virus multiplies. Hemagglutinin plays a key role in determining whether the strain is mild or severe.
Neuraminidase - The N in a flu virus's name, a surface protein that breaks the new viruses out of an infected cell, allowing disease to spread.
© Copyright 2004 Bell Globemedia Publishing Inc. All Rights Reserved.
http://www.theglobeandmail.com/servlet/story/RTGAM.20041117.wpan11
17/BNStory/specialScienceandHealth/?pageRequested=2
Comment
From Patricia Doyle, PhD
11-20-4
Hello Jeff -
I think the Helen Branswell article is rooted in fear. The fear is that a "naturally occurring" influenza pandemic will occur. It may very well occur. However, the real risk is that a lab-created genetically altered Influenza virus will appear in the general populace after its escape via infected lab workers returning to their communities and homes after work. This is basically what occurred with SARS on three separate occassions.
Labs are now genetically altering influenza viruses and working with the most deadly influenza strains, inserting lethal genes into them. This is asking for a catastrophe.
The most appalling recent research is the inserting of lethal genes (i.e. genes that gave the 1918 bird flu its lethality, and caused the bird flu to jump species) into contemporary influenza virus. Should this "hybrid" or "chimera virus" escape, we would, indeed, have a major pandemic with millions of casualties. BUT, but...this pandemic could have been prevented.
Should such an event occur, it would probably be compounded with denial of the origin of the pandemic, lying as to the efficacy of vaccine, and then covering up the true numbers of dead.
Furthermore, chaos would erupt in the medical community and public health would be in the same "impotent" mode as was the case when the US learned there was a flu vaccine shortage. Public health was in turmoil. The experts could not figure out how to get existing supplies of vaccine to the public. Actually, the loss of the vaccine was the best news of all for the "health" of the public
regarding the coming flu season. It has been well-noted that people who did not have flu shots in 1918 generally were able to evade the flu while vaccinated soldiers took the highest number of casualties.
I am sure that hospitals and public health would not be able to get medications to those with influenza complications and a health care system in chaos would be the real culprit in loss of life.
It would serve the public far better if public health would stop stirring up fear using the media and concentrate on containing and treating influenza patients. The same public health experts need to be honest with the public and inform the public on the best way to support the immune system which is going to be the first line of defense against any "pandemic" influenza bug. Diet, exercise and reduction of air and body pollutants should be in the front line arsenal for use against the flu bug.
US epidemiologist Michael Osterholm and the CDC need to stop concentrating on, and talking about, the 'MILLIONS OF DEATHS' and start to calculate how best to help people fight the flu without vaccines and how people can better support their immune systems. Constant reports about MILLIONS and MILLIONS of deaths from some POTENTIAL influenza outbreak does not help the situation.
And how about putting a stop to genetic research? Digging up previously eradicated virus samples, genetically altering their lethal genes, and then inserting those death genes into contemporary influenza is the REAL risk of a global pandemic.
Patricia Doyle
Re: Rise of the New Plagues Continues
Post by bigbunny on Nov 21, 2004, 6:56pm
Rare STD Now Spreading Among Gay Men
Infectious Disease News.com
11-21-4
A rare sexually transmitted disease (STD), lymphogranuloma venereum, (LGV) among men who have sex with men (MSM) has been reported in the Netherlands, according to the CDC.
LGV is a systemic STD caused by specific strains of Chlamydia trachomatis that rarely surface in the United States.
Typically, fewer than five cases are diagnosed in the Netherlands per year, but as of September 2004 there had been 92 confirmed LGV cases during the preceding 17 months among MSM there.
Belgium, Sweden and France have also reported LGV infections. It is difficult to determine whether the United States is experiencing a similar increase because LGV is not reportable.
However, the CDC did identify a L2 LGV strain on a U.S. patient,s rectal swab this past July. The patient was experiencing signs and symptoms similar to the Dutch patients, but did not have known exposure to European MSM. The patient,s contacts were evaluated and treated for LGV.
The first 13 reported cases in the Netherlands were diagnosed from April to November 2003, an additional 17 confirmed cases and 40 possible cases were identified later.
Researchers diagnosed the confirmed, probable and possible cases by conducting polymerase chain reaction (PCR) tests on rectal swab specimens and analyzing the genotype.
Confirmed cases met three criteria: contact with a patient confirmed to have LGV or proctitis; a positive PCR test for C. trachomatis; and L1, L2 or L3 genotype determined by PCR. Possible cases were defined as MSM who met only the first criteria and had a positive serologic test.
In all of the Rotterdam cases, LGV was associated with high-titer antibodies to C. trachomatis in sera, as determined by peptide enzyme immunoassay.
Epidemiological preliminary findings indicated that all the patients were white. Of 30 MSM whose HIV status was known, 23 (77%) were HIV-positive. Almost all of the men reported risky sexual behaviors.
Health care providers who identify possible LGV cases are urged to contact their local health department and the CDC at (404) 639-2059.
Etiology, Clinical Manifestations, Diagnosis and Treatment of Lymphogranuloma Venereum (LGV)
Etiology LGV is caused by Chlamydia trachomatis serovars L1 to L3. (C. trachomatis serovars B and D-K are responsible for the syndromes of nongonococcal urethritis and cervicitis). Clinical manifestations The primary lesion produced by LGV is a small, nonpainful genital papule, which can ulcerate at the site of inoculation after an incubation period of 3-30 days. This lesion can remain undetected within the urethra, vaginal vault or rectum. Common clinical manifestations include tender, unilateral or bilateral inguinal and/or femoral adenopathy, which can become fluctuant; and hemorrhagic proctitis or proctocolitis, which is associated with receptive anal intercourse (1). The clinical and histologic presentation of LGV proctocolitis can be similar to the initial manifestation of inflammatory bowel disease (2). Diagnosis Diagnosis is based primarily on clinical finding; routine laboratory confirmation might not be possible. Serologic tests for C. trachomatis (ie, microimmunofluorescence or complement fixation) can support diagnosis. Direct identification of C. trachomatis from a lesion (ie, bubo) or site of the infection (eg, rectum) can be made by using culture or by using nonculture nucleic acid testing; however, neither method is specific for LGV, and use of rectal swabs for nucleic acid testing is not cleared by the FDA. Treatment The recommended treatment is administration of 100 mg of doxycycline, twice a day for 21 days. Alternative treatment is 500 mg of erythromycin base orally, four times a day for 21 days. Some specialists in sexually transmitted diseases believe 1 g of azithromycin (Zithromax, Pfizer), administered orally once weekly for 3 weeks, is effective; however, clinical data are lacking. Sex partners who had contact with the patient within 30 days of the patient,s onset of symptoms should be treated with either 1 g of azithromycin in a single dose, or 100 mg of doxycycline, twice a day for 7 days. References: Perine PL, Stamm WE. Lymphogranuloma venereum. In: Homes KK, Mardh PA, Sparling PF, et al, eds. "Sexually Transmitted Diseases. New York, NY: McGraw-Hill; 1999:423-432. Bauwens JE, Lampe MF, Suchland RJ, et al. Infection with Chlamydia trachomatis lymphogranuloma venereum serovar L1 in homosexual men with proctitis: molecular analysis of an unusual case cluster. Clin Infect Dis. 1995;20(3):576-581.
For more information: CDC. Lymphogranuloma venereum among men who have sex with men Netherlands, 2003-2004. MMWR. 2004;53(42):985-998.
http://www.infectiousdiseasenews.com/200411/frameset.asp?article=lgv.asp
Re: Rise of the New Plagues Continues
Post by bigbunny on Nov 21, 2004, 6:58pm
Rare STD Now Spreading
Among Gay Men
Infectious Disease News.com
11-21-4
A rare sexually transmitted disease (STD), lymphogranuloma venereum, (LGV) among men who have sex with men (MSM) has been reported in the Netherlands, according to the CDC.
LGV is a systemic STD caused by specific strains of Chlamydia trachomatis that rarely surface in the United States.
Typically, fewer than five cases are diagnosed in the Netherlands per year, but as of September 2004 there had been 92 confirmed LGV cases during the preceding 17 months among MSM there.
Belgium, Sweden and France have also reported LGV infections. It is difficult to determine whether the United States is experiencing a similar increase because LGV is not reportable.
However, the CDC did identify a L2 LGV strain on a U.S. patient,s rectal swab this past July. The patient was experiencing signs and symptoms similar to the Dutch patients, but did not have known exposure to European MSM. The patient,s contacts were evaluated and treated for LGV.
The first 13 reported cases in the Netherlands were diagnosed from April to November 2003, an additional 17 confirmed cases and 40 possible cases were identified later.
Researchers diagnosed the confirmed, probable and possible cases by conducting polymerase chain reaction (PCR) tests on rectal swab specimens and analyzing the genotype.
Confirmed cases met three criteria: contact with a patient confirmed to have LGV or proctitis; a positive PCR test for C. trachomatis; and L1, L2 or L3 genotype determined by PCR. Possible cases were defined as MSM who met only the first criteria and had a positive serologic test.
In all of the Rotterdam cases, LGV was associated with high-titer antibodies to C. trachomatis in sera, as determined by peptide enzyme immunoassay.
Epidemiological preliminary findings indicated that all the patients were white. Of 30 MSM whose HIV status was known, 23 (77%) were HIV-positive. Almost all of the men reported risky sexual behaviors.
Health care providers who identify possible LGV cases are urged to contact their local health department and the CDC at (404) 639-2059.
Etiology, Clinical Manifestations, Diagnosis and Treatment of Lymphogranuloma Venereum (LGV)
Etiology LGV is caused by Chlamydia trachomatis serovars L1 to L3. (C. trachomatis serovars B and D-K are responsible for the syndromes of nongonococcal urethritis and cervicitis). Clinical manifestations The primary lesion produced by LGV is a small, nonpainful genital papule, which can ulcerate at the site of inoculation after an incubation period of 3-30 days. This lesion can remain undetected within the urethra, vaginal vault or rectum. Common clinical manifestations include tender, unilateral or bilateral inguinal and/or femoral adenopathy, which can become fluctuant; and hemorrhagic proctitis or proctocolitis, which is associated with receptive anal intercourse (1). The clinical and histologic presentation of LGV proctocolitis can be similar to the initial manifestation of inflammatory bowel disease (2). Diagnosis Diagnosis is based primarily on clinical finding; routine laboratory confirmation might not be possible. Serologic tests for C. trachomatis (ie, microimmunofluorescence or complement fixation) can support diagnosis. Direct identification of C. trachomatis from a lesion (ie, bubo) or site of the infection (eg, rectum) can be made by using culture or by using nonculture nucleic acid testing; however, neither method is specific for LGV, and use of rectal swabs for nucleic acid testing is not cleared by the FDA. Treatment The recommended treatment is administration of 100 mg of doxycycline, twice a day for 21 days. Alternative treatment is 500 mg of erythromycin base orally, four times a day for 21 days. Some specialists in sexually transmitted diseases believe 1 g of azithromycin (Zithromax, Pfizer), administered orally once weekly for 3 weeks, is effective; however, clinical data are lacking. Sex partners who had contact with the patient within 30 days of the patient,s onset of symptoms should be treated with either 1 g of azithromycin in a single dose, or 100 mg of doxycycline, twice a day for 7 days. References: Perine PL, Stamm WE. Lymphogranuloma venereum. In: Homes KK, Mardh PA, Sparling PF, et al, eds. "Sexually Transmitted Diseases. New York, NY: McGraw-Hill; 1999:423-432. Bauwens JE, Lampe MF, Suchland RJ, et al. Infection with Chlamydia trachomatis lymphogranuloma venereum serovar L1 in homosexual men with proctitis: molecular analysis of an unusual case cluster. Clin Infect Dis. 1995;20(3):576-581.
For more information: CDC. Lymphogranuloma venereum among men who have sex with men Netherlands, 2003-2004. MMWR. 2004;53(42):985-998.
http://www.infectiousdiseasenews.com/200411/frameset.asp?article=lgv.asp
Re: Rise of the New Plagues Continues
Post by bigbunny on Nov 25, 2004, 7:51am
.
H5N1Pandemic Potential
(click on title above for assocciated media stories)
>>Between a quarter and a third of the world's population will fall ill, according to new World Health Organization estimates, and 1 per cent of the sick will die.<<
A 1% case fatality rate for is a VERY optimistic number. Most of the current worry centers on H5N1 and the case fatality rate in Asia is in the 70-80% range, which would put human fatalities well north of 1 Billion. There really is little support for this rate to fall to 1% as the virus acquires human to human transmission. Although much has been made of re-assortments emerging from dual infections, the virus really evolves via recombination. Acquiring human receptor binding sequences via recombination would not be difficult and would involve a very small portion of the H gene. Such a recombinant could achieve efficient human to human transmission without significant change in the rest of H and no change in the other genes. Thus maintaining a case fatality rate of 70-80% would not be difficult.
Many factor favor such a scenario. The current case fatality rate is the highest recorded for human influenza infections. Those who have died have been children and young adults, indicating that the virus is not well recognized by human immune recognition systems. H9N2 viruses with H5N1 genes have been reported, as have H5N1 viruses with H9N2 genes. Since some H9N2 viruses already have receptors that target humans, creation of recombinants would not require mammalian infections.
The number of reported H5N1 infections in birds was at an all time high last season and recent lab experiments show that the H5N1 isolates that are lethal in humans in Vietnam and Thailand can grow to high titers in duck intestines without causing disease in the ducks. A second infection in these asymptomatic ducks can lead to recombinants that are shed in large amounts.
Thus, the migration of birds provide new flu sequences for the creation of novel recombinants which could retain the high case mortality rate seen in 2004 coupled with the ability to efficiently transmit from human to human.
http://www.recombinomics.com/pandemic_potential.html
Re: Rise of the New Plagues Continues
Post by bigbunny on Nov 28, 2004, 5:37pm
AIDS Strategy Failing As Disease Becomes Female Epidemic
By Jeremy Laurance
Health Editor
The Independent - UK
11-28-4
Global efforts to curb the spread of HIV/Aids are failing because the world has not recognised that it is a female epidemic, a report said yesterday.
Aids claimed 3.1 million lives last year, the highest ever, and the rate at which women and girls are affected is accelerating. The spread of the disease shows no sign of slowing, despite billions of pounds invested in treatment and prevention.
The annual report on the Aids epidemic, published by UNAids and the World Health Organisation yesterday, says a record 39.4 million people are living with HIV, up from 36.6 million two years ago.
Today, the Health Protection Agency will publish figures showing the number of people living in the UK with HIV has also reached a record high, above 50,000 for the first time.
Globally, the fastest increase in infections is among women and girls. They account for 57 per cent of all those infected in sub-Saharan Africa, the worst-hit region, and for 75 per cent of those aged 15 to 24.
In every region of the world, rates of infection in women are rising faster than among men. In Russia, which has the biggest HIV epidemic in Europe, affecting 860,000 people, the proportion of women infected has leapt from 24 per cent to 38 per cent in two years.
The "feminisation" of Aids has dawned slowly on the major international organisations committed to tackling it. Until now they have placed the ABC strategy - Abstain, Be faithful, use a Condom - at the centre of their prevention efforts.
Yesterday's report from UNAids said the ABC approach was "insufficient" and left "serious gaps". The strategy to prevent one of the worst diseases in human history must be rewritten with a new focus on women, it says. Kathleen Cravero, deputy executive director of UNAids, told a press conference in London to launch the report: "The prevention strategies are missing the point. They are not responding to the realities of women's lives. Women do not have the economic power or social choices over their lives to put the information [about HIV prevention] into practice."
Aids began as a mainly male disease, concentrated among homosexuals in the United States, drug users in Russia and the Far East who injected, and men who used prostitutes in Africa. But, as the epidemic has lengthened, the disease has taken hold among women. The number infected globally is about to overtake men.
Women are biologically twice as likely to become infected during sex as they are exposed to a larger dose of virus, and are more prone to be cajoled or forced into sex because of their lack of social power. When sex is violent and non-consensual, abstention is not an option.
Wives of men who die of Aids may be forced out of the family home, which may pass to the husband's relatives, leaving them destitute and forced to resort to sex for economic survival.
Studies in South Africa showed that women under 20 who were married - usually to older men - had higher rates of infection than those who were unmarried but sexually active, because the latter were better able to negotiate condom use.
Ms Cravero said: "We tell women to abstain when they have no right. We tell them to be faithful when they cannot ask their partners to be faithful. We tell them to use a condom when they have no power to do so."
"We need to give women power, to reduce levels of violence against them and to protect their property and inheritance rights. We are still not keeping pace with the epidemic and we need to tackle the problem in women and girls."
The emphasis on women is a major shift for UNAids which up to now has focused on changing the behaviour of men. But the feminisation of the epidemic has forced it to confront the failure of that strategy.
Without an Aids vaccine, the best technical hope for women is a microbicide to prevent transmission and provide them with a method they could control. The report says a first generation microbicide could be ready in five years if investment in research were expanded. A microbicide that was 60 per cent effective and used by one in five women could prevent about 2.5 million infections over three years, it says.
Emma Thompson, the actress and Aids campaigner who attended the UNAids launch, said: "Women's economic independence is vital in this struggle. I know a girl who gave her body to a man for an apple. If we have girls who have absolutely nothing we are not going to protect them."
Alvaro Bermejo, head of the International HIV/Aids Alliance said: "The report makes clear that too many strategies assume a greater level of choice about sex, particularly among women, than exists. Everyone must recognise this in their programmes - and work to change these economic and social realities. If we don't, we cannot have the greatest impact on the epidemic."
© 2004 Independent Digital (UK) Ltd
http://news.independent.co.uk/world/science_technology/story.jsp?story=586049
Re: Rise of the New Plagues Continues
Post by bigbunny on Nov 28, 2004, 5:45pm
Killer Bullfrogs On The Loose In BC
By Mark Hume
Globe and Mail Update
11-27-4
VANCOUVER -- When American bullfrogs were first imported to British Columbia in the 1930s, the idea was that their legs would end up on dinner plates. Instead, the frog farms failed; the stock got free, and now the giant bullfrogs are the ones doing the eating, attacking everything from tiny tree frogs to waterfowl.
Some municipalities are talking of halting the bullfrog invasion by building "control corridors," where the rapidly expanding population would be electroshocked and killed by freezing.
Clyde Burton, a naturalist in Powell River, said such controls might have helped if they had been in place years ago on the Sunshine Coast, where bullfrogs are blamed for wiping out the Cranberry Lake duck population.
"They will eat just about anything," said Mr. Burton, who over the seasons has heard the deep, honking sound of bullfrogs displace the songs of water birds on the lake, about 120 kilometres north of Vancouver.
"A small duck doesn't stand a hope in hell. They are like alligators. I'll tell you, boy, don't put your fingers over the side of the boat."
Mr. Burton said he first realized bullfrogs were eating birds a few years ago. He was standing in a marshy area on Cranberry Lake when a flock of small sandpipers landed.
"There was a big splash, and the flock took off," Mr. Burton recalled. "By the time I got over there to have a look, here was this bullfrog with a sandpiper in its mouth, just the corner of the wings sticking out."
Mr. Burton said he started catching bullfrogs after that to study stomach contents because he wanted to know if the sandpiper incident was just a case of one killer frog.
He soon found grisly proof that the scientific name for American bullfrogs, Rana catesbeiana, might as well be Latin for ready to eat anything.
"We had one with two newly hatched wood ducks in its belly. We got one with a male yellow-rumped warbler. We got mice."
Mr. Burton blames the bullfrogs, which he said stretch 40 centimetres toe tip to toe tip, for the lack of waterfowl on what was once a busy duck pond.
"I used to go over there on Mothers' Day and count 150 ducklings. Now you see zero," Mr. Burton said.
Wayne Campbell, former chief ornithologist of B.C. and the author of numerous bird books, said he went to investigate the stories of the Cranberry Lake bullfrogs a few springs ago, and was shocked by what he found.
"There was a big bullfrog floating on the surface, dead. Turns out it had choked, trying to swallow a gosling."
He said he heard stories about bullfrogs jumping at small songbirds.
Mr. Campbell said bullfrogs have spread from Vancouver to Powell River on the mainland coast and from Victoria to Campbell River, on Vancouver Island.
Although found naturally in much of southeastern Canada, the bullfrogs are an alien species in B.C. and Mr. Campbell said cold temperatures should stop them from spreading much farther.
But they are already posing a serious environmental problem because of their voracious appetite, he said.
"It's a difficult problem that should be tackled. It requires a team [of experts] to get together. But I don't know how you get rid of these darned things."
Purnima Govindarajulu, a University of Victoria PhD student studying bullfrogs in B.C., said any chance of containing them was lost when the frog farms set them free.
Since then, they have migrated along ditches and with human help.
"People are moving them from place to place," she said. "They have heard frog populations are dwindling, so they think they will help out by introducing them to a local lake or pond. In fact, it has the opposite effect, because native red-legged frogs are a main part of their diet."
Ms. Govindarajulu said people have also helped the bullfrogs by removing trees and brush, creating more favourable conditions by warming the water.
In Greater Victoria, Stan Orchard, an expert on amphibians, has proposed a long-term eradication project modelled on the program Alberta uses to keep rats out of the province.
Ms. Govindarajulu doubts it will work.
"Once bullfrogs are established, they are almost impossible to eradicate," she said. "Each female lays about 13,000 eggs. So you just need one breeding pair to escape and the population will explode again."
© Copyright 2004 Bell Globemedia Publishing Inc. All Rights Reserved.
http://www.theglobeandmail.com/servlet/s..../BNStory/Front/
Re: Rise of the New Plagues Continues
Post by bigbunny on Nov 29, 2004, 10:19pm
Archive Number 20041124.3146
Published Date 24-NOV-2004
Subject PRO/AH/EDR> Undiagnosed illness, avian - USA (FL)
http://www.promedmail.org/pls/askus/f?p=2400:1001:8517773668604153177::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1010,27280
UNDIAGNOSED ILLNESS, AVIAN - USA (FLORIDA)
******************************************
A ProMED-mail post <http://www.promedmail.org>
ProMED-mail is a program of the International Society for Infectious Diseases
<http://www.isid.org>
Date: 24 Nov 2004
From: ProMED-mail <promed@promedmail.org>
Source: ABC, 11 Nov 2004 [edited]
<http://www.nbc-2.com/articles/readarticle.asp?articleid=1841&z=3&p=>
Mysterious illness strikes birds
--------------------------------
A mysterious illness is making a number of wild birds sick, but it is only affecting one species, the double crested cormorant. Wildlife watchers are baffled, because no theory about the illness makes perfect sense.
Workers at the Conservancy of Southwest Florida's Wildlife Rehab Center are helping an unusual number of double crested cormorants. The birds are starving, thin, and lack energy. No one knows what's causing the mysterious ailment. Workers hydrate the birds and feed them. Some of them are eating willingly; others have to be force-fed. Despite all their best efforts, about half the birds that have gone into the rehab center have died. "Even though you know you're doing all you can, it's frustrating for some not to make it," said Joanna Fitzgerald of the Wildlife Rehab Center. The main theory is that red tide in the gulf is making the double crested cormorants sick. "The typical signs we see with red tide we just aren't seeing with these birds. I'm not 100 percent convinced it's red tide," said Fitzgerald.
Double crested cormorants are the birds you see on the side of a lake with their wings spread out. "These are the ones that dry their wings, they'll spread their wings to dry after they've been hunting or fishing," said Fitzgerald.
One of the birds regained enough strength to be able to be released into the wild in Port Royal. "It's very rewarding when you see them go," said Rebecca LeBlanc of the Wildlife Rehab Center.
[Byline: Tom Roussey]
--
[One would hope that these biologists are having the birds necropsied and some diagnostic tests run. The article here does not give enough specifics for speculation.
Avian Vacuolar Myelinopathy (AVM) may be a possibility. If a bird recovered, then it seems likely that AVM and botulism could be ruled out.
Certainly, if there is any more authoritative information on this situation, we would appreciate it. - Mod.TG]
Re: Rise of the New Plagues Continues
Post by bigbunny on Nov 30, 2004, 12:25am
SARS Vaccine Damages Liver In Animal Testing
The Globe and Mail
11-29-4
TORONTO (CP) -- A SARS vaccine designed by Canadian scientists triggered severe liver inflammation when tested in ferrets - an unexpected problem that should give pause to others working to develop a vaccine against the disease.
The team, which reported its findings in the Journal of Virology, stumbled upon the problem by accident when one of the scientists insisted on running unplanned blood chemistry tests on the vaccinated ferrets.
The director of the Canadian SARS Research Network says the results are a red flag to all working on vaccines for the disease.
"This is really important because it really is saying: proceed cautiously in people," said Dr. Mark Loeb, an infectious disease specialist at Hamilton's McMaster University. Dr. Loeb was not involved in the work.
The team was drawn from the Canadian Science Centre for Human and Animal Health, the Winnipeg complex which houses the National Microbiology Laboratory and the National Centre for Foreign Animal Disease.
Research scientist Jingxin Cao constructed the recombinant vaccine by genetically modifying a pox virus to produce a protein - called the spike protein - which is made by the SARS coronavirus. The spike protein is the key protein on the SARS virus that triggers an immune response.
Mr. Cao chose the modified pox virus, called MVA, because it has been widely - and safely - used in development of other vaccines.
"It's really safe, even in the so-called immune compromised, like AIDS patients," he said in an interview.
The team then put the vaccine to the test, vaccinating ferrets, which are believed to suffer disease similar to that experienced by humans who contract SARS. They then waited to see whether the animals developed antibodies to the virus when they were exposed to SARS in what's called a challenge test.
On that front, things went smoothly.
"We had quite nice antibody levels against this protein," said Hana Weingartl, head of special pathogens in the centre for foreign animal disease.
But then colleague Markus Czub insisted on running the blood chemistry tests and found evidence of severe hepatitis - inflammation of the liver. Autopsies on the animals confirmed the finding.
And there was another hitch. Their control ferrets - the unvaccinated animals - didn't show signs of disease, leading the team to wonder whether they are indeed a good model for human SARS.
"They certainly do replicate the virus but they did not get sick," Ms. Weingartl said.
That isn't the experience of another Canadian researcher working on a SARS vaccine.
Brett Finlay, a molecular biologist at the University of British Columbia, said ferrets his team tested developed symptoms similar to human SARS.
"They got sick; they got lung disease, just like people do," said Mr. Finlay, whose team worked on different kinds of vaccines, including one based on a killed coronavirus and another on a modified adenovirus.
"You crack open the lungs and it's all inflammed and yucky, just like you see in SARS."
His team's results are not yet published, so they haven't been confirmed by outside experts through a scientific journal's peer review process. But he says they did not see liver inflammation - and they checked.
"We did not see what they saw. We'd heard about that, so we were looking."
Mr. Finlay agreed with Dr. Loeb that all teams working on a SARS vaccine will have to check for liver inflammation from now on.
"We'd be dumb not to," he insisted.
As for the Winnipeg team, they cannot say whether the problem they saw relates strictly to their vaccine or is indicative of a wider challenge to the development of a SARS vaccine.
"We don't know whether or not this association of vaccination with enhanced hepatitis is only related to the MVA base," Mr. Cao said. "Could be if you tried a different way - for example, adenovirus-based, another virus based - you won't see this. We don't know."
© Copyright 2004 Bell Globemedia Publishing Inc. All Rights Reserved.
http://www.theglobeandmail.com/servlet/story/R
TGAM.20041128.wsars1128/BNStory/National/
Re: Rise of the New Plagues Continues
Post by bigbunny on Nov 30, 2004, 6:05pm
Salmonella Uses Hydrogen As An Energy Source, New Study Shows
New research, headed by microbiologists from the University of Georgia, show for the first time that Salmonella – a widespread and often deadly bacterial pathogen – use molecular hydrogen to grow and become virulent. The discovery represents a way that diseases caused by Salmonella and other enteric infections could be lessened or even eliminated.
![[image]](http://www.sciencedaily.com/images/2004/11/041129112654.jpg "[image]")
Color-enhanced scanning electron micrograph showing Salmonella typhimurium (red) invading cultured human cells. (Credit: Rocky Mountain Laboratories, NIAID, NIH)
The research, just published in the journal Infection and Immunity, was led by Rob Maier, Georgia Research Alliance Eminent Scholar and Ramsey Professor of Microbiology at UGA. Other authors of the paper from UGA were and researcher Adriana Olczak and research coordinator Susan Maier; and Shilpa Soni and John Gunn from Ohio State University.
"This builds on our earlier findings that major human pathogens are using an unexpected energy source," said Maier. "This new work expands our knowledge that molecular hydrogen is very important in the process of diseases caused by these organisms."
Such enteric pathogens as Salmonella are responsible for an estimated 2 million deaths a year and cause millions more cases of diarrheal illnesses, even in developed countries. Maier was the first to discover that hydrogen is not lost from the body as a waste product, as researchers previously thought, but remains at substantial levels and is an energy source for pathogenic bacteria. This knowledge that human pathogens can grow on hydrogen while residing in an animal may have profound implications for the treatment of some diseases.
In 2002, Maier published in the journal Science evidence that the gastric bacterium Helicobacter pylori, which gives rise to peptic ulcers, gastritis and some kinds of gastric cancers, needs hydrogen as an energy source. The new research extends those earlier findings to Salmonella.
The work has been possible because of the increasing number of entire genomes that are being sequenced for everything from bacteria to humans. Knowing the exact position of individual genes on the entire genome allows scientists a much richer understanding of how disease processes work than ever before.
"From the gene sequence we found that Salmonella was predicted to have three distinct membrane-associated enzymes that split molecular hydrogen using a unique metal center, which is composed of nickel, iron, cyanide and carbon monoxide," said Maier. "Humans don't make this kind of metal cluster in cells, and so it's an excellent target for therapeutic intervention. Also, making nickel unavailable to the cells by use of metal sequestering agents would be expected to stop the hydrogen using reactions required for growth of the bacterium."
The new research showed that each of the three membrane-associated, hydrogen-utilizing enzymes in Salmonella is coupled to a respiratory pathway that uses oxygen as the terminal electron acceptor. This permits growth of the pathogen.
Maier believed that these enzymes might enable bacteria to glean energy from the splitting of molecular hydrogen. Because the high-energy gas produced by the reactions of normal flora bacteria in the intestinal tract is freely diffusible, it can be measured within tissues colonized by pathogens. So, using mice as a model system, Maier and his colleagues were able to find that, indeed, Salmonella use molecular hydrogen as an energy source to grow and cause disease.
It should be noted that the team studied a type of Salmonella enterica called Typhimurium, a common food-poisoning bacterium closely related to a different strain of Salmonella that causes typhoid fever.
http://www.uga.edu/news/artman/publish/041129maier.shtml
Re: Rise of the New Plagues Continues
Post by bigbunny on Dec 4, 2004, 10:00am
Rocket Fuel Chemical Found In Organic Milk
Rocket Fuel Chemical Found In Lettuce From Arizona,
Organic Milk From Maryland, And In Spring Water.
12-1-4
WASHINGTON - The government has found traces of a rocket fuel chemical in organic milk in Maryland, green leaf lettuce grown in Arizona and bottled spring water from Texas and California. What's not clear is the significance of the data, collected by the Food and Drug Administration through Aug. 19.
Sufficient amounts of perchlorate can affect the thyroid, potentially causing delayed development and other problems.
But Environmental Protection Agency official Kevin Mayer called for calm, saying in an interview Tuesday: "Alarm is not warranted. That is clear."
"I think that it is important that EPA and FDA and other agencies come to some resolution about the toxicity of this chemical," Mayer said. "That has been, frankly, a struggle for the last few years."
The FDA found that of the various food items it tested, iceberg lettuce grown in Belle Glade, Fla., had the highest concentrations of perchlorate. The greens had 71.6 parts per billion of the compound, the primary ingredient in solid rocket propellent. Red leaf lettuce grown in El Centro, Calif., had 52 ppb of perchlorate. Most of the purified, distilled and spring bottled water tested around the nation tested had no detectable amount of perchlorate.
Whole organic milk in Maryland, however, had 11.3 ppb of perchlorate.
Asked whether that level of chemical in milk was worrisome, Mayer, the EPA's regional perchlorate coordinator for Arizona, California, Hawaii and Nevada, said, "The answer is, we don't know yet."
The FDA said in a statement that consumers should not change their eating habits in response to the test results, posted on the agency's Web site Friday.
The testing comes as federal agencies try find how much perchlorate people are exposed to from food so they can determine whether action is needed to protect the public health. Federal agencies have been trying since the early 1990s to determine what level of perchlorate is safe.
The state of California, meanwhile, set a standard of no more than 10 ppb of perchlorate in drinking water. That was lowered to 6 ppb in drinking water to account for the chemical also lacing food, Mayer said.
A more conservative suggestion, in a draft from the EPA, would allow no more than 1 ppb of perchlorate in drinking water.
The FDA tested lettuce samples collected at farms and packing sheds and bottled water from retail stores. Raw milk samples came from a research facility in Maryland and other milk samples were obtained from retail stores.
"These data are exploratory and should not be understood to be a reflection of the distribution of perchlorate in the U.S. food supply," the agency said in a statement. "Until more is known about the health effects of perchlorate and its occurrence in foods, FDA continues to recommend that consumers eat a balanced diet, choosing a variety of foods that are low in trans fat and saturated fat, and rich in high-fiber grains, fruits and vegetables."
http://abcnews.go.com/Health/wireStory?id=293356
Re: Rise of the New Plagues Continues
Post by bigbunny on Dec 7, 2004, 12:02am
MS risk 'linked to birth month'
Children born in May have an increased risk of going on to develop multiple sclerosis, research has suggested.
The analysis of MS rates among over 42,000 people born in the northern hemisphere showed a significantly lower risk for those born in November.
The effect was most evident in Scotland, where the prevalence of MS was the highest.
The study, published online by the British Medical Journal, was carried out by Oxford University researchers.
The team suggest that complex interactions between genes and the environment before or shortly after birth may help to explain the links they found.
This adds weight to the accepted view that something related to the environment - including around the time of birth - may influence the development of MS
Mike O'Donovan, MS Society,
They analysed data on the birth month, medical and family histories of 17,874 Canadian patients and 11,502 British patients with MS.
They were compared with a matched group of people from the general population and unaffected brothers and sisters of those with MS
In Canada, significantly fewer people with MS were born in November compared with the general population or sibling groups.
And in Britain, fewer people with MS had been born in November and significantly more had been born in May.
The number born in December was also significantly lower.
The researchers also looked at data from Denmark and Sweden, which again showed a May peak and a November fall.
'Complex jigsaw'
Overall, it was found that around 10% more people born in May and 10% fewer people born in November went on to develop MS, compared to rates seen in the other months of the year.
The researchers, led by Professor George Ebers of the department of clinical neurology at the Radcliffe Infirmary at the University of Oxford, said the explanation for the difference remained unclear.
But writing in the BMJ, they said: "The risk factors for the effects of the timing of birth must vary seasonally and probably interact with the development of the central nervous system or immune systems, or both."
The team said other studies had suggested exposure to the sun or seasonal variations in a mother's vitamin D levels during pregnancy may have an impact on brain development.
Mothers of babies born in May would be exposed to less sunlight because they are pregnant during the winter.
Professor Ebers added: "MS is an adult-onset disease. So you wouldn't think that happened right back at the beginning would be a risk factor.
"But this study does show that the month in which people are born appears to have an effect."
And he said people who had MS in their family may use the information to decide when they would try to conceive.
Mike O'Donovan, chief executive of the MS Society, said, "This is an interesting study which adds weight to the accepted view that something related to the environment - including around the time of birth - may influence the development of MS.
"It is also worth noting it does not negate the likelihood of environmental factors operating at other times as well. It is another piece in a very complex jigsaw of research."
It affects around 85,000 people in the UK and is most often diagnosed in people between the ages of 20 and 40. Women are almost twice as likely to develop MS as men.
Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/health/4072819.stm
Published: 2004/12/07 00:05:13 GMT
Re: Rise of the New Plagues Continues
Post by bigbunny on Dec 7, 2004, 12:06am
6 December 2004
Shampoo Washes Neurons Down The Drain
An antimicrobial agent found in many shampoos and widely used in industrial applications inhibits the development of neuron structures that are essential for transmitting signals between cells, says a University of Pittsburgh study presented at the Cell Biology 2004 meeting.
Exposure to low levels of methylisothiazolinone (MIT) restricted growth of axons and dendrites of immature rat nerve cells in culture, apparently by disengaging the machinery of a key enzyme that is activated in response to cell-to-cell contact, and may have potentially damaging consequences to a developing nervous system, the researchers report. "Our results thus far suggest there is potential that everyday exposure to the chemical could also be harmful to humans. I would be particularly concerned about occupational exposure in pregnant women and the possibility of risk to the fetus," said the study's senior author Elias Aizenman, at the University of Pittsburgh School of Medicine.
As an antimicrobial agent, MIT and related compounds kill harmful bacteria that grow near moisture or water. As such, they often are found in personal care products, as well as in water-cooling systems and at factories that require water for manufacturing. Since learning about MIT, Dr. Aizenman has not found any published neurotoxicity reports, or data in any public documents filed with the Environmental Protection Agency. The first set of studies he and his team published in 2002 in The Journal of Neuroscience involved acute exposure to mature rat neurons. They reported that 10-minute exposure at a high concentration - roughly 100 times the dose used in their current study - was lethal to these cells.
For the current study, the researchers kept immature, developing neurons in a media solution containing low concentrations of MIT for 18 hours. In a standard culture, an immature neuron will in such time develop an axon, the extension from the cell body used for sending signals to other cells, and several dendrites, elaborate projections that receive incoming information. But after exposure to MIT, the cells had few, if any, axons and dendrites.
The researchers plan additional research to further understand the molecular mechanisms underlying MIT's neurotoxic effect on cells, as well as studies involving whole animals. "This chemical is being used more and more extensively, yet there have been no neurotoxicity studies in humans to indicate what kind and at what level exposure is safe. I realize it's a big leap to suggest there may be a parallel between environmental exposure and the noticeably higher rates of diagnosed childhood developmental disabilities, but I would caution that based on our data, there very well could be neurodevelopmental consequences from MIT," concluded Dr. Aizenman.
http://www.scienceagogo.com/news/20041105213742data_trunc_sys.shtml
Re: Rise of the New Plagues Continues
Post by bigbunny on Dec 9, 2004, 1:38am
Pesticide In Cola Leads To Cancer
IOL | December 7 2004
http://prisonplanet.com/articles/december2004/071204leadstocancer.htm
New Delhi - India's highest court has ordered Pepsi and Coca-Cola to print warnings on their bottles sold in the country that the contents may contain pesticide residues.
The Supreme Court ruling late on Monday upheld a judgment by the Rajasthan High Court in November.
The two soft drink giants have two weeks to give the lower court proposed drafts of the pesticide warnings.
In February 2003 a parliamentary probe found soft drinks sold in India by the United States beverage giants contained pesticide residues and urged tougher national health standards.
The inquiry was ordered after the Centre for Science and Environment, alleged 12 of the companies' soft drinks had such high pesticide levels they could lead to cancer.
The parliamentary committee concluded that the group "stands corroborated on its finding of pesticide residues".
Coca-Cola and Pepsi have consistently denied their drinks pose any health hazards.
Their lawyer, Harish Salve, said during court proceedings that extensive use of pesticides in agriculture had resulted in a high degree of their presence in sugar. He said no pesticide was added to the drinks in the manufacturing process. - Sapa-AFP
Re: Rise of the New Plagues Continues
Post by bigbunny on Dec 9, 2004, 2:54am
Is Asian Bird Flu the Next Pandemic?
Stefan Lovgren
for National Geographic News
December 7, 2004
When a top World Health Organization official warned late last month that the bird flu virus that has plagued Asian countries might unleash a pandemic that could kill up to 50 million people, one thing that did not break out was mass panic.
After all, it's hardly the first time such a catastrophic prediction has been issued. Last year it was the SARS virus, now the potential mass killer is the H5N1 avian flu virus.
While most health experts agree that the bird flu virus represents a grave danger and is highly likely to spread unless urgent steps are taken, some virologists caution that alarmist warnings could harm preparedness plans.
"The danger is that people might get blasé about the message," said Ian Moore, a virology professor at the University of Reading in England. "They'll think, Yeah, yeah, I've heard it before. It didn't come then, and it won't come this time."
Genetic Change
The H5N1 virus, a subtype of the avian influenza virus, is found in poultry. Scientists at first believed it was impossible for birds to directly infect humans with the virus. But an outbreak in Hong Kong in 1997 that killed 6 of 18 people infected with the virus proved the contrary.
Since then outbreaks have forced the slaughter of millions of chickens, ducks, and other birds across Asia. This year there have been 44 confirmed human cases of H5N1 flu in Thailand and Vietnam. Of these, 32 people died. There is not yet a vaccine for the disease.
Meanwhile the virus has undergone huge genetic changes and become even more pathogenic. It now affects not only birds, but also cats, pigs, and even tigers.
Experts fear the disease will mutate into a form that can leap between humans and sweep populations with no immunity. The adaptation could occur through a few genetic changes or what is known as "re-assortment" of the genes of the avian strain and the human strain. Domestic ducks and pigs are seen as likely transmitters.
"All virologists agree that this is a very dangerous time for H5N1," Moore said.
"Alarmist"
There is some evidence that influenza pandemics occur on a regular cycle, with one every 20 to 30 years. The notorious Spanish flu killed at least 20 million people worldwide in 1918. Outbreaks in the late 1950s and late 1960s resulted in tens of thousands of deaths in the United States alone.
Now the world may be due for another outbreak.
"Almost everyone in the field feels that an influenza pandemic is virtually inevitable, and that we need to be prepared for it," said Stephen Morse, the director of the Center for Public Health Preparedness at Columbia University in New York.
The World Health Organization estimates the H5N1 virus could infect up to 30 percent of the world's population. Shigeru Omi, the WHO official who issued last month's warning, said that estimates of 2-7 million deaths were "conservative" and that the maximum range could go as high as 50 million deaths.
Some virologists, however, take issue with his warning.
"This alarmist warning is irresponsible in using this language to rouse the public's fear," said Michael Lai, a virologist at the University of Southern California in Los Angeles.
He says the warnings of an impending flu pandemic have circulated since the Hong Kong outbreak in 1997, but no major outbreak among humans has yet happened.
Furthermore no one actually knows what would happen to the virus if it adapted to grow in humans. It might be as lethal as it is now, or it might become far less pathogenic.
Since palliative care, or disease treatment, is much better today than in 1918, deaths are likely to be far fewer, some health experts argue.
Get Ready
Still, any pandemic is likely to spring from developing countries with limited means to fight it.
"There is at present no effective way to control the poultry endemicity for southeast Asia due to the lack of resources or political conviction," said Kwok-yung Yuen at the Center of Infection at the University of Hong Kong. "Only Hong Kong has [successfully maintained] bio-security in farms and markets."
The strong warnings, therefore, are mainly directed at governments rather than the general public, says Dick Thompson, a WHO spokesperson in Geneva, Switzerland.
"What we are trying to do is alert governments that steps need to be taken to prepare for the next pandemic," he said.
If that means warning of worst-case scenarios, so be it.
"Are we scaring people? I don't know," he said. "But rather than springing on people some terrible event, it's better that they get emotionally ready for what they could face. We think a pandemic is coming. Nobody knows when. But it is good to get people prepared before it arrives."
http://news.nationalgeographic.com/news/2004/12/1207_041207_birdflu.html
Re: Rise of the New Plagues Continues
Post by bigbunny on Dec 10, 2004, 4:04am
Child cancers steadily increasing
The rate of childhood cancer has slowly increased over the last three decades, research has found.
The International Agency for Research on Cancer, based in France, examined data from 19 European countries.
It found cancer rates increased by around 1% a year for children, and 1.5% a year for adolescents between the 1970s and 1990s.
The research, which stresses cancer before age 20 is still rare, is published in The Lancet.
It is likely that a complex combination of environmental and genetic factors are involved.
Professor John Toy
The scientists say no single factor can be held responsible for the rise, and the underlying causes are likely to be highly complex.
But they suggest exposure to infections and changes in birth weight may play a role, as may mixing of different populations.
Some - but not all - of the rise might be explained by better diagnosis of the disease, and better record keeping.
They analysed 113,000 cancers in children, and over 18,000 cancers in adolescents during the 1970s, 1980s and 1990s.
They found the incidence rate by the 1990s was 140 per million for children and 157 per million for adolescents.
The increases were recorded for virtually all tumour types in children.
In adolescents the major changes were seen for:
* Carcinomas that develop in tissues covering or lining organs of the body, such as the skin, the uterus, the lung, or the breast.
* Lymphomas that develop in the lymphatic system, such as Hodgkins disease.
* Soft tissue sarcomas that begin in the muscle, fat, fibrous tissue, blood vessels, or other supporting tissue of the body.
* Germ-cell cancers that develop in the testicles or ovaries.
* Tumours of the central nervous system.
Over the three decades studied survival rates increased substantially, reaching a five-year survival rate of 75% for children in western Europe, and 64% in eastern Europe.
Survival rates for adolescent patients were similar.
Lead researcher Dr Eva Steliarova-Foucher said: "Our results are clear evidence of an increase of cancer incidence in childhood and adolescence during the past decades, and of an acceleration of this trend."
Devastating disease
Professor John Toy, medical director at the charity Cancer Research UK, said: "Childhood cancer is uncommon but when it does occur it is devastating for all those involved.
"While it is good news that survival is dramatically improving the increase in incidence rates reported in this study are a cause for concern.
"The study shines light on some possible causes for the increase, such as population mixing and socioeconomic status.
"It is essential that researchers investigate these leads in order to develop future prevention strategies.
"It is likely that a complex combination of environmental and genetic factors are involved."
Also writing in The Lancet, Dr Catherine Cole, of the Princess Margaret Hospital for Children in Perth, Australia, said most children with cancer lived in developing countries.
And while 80% of children with cancer survived in the west, most in developing countries die from lack of medical care.
"The challenge now is to ensure equity of access to cancer care for all children.
"Centres of excellence should be developed in low-income countries to train staff."
Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/health/4079343.stm
Published: 2004/12/10 00:43:15 GMT
Re: Rise of the New Plagues Continues
Post by bigbunny on Dec 11, 2004, 5:13am
Atypical Scrapie Now Confirmed In The UK
From Patricia Doyle, PhD
dr_p_doyle@hotmail.com
12-11-4
Hello, Jeff - We discussed this when it first broke about 3 years ago. Whenever I am told by the food industry that:
1. Although consistent with BSE, there is no indication at this time to believe it is BSE in sheep, and
2. Eating Lamb is safe... I really begin to worry about the safety of the food.
The following paragraph is really an indication that there IS a problem and the meat is really unsafe. I think we need to be VERY CONCERNED.
"Senior officials with both DEFRA and the Scottish Executive's environment and rural affairs department were at pains to stress, however, that the discovery is not linked to BSE and that there is no need for consumer concerns over food safety."
Patricia Doyle
From ProMED-mail
New Strain Of Scrapie Hit Sheep Industry
By Dan Buglass The Herald - UK
12-11-4
The sheep industry was set on edge yesterday following an announcement by the Department of the Environment, Food and Rural Affairs [DEFRA] in London that tests had detected a new strain of scrapie, the fatal brain disease of sheep associated with BSE in cattle and, by implication, variant CJD in the human population.
Senior officials with both DEFRA and the Scottish Executive's environment and rural affairs department were at pains to stress, however, that the discovery is not linked to BSE and that there is no need for consumer concerns over food safety.
What is of major concern is that the government-funded Veterinary Laboratories Agency in Weybridge, Surrey, has confirmed that 83 "atypical" cases of scrapie have been found over the past 3 years in samples from 110 000 sheep brains tested. More worrying is the acknowledgement that of those 83 abnormal results, 12 have been found in sheep with the genotype normally associated with the highest degree of resistance to scrapie.
A statement from DEFRA confirmed that the National Scrapie Plan, which aims to rid the UK sheep flock of 37 million of the disease, will continue in its current form.
The UK, with the largest sheep flock in the European Union, is ahead of all other member states -- with the exception of the Netherlands -- in achieving its goal of scrapie-free status within a decade.
3 years ago the UK government and the devolved administrations drew up a contingency plan that, in the event of a proven link between scrapie and BSE, virtually every sheep would be slaughtered. That plan, in time, proved to be based on a seriously flawed scientific assessment.
The UK is obliged, under direction from the European Commission, to conduct brain tests each year on 10 000 sheep over 18 months of age which are processed in abattoirs, as well as a similar total which die on farms. Results have shown that only 0.3 per cent of these sheep have been infected with scrapie, with many devoid of clinical symptoms.
But it has been almost impossible to trace back the 83 "atypical" cases back to the farm of origin. This has prompted fears that the commission will insist the UK puts in place an individual identification scheme for sheep. This has been resisted by the UK on the grounds that no other member state runs sheep on an extensive regime such as in the Highlands and in the Welsh mountains, where stocking rates are very low. Tagging every lamb at birth and recording maternal details would be impossible.
A spokesperson for National Farmers Union (NFU) Scotland expressed support for the National Scrapie Plan (NSP). "We knew that abnormal cases could be thrown up, given the scale of the testing regime which promotes the most resistant genotypes. These will not be guaranteed as totally resistant, but they represent the best options for producers."
For details on the NSP, go to http://www.defra.gov.uk/animalh/bse/othertses/scrapie/nsp/index.html.
[2]
Department Confirms New Strain Of Scrapie In Sheep
Ireland On-Line
12-11-4
The Department of Agriculture has confirmed that a new strain of scrapie is emerging in Irish sheep. The disease is a fatal, degenerative illness affecting the central nervous system of sheep and goats and [like] BSE in cattle and CJD in humans [is caused by a mutated prion protein].
The department's confirmation of the existence of the illness in Ireland came just hours after the British authorities said that 80 cases of an unknown strain of scrapie had been found in sheep there.
ProMED-mail promed@promedmail.org
Atypical cases of scrapie have been reported, since 2003, also from Norway, France, and Switzerland. So far, the scrapie strains involved in these cases have not been shown to be related to BSE.
Following the recently published findings by a research group in France that they suspect the presence of a TSE (transmissible spongiform encephalopathy) infection in a goat's brain which tests cannot distinguish from BSE, the European Commission submitted data received from the French authorities to the Community Reference Laboratory (CRL) for TSEs based in Weybridge, England, for an evaluation by an expert group. The issue was discussed during the 85th meeting of the Spongiform Encephalopathy Advisory Committee (SEAC), held in Cardiff on 30 Nov 2004. The committee was informed that, although the data available are consistent with BSE, a definitive interpretation could not be provided until further data from mouse bioassays were available in about 2 months. - Mod.AS
Re: Rise of the New Plagues Continues
Post by bigbunny on Dec 13, 2004, 4:17am
Well the manufactured virus SARS didn't work so now the latest greatest threat to humanity is BIRD FLU. If you have been reading this and similar threads you will note that much of what is now being reported as breaking news has already been reported in the past. I just wonder whose side the WHO is really on:
Title : WHO urges countries to prepare against flu pandemic threat
By :
Date : 09 December 2004 1212 hrs (SST)
URL : http://www.channelnewsasia.com/stories/afp_world/view/121395/1/.html
MANILA : With up to 50 million people expected to die from the next influenza pandemic, the World Health Organisation (WHO) is to convene a meeting of international experts in Geneva next week to plan how best to meet the threat, it said in a statement Thursday.
Although it cannot predict when the next pandemic will strike, the WHO said the arrival of the avian influenza or "bird flu" virus, which is now widely entrenched in Asia, signals "the world has moved closer to the next pandemic."
"While it is impossible to accurately forecast the magnitude of the next pandemic, we do know that much of the world is unprepared for a pandemic of any size," the statement released from the WHO's Western Pacific headquarters in Manila said.
Estimates of the number of people expected to die from the next pandemic vary from two million to 50 million with between 20 percent and 50 percent of the world's population ultimately affected, the WHO said.
Next week's meeting will examine how prepared the world is to fight a pandemic.
Although the global spread of a pandemic cannot be stopped, the preparedness of countries will reduce its impact, the WHO said.
In the coming weeks it will publish an assessment tool to evaluate and focus national preparedness efforts.
It will also give guidance on stockpiling antivirals and vaccines.
The WHO called for speeding up research "to understand the mechanisms of emergence and spread of influenza pandemics."
It also said, "some have already developed structures and processes to counter the threat of a pandemic, but some plans are far from complete and many member states have yet to begin."
Influenza experts are concerned that the recent appearance and wide distribution of an avian influenza virus (A/H5N1) has the potential to ignite the next pandemic, the statement said.
"Given the current threat, WHO has urged all countries to develop or update their influenza pandemic preparedness plans for responding to the widespread socioeconomic disruptions that would result from having large numbers of people unwell or dying," it said.
In the last major flu pandemic in 1968 estimates vary from one million to four million deaths while the Spanish flu pandemic of 1918 the toll was between 20 million to well over 50 million.
"Extrapolations are problematic because the world in 2004 is a different place from 1918," the WHO said.
"The impact of greatly improved nutrition and health care needs to be weighed against the impact the increase in international travel would have in terms of global spread.
"The specific characteristics of a future pandemic virus cannot be predicted. It may affect between 20-50 percent of the total population.
"But the level of preparedness will influence the final death toll," the WHO said. - AFP
Re: Rise of the New Plagues Continues
Post by bigbunny on Dec 13, 2004, 4:18am
Warning as bird flu crossover danger escalates
The poultry farms of Asia are the breeding ground for the avian influenza virus, which is likely to spread across species - and to the West
Robin McKie and Jo Revill in London, John Aglionby in Bangkok and Jonathan Watts in Beijing
Sunday December 12, 2004
The Observer
Wanphen Sripirom has struggled for years to scrape a living as a subsistence farmer in Phichit province, north of Bangkok. Chickens have provided her with a lifeline that has been crucial for survival.
But last week Wanphen had to face a heart-breaking prospect: the slaughter of her brood. 'They're going to be killed tonight,' she said. It was a bitter blow, although the farmer is not alone in the privations she faces.
Thousands of others across Asia have already had their livelihoods devastated because their poultry has become infected by H5N1, the bird flu virus. Tens of thousands of ducks and chickens have been infected and tens of millions have been culled this year in a bid to stop the disease spreading. Economists believe this price tag for China alone has been £31 billion. The figure for the whole of South-East Asia is double that.
Health officials are unrepentant, however, for they are desperate to stop the disease spreading - not just to other poultry but to humans. The farms of South-East Asia, where humans and animals live beside each other in tiny yards and huts, have become a vast reservoir for the H5N1 virus, and that chills not just local officials but the world's health authorities.
The planet, they believe, is poised on the brink of a new flu pandemic whose source will be the infected farm birds of Thailand, Vietnam and China.
Already 44 confirmed human cases of H5N1 infection have been documented in Thailand and Vietnam (the only countries to report human cases). Of these, 32 have died, a fatality rate of 73 per cent. No wonder the World Health Organisation and other international medical groups have become fixated about South-East Asian agriculture.
'No man is an island,' said John Oxford, professor of virology at Queen Mary Westfield school of medicine, London. 'It doesn't matter where it starts - it will be on our doorstep within 12 hours. You can't argue that it isn't our problem.'
The struggle for survival of Wanphen Sripirom, and the thousands of other South-East Asian subsistence farmers, is a matter of direct consequence for us all, in other words. 'I noticed the symptoms of the virus in one of my birds one morning and by nightfall 50 had died,' Wanphen told The Observer. 'The following day another 30 died, and then another 30 the following day.
'Their bodies began shaking; it was as if they were suffocating and thick saliva starting coming out of their mouths. We tried to give the hens herbs to make them better, but it made no difference. The faces then went dark green and black, and then they died.'
Wanphen and her husband, Ban Noensai, were relatively lucky, however. They are still alive. The case of Pranee Thongchan, in the north Thai province of Kamphaengphet, presents a far more worrying example for health authorities. Pranee had no contact with poultry but had spent several days looking after her dying daughter Sakuntala. The 11-year-old had become ill after playing with infected hens. Doctors believe she was a bird flu victim, although Sakuntala was cremated before final tests could be carried out.
Then Pranee became ill and was taken to hospital, where she died several days later. Post-mortem tests showed she carried the H5N1 virus. Given Pranee's history and given the facts of her daughter's death, doctors conclude she was one of the first recorded victims of the human-to-human transmission of the H5N1 virus. The prospect of this being repeated in other cases terrifies doctors, although local officials are still desperately trying to calm the situation.
'From all the evidence that we have learnt, human-to-human transmission is very difficult,' affirmed Dr Supanit Chunsuttiwat, who works for Thailand's department of disease control.
World Health Organisation officials are not convinced, however. WHO's western Pacific director, Shigeru Omi, warned regional health ministers this month that there are genuine concerns that the virus could mutate into a form that could spread easily between humans and thus lead to a global pandemic.
'We are talking at least seven million (deaths), but maybe more - 10 million, 20 million and the worst case 100 million,' he said. And Shigeru was backed by Henk Bekedam, the Beijing WHO representative. 'This is a very real threat,' Bekedam told The Observer .
A bird flu pandemic could erupt next year or the following one or the one after that, say doctors. No one can be sure when. But what is certain is that a world outbreak is inevitable, given that the region has become such a vast reservoir for H5N1.
Not surprisingly, officials are now desperate to control and ultimately eradicate the virus, although conditions in the region are so chaotic such prospects look slim.
Consider the example of China. It has reported far fewer cases of avian flu than have been highlighted by other countries in South-East Asia. However, it is impossible to be sure about the extent of cases there because 80 per cent of the nation's chickens and ducks are reared in small, remote and poorly regulated farms.
'Good reporting is crucial to deal with this problem,' Bekedam said. 'But what are the incentives to report? Nil. If farmers tell officials, they risk losing their stocks. And if local officials tell the central government, they face trade bans.'
Re: Rise of the New Plagues Continues
Post by bigbunny on Dec 13, 2004, 4:18am
In addition, poorly planned vaccination programmes for poultry are making matters worse. Many farmers are buying black-market vaccines that have not been developed for H5N1.
These products keep the birds alive, even if they have the virus, which raises the risks of contagion when they are sold or transported. Farmers have also been sold fake vaccines that served only to make them falsely complacent about the poultry's safety.
The risks of the disease spreading to humans is also compounded by the poor living conditions in much of rural China, where average incomes are less than a quarter of those in the cities, and health insurance is almost non-existent.
Migratory birds also pose the problem of carrying the virus around the region, as do fighting cocks, a huge pastime in Thailand. 'People will go to great lengths to smuggle birds through cordons to get them to a fight,' said Priecha Asawametha, head of the Phichit provincial livestock office. 'It is very difficult to stop.'
Containment is clearly going to be extraordinarily difficult, if not impossible. So if the disease cannot be managed at source, the world must find ways to deal with an outbreak once it has begun to spread. Anti-viral drugs and vaccines offer the best hopes.
In the former case, one of the most successful anti-flu agents is Tamiflu, also known as oseltamivir. It is manufactured by Roche. It can alleviate victims' symptoms and prevent them from passing the virus to others.
Unfortunately, Roche's factory in Basel has had to double in size this year, and will double again next year simply in an attempt to keep up with demand. Nevertheless, a serious shortage seem inevitable. Another treatment, Relenza, which is made by GlaxoSmithKline, is also available but this is difficult to administer.
And despite the grim warning signs from South-East Asia, it is clear that many countries have not yet stockpiled anti-viral drugs. The UK, for example, has been in negotiations with Roche for months. Even if Britain buy enough doses only to cover between 10 to 20 per cent of its population, that bill will still come to millions of pounds. Yet no virus has actually emerged.
Vaccines, by contrast, will take time to develop. The problem is that, until the strain of H5N1 virus appears in this country, no one can create a vaccine against it, although scientists say that those that provide protection against existing strains could provide partial protection against the new one.
Britain also has a strong network of public health groups and is well placed to implement the plans that it is currently working on for dealing with the emergence of a flu pandemic.
By contrast, the United States looks ill-prepared and has bought antivirals to treat only one million of its 300 million citizens. 'We're all holding our breath,' said Julie Gerberding, head of the Centres for Disease Control and Prevention. Australia and the Netherlands have stockpiles that meet the demands of around one-third of their populations.
Given the death rates that the WHO is predicting, some of these preparations may seem poor. Professor Oxford counsels caution, however. It is not time for hysteria yet. 'There has never been better monitoring than there is at present. For the first time in history we will watch the emergence of a human virus, step by step, and we now have this window of opportunity to meet that challenge.'
Canada, which took such a battering, both economically and morale-wise over the recent Sars epidemic, provides a good example. It has learnt a great deal over the last year and has produced a pandemic plan. This is a prudent course of action, given that it has a large immigrant population from South-East Asia and is therefore badly exposed to the threat that bird flu poses.
Among the measures it plans to carry out is the publication of guides for helping people react should an outbreak occur. Measures include ensuring good hand-washing to prevent the spread of germs. If people fall ill, they should not go to work. If they fall into one of the high-risk categories - the elderly, the asthmatic, the immuno-suppressed - they should seek medical attention.
The point is that you cannot totally rely on drugs or the promise of a vaccine to lessen the risk, said Dr Theresa Tam, of the Immunisation and Respiratory Infections Division at the Public Health Agency of Canada. Behaviour has an enormous effect on the direction of an epidemic.
As to identifying who should be the first to get anti-viral treatments, the Canadians have asked a group of ethicists to help them draw up the plans.
As Tam told The Observer: 'We involved them, because these are not decisions that are purely scientific.'
On the other hand, the world has only limited time before that great flu epidemic erupts.
As every scientist, epidemiologist and doctor has told The Observer over the past few days, it is not a matter of if H5N1 erupts upon the world; it is simply a matter of when. We have time, but not a great deal, and should make the very most of it while we can. Politicians therefore need to pursue their plans with urgency, as Professor Oxford warned.
'This is the time to act. It's like an insurance policy; you don't wait until you've been burgled before you buy proper cover for your contents.'
http://observer.guardian.co.uk/print/0,3858,5084041-102275,00.html
Re: Rise of the New Plagues Continues
Post by bigbunny on Dec 13, 2004, 4:19am
Flu pandemic 'could wreck ecosystem'
Date: 11/12/04
A medical expert has warned that the next flu pandemic could wreck the global ecosystem, in addition to killing millions of people worldwide, a newspaper reported.
The World Health Organisation warned last week that bird flu is the mostly likely candidate to combine with a human virus, creating a new strain that could trigger a worldwide pandemic and kill as many as seven million people.
Microbiologist Kennedy Shortridge told a convention in Hong Kong Friday that he feared such a pandemic could destroy the global ecosystem in addition to causing human deaths, the South China Morning Post reported.
"I am very worried about the present situation we are in. We are on a knife-edge at the moment.
"If it goes the wrong way, we could have a very severe pandemic," Shortridge, an honorary professor at both the University of Hong Kong and the University of Auckland in Australia, was quoted as saying.
"If this virus gets into bird life beyond poultry, we could wreck the global ecosystem and we could be on the verge of an 'ecocide'," Shortridge, who helped Hong Kong fight a 1997 bird flu outbreak that crossed over to humans and killed six people, said without further elaboration.
Meanwhile, Hong Kong and mainland researchers said they have developed a new and quicker diagnostic test for the bird flu virus, which could detect whether someone is infected by the virus within two hours, another newspaper reported.
The new diagnostic test for the H5N1 bird flu virus has a 90 per cent accuracy rate and is much quicker in yielding results than current tests, which take three to five days, the Apple Daily quoted University of Hong Kong microbiologist Guan Yi as saying.
Guan declined to confirm the report, saying an announcement would be made later.
Bird flu this year has killed 32 people in Thailand and Vietnam, and millions of chickens across Asia.
However, there has been no concrete evidence yet of human-to-human transmission of the disease.
Shortridge said low hygiene standards have helped the virus to spread throughout the region and urged regional governments to improve transparency in their fight against the disease.
Copyright © 2004 AAP
http://seven.com.au/news/worldnews/141921
Re: Rise of the New Plagues Continues
Post by bigbunny on Dec 13, 2004, 4:26am
Further light reading on the much heralded forthcoming pandemic:
How Dire Is the Asian Bird Flu Threat?
http://news.nationalgeographic.com/news/2004/12/1207_041207_birdflu.html
Warning as bird flu crossover danger escalates
http://observer.guardian.co.uk/international/story/0,6903,1371917,00.html
Aventis, Chiron to Test Bird Flu Vaccine on Humans
http://story.news.yahoo.com/news?tmpl=st....alth_birdflu_dc
Chinese develop rapid bird flu test
http://feeds.bignewsnetwork.com/?rid=026a5b5753ae6ac4&cat=a1e025da3c02ca7c
Poultry exporters set sights on HK, South Korea
http://www.philstar.com/philstar/News200412130704.htm
Growing fears over bird flu
http://www.smh.com.au/news/Health/Growin....2182430964.html
Campaigners Call for Wild Bird Import Ban
http://news.scotsman.com/latest.cfm?id=3869398
America's role in Asia: A peek into the future
http://www.orlandosentinel.com/news/opin....inion-headlines
Google:
http://news.google.com/news?hl=en&ned=us&q=asian+bird+flu&btnG=Search+News
Re: Rise of the New Plagues Continues
Post by bigbunny on Dec 13, 2004, 5:25am
Simian Virus 40 and Human Disease
Keerti V. Shah
Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland
The inadvertent and unrecognized presence of simian virus 40 (SV40) in the commercial inactivated Salk poliovaccines administered between 1955 and 1963 resulted in the potential exposure of millions of individuals, in the United States and elsewhere, to this polyomavirus of the rhesus macaque [1]. Many of the monkey-kidney cultures used to prepare poliovirus pools were infected with the indigenous SV40. Soon after its discovery in 1960 [2], SV40 was found to be oncogenic in laboratory animals [3]. Therefore, the possibility that SV40 may cause human disease, particularly cancers, has been a topic of interest since the 1960s [4]. This debate has intensified during the past decade because several groups of investigators, using polymerase chain reaction (PCR) amplification methodology, have detected SV40 genomic sequences in a number of human cancers. These investigators have suggested that the virus contributes to the development of mesothelioma, osteosarcoma, pediatric and adult brain tumors, and non-Hodgkin lymphomas [5–8]. The reported presence of SV40 in tumors in individuals born after 1963 would seem to imply that SV40 is now established as a human infection circulating in communities via person-to-person contact [8]. Other investigators have been skeptical of these claims [9–12]; several groups have not been able to detect SV40 sequences in the aforementioned tumors [13–20], and epidemiologic studies have not revealed an increased risk of these cancers in populations exposed to SV40-contaminated poliovaccines or adenovirus vaccines [21–23]. In addition to a large number of scientific publications, the controversy has spawned a report by the Institute of Medicine [24], a book in the popular press [25], and litigations. The evidence for the pathogenicity of SV40 in humans can be conveniently examined in 3 parts: (1) the nature of the human response after exposure to SV40, (2) the evidence that infection with SV40 has become established in humans, and (3) the evidence that infection with SV40 contributes to the development of human cancers.
HUMAN RESPONSE TO SV40
That individuals exposed to SV40 may develop a transient infection was documented during the 1960s. Morris et al. [26] found that, after intranasal inoculation of live SV40 (which was an inadvertent contaminant of an experimental respiratory syncytial virus vaccine), ∼60% of the volunteers developed neutralizing antibodies to the virus. The antibody titers in the positive sera were low: small amounts of infectious virus were recovered from throat swabs of some of the individuals 7 or 11 days after inoculation; virus was not recovered from rectal swabs. After oral administration of SV40 (which was a contaminant of the experimental lots of the Sabin attenuated poliovaccine) to children, small amounts of virus were recovered intermittently, for up to 5 weeks, from the stools of some of the volunteers, but none of the children developed an antibody response [27, 28]. Both the serological study of American zoo workers that is reported by Engels et al. [29] in this issue of the Journal and an earlier study of employees of monkey-export firms in India [30] suggest that infection with SV40 may also be acquired by contact with (presumably) naturally infected primates. Engels et al. [29] were able to show (1) that the prevalence of SV40 antibody in "nonhuman-primate zoo workers" (i.e., "those currently working specifically with either nonhuman primates or a larger class of animals including nonhuman primates and those in senior administrative positions, which were assumed to be filled by individuals with extensive animal-handling experience") was higher than that in "other zoo workers" (i.e., "those currently working with classes of animals not including nonhuman primates and those performing maintenance, clerical, or visitor service") and (2) that the SV40-reactive antibodies in the sera of the nonhuman-primate zoo workers were more likely to be SV40 specific (see below) than were those in the sera of the other zoo workers.
IS SV40 ESTABLISHED AS A HUMAN INFECTION?
Although SV40 may produce transient infection in exposed individuals, the results of serological and virological studies indicate that SV40 has not become established in the human population. It is very likely that the low levels of SV40-reactive antibodies described in human sera in many previous investigations [31–33] are the result of cross-reactivity between SV40 and the widely prevalent human polyomaviruses BKV and JCV [34]. Sera of rhesus macaques naturally infected with SV40 react strongly with SV40 viruslike particles (VLPs), but they also react—to a lesser degree but unambiguously—with BKV VLPs and with JCV VLPs [35, 36]. Rhesus serum's reactivity with BKV VLPs and with JCV VLPs is decreased by preadsorption with both SV40 VLPs and either BKV VLPs or JCV VLPs. Conversely, the low-level SV40 reactivity of human sera was clearly correlated with reactivity to BKV and JCV and, whenever measured, was significantly decreased by preadsorption with either BKV VLPs or JCV VLPs [35–38]. Investigators who have tested human sera against all 3 viruses—SV40, BKV, and JCV—have concluded that the serological evidence does not support the notion of widespread prevalence of SV40 in humans. In their study of 2054 serum samples collected in England and Wales, Knowles et al. [39] found 79 samples with neutralizing antibodies against SV40, but only 1 of these was negative for both antibody against BKV and antibody against JCV. They concluded that "[t]here is no serological evidence that SV40 entered the human population during the past 80 years" (p. 115). Carter et al. [36] reported that 46 of 699 serum samples from the United States were reactive against SV40 in VLP-based ELISA but that "none of these samples could be confirmed as having authentic SV40 antibodies following pre-adsorption with JCV or BKV VLPs" (p. 1522) and that their data "do not provide support for SV40 being a prevalent human pathogen" (p. 1522). Sanjose et al. [37] tested 1107 serum samples from Spain with SV40 VLPs and stated that "[t]here was no serological evidence for widespread circulation of SV40...in Spain" (p. 522).
If SV40 infection were responsible for a tumor, the probable sequence of events would include SV40 viremia, for the virus to reach the target organ, and virus multiplication at the site of the tumor, before the clonal expansion of transformed cells. These events should then lead to a higher prevalence of antibodies in these patients than in control subjects or other groups. However, previous studies have not shown that either the sera of patients with mesothelioma [40], osteosarcoma [36, 40], or lymphomas [37, 38] or the prediagnostic sera of patients with brain cancer [41] have greater reactivity to SV40 than do the sera of other groups.
There is no consistent virological evidence that SV40 circulates in the community. Large amounts of infectious human polyomaviruses BKV and JCV are present in the urine of immunocompromised patients, and urinary virus shedding is accompanied by a serological response. We did not recover SV40 sequences from any of 166 urine samples from HIV-seropositive or HIV-seronegative individuals, but we were able to identify SV40 sequences in all 17 masked urine specimens that were spiked with ∼200 copies of SV40; BKV was detected in 14% of these specimens, JCV in 34% [42]. Similarly, Bofill-Mas et al. [43] did not detect SV40 sequences in any sewage samples collected in different geographic areas of Europe and in South Africa, but BKV sequences and JCV sequences were recovered from most of the same samples. These results are consistent with the negative results described above. In contrast to these negative results, there are reports of recovery of SV40 sequences from urine, peripheral-blood cells, and other tissues from normal healthy individuals, as well as from patients with renal disease [44–46]. However, fully documented and serologically confirmed human SV40 infections have not yet been described.
Re: Rise of the New Plagues Continues
Post by bigbunny on Dec 13, 2004, 5:26am
SV40 AND HUMAN CANCERS
The most puzzling aspect of the controversy—and the heart of the problem—has been a lack of agreement on whether authentic SV40 sequences are present in human tumors. The studies with positive results have reported small copy numbers (often estimated as being <1 copy/10–100+ cells) of T antigen–coding sequences in a wide variety of unrelated tumors. Relatively few studies have attempted to identify SV40 transcripts or T protein in the tumor tissue, and the results of these studies have been inconclusive. On the other hand, employing similar or more-sensitive methods, several recent studies of mesothelioma [13–16], lymphomas [17, 18], and brain tumors [19, 20] have shown largely or completely negative results. Contamination with laboratory plasmids has now been identified as one reason for the discrepancy. At a 1997 meeting organized by the US Food and Drug Administration to examine SV40 as a possible human pathogen, Griffiths et al. [47] and Volter et al. [48] independently suggested the possibility that false-positive results may follow such contamination, because fragments of the SV40 genome—especially of the early region coding for large T antigen—have been used in the construction of hundreds of expression vectors worldwide. The reality and magnitude of this hypothesized risk have now been confirmed: in a recent study of mesothelioma, Lopez-Rios et al. [15] demonstrated conclusively that their initial observation of SV40 sequences in a majority of cases did not reflect the presence of genuine SV40 genomes but, instead, was due to contamination by SV40 sequences in a specific plasmid (i.e., pGL2) used in their laboratory; they also provided evidence that contamination by similar plasmid-derived SV40 sequences was responsible for the positive results that had been reported by another group of investigators. The report by Lopez-Rios et al. [15] should stimulate a reappraisal of previous studies showing positive results—and should lead to modification of the PCR primer sets employed in future studies.
CONCLUSION
Individuals exposed to SV40 by contact with the virus or with its animal hosts may contract the infection, but currently available evidence does not suggest that SV40 circulates in the community by person-to-person contact or that it contributes to the development of any human cancer. However, there is room for doubt, because the interpretation of the results of previous studies is limited by the uncertainties surrounding the assessment of exposure to SV40. Generally, individual investigations have measured viral DNA, circulating antibodies, or other markers of presumed exposure to SV40 but have rarely incorporated multiple markers of such exposure. Additionally, the presence of antibodies against SV40 T antigen has not been adequately evaluated as a marker of SV40-associated malignancy. These uncertainties in the assessment of exposure to SV40 may be clarified by future studies that (1) investigate the "full signature" of infection with SV40 [49], by using masked specimens from cancer cases and control subjects and correlating data for all markers of exposure to SV40 (e.g., genomic sequences, transcripts, antibodies to VLPs and T antigen, and T cell response [50]), and (2) incorporate strict monitoring of the assays for sensitivity, specificity, and reproducibility. A closer study of individuals with exposure to nonhuman primates (individuals similar to those described by Engels et al. [29])—and of these individuals' families—may help define the characteristics of human SV40 infection and its transmissibility. It is necessary to determine, with certainty, whether a potentially oncogenic virus inadvertently introduced into the population during the course of administration of a highly successful vaccine does or does not cause any unanticipated adverse effect.
References
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Re: Rise of the New Plagues Continues
Post by bigbunny on Dec 13, 2004, 5:26am
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http://www.journals.uchicago.edu/JID/journal/issues/v190n12/33484/33484.html
Re: Rise of the New Plagues Continues
Post by bigbunny on Dec 13, 2004, 5:31am
Hep B virus mutating, new drug in the pipeline :
New Delhi, Dec 9 : The virus causing the dreaded Hepatitis B has mutated even as scientists across the world are working on new drugs that are more effective in conquering the disease, a liver expert said today.
"The virus causing Hepatitis B has changed over the years due to mutation. This means virus would become more difficult to treat," Dr S K Sarin, Head of the Gastroenterology Department at the G B Pant Hospital told reporters, announcing the Asia's largest liver conference beginning this Saturday.
About 30-40 per cent of Hepatitis cases in Asia are due to the mutated virus, Sarin said adding virus was also becoming resistant to drugs.
However, scientists across the world were working on new drugs which were likely to get approval of the US' Federal Drug Authority by 2005-07, he said.
New drugs would increase the success rate of drugs and would target the mutated viruse, Sarin said adding G B Pant Hospital was also participating in the clinical trial of a new drug called "Entecavir" which was being tried for the past five-six years.
The drug, developed by a US company, was also being tried in other countries and was likely to get approved in the US next year. After that, it would need approval by Indian drug authorities, he said.
The drug, taken orally, gives a success of about 40-45 per cent. It supresses viral multiplication.
The success rate with available drugs was more in Hepatitis C cases at 90 per cent, he said. PTI
http://www.teamindia.net/news/index.php?action=fullnews&id=42595
Re: Rise of the New Plagues Continues
Post by bigbunny on Dec 18, 2004, 5:56pm
Source: Johns Hopkins Medical Institutions
Date: 2004-10-21
URL: http://www.sciencedaily.com/releases/2004/10/041021084911.htm
Antipsychotic Drugs Linked To Insulin Resistance In Children
Researchers from the Johns Hopkins Children's Center say a group of drugs known as "atypical antipsychotics" that are commonly used to treat children with aggression, bipolar disorder, and schizophrenia may trigger insulin resistance, a condition that increases the risk of developing Type 2 diabetes and heart disease later in life.
Results of the study linking insulin resistance to the use of these antipsychotics are scheduled for presentation October 20th during the annual meeting of the American Academy of Child and Adolescent Psychiatry in Washington, D.C. (October 19-24)
For the study, the Johns Hopkins team evaluated 11 children, some overweight and others obese, who gained significant amounts of weight (a 10 percent weight increase) while taking the new-generation, or atypical, antipsychotic drugs olanzpine, quetiapine, and risperidone. Considerable weight gain is a common side effect of atypical antipsychotic medications, and is also one of the many factors that can contribute to insulin resistance.
All six children on moderate or high doses of one of these drugs, and three of five children on low doses, had evidence of insulin resistance, a condition in which the body cannot properly use the insulin it produces. This evidence included hypertension, high levels of triglycerides, low levels of high density lipoprotein cholesterol ("good" cholesterol) and increased levels of protein in the urine.
"The insulin resistance seen in these children was greater than what would be expected from weight gain alone, suggesting there is a factor distinct from excess weight that directly induces insulin resistance," says the study's lead author, Mark A. Riddle, M.D., director of the division of child and adolescent psychiatry at the Children's Center.
In general, this group of new-generation antipsychotics creates fewer side effects than older drugs used to treat debilitating psychiatric conditions such as schizophrenia, Riddle says. The drugs, which balance certain chemicals in the brain and stabilize mood, have successfully treated countless numbers of children since being introduced in the 1990s, he notes.
"Treatments are always a matter of risk and benefit balance. Clearly these drugs are an important treatment option. But diabetes and heart disease are serious health issues, so it's important to further investigate this apparent relationship between atypical antipsychotics and insulin production and consumption," he adds. "We may need to reexamine how we are prescribing these drugs to see if dosage changes can be made to ensure children will continue to receive the benefits of these medications while not putting them at risk for developing other health problems in the future."
If the study's findings are confirmed by larger follow-up studies, Riddle says he would expect monitoring of metabolic side effects to become standard practice among clinicians prescribing atypical antipsychotics to children.
Insulin resistance occurs when muscle, fat, and liver cells do not properly use insulin, the hormone produced by the pancreas that helps cells absorb glucose and provides a source of energy to the body. The pancreas tries to keep up with the demand for insulin by producing more. Eventually, the pancreas cannot keep up with the body's need for insulin, and excess glucose builds up in the bloodstream. Excess weight, lack of exercise, and a family history of diabetes all contribute to insulin resistance. The condition is associated with an increased risk of developing Type 2 diabetes, heart disease, and stroke.
Study co-authors were David Cooke, M.D., and Helen Courvoisie, M.D., from the Johns Hopkins Children's Center.
Re: Rise of the New Plagues Continues
Post by bigbunny on Dec 23, 2004, 10:33am
Home Exposure To Radon Linked To Lung Cancer Deaths
BBC News
12-21-4
Domestic exposure to radon gas is responsible for a significant number of lung cancer deaths, research has found.
The risk appears to be much higher for smokers.
The researchers conclude radon in the home causes approximately 20,000 lung cancer deaths in the European Union each year - about 1,000 in the UK.
The British Medical Journal study, funded by Cancer Research UK and the European Union, is the largest ever of its type.
Radon is a naturally occurring, colourless, odourless, radioactive gas found at varying levels in all houses in the UK and across Europe. This research combines information from 13 smaller studies across Europe, which involved 7,000 people who had developed lung cancer and 14,000 without the disease.
It found that radon exposure can cause lung cancer in lifelong non-smokers, but the risk is low.
However, for any given level of exposure to radon, smokers have about 25 times the risk of developing lung cancer than those who do not smoke.
Previous studies of radon in homes have not been large enough to assess the risks reliably.
Nor have they been able to examine risks separately in smokers and non-smokers.
Professor Sarah Darby, of the University of Oxford, who led the collaboration, said: "By putting together many different studies we have shown that radon in ordinary homes is causing about 9% of lung cancer deaths each year in Europe, which is 2% of all cancer deaths.
"In the UK, where radon levels are lower than in many European countries, radon in ordinary homes causes about 1,000 deaths each year, which is about 1% of all cancer deaths."
Smokers' risks
Professor Sir Richard Peto, also at Oxford University, said that on average in Europe the absolute risks of getting lung cancer by age 75 years at usual radon concentrations of 0, 100, and 400 becquerels per cubic metre (Bq/m 3 ) would be about 0.4%, 0.5%, and 0.7%, respectively, for lifelong non-smokers.
However, for cigarette smokers the risks are about 25 times greater - 10%, 12% and 16%.
Radon is formed from the natural disintegration of uranium, which is present in ordinary surface rocks and in soil.
Radon that diffuses into the atmosphere usually disperses rapidly but it can accumulate indoors, especially in small buildings such as houses.
Lung damage
As radon decays it creates particles that can damage the cells lining the airways of the lung.
This damage can lead to cancer and, as the lungs of smokers may have many cells that are already somewhat damaged, the extra risk from radon is much greater for them than it is for non-smokers.
The UK's National Radiological Protection Board (NRPB) has estimated around 100,000 properties in Britain are significantly affected by radon.
Earlier this year the NRPB reported concentrations of radon up to 85 times higher than recognised safety limits in two homes in Cornwall.
High radon levels in existing houses can usually be reduced by changes to the ventilation system, such as improving underfloor air bricks and extracting radon from beneath the building with a fan, although this can cost up to £1,000 to install and £50 per year to run.
When constructing new buildings, however, low concentrations can usually be achieved by enhancing the damp-proof membrane across the full footprint of the building, at an extra cost of only around £100.
The researchers found lung cancer risk to be raised by 16% for every 100 Bq/m 3 of radon present in the home.
Professor Darby said: "We also found that there is a detectable risk even in homes with levels below 200 Bq/m 3, which is the currently recommended 'action level' in the UK.
"Indeed we estimate that about ninety per cent of radon-induced lung cancers occurred in homes with levels of radon below 200 Bq/m 3."
© BBC MMIV
http://news.bbc.co.uk/2/hi/health/4113765.stm
Re: Rise of the New Plagues Continues
Post by bigbunny on Dec 23, 2004, 10:38am
Given the recent press releases on SARS this latest discovery paints SARS as a VERY dangerous virus:
SARS Continues To Live In The Dead
The Globe and Mail
12-21-4
TORONTO (Canadian Press) -- Autopsies on 19 patients who died during the SARS outbreak in Toronto last year found the SARS coronavirus was present in the lungs of all of them, according to a study published in the Journal of Infectious Diseases.
The virus was detected in 73 per cent of the bowel samples examined, 41 per of liver samples and 38 per cent of kidney samples.
"People that died of SARS continued to have virus in their lungs as long as 51 days after the onset of illness," co-author Dr. Kevin Kain, director of the McLaughlin-Rotman Centre for Global Health in Toronto, said in an interview Monday.
"That is quite unusual for a viral infection. Usually, they come, they make you sick, they often clear. You may go on and die, but the virus is usually long gone. The virus is still there in these people. It likely is playing a direct role in their illness."
Autopsies were performed on 21 of the 44 people who died after severe acute respiratory syndrome hit the city in the spring of 2003.
"Nineteen of those 21 had died less than 51 days (after onset of disease)," said Dr. Kain. "All 19 people that died within 51 days had virus in their lung, often at very high viral load."
He said the higher the viral load in a person, the more likely they were to progress to death and have the virus in other organs in the body.
The findings are significant because they show there was a risk the virus could be transmitted to caregivers even weeks and months after the onset of illness, Dr. Kain noted. As well, those handling the patient after death and conducting post mortems would need to be protected from possible infection.
Dr. Kain said the finding that the SARS coronavirus was in the bowel was also noteworthy.
"Over 70 per cent had virus identified in their small intestine and in their large intestine. It helps explain why people with SARS develop gastero-intestinal symptoms."
Again, he indicated it would have been important for caregivers to be aware of the risks when SARS patients had diarrhea and similar problems.
"That becomes important in terms of transmission," he said. "It isn't just respiratory; it could be fecal-oral. There were issues like this in Hong Kong.
Around the globe, there were 8,098 probable SARS cases diagnosed in 29 countries, the bulk in China, Hong Kong, Taiwan, Canada and Singapore; 774 people died.
Dr. Kain said very few autopsies were performed around the world on SARS patients because "they were so apprehensive about it."
"I think that's a testament to the pathologists at [Toronto's] University Health Network ... most places didn't do autopsies."
© Copyright 2004 Bell Globemedia Publishing Inc. All Rights Reserved.
http://www.theglobeandmail.com/servlet/story/RTGAM
.20041220.wsars1220/BNStory/National/
Influenza images:
http://phil.cdc.gov/Phil/default.asp.
Re: Rise of the New Plagues Continues
Post by bigbunny on Dec 24, 2004, 5:09pm
Alcohol 'aids HIV cell infection'
Exposure to alcohol makes mouth cells more susceptible to HIV infection during oral sex, research has shown.
Earlier studies focused on how alcohol consumption increased the chance of someone having unprotected sex and therefore risking HIV infection.
But the team from the University of California at Los Angeles (UCLA) looked at how alcohol affected cells.
The research is published in the Journal of Acquired Immune Deficiency Syndrome.
We urge people to enjoy the festive season safely
Deborah Jack, National Aids Trust
Cells from the lining of the mouth, the epithelium, were obtained from people who were HIV negative.
The cells were then exposed to various concentrations of alcohol, similar to those found in beers, and then to a strain of HIV which had been modified with green fluorescent protein so that researchers could see if it infected cells.
It was found that epithelial cells which had been exposed to 4% of ethanol for 10 minutes showed between a three to six-fold greater susceptibility to infection from the HIV strain.
CD4 count
HIV attacks a particular type of white blood cells called CD4+ cells.
White blood cells adhere to endothelial cells.
HIV hijacks the cell, inserting its own genes into the cell's DNA and uses it to manufacture more virus particles. These go on to infect other cells.
The CD4+ host cells eventually die, although scientists do not know exactly how.
The body's ability to fight diseases decreases as the number of CD4+ cells drops, until it reaches a critical point at which the patient is said to have Aids - Acquired Immune Deficiency Syndrome.
Deborah Jack, chief executive of the National Aids Trust, said the UCLA study was useful.
"We always welcome new research into the risks of HIV transmission, but these are very early findings and much more work needs to be done to prove a biological link between alcohol and HIV transmission.
"However, the influence of alcohol on the decision whether or not to have unprotected sex has already been established and particularly at this time of year we urge people to enjoy the festive season safely. "
Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/health/4123193.stm
Published: 2004/12/24 11:19:14 GMT
Re: Rise of the New Plagues Continues
Post by bigbunny on Dec 24, 2004, 5:20pm
Undercooked Turkeys Can Harbor Superbugs
NewScientist.com News Service
12-23-4
High proportions of bacteria found in US turkeys are "superbugs", resistant to many of the antibiotics used on farms and to treat people.
The study sampled over 1000 turkey carcasses from two undisclosed turkey-processing plants in the US Midwest. Of these, 94 birds "were found to contain strains of both Campylobacter and Salmonella", says Catherine Logue, head of the team at North Dakota State University in Fargo, US, which conducted the study.
It is well established that commercial poultry - including turkeys - can contain bacteria that cause serious gastrointestinal upsets if it is not cooked properly. But this latest finding raises the possibility that antibiotic-resistant bacteria might find their way from turkeys into the human food chain, and possibly into hospitals.
Each year, Campylobacter and Salmonella make 2 to 4 million US citizens ill, and could prove much more difficult to treat if they become resistant to clinical antibiotics, such as erythromycin, ciprofloxacin, gentamicin and tetracycline.
Gene scavenging
Of the Salmonella samples grown from the infected birds, many were resistant to several antibiotics - 88% of Salmonella samples from one plant were resistant to tetracycline, and 35% from the other. Around 45% of the samples from one plant were simultaneously resistant to four antibiotics.
Logue says that resistance in Salmonella may be so abundant because 68% of the strains her team grew had genes for making class I integrase. This enzyme enables bacteria to scavenge "cassettes" of genes that confer resistance to antibiotics, either from the environment or from other bacteria.
Of the Campylobacter samples, 58% from one processing-plant were resistant to at least one antibiotic, while more than 10% of samples from the other plant were resistant to no less than 8 antimicrobials.
Although no Campylobacter had the class I integrase gene, more than a third had "efflux pump" genes which enable bacterial cells to survive by ejecting antibiotics.
Faster fattening
Logue says that the scale of the risks posed by resistant bacteria in turkeys is difficult to assess. In a previous study by her group published in 2003, she found that around 17% of processed birds were infected with Salmonella, while a parallel study found that 35% of birds carried Campylobacter.
Antibiotics have been routinely given to turkeys to fatten them up faster and keep them healthy. But this practice pushes the bacteria to evolve resistance to the farmyard antibiotics, and also to related drugs used in human medicine.
Europe banned a group of antibiotic growth promoters a decade ago to try to curb the rise of resistance. The US Food and Drug Administration is worried too, and in March 2004 upheld a 2000 decision to stop farmers giving poultry enrofloxicin, an antibiotic similar to the medically important fluoroquinolohe medically important fluoroquinolones.
Whatever the risk that resistant bacteria will spread from turkey farms to people to hospitals, Logue says that turkey is safe to eat provided it is thoroughly cooked. "Just make sure it's thoroughly de-frosted, and that you cook it right through, all the way to the core," she says.
Journal reference: Food Microbiology (vol 21, p779)
http://www.newscientist.com/article.ns?id=dn6820
Re: Rise of the New Plagues Continues
Post by bigbunny on Dec 24, 2004, 8:34pm
Source: Northwestern University
Date: 2004-11-26
URL: http://www.sciencedaily.com/releases/2004/11/041123115119.htm
Chronic Back Pain Shrinks 'Thinking Parts' Of The Brain, Study Finds
CHICAGO --- Chronic back pain, a condition afflicting many Americans, shrinks the brain by as much as 11 percent -- equivalent to the amount of gray matter lost in 10 to 20 years of normal aging, a Northwestern University research study found.
Loss in brain density is related to pain duration, indicating that 1.3 cubic centimeters of gray matter (the part of the brain that processes information and memory) are lost for every year of chronic pain, said lead researcher A. Vania Apkarian, associate professor of physiology at Northwestern University Feinberg School of Medicine and a researcher at the Northwestern University Institute of Neuroscience.
The study, the first to examine brain changes in chronic pain conditions, was published in the Nov. 23 issue of The Journal of Neuroscience.
At least 25 percent of Americans suffer from back pain; in one fourth of these individuals, back pain is chronic and unremitting. Although chronic pain greatly diminishes quality of life and increases anxiety and depression, it previously had been assumed that the brain reverts to its normal state after chronic pain stops.
Apkarian and co-researchers used structural magnetic resonance imagin