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Crafty_Dog
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« Reply #50 on: February 27, 2010, 12:34:25 PM »

A minor-league pitcher in his younger days, Richard Armbruster kept playing
baseball recreationally into his 70s, until his right hip started bothering
him. Last February he went to a St. Louis hospital for what was to be a
routine hip replacement.   By late March, Mr. Armbruster, then 78, was dead.
After a series of postsurgical complications, the final blow was a
bloodstream infection that sent him into shock and resisted treatment with
antibiotics.

“Never in my wildest dreams did I think my dad would walk in for a hip
replacement and be dead two months later,” said Amy Fix, one of his
daughters.

Not until the day Mr. Armbruster died did a laboratory culture identify the
organism that had infected him: Acinetobacter baumannii. The germ is one of
a category of bacteria that by some estimates are already killing tens of
thousands of hospital patients each year. While the organisms do not receive
as much attention as the one known as MRSA — for methicillin-resistant
Staphylococcus aureus — some infectious-disease specialists say they could
emerge as a bigger threat.  That is because there are several drugs,
including some approved in the last few years, that can treat MRSA. But for
a combination of business reasons and scientific challenges, the
pharmaceuticals industry is pursuing very few drugs for Acinetobacter and
other organisms of its type, known as Gram-negative bacteria. Meanwhile, the
germs are evolving and becoming ever more immune to existing antibiotics.

“In many respects it’s far worse than MRSA,” said Dr. Louis B. Rice, an
infectious-disease specialist at the Louis Stokes Cleveland V.A. Medical
Center and at Case Western Reserve University. “There are strains out there,
and they are becoming more and more common, that are resistant to virtually
every antibiotic we have.”

The bacteria, classified as Gram-negative because of their reaction to the
so-called Gram stain test, can cause severe pneumonia and infections of the
urinary tract, bloodstream and other parts of the body. Their cell structure
makes them more difficult to attack with antibiotics than Gram-positive
organisms like MRSA.  Acinetobacter, which killed Mr. Armbruster, came to
wide attention a few years ago in infections of soldiers wounded in Iraq.
Meanwhile, New York City hospitals, perhaps because of the large numbers of
patients they treat, have become the global breeding ground for another
drug-resistant Gram-negative germ, Klebsiella pneumoniae. According to
researchers at SUNY Downstate Medical Center, more than 20 percent of the
Klebsiella infections in Brooklyn hospitals are now resistant to virtually
all modern antibiotics. And those supergerms are now spreading worldwide.

Health authorities do not have good figures on how many infections and
deaths in the United States are caused by Gram-negative bacteria. The
Centers for Disease Control and Prevention estimates that roughly 1.7
million hospital-associated infections, from all types of bacteria combined,
cause or contribute to 99,000 deaths each year.   But in Europe, where
hospital surveys have been conducted, Gram-negative infections are estimated
to account for two-thirds of the 25,000 deaths each year caused by some of
the most troublesome hospital-acquired infections, according to a report
released in September by health authorities there.   To be sure, MRSA
remains the single most common source of hospital infections. And it is
especially feared because it can also infect people outside the hospital.
There have been serious, even deadly, infections of otherwise healthy
athletes and school children. !!!! By comparison, the drug-resistant
Gram-negative germs for the most part threaten only hospitalized patients
whose immune systems are weak. The germs can survive for a long time on
surfaces in the hospital and enter the body through wounds, catheters and
ventilators.

What is most worrisome about the Gram-negatives is not their frequency but
their drug resistance.

“For Gram-positives we need better drugs; for Gram-negatives we need any
drugs,” said Dr. Brad Spellberg, an infectious-disease specialist at
Harbor-U.C.L.A. Medical Center in Torrance, Calif., and the author of
“Rising Plague,” a book about drug-resistant pathogens. Dr. Spellberg is a
consultant to some antibiotics companies and has co-founded two companies
working on other anti-infective approaches. Dr. Rice of Cleveland has also
been a consultant to some pharmaceutical companies.

Doctors treating resistant strains of Gram-negative bacteria are often
forced to rely on two similar antibiotics developed in the 1940s — colistin
and polymyxin B. These drugs were largely abandoned decades ago because they
can cause kidney and nerve damage, but because they have not been used much,
bacteria have not had much chance to evolve resistance to them yet.

“You don’t really have much choice,” said Dr. Azza Elemam, an
infectious-disease specialist in Louisville, Ky. “If a person has a
life-threatening infection, you have to take a risk of causing damage to the
kidney.”

Such a tradeoff confronted Kimberly Dozier, a CBS News correspondent who
developed an Acinetobacter infection after being injured by a car bomb in
2006 while on assignment in Iraq. After two weeks on colistin, Ms. Dozier’s
kidneys began to fail, she recounted in her book, “Breathing the Fire.”
Rejecting one doctor’s advice to go on dialysis and seek a kidney
transplant, Ms. Dozier stopped taking the antibiotic to save her kidneys.
She eventually recovered from the infection.

Even that dire tradeoff might not be available to some patients. Last year
doctors at St. Vincent’s Hospital in Manhattan published a paper describing
two cases of “pan-resistant” Klebsiella, untreatable by even the
kidney-damaging older antibiotics. One of the patients died and the other
eventually recovered on her own, after the antibiotics were stopped.

“It is a rarity for a physician in the developed world to have a patient die
of an overwhelming infection for which there are no therapeutic options,”
the authors wrote in the journal Clinical Infectious Diseases.

In some cases, antibiotic resistance is spreading to Gram-negative bacteria
that can infect people outside the hospital.  Sabiha Khan, 66, went to the
emergency room of a Chicago hospital on New Year’s Day suffering from a
urinary tract and kidney infection caused by E. coli resistant to the usual
oral antibiotics. Instead of being sent home to take pills, Ms. Khan had to
stay in the hospital 11 days to receive powerful intravenous antibiotics.
This month, the infection returned, sending her back to the hospital for an
additional two weeks.

Some patient advocacy groups say hospitals need to take better steps to
prevent such infections, like making sure that health care workers
frequently wash their hands and that surfaces and instruments are
disinfected. And antibiotics should not be overused, they say, because that
contributes to the evolution of resistance.

To encourage prevention, an Atlanta couple, Armando and Victoria Nahum,
started the Safe Care Campaign after their 27-year-old son, Joshua, died
from a hospital-acquired infection in October 2006. Joshua, a skydiving
instructor in Colorado, had fractured his skull and thigh bone on a hard
landing. During his treatment, he twice acquired MRSA and then was infected
by Enterobacter aerogenes, a Gram-negative bacterium.

“The MRSA they got rid of with antibiotics,” Mr. Nahum said. “But this one
they just couldn’t do anything about.”
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ccp
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« Reply #51 on: February 27, 2010, 01:07:51 PM »

Safe Care Campaign.

Yes hand hygiene could help.  And yes more is and should be done towards this end.

Also of benefit may be to NOT sky dive for a living.

Kind of reminds me of the father of that young fellow in Iraq who had his head cut off on the internet blaming of course George Bush for it all.  He failed to remember his was walking around a war zone trying to start a computer business after the Iraq invasion.

Kind of fits the concept that no one wants to take responsibility for anything they do.  It is always some one else's fault.  The victimhood mentality.
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Body-by-Guinness
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« Reply #52 on: March 21, 2010, 12:34:05 AM »

Researchers Turn Mosquitoes Into Flying Vaccinators
Science Magazine ^ | 3/18/10 | Martin Enserink

Here's a study to file under "unworkable but very cool." A group of Japanese researchers has developed a mosquito that spreads vaccine instead of disease. Even the researchers admit, however, that regulatory and ethical problems will prevent the critters from ever taking wing—at least for the delivery of human vaccines.

Scientists have dreamed up various ways to tinker with insects' DNA to fight disease. One option is to create strains of mosquitoes that are resistant to infections with parasites or viruses, or that are unable to pass the pathogens on to humans. These would somehow have to replace the natural, disease-bearing mosquitoes, which is a tall order. Another strategy closer to becoming reality is to release transgenic mosquitoes that, when they mate with wild-type counterparts, don't produce viable offspring. That would shrink the population over time.

The new study relies on a very different mechanism: Use mosquitoes to become what the scientists call "flying vaccinators." Normally, when mosquitoes bite, they inject a tiny drop of saliva that prevents the host's blood from clotting. The Japanese group decided to add an antigen-a compound that triggers an immune response-to the mix of proteins in the insect's saliva.

A group by led by molecular geneticist Shigeto Yoshida of Jichi Medical University in Tochigi, Japan, identified a region in the genome of Anopheles stephensi-a malaria mosquito-called a promoter that turns on genes only in the insects' saliva. To this promoter they attached SP15, a candidate vaccine against leishmaniasis, a parasitic disease spread by sand flies that can cause skin sores and organ damage. Sure enough, the mosquitoes produced SP15 in their saliva, the team reports in the current issue of Insect Molecular Biology. And when the insects were allowed to feast on mice, the mice developed antibodies against SP15.

Antibody levels weren't very high, and the team has yet to test whether they protect the rodents against the disease. (Only very few labs have the facilities for so-called challenge studies with that disease, says Yoshida.) In the experiment, mice were bitten some 1500 times on average; that may seem very high, but studies show that in places where malaria is rampant, people get bitten more than 100 times a night, Yoshida points out. In the meantime, the group has also made mosquitoes produce a candidate malaria vaccine.

Other researchers are wowed by the achievement. "The science is really beautiful," says Jesus Valenzuela of the National Institute of Allergy and Infectious Diseases in Bethesda, Maryland, who developed the SP15 vaccine. David O'Brochta, an insect molecular geneticist at the University of Maryland, College Park, calls it "a fascinating proof of concept."

So why won't it fly? There's a huge variation in the number of mosquito bites one person received compared with the next, so people exposed to the transgenic mosquitoes would get vastly different doses of the vaccine; it would be a bit like giving some people one measles jab and others 500 of them. No regulatory agency would sign off on that, says molecular biologist Robert Sinden of Imperial College London. Releasing the mosquitoes would also mean vaccinating people without their informed consent, an ethical no-no. Yoshida concedes that the mosquito would be "unacceptable" as a human vaccine-delivery mechanism.

However, flying vaccinators-or "flying syringes" as some have dubbed them -may have potential in fighting animal disease, says O'Brochta. Animals don't need to give their consent, and the variable dosage would be less of a concern.

http://news.sciencemag.org/sciencenow/2010/03/researchers-turn-mosquitoes-into.html
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Body-by-Guinness
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« Reply #53 on: June 18, 2010, 02:44:09 PM »

I've posted before about how Western insecticide fetishes, particularly where DDT is concerned, leads to the deaths of millions of Africans, particularly children. This piece for the most part skirts around specifics, but brings home the scope of the situation.

Battling a Scourge
By Alex Perry / Apac
To reach the most malarial town on earth, head north from Kampala, cross the Victoria Nile and, just before you come to the refugee camps that mark the southern edge of Uganda's 20-year civil war, turn east to Lake Kwania. Africa's other Great Lakes are known for freshwater beaches and cool evenings, but Kwania is more of a giant swamp: shallow, full of crocodiles and choked with lily, papyrus and hyacinth. The malaria parasite loves it here.

Kwania's creeks, looking like a million silver fish bones from the air, are perfect for a deadly subspecies of mosquito, Anopheles funestus, which feeds almost exclusively on humans, with an appetite to shame a vampire. The nearby town of Apac is packed with a living blood bank of people. The average funestus bites human flesh 190 times a night. The average resident is bitten tens of thousands of times a year, including 1,586 bites — four a day — that carry malaria. (See TIME's photo-essay "The Most Malarial Town on Earth.")

Driving into Apac late on an August day last year, I saw a naked man lumbering toward me. Tall and thin, he was gray with dust, and his hair bristled with twigs and grass. He was talking to someone only he could see. Edging past, I was surprised by a second naked figure lurching out of a side street. He had the same cracked skin stretched over the same slender frame. Ahead, a third naked figure sat by the side of the road, his head in his hands. I felt as if I'd arrived in a town of zombies.

Apac's empty streets reinforced that impression. The town seemed to exist only for sickness and death: on one road I counted 12 medical centers, 10 drugstores and a crumbling, windowless nursing school. Soon I found a building that belonged to the Ministry of Health. I pulled in, entered and followed a dark corridor to a door marked "District Health Officer." I knocked. Behind two sets of fly screens and under a ceiling fan, Dr. Matthew Emer sat at his desk. I explained I was following a new campaign to rid the world of malaria and was in Apac to see what it was up against. Who were the naked men? I asked. "Brain damage," Dr. Matthew replied. "Severe malaria can do that to a baby. You never recover."

Dr. Matthew thought I should see some statistics. Apac is home to 515,500 people. Between July 2008 and June 2009, 124,538 of them were treated for malaria. That meant 2,000 to 3,000 patients a week for Dr. Matthew and his three fellow doctors, and the number rose to 5,000 in the rainy season. Of Apac's malaria patients, nearly half were under 5. (Read Dr. Mehmet Oz's explanation on why western diseases are spreading around the world.)

Signboards erected by the side of the road announced the presence of two foreign-assistance programs. One was a European-funded child-protection group, which had no malaria component to its program. The other was the National Wetlands Program (NWP), funded by Belgium. Partly because of NWP's influence, the draining of malarial swamps is banned — which amounts to preserving wetlands at the price of human life. Spraying houses with insecticide — which in 2008 cut malaria infections in half — is also forbidden. Why? Because of objections from Uganda's organic-cotton farmers, who supply Nike, H&M and Walmart's Baby George line. Chemical-free farming sounds like a great idea in the West, but the reality is that Baby Omara is dying so Baby George can wear organic.

The Problem with Helping
This, too often, is how aid goes: good intentions sidetracked by ignorance; a promising idea poorly executed; projects that are wasteful, self-regarding and sometimes corrupt. The people being helped often see things this way, as do the ones doing the helping, who ask why the hundreds of billions of dollars given to Africa since World War II have changed so little. It was in the face of such controversy that in 2007 the aid world unveiled one of its most ambitious goals: eradicating malaria.

The history of malaria is a long one. Originating in West Africa, it spread to half of humankind by the mid–19th century and has killed tens of millions and infected hundreds of millions more, including eight American Presidents. Malaria played a role in stopping Alexander the Great in India. It contributed to the fall of Rome, the relocation of the Vatican and the U.S. defeat in Vietnam. It still rages in the poverty-stricken world: it killed 863,000 people in 2008 — 89% of them African, and 88% of those people children under 5 — and infected 243 million more, says the World Health Organization (WHO). The lobbying group Malaria No More reckons that the disease costs Africa $12 billion a year — 1.3% of its economic growth. Fixing that would be the biggest boost to health and development in history. It would also be a stunning riposte to aid's critics.

It could happen. A previous campaign against malaria in the 1950s and '60s effectively eliminated the disease in Europe and the U.S. but made little progress in Africa and Asia, in part because health officials concluded that those places were simply too tough to fix. This time things are different. Now more than ever, it's unacceptable — indeed, immoral — to see Africa and Asia as beyond help. Today's funding is unprecedented, exceeding $10 billion. So is the leadership, from the U.S. President to the Sultan of Nigeria to soccer star David Beckham. Their goal is threefold: universal protection by the end of 2010 via the distribution of 700 million insecticide-treated bed nets; no more malaria deaths by the end of 2015; no malaria at all a decade or two after that. (See the latest on AIDS care, epidemic tracking and more.)

The logistics of such a plan are less complex than they seem, because while malaria affects half the world's countries, just seven — the Democratic Republic of Congo, Ethiopia, Kenya, Nigeria, southern Sudan, Tanzania and Uganda — account for two-thirds of all cases. So how might this malaria campaign succeed where so many others have come unstuck?

The Unlikely Leader
High above the Serengeti, Ray Chambers unclips his safety belt and beckons me to follow him to the back of the plane. At 67, Chambers, the U.N. special envoy for malaria, is graying and a little stiff, but with his square jaw, Clint Eastwood voice and the plane — his own — there is still something of the Master of the Universe about him. The son of a Newark, N.J., warehouse manager, Chambers was in his 20s when he came up with the idea of the leveraged buyout, a concept that made him fabulously rich — but not happy. In 1987 he found himself visiting a project for inner-city teenagers in Newark. He promised to pay the college tuition of 1,000 kids "if they stayed the path." That made him feel great. So in 1989 he closed his investment firm and became a philanthropist, giving away $50 million by 1993. (See TIME's photo-essay "The Most Malarial Town on Earth.")

In 2005, Chambers was looking at a photograph of sleeping Mozambican children taken by his friend the Harvard economist Jeffrey Sachs. "Cute kids," he remarked. "You don't understand," replied Sachs. "They're in malarial comas. They all died." Chambers was mortified. "So I said to Jeff, 'I'd like to kind of come up with business concepts to see if we can't save 1.3 million children a year.'" The next year, he established Malaria No More — a group that raises money, implements programs and stands as a case study of how aid can change.

The ethos of Malaria No More is that aid should be seen not as a noble act of charity but as something that's in everyone's interest. Eradicating disease boosts productivity, creates markets, stabilizes governments — even gives celebrities a point. It's a route to prosperity. Official endorsement of Chambers' approach came in 2008 when U.N. Secretary-General Ban Ki-moon appointed him special envoy. "You could see Ray was the guy to get this done," says WHO head Margaret Chan.

To be fair, he was not alone. Many companies are doing well by doing good, realizing that, say, an HIV program at a South African mine cuts absenteeism. A nuanced vision of a successful company is taking hold, one that elevates social responsibility to a core mission — and was backed with $14.5 billion in the U.S. in 2007, according to the Chronicle of Philanthropy.

Partly as a result of Chambers' prodding, that new way of giving aid has encouraged Western governments to open their wallets too. Funding for malaria has exploded from $50 million in 1997 to $6.6 billion for the Global Fund to Fight AIDS, TB and Malaria and $5.5 billion for the President's Malaria Initiative, a U.S. program launched in 2005. A good example of how aid is creeping into our lives in subtler ways is Unitaid. Founded in 2006 to raise money for AIDS, TB and malaria through small taxes on air tickets and check boxes on e-tickets, it has so far raised $870 million. (See the latest on AIDS care, epidemic tracking and more.)

Religion has caught the bug too — as it were. Rick Warren's Saddleback Church in Lake Forest, Calif., is training health workers in western Rwanda. The heads of the Muslim and Christian faiths in Nigeria are training hundreds of thousands of imams and priests in malaria care and net and drug distribution. Help also comes from retired politicians like Bill Clinton and Tony Blair, who have both set up aid foundations. Blair, whose Faith Foundation is assisting the Muslim-Christian collaboration in Nigeria, told Time, "The nature of help is changing. The malaria campaign is about as good an example as you get of rebalancing the respectability of the aid case."

Real Results
The payoff can be spectacular. malaria has been at least halved in nine African countries since 2000. Ethiopia and southern Sudan should reach universal protection this year; Chambers predicts global bed-net coverage in the first quarter of 2011, just months past his target. A visit last August by Chambers and Chan to the children's ward of a Zanzibar hospital produced whoops of joy from Chan. It was empty.

That success is hardly universal — or permanent. Zanzibar has eradicated malaria twice before but each time reimported it from mainland Tanzania. Kenya, an early success story, has slipped. Congo has only just got going. What do these failures have in common? Bad government. When Chambers visited Tanzania in August 2009, he found an approved $111 million Global Fund grant lying unclaimed for want of a single signature. In Uganda, Global Fund grants totaling $367 million were suspended over allegations — now before the courts — of corruption involving three health ministers and several aid groups. "The house is on fire," Chambers told a meeting of ministers and aid groups in Kampala last August. Chan was blunter: "We will hold you to account on behalf of the 350 women and children who die every day here." That, too, is a face of aid. (Read Dr. Mehmet Oz's explanation on why western diseases are spreading around the world.)

In Apac I visited the town hospital the morning after I arrived to find 30 newly admitted babies. When I returned that night, there were another 10. Martin, 27, was the only nurse on duty, and he was equipped only with quinine — long ago phased out in the West when malaria became resistant to it — headache pills and sugar solution. I watched him try to stick an IV needle into a 4-month-old girl, Doris Amang. He tried the backs of both her hands, then both sides of her head. Doris screamed and kicked. After pricking her 12 times, he gave up. Her veins had collapsed from dehydration. The windows were wide open. I watched a mosquito settle on Doris' cheek.

The next day, I returned. There were 50 babies now but no sign of Martin or any other staff member. The mothers were looking to me, but I had nothing to offer. I left the ward, walked quickly to my car and headed for the gates. Nearby was a naked street walker, feeling his way along the fence. As I roared past, I caught a glimpse of his startled expression, his emaciated face. I drove out of town and didn't stop until I reached Kampala.

Click to Print
Find this article at:
http://www.time.com/time/specials/packages/article/0,28804,1995199_1995197_1995176,00.html
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Rarick
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« Reply #54 on: June 19, 2010, 07:14:34 AM »

I remember reading a book way back in 6th grade that talked about "macroEngineering"  while the region mentioned in the previous post wasn't addressed, both the Sahara and Central Africa were.

The smaller of the 2 projects was the Quatrra(sp?) depression. It involved drilling tunnels/canals to the Mediterranean for water and runing said water thru turbines for electricity.  The water could then be deslinated with the electricity for irrigation, and the salt used for what salt is used for.  After the depression filled up in a few hundred years, you get a new great lake,  That lake could then be used as an irrigation reservoir.........  Macro with a big M engineering.  The angle that makes this germane to the thread would be that the increased availability of electrical power, irrigation, etc. would all raise the quality of living for the human population in the whole region.  That has always lessened the instance of disease, less instances makes for less mutation.  That would help stop both the spread and evolution of new diseases. This is the least active but here are some links:
http://en.wikipedia.org/wiki/Qattara_Depression
http://www.unu.edu/unupress/unupbooks/80858e/80858e0a.htm
http://www.springerlink.com/content/p162768711165022/
http://pielkeclimatesci.files.wordpress.com/2009/09/r-36.pdf

The larger of the projects was Lake Congo.  Dam up the congo river where it passes thru the gorge on the way to the coast.  That would drown 3 countries interior to africa, and incidentaklly some of the nastiest hell holes created by man and nature to date.  This area is the breeding ground of Filiarisis, HIV, Malaria, a large number of parasites, and who knows what new stuff is bubbling away in the rancid tidal swamp and swamplands of the congo river.  That dam alone would power a lot of the african coast from Lesotho on down to Nigeria it wouls also allow the congo alluvial plain to dry abnd be developed into some pretty rich farmlands like the Nile and Missisippi have along their banks eh? Once lake congo filled up you could tap the north end and develop hydro electric/irrigation to the chad region and restart the flow of the Niger river?  That would give a secondary supply of water to that whole region.......   The east and southern edges of the lake could be tapped too, that lake is basically in a tropical rainforest zone so you have a rain barrel practically overflowing and need to do something with that water............ Maybe all tha free clean power right on the equator could be used to build our first deliberately developed space/star port?  It would have a certain justice and balance about it wouldn't it? A small part of this would be the Inga Project
Links:
http://en.wikipedia.org/wiki/Congo_River
http://www.newsfromafrica.org/newsfromafrica/articles/art_10997.html
http://en.wikipedia.org/wiki/Congo_Basin

How many Trillions have we spent trying to help africans of all tribes and nations only to discover we are not getting anywhere?  Make a big project and a big dream and get them more interested in building rather than fighting.  In the process you get a whole bunch of apprentices who earn money and...... well we have brains.  2 bootstrap projects that could transform the part of the world that is the most miserable and let them join the rest of us...........

Hey it is a dream, but why not?
« Last Edit: June 19, 2010, 07:46:43 AM by Rarick » Logged
Crafty_Dog
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« Reply #55 on: July 09, 2010, 09:11:17 AM »

By MARK SCHOOFS
HIV research is undergoing a renaissance that could lead to new ways to develop vaccines against the AIDS virus and other viral diseases.

In the latest development, U.S. government scientists say they have discovered three powerful antibodies, the strongest of which neutralizes 91% of HIV strains, more than any AIDS antibody yet discovered. They are now deploying the technique used to find those antibodies to identify antibodies to influenza viruses.

Mark Schoofs discusses a significant step toward an AIDS vaccine, U.S. government scientists have discovered three powerful antibodies, the strongest of which neutralizes 91% of HIV strains, more than any AIDS antibody yet discovered.
The HIV antibodies were discovered in the cells of a 60-year-old African-American gay man, known in the scientific literature as Donor 45, whose body made the antibodies naturally. The trick for scientists now is to develop a vaccine or other methods to make anyone's body produce them as well.

That effort "will require work," said Gary Nabel, director of the Vaccine Research Center at the National Institute of Allergy and Infectious Diseases, who was a leader of the research. "We're going to be at this for a while" before any benefit is seen in the clinic, he said.

The research was published Thursday in two papers in the online edition of the journal Science, 10 days before the opening of a large International AIDS Conference in Vienna, where prevention science is expected to take center stage. More than 33 million people were living with HIV at the end of 2008, and about 2.7 million contracted the virus that year, according to United Nations estimates.

Vaccines, which are believed to work by activating the body's ability to produce antibodies, eliminated or curtailed smallpox, polio and other feared viral diseases, so they have been the holy grail of AIDS research.

Last year, following a trial in Thailand, results of the first HIV vaccine to show any efficacy were announced. But that vaccine reduced the chances of infection only by about 30%, and controversy erupted because in one common analysis the results weren't statistically significant. That vaccine wasn't designed to elicit the new antibodies.

The new discovery is part of what Wayne Koff, head of research and development at the nonprofit International AIDS Vaccine Initiative, calls a "renaissance" in HIV vaccine research.

Antibodies that are utterly ineffective, or that disable just one or two HIV strains, are common. Until last year, only a handful of "broadly neutralizing antibodies," those that efficiently disable a large swath of HIV strains, had been discovered. And none of them neutralized more than about 40% of known HIV variants.

But in the past year, thanks to efficient new detection methods, at least a half dozen broadly neutralizing antibodies, including the three latest ones, have been identified in peer-reviewed journals. Dennis Burton of the Scripps Institute in La Jolla, Calif., led a team that discovered two broadly neutralizing antibodies last year; he says his team has identified additional, unpublished ones. Most of the new antibodies are more potent, able to knock out HIV at far lower concentrations than their previously known counterparts.

HIV is a highly mutable virus, but one place where the virus doesn't mutate much is where it attaches to a particular molecule on the surface of cells it infects. Building on previous research, researchers created a probe, shaped exactly like that critical site, and used it to attract only those antibodies that efficiently attack it. That is how they fished out of Donor 45 the special antibodies: They screened 25 million of his cells to find 12 that produced the antibodies.

Donor 45's antibodies didn't protect him from contracting HIV. That is likely because the virus had already taken hold before his body produced the antibodies. He is still alive, and when his blood was drawn, he had been living with HIV for 20 years.
While he has produced the most powerful HIV antibody yet discovered, researchers say they don't know of anything special about his genes that would make him unique. They expect that most people would be capable of producing the antibodies, if scientists could find the right way to stimulate their production.

Dr. Nabel said his team is applying the new technique to the influenza virus. Like HIV, influenza is a highly mutable virus—the reason a new vaccine is required every year.

"We want to go after a universal vaccine" by using the new technique to find antibodies to a "component of the influenza virus that doesn't change," said NIAID director Anthony Fauci. In principle, Dr. Fauci said, the technique could be used for any viral disease and possibly even for cancer vaccines.

Some of the new HIV antibodies discovered over the past year attack different points on the virus, raising hopes that they could work synergistically.

In unpublished research, John Mascola, deputy director of the Vaccine Research Center, has shown that one of Dr. Burton's antibodies neutralizes virtually all the strains that are resistant to the antibody from Donor 45. He also found the reverse: The antibody from Donor 45 disables HIV strains resistant to one of Dr. Burton's best antibodies. Only one strain out of 95 tested was resistant to both antibodies, he said. Dr. Mascola is one of the authors of Thursday's papers.

Researchers say they plan to test the new antibodies, likely blended together in a potent cocktail, in three broad ways.

First, the antibodies could be given to people in their raw form, somewhat like a drug, to prevent transmission of the virus. But they would likely be expensive and last in the body for a limited time, perhaps weeks, making that method impractical for all but specialized cases, such as to prevent mother-to-child transmission in childbirth.

The antibodies could also be tested in a "microbicide," a gel that women or gay men could apply before sex to prevent infection.

 
The antibodies might even be tried as a treatment for people already infected. While the antibodies are unlikely to completely suppress HIV on their own, say scientists, they might boost the efficacy of current antiretroviral drugs.

Dr. Nabel said that the Vaccine Research Center has contracted with a company to produce an antibody suitable for use in humans so that testing in people could begin.

A second way to use the new research is to stimulate the immune system to produce the antibodies. Jonas Salk injected people with a whole killed polio virus, and virtually everyone's immune system easily made antibodies that disabled the polio virus. But for HIV, the vast majority of antibodies are ineffective. Now, scientists know the exact antibodies that must be made—those found in Donor 45 and in Dr. Burton's lab, for example. So researchers need "a reverse engineering technology" to find a way to get everyone to produce them, said Greg Poland, director of vaccine research at Mayo Clinic in Rochester, Minn.

That's what scientists at Merck & Co. have done. In a study published this year in the Proceedings of the National Academy of Sciences, the Merck Scientists knew that an old antibody, weaker than the newly discovered ones, attaches to a particularly vulnerable part of HIV. They created a replica of that piece of the virus to train the immune system to produce antibodies aimed at that exact spot. It was a painstaking process, requiring researchers to add chemical bonds to stabilize the replica so that it wouldn't collapse and lose its shape. Eventually, Merck was able to make experimental vaccine candidates capable of spurring guinea pigs and rabbits to produce antibodies that home in on the target site and neutralize HIV. Those vaccines weren't nearly powerful enough, but, said Dr. Koff, Merck's research provides a "proof of principle" that reverse engineering can work for the much stronger new antibodies.

There are other potential pitfalls. There is evidence that Donor 45's cells took months or possibly even years to create the powerful antibodies. That means scientists might have to give repeated booster shots or devise other ways to speed up this process.

Finally, there are experimental methods that employ tactics such as gene therapy. Nobel laureate David Baltimore is working on one such approach.
His team at the California Institute of Technology in Pasadena, Calif., has stitched genes that code for antibodies into a harmless virus, which they then inject into mice. The virus infects mouse cells, turning them into factories that produce the antibodies.

Write to Mark Schoofs at
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« Reply #56 on: July 12, 2010, 10:06:05 AM »

Buried in this piece are some really scary data about transmssion rates:
=========
WASHINGTON — President Obama will unveil a new national strategy this week to curb the AIDS epidemic by slashing the number of new infections and increasing the number of people who get care and treatment.

“Annual AIDS deaths have declined, but the number of new infections has been static and the number of people living with H.I.V. is growing,” says a final draft of the report, obtained by The New York Times.

In the report, the administration calls for steps to reduce the annual number of new H.I.V. infections by 25 percent within five years. “Approximately 56,000 people become infected each year, and more than 1.1 million Americans are living with H.I.V.,” the report says.

Mr. Obama plans to announce the strategy, distilled from 15 months of work and discussions with thousands of people around the country, at the White House on Tuesday.

While acknowledging that “increased investments in certain key areas are warranted,” the report does not propose a major increase in federal spending. It says the administration will redirect money to areas with the greatest need and population groups at greatest risk, including gay and bisexual men and African-Americans. The federal government now spends more than $19 billion a year on domestic AIDS programs.

On average, the report says, one person is newly infected with H.I.V. every nine and a half minutes, but tens of thousands of people with the virus are not receiving any care. If they got care, the report says, they could prolong their own lives and reduce the spread of the virus to others. By 2015 the report says, the United States should “increase the proportion of newly diagnosed patients linked to clinical care within three months of their H.I.V. diagnosis to 85 percent,” from the current 65 percent.

The first-ever national AIDS strategy has been in the works since the start of the administration. It comes in the context of growing frustrations expressed by some gay rights groups. They say that more money is urgently needed for the AIDS Drug Assistance Program, and they assert that the White House has not done enough to secure repeal of the law banning military service by people who are openly gay or bisexual.

The report tries to revive the sense of urgency that gripped the nation in the first years after discovery of the virus that causes AIDS. “Public attention to the H.I.V. epidemic has waned,” the report says. “Because H.I.V. is treatable, many people now think that it is no longer a public health emergency.”

The report calls for “a more coordinated national response to the H.I.V. epidemic” and lays out specific steps to be taken by various federal agencies.

Mr. Obama offers a compliment to President George W. Bush, who made progress against AIDS in Africa by setting clear goals and holding people accountable.

The program begun by Mr. Bush, the President’s Emergency Plan for AIDS Relief, “has taught us valuable lessons about fighting H.I.V. and scaling up efforts around the world that can be applied to the domestic epidemic,” the report says.

Mr. Obama’s strategy is generally consistent with policies recommended by public health specialists and advocates for people with H.I.V. But some experts had called for higher goals, more aggressive timetables and more spending on prevention and treatment.

The report makes these points:

¶Far too many people infected with H.I.V. are unaware of their status and may unknowingly transmit the virus to their partners. By 2015, the proportion of people with H.I.V. who know of their condition should be increased to 90 percent, from 79 percent today.

¶The new health care law will significantly expand access to care for people with H.I.V., but federal efforts like the Ryan White program will still be needed to fill gaps in services.

¶Federal spending on H.I.V. testing and prevention does not match the need. States with the lowest numbers of H.I.V./AIDS cases often receive the most money per case. The federal government should allocate more of the money to states with the highest “burden of disease.”

¶Health officials must devote “more attention and resources” to gay and bisexual men, who account for slightly more than half of new infections each year, and African-Americans, who account for 46 percent of people living with H.I.V.

¶The H.I.V. transmission rate, which indicates how fast the epidemic is spreading, should be reduced by 30 percent in five years. At the current rate, about 5 of every 100 people with H.I.V. transmit the virus to someone in a given year.

If the transmission rate is unchanged, the report says, “within a decade, the number of new infections would increase to more than 75,000 per year and the number of people living with H.I.V. would grow to more than 1.5 million.”

The report finds that persistent discrimination against people with H.I.V. is a major barrier to progress in fighting the disease.

“The stigma associated with H.I.V. remains extremely high,” it says. “People living with H.I.V. may still face discrimination in many areas of life, including employment, housing, provision of health care services and access to public accommodations.”

The administration promises to “strengthen enforcement of civil rights laws” protecting people with H.I.V.

One political challenge for the administration is to win broad public support for a campaign that will focus more narrowly on specific groups and communities at high risk for H.I.V. infection.

“Just as we mobilize the country to support cancer research whether or not we believe that we are at high risk of cancer and we support public education whether or not we have children,” the report says, “fighting H.I.V. requires widespread public support to sustain a long-term effort.”
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« Reply #57 on: July 26, 2010, 05:20:05 PM »

Scripps research study shows infectious prions can arise spontaneously in normal brain tissue
Scripps Research Institute ^ | July 26, 2010cimon

Metal surfaces spur conversion of normal prion protein into disease-causing prions

JUPITER, FL, July 26, 2010 – In a startling new study that involved research on both sides of the Atlantic, scientists from The Scripps Research Institute in Florida and the University College London (UCL) Institute of Neurology in England have shown for the first time that abnormal prions, bits of infectious protein devoid of DNA or RNA that can cause fatal neurodegenerative disease, can suddenly erupt from healthy brain tissue.

The catalyst in the study was the metallic surface of simple steel wires. Previous research showed that prions bind readily to these types of surfaces and can initiate infection with remarkable efficiency. Surprisingly, according to the new research, wires coated with uninfected brain homogenate could also initiate prion disease in cell culture, which was transmissible to mice.

The findings are being published the week of July 26, 2010, in an advance, online edition of the journal Proceedings of the National Academy of Sciences (PNAS).

"Prion diseases such as sporadic Creutzfeldt-Jakob disease in humans or atypical bovine spongiform encephalopathy, a form of mad cow disease, occur rarely and at random," said Charles Weissmann, M.D., Ph.D., chair of Scripps Florida's Department of Infectology, who led the study with John Collinge, head of the Department of Neurodegenerative Disease at UCL Institute of Neurology. "It has been proposed that these events reflect rare, spontaneous formation of prions in brain. Our study offers experimental proof that prions can in fact originate spontaneously, and shows that this event is promoted by contact with steel surfaces."

Infectious prions, which are composed solely of protein, are classified by distinct strains, originally characterized by their incubation time and the disease they cause. These toxic prions have the ability to reproduce, despite the fact that they contain no nucleic acid genome.

Mammalian cells normally produce harmless cellular prion protein (PrPC). Following prion infection, the abnormal or misfolded prion protein (PrPSc) converts PrPC into a likeness of itself, by causing it to change its conformation or shape. The end-stage consists of large aggregates of these misfolded proteins, which cause massive tissue and cell damage.

A Highly Sensitive Test

In the new study, the scientists used the Scrapie Cell Assay, a test originally created by Weissmann that is highly sensitive to minute quantities of prions.

Using the Scrapie Cell Assay to measure infectivity of prion-coated wires, the team observed several unexpected instances of infectious prions in control groups where metal wires had been exposed only to uninfected normal mouse brain tissue. In the current study, this phenomenon was investigated in rigorous and exhaustive control experiments specifically designed to exclude prion contamination. Weissmann and his colleagues in London found that when normal prion protein is coated onto steel wires and brought into contact with cultured cells, a small but significant proportion of the coated wires cause prion infection of the cells – and when transferred to mice, they continue to spawn the disease.

Weissmann noted that an alternative interpretation of the results is that infectious prions are naturally present in the brain at levels not detectable by conventional methods, and are normally destroyed at the same rate they are created. If that is the case, he noted, metal surfaces could be acting to concentrate the infectious prions to the extent that they became quantifiable by the team's testing methods.

###

The first author of the study, "Spontaneous Generation of Mammalian Prions," is Julie Edgeworth of the UCL Institute of Neurology. Other authors of the study include Nathalie Gros, Jack Alden, Susan Joiner, Jonathan D.F. Wadsworth, Jackie Linehan, Sebastian Brandner, and Graham S. Jackson, also of the UCL Institute of Neurology.

The study was supported by the U.K. Medical Research Council.

About The Scripps Research Institute

The Scripps Research Institute is one of the world's largest independent, non-profit biomedical research organizations, at the forefront of basic biomedical science that seeks to comprehend the most fundamental processes of life. Scripps Research is internationally recognized for its discoveries in immunology, molecular and cellular biology, chemistry, neurosciences, autoimmune, cardiovascular, and infectious diseases, and synthetic vaccine development. Established in its current configuration in 1961, it employs approximately 3,000 scientists, postdoctoral fellows, scientific and other technicians, doctoral degree graduate students, and administrative and technical support personnel. Scripps Research is headquartered in La Jolla, California. It also includes Scripps Florida, whose researchers focus on basic biomedical science, drug discovery, and technology development. Scripps Florida is located in Jupiter, Florida. See www.scripps.edu

http://www.eurekalert.org/pub_releases/2010-07/sri-srs072610.php
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« Reply #58 on: April 29, 2011, 09:38:29 PM »

The Shot Heard Round the World
By SCOTT GOTTLIEB


By 1947, smallpox in the U.S. was rare, but when two people died from the disease in New York, officials urged residents who hadn't been vaccinated in the past 7-10 years to get the shot. Above: Morrisania Hospital in the Bronx.

A vaccine that is intended to save countless lives. Parents suspicious of the shots, terrified of what the vaccine will do to their children. The government insisting on vaccinations for the general good.

Sounds like recent history, when a British doctor's study linking autism to the three-in-one vaccine for measles, mumps and rubella panicked some parents into barring their children from being vaccinated. But long before actress Jenny McCarthy prominently stirred fears about MMR shots, the vaccination campaign to eradicate smallpox was met with similar trepidation. One significant difference: The study that caused the anti-MMR hysteria has been proved to be bogus, while the smallpox vaccine used a century ago carried genuine dangers.

When some states introduced mandatory smallpox vaccinations during the epidemic of 1898-1903, Americans resisted by the thousands. The ensuing battles produced medical conventions and case law that altered the balance between government authority and medical practice, in favor of federal control. The effects of the smallpox fight continue to this day: The Obama health-care law and the infrastructure required to administer it rely on some of these century-old precedents.

In "Pox: An American History," Michael Willrich meticulously traces the story of how the smallpox vaccine was pressed into service during a major outbreak. Sometimes the shots were physically forced on people, outraging their sense of personal freedom and—when the vaccine sickened some and killed others—galvanizing suspicion of vaccination programs. The episode, Mr. Willrich says, prompted large swaths of Americans to insist that "the liberty protected by the Constitution also encompassed the right of a free people to take care of their own bodies and children according to their own medical beliefs and consciences."

Historical records show that smallpox was a human scourge for thousands of years. The virus produces high fever, severe back pain and scarring eruptions of flat red spots on the skin that turn into pustules and then into scabs—a two-week process during which the disease is highly contagious. Smallpox can vary in its severity, with some strains killing many sufferers and others relatively few. In the late 18th century, the British scientist Edward Jenner discovered that scratching the arms of healthy children with a bit of pus from cowpox immunized them against smallpox. The revelation was jeered by skeptics, but soon many governments were encouraging smallpox shots—and cowpox-based vaccines would eventually rout the disease from the modern world.

The smallpox outbreak in the U.S. that began in 1898 was not as virulent as some earlier ones, but memories of past horrors and mounting deaths across the country stirred officials to action. Over the epidemic's five-year course, an estimated 4,000 to 5,600 Americans died from smallpox, and tens of thousands suffered from nonfatal but often disfiguring infections.

Prior to the epidemic, public heath was largely the province of state and local authorities. But many officials proved incapable, or unwilling, to intervene when faced with the epidemic itself. In some cases, money was at issue. In other cases, racism. In the South and elsewhere, Mr. Willrich says, local officials refused to invest in stopping a virus that they saw as a blight of "dark people" who who were forced to live in close quarters with poor sanitary conditions. Mostly, though, the failure was a matter of ineptitude: Many doctors and others who focused on the infectious smallpox pustules didn't understand that the virus could be easily transmitted by a cough or a sneeze. And the vaccination programs were at best haphazard.

Walter Wyman, the U.S. surgeon general for two decades beginning in 1891, "railed against the short-sightedness of local and state officials who, he believed, had allowed smallpox to rage out of control," Mr. Wallrich writes. Whatever the cause of the anemic response to the epidemic, it prompted federal intervention in public-health matters—opening a door that has never closed.

Invoking what Mr. Willrich calls "a precedent in the American legal tradition of police power, which allowed for broad governmental intrusions into everyday lives of American citizens" when the public welfare was at stake, the feds stepped in. The government deployed "virus squads" of vaccinators who fanned out across the country, aided by Texas Rangers along the Mexico border and by billyclub-swinging policemen in New York. Health officials opened "pesthouses," where the ill were sequestered; sometimes whole towns were quarantined. The vaccinators visited factories and schools and railroad stations. In some cases, people who had been exposed to the smallpox virus were vaccinated at police gunpoint.

Pox: An American History

By Michael Willrich
Penguin Press, 422 pages, $27.95

Their reluctance was understandable: The smallpox vaccine was sometimes shoddily produced. In Camden, N.J., in 1901, the deaths of nine schoolchildren were linked by newspapers to a commercially produced vaccine tainted with tetanus. (Around that time, 13 children in St. Louis died of tetanus after being vaccinated for diphtheria.) It wasn't just civil libertarians who opposed the compulsory vaccinations; many practical people did the math and preferred to take a chance with the virus, not the vaccine. It was not just a fear of death that scared people: Reports of excruciating arm soreness caused by the vaccine made manual laborers, worried about having to miss work, avoid the shots. People produced fake vaccination certificates and sometimes injured their skin to simulate the telltale scar caused by the vaccine.

The feds realized that if they were going to mandate vaccination, the government would have to ensure that the shots were safe. In 1902, President Theodore Roosevelt signed the Biologics Control Act, the first federal law to regulate drug products. It was a precursor to today's Food and Drug Administration.

This being America, the vaccine tempest also gave rise to litigation. Mr. Willrich, a history professor at Brandeis University, says that the most significant of what became a series of legal rulings was the 1905 Supreme Court decision in Jacobson v. Massachusetts. The complex opinion gave the high court's blessing to compulsory-vaccination schemes. But the justices also established a set of standards for balancing governmental power and individual rights during public emergencies. The decision was invoked in 2004 by Justice Clarence Thomas in his dissent from the court's ruling in Hamdi v. Rumsfeld, granting certain rights to U.S. citizens detained as "illegal enemy combatants."

In the end, vaccination methods were dramatically improved, the epidemic was stopped—and over the next few decades smallpox was wiped out of human circulation by concerted vaccination campaigns and the swift isolation of the infected. Today, the virus is confined to frozen storage inside a lab in Atlanta and one in Koltsovo, Russia. But the federal role in the practice of medicine remains very much alive.

—Dr. Gottlieb is a clinical assistant professor at the New York University School of Medicine and an American Enterprise Institute resident fellow.

http://online.wsj.com/article/SB10001424052748703858404576214482670405722.html
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« Reply #59 on: April 30, 2011, 12:31:09 PM »

That was interesting BBG.
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« Reply #60 on: December 16, 2011, 12:38:51 PM »

At least someone is challenging the deed, and the difusion of the knowledge:

http://www.msnbc.msn.com/id/21134540/vp/45690564#45690564
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« Reply #61 on: January 05, 2012, 07:34:36 AM »

By BETSY MCKAY
The quest for a vaccine against AIDS is gaining momentum, with research published Wednesday identifying promising new candidates that protected monkeys against a powerful strain of the virus and that soon could be tested in humans.

The study, published in the online edition of the journal Nature, also shed light on how the first human vaccine to have conferred limited protection against the AIDS virus may have worked.

In the research, several experimental vaccines partially prevented infection in monkeys from a highly potent, highly immune-resistant strain of simian immunodeficiency virus, an unusual finding, researchers said. SIV is similar to human immunodeficiency virus, or HIV, the virus that causes AIDS, and SIV infection in monkeys resembles HIV infection in humans.

Decades of Progress and Setbacks
Recent advances have followed years of frustration in HIV research and prevention.

View Interactive
..The new vaccines, combining two different technologies to generate an immune response, reduced the chances that a monkey would be infected by the virulent SIV strain in each exposure by 80% to 83%, compared with a placebo. The vaccines also significantly reduced the amount of virus in the blood of monkeys who did become infected.

The protection was only partial—most of the vaccinated monkeys eventually became infected after multiple exposures. Still, the study was among the first to prevent infection against a virulent, highly immune-resistant SIV strain.

Plans are under way for clinical trials of a human-adapted version of one of the vaccines used in the monkeys, said Dan Barouch, professor of medicine at Harvard Medical School and Beth Israel Deaconess Medical Center, and lead author of the study. The vaccine will be tested in people both in the U.S. and internationally, including in populations in Africa where HIV infection rates are high, he said.

"There's more hope than ever before that an AIDS vaccine might be possible," said Dr. Barouch.

The findings are part of a renaissance in AIDS research, with multiple vaccine candidates under exploration and a landmark study published last year showing that AIDS drugs can reduce the spread of HIV from an infected person to others. But HIV researchers still don't fully understand how to prevent infection.

Vaccines, which work by spurring the body's ability to produce antibodies or immune cells, are considered the holy grail of AIDS research, because of the powerful role they played in eradicating smallpox and eliminating or sharply reducing the spread of other infectious diseases.

About 34 million people globally are infected with HIV, with about 2.7 million more infected each year, according to United Nations estimates.

In 2009, results of the first HIV vaccine to confer any protection against HIV were announced, after a large clinical trial in Thailand. That vaccine reduced the chances of infection only 31%, and prompted some controversy when one analysis found the results weren't statistically significant.

Still, the results helped rejuvenate the field. The latest study helps explain what many scientists suspected after the Thai trial: that the surface protein of the HIV virus, or its envelope, is involved in preventing infection.

"It clearly demonstrated you need to make antibodies against the outer coating of the virus," said Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, the part of the National Institutes of Health that oversees AIDS research and co-funded the latest study.

"It confirms what was seen in the Thai trial was real," said Louis Picker, associate director of the Vaccine and Gene Therapy Institute at Oregon Health & Science University, who reviewed the study led by Dr. Barouch but wasn't involved in it.

One strength of the study, said Dr. Fauci, was that the researchers made their vaccines with one strain of SIV and infected monkeys with another—replicating a likely real-world scenario, because the ever-mutating AIDS virus comes in many strains.

Many previous studies have used the same virus, but "that's not the way the real world works," he said. "There are so many different varieties of HIV out there. You've got to protect the person against potentially any strain."

While monkey models are considered highly reliable in HIV research and the findings resemble those of the Thai trial in humans, HIV researchers cautioned that it won't be known whether these vaccines work in humans until they are tried.

"HIV is progressively revealing its secrets and each time it gets us closer to the goal, but this isn't like a basketball game where it's the last two minutes," said Bruce Walker, a veteran HIV researcher and director of the Ragon Institute, an enterprise of Massachusetts General Hospital, the Massachusetts Institute of Technology and Harvard University. Ragon Institute helped fund the latest study and has raised $11 million of about $22 million needed for the clinical trials, Dr. Walker said.

Mark Schwartz, chairman and founding partner of MissionPoint Capital Partners, a private equity firm, donated $1 million of his own funds, together with his wife Lisa, toward the clinical trials. "Is it risky in a venture capital kind of way? Yes, it is," he said. But, he said," Ultimately, we think the real payoff is going to be in a vaccine."

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« Reply #62 on: January 08, 2012, 07:10:30 AM »


ALthough I have not studied the issue closely, I must say my intuitive reaction is the same.
=============================


Scientists have long worried that an influenza virus that has ravaged poultry and wild birds in Asia might evolve to pose a threat to humans. Now scientists financed by the National Institutes of Health have shown in a laboratory how that could happen. In the process they created a virus that could kill tens or hundreds of millions of people if it escaped confinement or was stolen by terrorists.

We nearly always champion unfettered scientific research and open publication of the results. In this case it looks like the research should never have been undertaken because the potential harm is so catastrophic and the potential benefits from studying the virus so speculative.

Unless the scientific community and health officials can provide more persuasive justifications than they have so far, the new virus, which is in the Netherlands, ought to be destroyed. Barring that, it should be put in a few government-controlled laboratories with the highest containment rating, known as biosafety level 4. That is how the United States and Russia contain samples of smallpox, which poses nowhere near the same danger of global devastation.

In the future, it is imperative that any such experiments be rigorously analyzed for potential dangers — preferably through an international review mechanism, but also by governmental funding agencies — before they are undertaken, not after the fact as is happening in this case.

The most frightening research was done by scientists at the Erasmus Medical Center in Rotterdam, who sought to discover how likely it is that the “bird flu” virus, designated A(H5N1), might mutate from a form that seldom infects or spreads among humans into a form highly transmissible by coughing or sneezing. Thus far the virus has infected close to 600 humans and killed more than half of them, a fatality rate that far exceeds the 2 percent rate in the 1918 influenza pandemic that killed as many as 100 million people.

Working with ferrets, the animal that is most like humans in responding to influenza, the researchers found that a mere five genetic mutations allowed the virus to spread through the air from one ferret to another while maintaining its lethality. A separate study at the University of Wisconsin, about which little is known publicly, produced a virus that is thought to be less virulent.

These findings led to an unprecedented request from an American federal advisory board that the researchers and the two scientific journals that plan to publish the studies omit any details that might help terrorists figure out how to unleash a devastating pandemic. That presumably includes details on how the engineered virus was made and details on the precise mutations that allowed it to go airborne.

We doubt that anything at all should be published, but it seems clear that something will be.

The two journals reviewing the papers seem inclined to follow the advisory board’s recommendations that the research be published in a redacted form, provided there is some way for researchers who need the information to gain access to the full details. The Erasmus team believes that more than 100 laboratories and perhaps 1,000 scientists around the world need to know the precise mutations to look for. That would spread the information far too widely. It should suffice to have a few of the most sophisticated laboratories do the analyses.

Defenders of the research in Rotterdam claim it will provide two major benefits for protecting global health. First, they say the findings could prove helpful in monitoring virus samples from infected birds and animals. If genetic analysis found a virus somewhere that was only one or two mutations away from going airborne, public health officials would then know to bear down aggressively in that area to limit human contact with infected poultry and ramp up supplies of vaccines and medicines.

But it is highly uncertain, even improbable, that the virus would mutate in nature along the pathways prodded in a laboratory environment, so the benefit of looking for these five mutations seems marginal.

A second postulated benefit is that the engineered virus can be used to test whether existing antiviral drugs and vaccines would be effective against it and, if they come up short, design new drugs and vaccines that can neutralize it. But genetic changes that affect transmissibility do not necessarily change the properties that make a virus susceptible to drugs or to the antibodies produced by a vaccine, so that approach may not yield much useful new information.

We cannot say there would be no benefits at all from studying the virus. We respect the researchers’ desire to protect public health. But the consequences, should the virus escape, are too devastating to risk.

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« Reply #63 on: March 04, 2012, 10:55:40 AM »



The Truth About the Doomsday Virus?
Published: March 3, 2012
o   

Two months ago we warned that a new bird flu virus — modified in a laboratory to make it transmissible through the air among mammals — could kill millions of people if it escaped confinement or was stolen by terrorists. Now Ron Fouchier, the Dutch scientist who led the key research team, is saying that his findings, which remain confidential, were misconstrued by the press.
Related
•   Genetically Altered Bird Flu Virus Not as Dangerous as Believed, Its Maker Asserts (March 1, 2012)
•   Health Guide: Avian Influenza
He says that the virus did not spread easily and was not lethal when transmitted from one ferret to another by coughing or sneezing, and that it became highly lethal only when big doses were injected into the animals’ windpipes.
That is hard to square with his original assertions. Experts who read his original manuscript say it reported that the new virus spread through the air and remained as virulent as the natural virus, which has killed 60 percent of the humans it has infected.
Dr. Fouchier’s new claims are only the latest bizarre twist in a global health debate that badly needs an objective, independent arbiter. The public needs to know whether this virus is a potentially big killer, and if so, how it should be contained. It needs to know what details can be published without giving terrorists a recipe for a biological weapon. And it needs to know that a mechanism will be put in place to assess all the risks and benefits of such research before it is approved — not after a new virus has been created.
The debate became public after a federal advisory board, the National Science Advisory Board for Biosecurity, recommended that papers prepared by Dr. Fouchier’s group and researchers doing similar work at the University of Wisconsin-Madison be published only after omitting details that might help terrorists. That drew charges of censorship from some scientists, and others warned that restricting the information would make it harder to track and combat an outbreak of a similar strain.
The World Health Organization convened a closed meeting of 22 experts last month, which concluded that the research should eventually be published in full. The group was dominated by participants with a clear stake in publication — including the researchers who made the viruses, the journals that want to publish their papers in full, and developing countries that want access to full details in exchange for having contributed the viruses that were studied.
Now this country’s National Institutes of Health, which financed the research and has its own reputation on the line, is asking the biosecurity advisory board to reconsider its call to redact details before publication.
We welcome a new appraisal from a board that has already shown considerable independence. We hope it will look beyond the security and terrorism issues and voice its opinion on what safety precautions should be required to prevent the virus from escaping and whether the work should proceed at multiple labs or possibly be halted.
These issues need to be resolved by experts who do not have institutional biases or turf to protect. The World Health Organization should be in the best position to oversee a response to what is a global problem. Its first effort was one-sided and disappointing, but it has pledged to convene further meetings with a much broader range of experts and interested parties. It must ensure that these forums are not rubber stamps for what the narrower special-interest group just concluded.
These are complicated issues, and the stakes are enormous. Governments and scientists have a clear responsibility to get this judgment and future efforts right.

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« Reply #64 on: June 21, 2012, 02:19:05 PM »



Bird Flu Type Could Be Transmitted Through Air .
By GAUTAM NAIK

In an experiment showing how the virus that causes bird flu might trigger a human pandemic, scientists induced five genetic changes in the bug, transforming it into a type capable of airborne transmission between mammals.

The findings signal how the virus, which has killed nearly 60% of about 600 people known to have been infected in more than a dozen countries since 2003, could pose a much greater public health risk in the future. Two of the mutations the scientists created in the experiment already circulate in birds and people, and natural evolution could bring about the remaining three mutations, researchers said.

The findings appear in the journal Science, which on Friday is publishing several papers and commentaries about the virus, which is also known as H5N1. The studies were funded by the U.S. National Institutes of Health and other groups.

The genetic-alteration paper in Science is one of two controversial experiments whose planned publication sparked fears it would give terrorists a blueprint for making a biological weapon. The first such paper described an alternative genetic technique for creating a pandemic version of H5N1 and appeared in Nature in May.

If public-health officials know which bird-flu genetic signatures to look for, they can obtain swabs from people infected with H5N1 and see whether the critical mutations have started to accumulate.

The authors of the latest studies caution that they cannot predict when or if the remaining three genetic mutations might emerge. Nor are these the only possible mutations that could start a pandemic, they say.

"We only know that it's within the realm of possibility that the [three mutations] could evolve in a human or other mammalian host," said Derek Smith of the University of Cambridge. In one of the Science papers, co-authored by Dr. Smith, a 15-year analysis of surveillance data found that two of the five mutations seen in the lab-engineered viruses had occurred in several existing bird flu strains.

The H5N1 virus, which causes bird flu, can move from birds to people through physical contact. But it isn't yet efficient at jumping from person to person, a necessary ingredient for sparking a pandemic.

The flu-surveillance benefit of the research "far outweighs the risk of nefarious" use posed by terrorists or anyone else pursuing a biological-weapons program, said Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, part of the NIH. Dr. Fauci and NIH director Francis Collins co-authored one of the commentaries in Science examining the benefits and risks of flu research.

The latest studies also indicate that the risk of an H5N1-pandemic may be greater than previously believed.

In the experiment published in Nature in May, scientists combined H5N1 and swine flu and came up with a hybrid bug that could leap from mammal-to-mammal. That experiment was based on the long-held notion that a pandemic strain is more likely to emerge when a flu virus mixes its genes with another virus in an animal host, such as a pig.

But one of the Science studies suggests that such "re-assortment" may not be necessary to give rise to a pandemic strain, and that it might emerge from mutations in H5N1 alone.

Scientists first changed three amino acids of H5N1 in a way they believed would boost the bug's affinity for human hosts, and then infected ferrets with the mutated virus. Ferrets are a good model because they sneeze like humans and show similar symptoms when infected by flu.

The researchers swabbed the noses of the infected ferrets and used virus samples from their bodies to infect another round of ferrets, thus "passaging" the virus several times through different ferrets. At each stage, they took tissue samples from the animals and analyzed how H5N1 was evolving.

"After about 10 passages, we found the virus had acquired the ability to transmit" from animal to animal, said Ron Fouchier of the Erasmus Medical Center in Rotterdam, Netherlands, and co-author of the study. That suggests that "in humans it would take a low number of transmissions for the mutations to accumulate."

Five mutations gave the virus the ability to jump from ferret to ferret: three of the initial amino-acid changes, plus two that emerged through evolutionary selection in the animals' bodies.

Four of the genetic substitutions were in hemagglutinin, a protein on the surface of H5N1 that helps it to enter host cells. The fifth was in the polymerase 2, a protein that helps the virus replicate its genetic material.

Although the lab-made virus had acquired the ability to leap between animals, it wasn't lethal and most of the infected ferrets eventually recovered from the flu. The animals succumbed only when large doses of the mutant virus were introduced directly into their throats.

Test-tube experiments also suggested that the engineered virus responded to the antiviral drug oseltamivir and to antbodies from ferrets that had received experimental H5N1 vaccines, according to the study by Dr. Fouchier and his colleagues.

Write to Gautam Naik at gautam.naik@wsj.com

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« Reply #65 on: October 06, 2012, 09:29:11 AM »



http://www.nytimes.com/2012/10/06/health/another-use-for-home-hiv-test-screening-partners.html?_r=1&nl=todaysheadlines&emc=edit_th_20121006
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« Reply #66 on: October 30, 2012, 10:35:10 AM »

http://www.nytimes.com/2012/10/30/health/a-weak-spot-in-hivs-armor-raises-hope-for-a-vaccine.html?nl=todaysheadlines&emc=edit_th_20121030
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« Reply #67 on: November 19, 2012, 07:53:04 PM »



By THOMAS M. BURTON and BETSY MCKAY
A government health panel on Monday for the first time recommended testing for the human immunodeficiency virus for all Americans aged 15 to 65, in an effort to slow its spread.


An estimated 200,000 people in the U.S. are infected with the virus that can cause AIDS and don't realize it. The U.S. Preventive Services Task Force said the new draft recommendation is aimed at preventing those people from infecting others or developing AIDS themselves.

The panel's recommendation is significant because, if finalized, private insurers would have to pay for the test. Past recommendations haven't always been embraced by doctors. But in this instance, the weight of medical evidence has already been trending in favor of screening and earlier treatment of people with HIV.

It is estimated that 1.1 million Americans have HIV, with about 50,000 new cases annually.

Focusing tests only on those at high risk hasn't been very effective, the panel said. "Targeted screening misses a substantial proportion of infected persons because of undisclosed or unknown risk factors," said an article in Annals of Internal Medicine published Monday to support the task force's recommendation.

Until now, the task force had only recommended that doctors screen all pregnant women for HIV, and that younger adolescents and older adults who are at increased risk also be screened. Those at high risk include men who engage in sex with other men, people who take drugs by injection, and those who have sex with infected people, the task force has said.

Monday's recommendation doesn't say precisely how often people should get HIV screening. "One reasonable approach," the task force wrote, "would be onetime screening of adolescent and adult patients to identify persons who are already HIV positive, with repeat screening of persons who are known to be at risk for HIV infections."

Anthony S. Fauci, director of the National Institute of Allergy and Infectious Diseases and a leading researcher and White House adviser on AIDS, said more than half of new HIV infections in the U.S. are a result of people who don't realize they have the virus. Testing and treating people, he said, "makes it highly unlikely that people with HIV will transmit their infection to their sexual partners."

Carl Schmid, deputy executive director of The AIDS Institute, a public-policy advocacy group, called the decision "a monumental shift in how HIV in the U.S. can be prevented, diagnosed and treated." He called the current risk-based approach "an ineffective screening strategy."

But there are many people who are skeptical about wider HIV testing, said Michael S. Lyons, an emergency room physician at the University of Cincinnati. "The benefits of diagnosing someone as early as possible are basically proven," he said, "but the difficulty is how do you do that?"

Mr. Lyons said many relatively poor people who show up at the emergency room may well be HIV-positive, "but emergency departments are very strained at this point. This is a compelling example of the tension between what would be good to do and what practically can be done."

The Centers for Disease Control and Prevention declined to comment on the significance of the recommendation because it is only in draft form and subject to public comment. Since 2006, the CDC has recommended routine HIV testing for everyone aged 13 to 64.

Jonathan Mermin, director of the CDC's HIV/AIDS prevention program, has said HIV testing should be "as routine as cholesterol screening."

From here, the task force's draft would have to become a final recommendation. At an unspecified time after that, insurance plans would be obligated to pay for the test. Ultimately, it would be up to doctors to order the test.

Robert Zirkelbach, spokesman for America's Health Insurance Plans, said, "If a physician orders a test, the insurer will cover it, and that won't change." The new Affordable Care Act requires insurers to pick up the costs.

The HIV tests are either blood or oral-swab tests, and the results of some are known in minutes. A 2010 study found that the quick test cost on average $48 for a negative test and $64 for a positive test, with the difference being the cost of counseling.
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« Reply #68 on: November 23, 2012, 10:27:12 AM »



How Fight to Tame TB Made It Stronger .
By GEETA ANAND in Mumbai and BETSY MCKAY in Atlanta

The World Health Organization's long-standing strategy for fighting tuberculosis is showing deadly unintended consequences: By focusing for years on the easiest-to-cure patients, it helped allow TB strains to spread that are now all but untreatable by modern medicine.


The WHO and a growing chorus of global health experts are now calling for a significant overhaul in the way nations with widespread drug-resistant TB combat the disease. It amounts to a de facto acknowledgment that the WHO's TB strategy, and the countries that use it, failed to adapt quickly enough as the disease formed more powerful, resistant strains.

"The TB community has been too conservative" on a global scale, said Puneet Dewan, until recently a senior officer in the WHO's India tuberculosis program. "We should have pushed sooner for a more aggressive, comprehensive approach" toward drug resistance, he said this month in an interview. "There was a cost in failing to do that. We're paying that cost today."

The WHO played a particularly sizable role in designing the tuberculosis program in India, which has seen a steep decline in regular TB. But India and other poor countries are now in the midst of an epidemic of drug-resistant strains—deadlier and harder-to-treat varieties of one of the world's top infectious-disease killers.

G.R. Khatri, who headed India's TB program more than a decade ago, called the epidemic of resistant TB in Mumbai "a recipe for disaster." The WHO should have known it was so bad and bears responsibility, he said. "What has the WHO been doing?"

In pilot testing across India this year of a new diagnostic method, some 6.6% of untreated TB patients were drug-resistant—suggesting far higher rates than the 2% to 3% levels India and the WHO have cited for years. The test was a collaboration of international aid groups and India's government.

At one clinic in Mumbai, research showed more than one quarter of 566 TB patients tested in recent months were resistant to the most powerful treatment, according to data obtained by The Wall Street Journal through India's Right to Information Act. The results are preliminary, but in the absence of any nationwide survey they offer a sense of what India's drug-resistance rates might be.

Enlarge Image


Close.The WHO is in the midst of a "complete rethinking" of its strategy toward drug resistance that involves helping countries move more quickly to address their epidemics, said Mario Raviglione, the WHO's top tuberculosis official. Countries with the largest epidemics, such as India, China, South Africa and Russia, haven't moved rapidly enough against drug resistance, he said. "That is why you see no global progress."

Dr. Dewan said that perhaps he and others should have recognized Mumbai's epidemic sooner. But partly because drug-resistant TB was a slow-moving emergency, he said, it was hard to get a full sense of the scope.

"It's a bit like the frog in a pot on a stove," Dr. Dewan said. "If you turn up the heat fast, the frog jumps out. If you turn up the heat slowly, the frog doesn't jump out, it slowly dies."

Only now is India planning its first national survey of drug resistance in TB patients, according to Prahlad Kumar, director of the National Tuberculosis Institute, the government's Bangalore-based research center. A timetable hasn't yet been set.

In-Depth: A Killer Quietly Gains Strength
The Wall Street Journal is chronicling the world's imperfect response to the rise of drug-resistant tuberculosis, an ancient disease that modern medicine, until recently, could defeat.

A selection of reports:

One woman's case of nearly incurable tuberculosis echoes around the world. (9/8/12)
India's slow reaction appears to be nurturing an all-but-untreatable strain of TB, raising the prospect of a global health hazard. (6/20/12)
A top doctor in Mumbai reports finding 12 cases of tuberculosis that are all but untreatable by current methods. (1/19/12)
.The policy changes are vindication for Zarir Udwadia, a prominent Indian physician whose controversial findings earlier this year—he identified several patients in Mumbai who were so drug-resistant that virtually none of the usual medicines worked—helped sound the alarm. Patients like these reflect the way drug-resistant TB "is mismanaged in India," Dr. Udwadia said.

Dr. Dewan said he has been taken by surprise by "crazy" levels of resistance like those identified by Dr. Udwadia. Dr. Dewan's own views have shifted quickly: As recently as last year, he said at a presentation in India that there was too much "hype" regarding drug-resistant TB.

Globally, studies suggest that drug-resistant TB is likely far more common than the WHO's own estimate of 3.7% of previously untreated patients. Resistance is worsening in many countries, the research indicates, even as the WHO's widely praised program to fight regular TB has succeeded in reducing the overall number of TB cases since the 1990s.

For decades, the WHO, aid groups and nations have been fighting TB world-wide. But the governmental effort focused almost exclusively on traditional, treatable strains, which are inexpensive to diagnose and defeat with drugs. However, this approach largely ignored drug-resistant strains.

In India, that has left the lives of patients like 22-year-old Amol Dhuri hanging in the balance. In January he was diagnosed with extensive drug-resistance—but the lab that tested him hasn't yet been accredited by the government to do this kind of testing. In fact, Mumbai, India's largest city, doesn't yet have a single lab accredited to diagnose extensive drug-resistance.

Because India's government will give patients the more powerful drugs only if they are tested by an accredited lab, Mr. Dhuri hadn't until this week started taking the drugs that have a shot at curing his strain.

More
Mumbai Grapples With Drug Resistant TB Strain
The Wall Street Journal's Investigation on Tuberculosis
.He was taking a cocktail of drugs provided by the government at no charge, most of which he was resistant to.

"I just don't understand why I'm taking these medicines and they're having no effect at all," Mr. Dhuri said.

Mr. Dhuri's drug regimen wasn't merely ineffective, it was potentially dangerous. Giving a patient medicines not strong enough to kill the TB bacteria increases the chance that it will mutate into drug-resistant strains.

It also left Mr. Dhuri wandering around, possibly spreading his drug-resistant disease to others. The average TB patient infects 10 to 15 people a year, according to the WHO.

Neither Ashok Kumar, head of India's TB program, nor P.K. Pradhan, secretary of the Ministry of Health & Family Welfare, returned calls seeking comment on Mr. Dhuri's case. But after the Journal's inquiries, Mr. Dhuri's drug-resistance report from an accredited lab elsewhere in the country showed up by email late last week, confirming his extensive drug resistance, Mumbai TB officials said. They said they would put him on the correct treatment this week.

The WHO, the United Nations agency dedicated to public health, once insisted that countries tackle only regular TB first before trying to treat resistant strains. Now, it urges poor countries to treat both simultaneously.

That, however, requires much more money. There will be a shortfall of $3 billion a year out of the $8 billion a year needed to fight TB in developing countries between 2013 and 2015, according to the WHO's Dr. Raviglione.

In India, medicines to treat regular TB cost $9 a month, compared with $2,000 for resistant strains.

Globally, TB receives much less money from international donors than other major deadly infectious diseases, according to data from the Institute for Health Metrics and Evaluation at the University of Washington. International assistance for TB was $1 billion in 2009. By contrast, malaria, which killed nearly half as many people, received $2 billion that same year. HIV received $6.5 billion, although HIV also costs more to treat and kills about 20% more people a year.

"There needs to be a giant leap in funding, thinking and innovation," said Soumya Swaminathan, director of the National Institute of Research in Tuberculosis, one of the Indian government's premier research centers.

Tuberculosis, an ancient, airborne disease that mostly affects the lungs, is spread by coughing and sneezing. In the 19th century, it was the biggest killer of adults in most of Europe.

In the 1940s researchers discovered they could cure it, over many months, with a cocktail of medicines. In many western nations, TB went into retreat. But in poor countries, it thrived and spread amid poverty and a lack of treatments and diagnostic tools.

The WHO in 1993 declared TB a global public-health emergency, following a resurgence driven largely by the HIV epidemic. At the time, there were approximately eight million cases a year world-wide.

Globally, there was almost no funding for TB, no unified strategy to fight it, and hundreds of treatment regimens in effect. Arata Kochi, the WHO's TB chief at the time, called it "treatment chaos."

The solution, many believed, was to devise a standard, simple-to-understand treatment cheap enough to work in the world's poorest places. The WHO developed a strategy known as DOTS, or Directly Observed Therapy Short-Course, so named because patients were to be directly supervised to make sure they took their medicine. Skipping doses, even briefly, gives the disease a chance to mutate and become drug-resistant.

The WHO, which produces health standards and policies, urged countries to adopt its DOTS program, though it can't oblige them.

The WHO played a particularly large role in India because of the size of the country's TB burden. Dozens of WHO consultants provided technical support nationwide.

Under DOTS, India relied on a rudimentary but affordable diagnostic—peering at a patient's spit under a microscope to spot the bacteria. Patients got a six-month treatment of four standard medicines. Anyone still sick went back on the same regimen for eight more months, plus one additional drug.

This could cure most people with regular TB. But it wasn't strong enough to cure multi-drug resistant, or MDR, strains.

The WHO decided that tackling MDR was unfeasible in places with poor infrastructure, little money and millions of patients lacking even basic treatment.

At that time, "there were two million new cases of TB in India each year"—almost none of which were being treated effectively—and "97% of them weren't MDR," said Thomas Frieden, the physician who spearheaded the India program on behalf of the WHO in its initial years. He is now director of the Centers for Disease Control and Prevention in Atlanta.

Dr. Khatri, who set up the India DOTS program with Dr. Frieden in 1997, agreed with the WHO's philosophy of treating regular TB first. "Every one minute, a patient was dying of TB in India," he said. "So I believed we should not plow a penny into MDR TB in India—and I did not." Dr. Khatri now heads the nonprofit World Lung Foundation for South Asia.

"It was well-intentioned reasoning in a resource-limited world," said Dr. Dewan, who left the WHO in recent weeks to join the Bill & Melinda Gates Foundation's TB program in India.

Dr. Raviglione, too, supports the WHO's original strategy. Without it, he said, drug resistance would now be "enormous." DOTS eliminated many of the slipshod medical practices that let the bacteria to mutate into super-resistant strains.

Meanwhile, however, evidence showed drug resistance emerging globally. Resistance was found in all 35 countries surveyed for a 1997 WHO-affiliated report. In 2000, a subsequent report found worrisome resistance rates in several countries, including parts of China and India.

In 2000, the WHO began a new program to tackle drug resistance and to "mop up" the damage caused by TB programs that had been "careless in how they treat the disease." But that program was never widely implemented, aside from some pilot programs.

This pilot program didn't even reach Mumbai, India's largest city, until mid-2010.

Around the same time, evidence emerged that resistant strains were more lethal than thought.

In one South Africa neighborhood, some 40% of patients with multi-drug-resistant TB—and 51% with higher levels of resistance—were dead within 30 days of their initial TB diagnosis, a 2010 study showed.

If that many people were dying within just 30 days, India's pilot program looked inadequate: It waited 14 months from initial diagnosis before even testing for resistance.

"We knew it was bad, but we didn't know it was this bad," Dr. Dewan said of the study.

Then, this year Dr. Udwadia and others at Mumbai's P.D. Hinduja National Hospital & Medical Research Center identified an even more menacing threat. The researchers called it "total drug resistance," because virtually none of the 12 treatments used to treat TB worked.

The report "sounded an alarm" globally, Dr. Dewan said. India quickly formulated a plan to increase its TB spending fourfold over five years, although that plan is still awaiting funding. It would establish more labs and 120 drug-resistance specialty centers.

Because most TB patients bypass the government's program when they first seek treatment, the new plan emphasizes engaging India's burgeoning private health-care providers.

Still, even this proposal falls short. By 2017, the plan says, India would only be able to treat fewer than half its estimated 100,000 multi-drug-resistant cases annually. Meanwhile India is home to the world's largest population of TB patients—2.2 million of last year's 8.7 million new cases—and treatment delays remain typical.

Last year the WHO began overhauling its "global architecture" for fighting drug resistance, Dr. Raviglione said. Instead of one committee in Geneva advising the world, regional expert groups will work with governments to help them develop and fund programs to attack drug resistance.

The WHO is also helping countries implement a new test, GeneXpert, that can diagnose TB and a common form of resistance in just 100 minutes, instead of several weeks. This marks the first major diagnostic advance in more than a century.

Eleven new or repurposed TB drugs are also in clinical trials. Dr. Raviglione said a task force is now studying how best to use them without fostering more drug resistance. Meanwhile, India's central TB office says it has established 43 testing labs and plans to build 30 more by 2015.
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« Reply #69 on: December 10, 2012, 08:33:02 AM »




By CARL F. NATHAN
 
Published: December 9, 2012


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I hope you never have this experience: a loved one is hospitalized. Her doctors tell you her infection is resistant to antibiotics. She dies. More than 60,000 American families go through that experience each year — and the number is almost certain to rise.






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Multidrug-resistant organisms are showing up in top-flight hospitals — like the klebsiella found in the National Institutes of Health’s Clinical Center this year, which may have led to the deaths of seven patients. Even infections that used to be a breeze to treat, like gonorrhea, are becoming incurable.

In much of the world, of course, bacterial disease is a routine cause of tragedy. Tuberculosis alone kills 1.4 million people a year. One reason for this staggeringly high figure is that most people in the world are too poor to pay for most medicines. But another reason is that some strains of tuberculosis bacteria have become resistant to most of the drugs we have. Even after two years of toxic treatment, drug-resistant tuberculosis has a fatality rate of about 50 percent.

What makes the rapid loss of antibiotics to drug resistance particularly alarming is that we are failing to make new ones. We are emptying our medicine chest of the most important class of medicines we ever had. And the cause can be traced, for the most part, to two profound problems.

The first is economic. Historically, the drug industry thrived on antibiotics. But if an antibiotic is useful against only one type of bacterium, relatively few people need it during its patent life. And if an antibiotic is “broad spectrum,” meaning it works on many different types of bacteria, wider use shortens its commercial life because it quickens the pace at which bacteria develop resistance. Moreover, antibiotics are designed to cure an acute disease — not to palliate a chronic one — so people need them only for a limited time. Compared with drugs that are used for years to treat widespread conditions like high cholesterol or asthma, antibiotics pale as a corporate investment.

The second challenge stems from the nature of bacteria. Though brainless, they are brainy, enjoying a highly effective collective intelligence. Large numbers of independently mutating bacteria test adaptations to group problems, like how to survive antibiotics. What works — like modifying the bacterial proteins to which antibiotics would otherwise bind — wins. As bacteria become more adept at evading antibiotics, it has become much harder to find drugs that can beat them back.

Merge these two problems — scientific and economic — and the result is a drug-development disaster: the prospects are so discouraging that few companies bother to try anymore.

How can we confront the critical shortage of new antibiotics when both the scientific approach and the economic model are letting us down? We can change both paradigms.

Drug makers survive by selling what people or governments buy in amounts and at prices that maximize profit. Monopoly protects the ability to set price for profit. Patents allow monopoly. Secrecy protects intellectual property until it is patented.

But what if we take a page out of the pathogen playbook? Many pathogens exchange DNA, sharing what they learn. Drug makers can operate in the same way: they can do science “open lab”-style, working in teams with academic and government scientists and other drug companies to share what they learn and to bring fresh scientific ideas and technological tools to bear. Relaxing the traditional insistence on secrecy allows collaboration, and with it, innovation.

Did I hear you say, “It’ll never happen”? It already has. GlaxoSmithKline opened its campus at Tres Cantos, Spain, to outside academic, government and biotech scientists in order to collaborate on finding antibiotics for neglected infectious diseases. The independent Tres Cantos Open Lab Foundation selects the projects and helps cover visiting researchers’ expenses.

In another version of the open lab concept, the Bill and Melinda Gates Foundation organized a TB Drug Accelerator program that brings together research teams from seven major companies (Abbott Laboratories, AstraZeneca, Bayer, Eli Lilly, GlaxoSmithKline, Merck and Sanofi) with scientists from four academic and government institutions. The companies have exchanged more than a thousand compounds and provided the academic and government scientists with access to millions.

These experiments show that even competing research teams can share knowledge, risk and reward in anti-infective drug development, test diverse approaches and avoid redundant efforts. (I’m involved in both of these projects.)

Philanthropic efforts have financed these open labs, but they can’t substitute for market forces. Nor can the current economic model give antibiotic development a permanent, prominent place in drug company portfolios.

There are, however, other ways for drug makers to profit beyond using monopoly to protect prices. As Thomas Pogge of Yale and Aidan Hollis of the University of Calgary have pointed out, an intergovernmental fund for drug discovery could reward drug makers for products in proportion to their impact in reducing the loss of healthy years of life. The lower the cost of a lifesaving drug, the greater the number of people who could use it; the more lives protected, then, the greater the monetary reward. An investment of $20 billion a year could encourage more open-lab collaborations to find new medicines in challenging settings like antibiotic discovery and make them accessible to all who need them.

If we don’t make new antibiotics, we will lose the ability to practice modern medicine. A new collaborative model for drug discovery can help make sure this doesn’t happen.


Carl F. Nathan is chairman of the department of microbiology and immunology at Weill Cornell Medical College.
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« Reply #70 on: March 10, 2013, 10:28:01 PM »

http://www.usatoday.com/story/news/nation/2013/03/05/superbugs-infections-hospitals/1965133/

I raise once again the possibility that a major factor to this long threatened appararently now imminent disaster is that massive use of antibiotics by the beef and poultry agro-industries , , ,
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« Reply #71 on: April 07, 2013, 10:44:07 AM »

I gather the avian bird flu thing is happening again in China  , , ,
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« Reply #72 on: April 09, 2013, 08:16:55 AM »

In China, a New Bird Flu Emerges
April 9, 2013 | 1045 GMT



Summary
 


The first three human cases of H7N9, a new strain of bird flu, were reported in eastern China at the end of March. The emergence of a new disease in China can bring back the fears associated with the 2003 outbreak of Severe Acute Respiratory Syndrome, or SARS. But there are key differences in this case, including the mode of infection and the governmental response. Any impact will be from preventative or reactive actions and not from the disease itself.
 


Analysis
 
China notified the World Health Organization on March 31 of three human cases of H7N9 in Shanghai and neighboring Anhui province. The two Shanghai cases resulted in deaths. As of April 8, 24 cases and 7 deaths have been reported in eastern Chinese provinces, and the disease has been detected in Jiangsu and Zhejiang provinces as well. New cases of H7N9 are likely to be identified frequently in the near term, since the region and the virus are under scrutiny.
 
While the disease is still new in humans, hundreds of people who have come into contact with the infected individuals are being monitored and there have been no confirmed infections.  This indicates strongly that H7N9 cannot be transmitted between humans, and the World Health Organization has said that there is no proof of human-to-human transmission. Although the possibility of an eventual mutation cannot be ruled out, the current lack of human-to-human transmission is an important difference between this flu strain and the SARS virus, which infected more than 8,000 people in 2003. The H7N9 virus is more similar to its H5N1 bird flu cousin, which also is not typically transmitted between humans.
 






.
 

Official Responses and Precautions
 
Another apparent difference between the first occurrence of SARS in China and the new H7N9 virus is the response from Beijing. With the SARS outbreak, several months lapsed between the first case (November 2002) and identification of the disease (March 2003), despite a cluster of 305 cases of an unknown respiratory illness in February 2003 in Guangdong. These delays, along with the fact that the disease could be passed between humans, enabled SARS to spread to Hong Kong and Vietnam. With H7N9, there was less than a month between infection and identification of the disease. 
 
Moreover, international health organizations, such as the World Health Organization, appear to be very involved and informed with this case. The Chinese government did not disclose information regarding the SARS virus as readily as it has with the H7N9 virus. The ready exchange of information aids in the prevention of pandemics. For instance, the World Health Organization Collaboration Center in China has determined that while there is no vaccine, H7N9 does appear to be susceptible to anti-viral treatment. Additionally, the Centers for Disease Control and Prevention has taken measures to prepare a vaccine if necessary, although making the vaccine would take at least six months. Even so, the ongoing openness and sharing of relevant information will be key to proper management of the disease. 
 
In the wake of announcements about H7N9, surrounding countries have begun to take preventive measures. Vietnam has banned poultry imports from China, although illicit trade is prevalent in the area. Japan is taking precautions at its airports, which are on heightened alert for people with flu-like symptoms coming from China.
 
Potential Economic Effects
 
The H7N9 virus has been detected in a pigeon in Shanghai, the first detection in an animal since a person contracted the virus. This detection has resulted in the culling of more than 20,000 birds in the Shanghai markets and closures of live poultry markets in Shanghai and Nanjing, Jiangsu province. More than 400 million birds were culled after the H5N1 version of bird flu was first detected in 2003. For China, a large producer of poultry, the birds culled since the H7N9 outbreak make up a relatively small portion of the industry; the country produces on average a little more than 300,000 metric tons of poultry a week. 
 
A key difference between H7N9 and H5N1 is that H7N9 does make the birds visibly sick. Infected birds could then act as carriers without outward symptoms. This could result in broader culling to prevent the spread of the disease between birds. Poultry is a large source of protein in China, and large-scale culling could lead to higher prices for consumers.
 
The H7N9 outbreak could have more economic effects if culling continues and escalates or if the movement of people changes because of either policy or fear, which could come from the spread of misinformation. International markets for corn and soy fell following news of the culling, since China's poultry industry is a large consumer of both products for poultry feed. Since the announcement of the discovery of the virus, stock prices for Chinese airlines have also fallen.
 
In studies of the overall economic impact of the SARS outbreak, models have shown that the short-term economic impact was 1 percent of gross domestic product for China and 2.6 percent of GDP for Hong Kong. This would amount to more than $16 billion in losses for China that would have been temporally and geographically acute, most likely affecting specific regions of the country. Overall, China's GDP still grew 10 percent in 2003, and Hong Kong saw growth of 3 percent that same year. Tourism was greatly affected, with travel to infected areas decreasing by more than 50 percent during the peak of the outbreak.
 
At this point, the overall economic impact of H7N9 appears to be minimal. As measures continue to be taken to prevent any potential pandemic, it is possible that certain sectors, such as tourism and the poultry sector, could see short-term losses. But barring a shift in the behavior of the new virus, the long-term macroeconomic impact is likely to be minimal.
.

Read more: In China, a New Bird Flu Emerges | Stratfor
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« Reply #73 on: April 15, 2013, 06:03:23 AM »

http://www.newyorker.com/online/blogs/elements/2013/04/the-green-death.html

From the article:

In 2005, Experiment Station researchers were unnerved to learn that a bacterial disease called citrus greening had arrived in Florida citrus groves. Citrus greening, also called huanglongbing or yellow dragon disease, is carried by an insect called the Asian citrus psyllid. It cannot, as yet, be cured; while infected trees may not show symptoms for months or years, they eventually begin to produce yellow foliage and misshapen, bitter fruit that drops prematurely to the ground. Researchers consider greening a mortal threat: it is so damaging to fruit crops that in 2003, the U.S. classified the bacteria that causes it as a bioterror tool.
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« Reply #74 on: April 26, 2013, 08:48:59 AM »

OPINION
April 25, 2013, 7:15 p.m. ET.
The Changing Bird Flu Threat
Why China and the U.S. may be better equipped today for a pandemic than a decade ago..
By TEVI TROY

The outbreak of avian flu in China has killed at least 22 people and infected more than 108—including a man in Taiwan who had traveled in the eastern Chinese city of Suzhou. For two months airline stocks have been buffeted and officials have raised concerns about a possible pandemic. So why does the American public seem so unconcerned?

There are some good and some bad reasons for the relatively blasé reaction. Most obvious is that the disease seems far away. In addition, talk of pandemics is often overblown. The 2009 swine flu was bad but nowhere near the disaster that some experts feared.

On the positive side, public health has made significant advances in dealing with flu. These suggest cause for optimism about this outbreak and possible future ones.

The first major improvement is in the cooperative posture of the Chinese government—a far cry from the unfortunate experience with the SARS virus a decade ago. Back then, Beijing kept outside organizations such as the World Health Organization in the dark about the outbreak, which ultimately infected 8,000 people and killed about 800.

SARS spread across the Pacific (to Canada) and cost the global economy as much as $50 billion. A quicker and more open Chinese response could have limited the outbreak.

This time, by contrast, China is sharing information with the World Health Organization, closely monitoring the disease and aggressively culling flocks of chickens that could be infected.

Not that we should all sing kumbaya. Shanghai, where this flu began, is a relatively open part of China, which may account for some of the government's new transparency. In addition, the current director-general of the World Health Organization is China's own Margaret Chan. Her successors may not be viewed as favorably by Beijing.

Another positive story has to do with vaccine development and production. Thanks in large part to a push for greater vaccine capacity during the Bush administration, the United States now has a more reliable annual supply of the regular flu vaccine. Researchers in the U.S. have also seen improvements in cell-based vaccine technology that can supplement and perhaps even supplant traditional egg-based vaccines—meaning that vaccine quantity wouldn't be limited by the supply of eggs and wouldn't risk harming people with food allergies.

Regarding this outbreak's particular strain (H7N9), Chinese authorities have shared the virus with international flu labs, and U.S. health officials are developing lab strains that would allow American manufacturers to produce large amounts of a vaccine if needed.

The U.S. Biomedical Advanced Research and Development Authority and Novartis NOVN.VX -0.58%have a partnership that enabled them to start creating a vaccine before H7N9 even left China, based on the posted genetic sequence. This virus is particularly concerning because the H7 strain is hard for vaccine makers to match (and this year's flu vaccine had a not atypical effectiveness rate of only 62%). Still, Americans are much better off than they were just a decade ago.

The third cause for optimism is that there have been no recorded cases of so-called sustained human-to-human transmissions, meaning the movement of the virus from a single infected person to more than one other person. That occurred with SARS but not in previous cases of avian flu. If it did, it would be the nightmare scenario for public-health officials.

We aren't out of the woods just yet. While China has been tracking severe cases, it is unknown whether any individuals are mildly affected—having few symptoms but still being contagious. A recent World Health Organization report revealed that 40% of those infected had no obvious interactions with poultry, but they must have been infected somehow. The source of those transmissions is unknown.

Because of the uncertainties about transmission, the difficulties in matching H7 strains, and concerns about asymptomatic transmitters, the H7N9 outbreak bears careful watching. But the global public-health system is far more capable of dealing with flu than it was 10 years ago. Here's hoping that the current outbreak doesn't spread and test the limits of this improved system.

Mr. Troy is a senior fellow at the Hudson Institute and a former deputy secretary of Health and Human Services
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« Reply #75 on: April 27, 2013, 12:48:00 PM »

Another health threat.

It is still contained but if it gets into community settings like MSRA has there will be big problems.  No antibiotics are consistently effective for this and the death rate is reported at 50%.  I've read the development of new antibiotics are several years away at least.   

http://www.cdc.gov/HAI/organisms/cre/
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« Reply #76 on: May 10, 2013, 07:46:53 AM »

The Next Contagion: Closer Than You Think
By MICHAEL T. OSTERHOLM
Published: May 9, 2013

THERE has been a flurry of recent attention over two novel infectious agents: the first, a strain of avian influenza virus (H7N9) in China that is causing severe respiratory disease and other serious health complications in people; the second, a coronavirus, first reported last year in the Middle East, that has brought a crop of new infections. While the number of human cases from these two pathogens has so far been limited, the death rates for each are notably high.

Alarmingly, we face a third, and far more widespread, ailment that has gotten little attention: call it “contagion exhaustion.” News reports on a seemingly unending string of frightening microbes — bird flu, flesh-eating strep, SARS, AIDS, Ebola, drug-resistant bugs in hospitals, the list goes on — have led some people to ho-hum the latest reports.

Some seem to think that public health officials pull a microbe “crisis du jour” out of their proverbial test tube when financing for infectious disease research and control programs appears to be drying up. They dismiss warnings about the latest bugs as “crying wolf.” This misimpression could be deadly.

It’s important to understand our relationship with the microbial world. Most microscopic organisms benefit humans, other organisms or the environment in some way — for example, they help us digest our food and keep bad bugs in check.

At the same time, we are never far away from one of the 1,400 kinds of disease-causing microbes that are capable of infecting people; many infect animals, too. Of these microbes, known as pathogens, about 500 can be transmitted from humans to other humans. And around 150 of them can cause epidemics — rapidly spreading outbreaks of serious, sometimes life-threatening, disease.

Each pathogen has its own “footprint” (or potential footprint) on our human health and social, political and economic landscapes. Far too often the public — and policy makers and journalists — confuse those infectious diseases that can be life-threatening for a limited number of individuals with those that can cause widespread damage to society as a whole.

A disease in the former category is “flesh-eating strep” (invasive group A streptococcal disease). Approximately 9,000 to 11,500 cases are recognized each year in the United States, and about 1,000 to 1,800 of these patients die. When outbreaks of this type occur in this country, particularly if they affect schools or day-care centers, they generate front-page news and widespread concern.

Conversely, last year worldwide 1.7 million of the 34 million people infected with H.I.V. died from AIDS. There was little front-page news coverage about these cases. Nor was there much coverage last year of the estimated 1.5 million tuberculosis-related deaths, of the 1.1 million young children who died of infectious diarrheal illness, or of the 825,000 deaths from malaria. Infectious diseases like these plague the world but, because they don’t occur in our backyard, they remain relatively invisible to Americans.

In the case of the two latest threats — the H7N9 influenza virus and the new coronavirus — the number of infected people is small, and the infections are occurring thousands of miles away from the United States. Yet we should be seriously concerned about both.

Diseases like H7N9 influenza and the new coronavirus are different from noninfectious causes of serious illness and death — and even most microbial causes of disease. They can kill large numbers of people quickly and simultaneously around the world. The 1918 flu pandemic killed an estimated 50 million people worldwide in less than 18 months. The 2003 SARS pandemic, while more limited, resulted in more than 8,275 cases and 775 deaths.

Why does this suddenly happen? Both animal influenza and coronaviruses normally infect animals, not humans. But when these viruses undergo very specific genetic changes that occur as a result of everyday microbial evolution, we have a whole new ballgame; one that is largely played by their rules and on their schedule. Now a virus that once could infect only animals and maybe very rarely infect humans is readily transmitted by people to other people. You could get infected just by breathing shared air with the airplane passenger next to you, or by standing next to the wrong person in an elevator or even by lying next to your sleeping mate. We call this respiratory transmission.

Consider how quickly the H1N1 influenza virus spread in 2009: within the first month of that pandemic, the virus had infected people in at least 42 countries. The only thing keeping these viruses from becoming pandemic killers is their genetics. With few exceptions, all the current human H7N9 and coronavirus cases represent sporadic animal-to-human transmission. But if these viruses continue to spread in their respective animal reservoirs, repeated transmissions of the viruses to humans may lead to the genetic changes that will make either virus readily transmitted by humans to humans. Add in the fact that humans have little to no natural immunity to these viruses, and we could have the next pandemic.

Our public health tools to fight these viruses are limited. We have no vaccines or effective drugs readily available to stop or treat the new coronavirus in the Middle East. And while we have influenza vaccines, my colleagues and I have detailed in an article this week in the Journal of the American Medical Association why we most likely will have limited global impact on an H7N9 pandemic with our current outdated influenza vaccine technology.

In short, we won’t be saved by vaccines if a pandemic emerges from these two new threats. At best, in the case of H7N9, we can only hope that vaccines can help somewhat.

The toll is economic, not just human. Studies have shown that a severe global pandemic, caused by viruses like influenza or coronavirus, could bring the global economy, which is ever reliant on global communications and transportation networks, to its knees. When people are too sick or too afraid to work, borders are closed and global supply chains break, and trade falls. Over months, the economic costs could send the world into recession.

Are either H7N9 or coronavirus pandemics inevitable? We don’t know. But each time one of these viruses infects a human or even another mammal, it’s one more throw at the genetic roulette table.

To reduce the odds of a pandemic, China and the Middle Eastern countries where these viruses are now circulating in animals must do everything they can to identify the animal sources and use every tool they have to eliminate the spreading of the disease. To cull millions of apparently healthy chickens or other domestic animals is not easy, but it is essential.

The world as whole must invest in a new generation of effective influenza and coronavirus vaccines. They are the ultimate insurance policy against similar future emerging viruses. These viruses may seem far away, but tomorrow they could be at America’s doorstep.

Michael T. Osterholm, an epidemiologist, is a professor of environmental health sciences in the School of Public Health, and the director of the Center for Infectious Disease Research and Policy, at the University of Minnesota. .
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« Reply #77 on: May 16, 2013, 10:49:08 PM »

As Hepatitis C Spreads, Scotland Steps In
By JEANNE WHALEN

DUNDEE, Scotland—Sam Nicoll, an unemployed laborer with a history of heroin use in this down-and-out city, has recently been released from prison. He's just become a father. And on a recent morning, he ran out of injection needles.
[image]

But a nurse here, Brian Stephens, wants the 24-year-old to focus on a different problem: hepatitis C.

Mr. Nicoll recently took a blood test for the virus at a local needle exchange, and it came back positive. In most parts of the world, he wouldn't be diagnosed or considered for treatment. Few countries conduct widespread testing of injection drug users or offer them medication for hepatitis C, in part because they are considered too unreliable to turn up for appointments or to stick to the costly, monthslong treatment regimen.



Scotland, however, is ignoring conventional wisdom and making a bold push to control a virus that may be one of the biggest ticking time bombs in medicine. Hepatitis C kills about 350,000 people a year globally, and in many Western countries it infects far more people than HIV. The disease can lead to cirrhosis or cancer of the liver and is the leading cause of liver transplants in many countries.

Yet because the virus often strikes injection drug users, the homeless and other hard-up populations, efforts to tackle the problem have lagged behind, health experts say. While hepatitis C now kills more Americans each year than HIV does, the U.S. Centers for Disease Control and Prevention spends only about $30 million a year on prevention of viral hepatitis, compared with almost $800 million for HIV.

For its part, Scotland, with a population of only five million, has launched a £100 million (about $150 million) program, running from 2008 to 2015, to diagnose and treat hepatitis C, regardless of the patient's history. Medication alone can cost anywhere from $10,000 to $40,000 per patient.

Because Scotland was hit with a wave of hepatitis C in the 1980s and it can take 20 years or more for infections to seriously damage the liver, the country is "just at the moment beginning to see this increase in end-stage liver disease," says David Goldberg, head of Health Protection Scotland's hepatitis C and HIV programs and professor of public health at University of Glasgow. "That clearly is going to have a major impact on demand for liver transplants over the next decade."
[image]

The country's taxpayer-funded health system is scrambling to find and treat infections in all hepatitis-prone communities, including Pakistani immigrants and people who received blood transfusions before the virus was discovered in 1989. But it is mostly focusing on current and former injection drug users, who account for about 90% of infections here.

Cities such as Dundee and Edinburgh—setting of the heroin-drenched 1996 film "Trainspotting"—have been particularly hard hit by injection drug use since an economic downturn in the 1980s. Within the European Union, Scotland has one of the highest reported prevalence levels of injection drug use, according to the European Monitoring Centre for Drugs and Drug Addiction.

Early results of the Scottish program are promising. About half of the 38,000 Scots estimated to have been chronically infected have now been diagnosed, compared with 39% in 2007. Of those, about 1,100 new patients a year are receiving treatment, nearly triple the number from 2007. Dr. Goldberg says the aim is to reach 2,000 new patients a year, which should help prevent up to 5,200 cases of cirrhosis by 2030.

Tackling hepatitis C is a difficult assignment. It typically is spread when an infected person's blood enters another person's body, as often happens when drug users share needles. According to the U.K.'s National Health Service, the virus can also be found in some other body fluids, including saliva and semen, but this is far less common, making sexual transmission more rare than it is with HIV.

Because symptoms often don't surface until decades after infection, many people don't know they are infected.

To find infections in current drug users, Scotland is blanketing needle exchanges with simple finger-prick diagnostic kits. After identifying people with infections, many parts of Scotland try to start weaning them off heroin before offering hepatitis C medication. The typical approach is to prescribe methadone, a synthetic opiate that can help reduce heroin cravings, and wait for the patient to gain some stability, says John Dillon, a doctor in Dundee who helps run the hepatitis C program, which is staffed with about 85 doctors and nurses.

But Dundee and other regions have started treating drug users without necessarily trying to stabilize them on methadone first. They are motivated by research from University of Bristol, London School of Hygiene and Tropical Medicine and other institutions suggesting that if just 20 out of 1,000 active injection drug users are treated each year, it could stop them infecting others and reduce the rate of hepatitis C prevalence by nearly 30% in 10 years.

Doing that requires a ton of support, says Mr. Stephens, 41, the nurse at the hepatitis C program in Dundee. But for many, it may be years before they are ready to quit their drug habit, he says. "And how many people will they have infected in that time?"

Much of the program involves sending nurses like him out into the field. A 16-year veteran in nursing, he is known for going to extremes to stay in touch with patients, sometimes phoning them many times to remind them to turn up for appointments. He gives them his cellphone number, answers their calls on weekends, helps them inject the weekly interferon shots they need to kill the virus and sometimes spends hours at needle exchanges and methadone clinics waiting in vain for them to appear.

On a recent morning, Mr. Stephens met with Mr. Nicoll, who had come to a needle exchange program for a new set of syringes. Mr. Stephens invited him into a private room to discuss the results of the blood test he had taken at the exchange about seven months previously, which indicated that he probably had the hepatitis C virus. Mr. Nicoll had missed several appointments to return for a second test needed to confirm the infection. "I've been quite scared to come back," he acknowledged.

Mr. Stephens seized the moment and drew the blood on the spot, explaining what treatment would involve. Clutching a small bag of syringes, Mr. Nicoll mentioned that his life was about to get more hectic: "I've got a baby daughter coming. She's due soon."

About two weeks before meeting Mr. Stephens, Mr. Nicoll had started taking methadone in an effort to tame his drug habit. But like many methadone recipients—particularly in the early stages of treatment—he was continuing to use heroin. Mr. Stephens said that wouldn't disqualify him from hepatitis C treatment. "If someone is continuing to use heroin and they continue to come to appointments, we don't really care. We'll go ahead and treat them anyway," he said. (In a subsequent interview, Mr. Nicoll said he had stopping using heroin, which Mr. Stephens said was confirmed in a urine test. The two are awaiting more blood test results before deciding on the next step in his hepatitis treatment.)

Mr. Stephens said he wound up specializing in hepatitis C after a London surgeon once told him: "Whatever you do, get into hepatitis, because it's going to be huge." The work takes its own form of patience: At a nearby methadone clinic that afternoon, Mr. Stephens met with George Nelson, a 44-year-old addict who was successfully cured of hepatitis C a few years ago, only to find recently that he had reinfected himself through risky drug use.

"I remember getting cleared last time and saying, 'I'll never do that again,'" Mr. Nelson told Mr. Stephens. "For 14 months I was clean. Then I put myself at risk again."

Many countries don't treat active drug users or patients taking methadone because of this risk: they fear the money and effort will be wasted if the person continues using illicit drugs and gets reinfected. "There's been an argument, if you have constrained resources, who would you treat first? Obviously not drug users. But actually there's an argument that you should treat them first," says Charles Gore, president of the World Hepatitis Alliance in London. In Scotland and many places, injection drug use is by far the biggest source of the virus's transmission. Stopping that transmission is "a way to turn off the tap, and then we can empty the pool," Mr. Gore says.

In a recent study, University of Dundee analyzed treatment results for 291 patients in the region, comparing outcomes for people who had never injected drugs to those of active and former users. They found that 61% of noninjection-drug-users achieved a sustained virological response, or SVR, the clinical term for a cure. About 55% of former users and 47% of active users obtained an SVR, the study showed. The authors concluded that active injection drug use "is not a barrier to treatment or a successful achievement of SVR."

In the U.S., few doctors offer hepatitis C treatment to people taking drugs or methadone, says Michael Ninburg, executive director of the Hepatitis Education Project in Seattle. There are also few needle exchanges or methadone clinics in many communities, and even those that do exist don't typically test people for hepatitis C. John Ward, director of the CDC's viral hepatitis division, says the disease is simply "underrecognized, undermanaged and undertreated."

Still, the Scottish approach is being tried in a few places.

Diana Sylvestre, an assistant clinical professor of medicine at University of California, San Francisco, runs a nonprofit clinic in Oakland that treats many people with drug addictions. When she started the clinic 15 years ago, "it became apparent hepatitis C was a huge problem," she says. She started out treating people who had achieved some stability in their lives while taking methadone, later branching out to addicts in more of a "state of disarray," she says. The clinic conducts blood tests and doles out medicine at weekly meetings that also include lunch and hepatitis C education sessions.

"We find that some people you would never predict are able to organize themselves around this schedule," she says, adding that "virtually 100%" of patients who start treatment complete it, and that 80% to 85% are cured.

The lack of medical insurance among many U.S. drug users makes it hard to tackle the hepatitis C problem in a comprehensive way, says Brian Edlin, an associate professor at Weill Cornell Medical College in New York who treats injection drug users for hepatitis C.

Indeed, in a recent study he led to evaluate hepatitis C treatment in active drug users, some of the patients didn't have health insurance, Dr. Edlin says. He provided free care to everyone in the study and helped eligible patients get enrolled in Medicaid to cover the cost of medication. For those who weren't eligible, he obtained free drugs from manufacturers. He also offered mental-health and substance-abuse treatment to anyone who wanted it. Overall, 72% of the patients were cured of hepatitis C, a result he called "very successful." Next he is aiming to recruit up to 200 injection drug users for a larger trial that will more rigorously test the benefits of treatment.

"Doctors raise legitimate uncertainties about treating this population that need to be addressed through research," Dr. Edlin said.

In Dundee, Mr. Stephens and his colleagues are also attempting to enroll injection drug users in a similar study. To encourage them to sign up, they are offering participants a regular supply of high-protein drinks and vouchers to buy food at supermarkets. That is an incentive because "heroin users don't eat very well," Mr. Stephens says. "They spend most of their money on drugs."

Still, recruitment so far has been tough. One young woman he was hoping to enroll didn't turn up for a meeting at the needle exchange. Later, he learned she was due in court on charges she had assaulted a shopkeeper after she had been caught stealing. He ultimately tracked her down and enrolled her in the study. If she goes to prison, he says, "we'll continue her treatment" there.

Meanwhile, Mr. Stephens says he has seen anecdotal evidence that current and recent heroin users can make it through treatment. One patient recently cured, 35-year-old Leanne Petrie, took heroin for 16 years before quitting in late 2011. In an interview, she said she tested positive for hepatitis C around the age of 25 but didn't seek treatment for years.

In 2010, while living in the Scottish county of Fife, she was taking methadone to try to withdraw from heroin, and attending hepatitis C support meetings to learn about treatment. But because she was drinking heavily, her substance-abuse counselor cut off her methadone, which she says prompted her to drink more—about a bottle of vodka a day. She was also still dabbling in heroin.

In 2011, she says she got involved with a violent man who also took heroin. In December 2011, he burned her hand with a cigarette and wrecked her apartment, she says. A few days later, she took an overdose of sleeping pills. "I felt I couldn't get out," she says.

She woke up in the hospital, and, at the encouragement of her family, decided to move to Dundee to say with her cousin. She stopped drinking and taking heroin, and in January 2012, sought treatment for hepatitis C. In the middle of her treatment, she had to leave her cousin's house and stay in a homeless shelter for three months, but she eventually got an apartment from social services. She completed her treatment in November.

Seeing progress with her hepatitis C treatment helped her cope with the instability in her life and stay off drugs, she says. "Since I moved to Dundee I've achieved a lot," she says. "When you see the treatment is working, it helps you keep going."
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« Reply #78 on: May 28, 2013, 10:15:31 PM »

http://edition.cnn.com/2013/05/28/health/france-coronavirus-death/index.html?sr=fb052813francecoronvirus730p
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« Reply #79 on: July 05, 2013, 10:26:46 AM »




BAKERSFIELD, Calif. — In 36 years with the Los Angeles police, Sgt. Irwin Klorman faced many dangerous situations, including one routine call that ended with Uzi fire and a bullet-riddled body sprawled on the living room floor.


But his most life-threatening encounter has been with coccidioidomycosis, or valley fever, for which he is being treated here. Coccidioidomycosis, known as “cocci,” is an insidious airborne fungal disease in which microscopic spores in the soil take flight on the wind or even a mild breeze to lodge in the moist habitat of the lungs and, in the most extreme instances, spread to the bones, the skin, the eyes or, in Mr. Klorman’s case, the brain.

The infection, which the Centers for Disease Control and Prevention has labeled “a silent epidemic,” is striking more people each year, with more than 20,000 reported cases annually throughout the Southwest, especially in California and Arizona. Although most people exposed to the fungus do not fall ill, about 160 die from it each year, with thousands more facing years of disability and surgery. About 9 percent of those infected will contract pneumonia and 1 percent will experience serious complications beyond the lungs.

The disease is named for the San Joaquin Valley, a cocci hot spot, where the same soil that produces the state’s agricultural bounty can turn traitorous. The “silent epidemic” became less silent last week when a federal judge ordered the state to transfer about 2,600 vulnerable inmates — including some with H.I.V. — out of two of the valley’s eight state prisons, about 90 miles north of here. In 2011, those prisons, Avenal and Pleasant Valley, produced 535 of the 640 reported inmate cocci cases, and throughout the system, yearly costs for hospitalization for cocci exceed $23 million.

The transfer, affecting about a third of the two prisons’ combined population, is to be completed in 90 days, a challenge to a prison system already contending with a federal mandate to reduce overcrowding. Jose Antonio Diaz, 44, who has diabetes and was recently relocated to Avenal, is feeling “very scared of catching it,” said his wife, Suzanne Moreno.

Advocates for prisoners have criticized state agencies for not moving the inmates sooner. “If this were a factory, a public university or a hotel — anything except a prison — they would shut these two places down,” said Donald Specter, the executive director of the Prison Law Office, which provides free legal assistance to inmates.

The pending transfer has underscored the complexities and mysteries of a disease that continues to baffle physicians and scientists. In Arizona, a study from the Department of Health Services showed a 25 percent risk of African-Americans with newly diagnosed valley fever developing complications, compared with 6 percent of whites.

“The working hypothesis has to do with genetic susceptibility, probably the interrelationships of genes involved in the immune system,” said Dr. John N. Galgiani, a professor at the University of Arizona and the director of the Valley Fever Center for Excellence, founded in 1996. “But which ones? We’re clueless.”

Kandis Watson, whose son Kaden, 8, almost died, had a gut feeling that “something was not right,” she said, when Kaden began feeling sick two years ago. The pediatrician prescribed antibiotics, but Kaden’s health deteriorated, with a golf ball-size mass developing at the base of his neck. The infection enveloped Kaden’s chest, narrowing his trachea.

Kaden was essentially breathing through an opening the size of a straw, said Dr. James M. McCarty, the medical director of pediatric infectious diseases at Children’s Hospital Central California in Madera, where Kaden spent six months. Today the boy is back to his mischievous self, surreptitiously placing a green plastic lizard in his mother’s hair.

But how he contracted valley fever is still guesswork. “I think he got it being a boy, digging in the dirt,” Mrs. Watson said.

Kern County, where Bakersfield is located, had more than 1,800 reported cases last year. At Kern Medical Center, Dr. Royce H. Johnson and his colleagues have a roster of nearly 2,000 patients. Many, like Mr. Klorman, have life-threatening cocci meningitis.

“I got a bad break,” said Mr. Klorman, who is known as Joe. Until illness forced his retirement, he preferred a squad car to a desk job. Now he travels four hours round trip three times a week so Dr. Johnson can inject a powerful antifungal drug into his spinal fluid. In other patients, the disease has been known to eat away ribs and vertebrae.

“It destroys lives,” said Dr. Johnson, whose daughter contracted a mild form. “Divorces, lost jobs and bankruptcy are incredibly common, not to mention psychological dislocation.”

Once athletic, Deandre Zillendor, 38, dropped to 145 pounds from 220 in two weeks, and lesions erupted on his face and body. “You keep it forever, like luggage,” he said of the disease.

================================

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Todd Schaefer, 48, who produces award-winning pinot noirs in Paso Robles, was told by his doctors that he had 10 years to live. That was 10 years ago. But valley fever has disseminated into his spinal column and brain, and his conversation is interrupted by grimaces of pain. Ruggedly handsome, he still outwardly resembles the archetype of the California good life. But Mr. Schaefer has had a stroke, a hole in his lung, two serious heart episodes and relapses that “put me on the edge of life,” he said.



Mr. Schaefer, 48, has had serious heart problems, and can no longer drink the wine he and his wife, Tammy, produce.


He believes he got infected with valley fever atop a tractor during the construction of Pacific Coast Vineyards, which he runs with his wife, Tammy. One doctor initially suggested bed rest, chicken soup and cranberry juice.

Today Mr. Schaefer can no longer can drink wine, and he begins every morning retching. “I told her to leave me,” he said at one low point, of his wife, who is 37. “She’s too young, too beautiful.”

Dr. Benjamin Park, a medical officer with the C.D.C., said that the numbers of cases are “under-estimates” because some states do not require public reporting. They include Texas, where valley fever is endemic along the Rio Grande. In New Mexico, a 2010 survey of doctors and clinics by the state’s public health department revealed that 69 percent of clinicians did not consider it in patients with respiratory problems.

Numbers spike when rainfall is followed by dry spells. Many scientists believe that the uptick in infections is related to changing climate patterns. Kenneth K. Komatsu, the state epidemiologist for Arizona, where 13,000 cases were reported last year, said that another factor may be urban sprawl: “digging up rural areas where valley fever is growing in the soil,” he said.

In Avenal, citizens have become activists, looking into possible environmental factors, including a regional landfill that accepts construction waste. Three of the four children of James McGee, a teacher, have contracted the disease, including Marivi, 17, who was found convulsing in the ladies’ room at school. Dr. McCarty of Children’s Hospital is seeing an increasing number of children from Avenal.

Valley fever was a familiar presence during the Dust Bowl, and in Japanese internment camps throughout the arid West. Yet there is still no cure, and research on a fungicide and a potential vaccine have been stalled by financing issues. One company, Nielsen Biosciences Inc., has developed a skin test to identify cocci but has not yet been able to make it financially viable.

Part of the difficulty is that cocci is “a hundred different diseases,” Dr. Johnson said, depending on where in the body it nests. His patients include farm workers, oil field workers and construction workers.

One of his patients, Barbara Ludy, 61, had a job that involved taking care of a man who is quadriplegic. She was strong enough to lift his 175-pound frame, plus his wheelchair, into a van. Cocci meningitis affected her ability to think, to remember, to walk, to live independently. When her weight dropped to 71 pounds, her distraught daughters went to Goodwill to buy their mother size zero clothes.

One daughter, Jennifer Gillet, now takes care of her mother full time. Ms. Ludy is recuperating, slowly. And things are looking up: She is now a size 10.
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Crafty_Dog
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« Reply #80 on: July 17, 2013, 07:53:43 PM »

I have no idea of the reliability of this site:

http://www.realfarmacy.com/cdc-admits-98-million-americans-received-polio-vaccine-contaminated-with-cancer-virus/#VgfMOhOPiMr3RBqP.01
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« Reply #81 on: July 18, 2013, 08:24:20 PM »



http://www.reagancoalition.com/articles/2013/20130718005-distract-obama-eo.html
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« Reply #82 on: July 20, 2013, 12:35:19 PM »

Fifteen Years After Autism Panic, a Plague of Measles Erupts
Legions spurned a long-proven vaccine, putting a generation at risk
By JEANNE WHALEN and BETSY MCKAY
   
PORT TALBOT, Wales—When the telltale rash appeared behind Aleshia Jenkins's ears, her grandmother knew exactly what caused it: a decision she'd made 15 years earlier.

Ms. Jenkins was an infant in 1998, when this region of southwest Wales was a hotbed of resistance to a vaccine for measles, mumps and rubella. Many here refused the vaccine for their children after a British doctor, Andrew Wakefield, suggested it might cause autism and a local newspaper heavily covered the fears. Resistance continued even after the autism link was disproved.

The bill has now come due.

A measles outbreak infected 1,219 people in southwest Wales between November 2012 and early July, compared with 105 cases in all of Wales in 2011.

One of the infected was Ms. Jenkins, whose grandmother, her guardian, hadn't vaccinated her as a young child. "I was afraid of the autism," says the grandmother, Margaret Mugford, 63 years old. "It was in all the papers and on TV."
More

    Brooklyn Measles Outbreak Shows Risks

The outbreak presents a cautionary tale about the limits of disease control. Wales is a modern society with access to modern medical care and scientific thought. Yet legions spurned a long-proven vaccine, putting a generation at risk even after scientists debunked Dr. Wakefield's autism research.

The outbreak matters to the rest of the world because measles can quickly cross oceans, setting back progress elsewhere in stopping it. By 2000, the U.S. had effectively eliminated new home-grown cases of measles, though small outbreaks persist as travelers bring the virus into the country. New York City health officials this spring traced a Brooklyn outbreak to someone they believe was infected in London.

Measles outbreaks are a "canary in the coal mine," says James Goodson, the lead measles expert at the U.S. Centers for Disease Control and Prevention. People who refuse one vaccine may be spurning others, setting communities up for outbreaks of other dangerous diseases that are slower to propagate, he says, such as diphtheria and whooping cough.

"Despite the fact that it's one of the greatest health measures ever invented by man or woman, there seems to still be a small residue of humanity that objects to the very idea of immunization," says Dai Lloyd, a doctor in Wales who treated many of the recent measles cases. "If you go around the cemetery you can see the historical evidence of childhood slaughter from pre-immunization days."

Measles is a respiratory condition causing fever, cough and rash. Most people who catch it recover fully. But measles can lead to deafness and pneumonia, and, in about one in 1,000 cases, death. It is one of the most contagious diseases, spread by coughing and sneezing.

It is also among the most preventable, with an effective inoculation since the 1960s that is now commonly given with mumps and rubella vaccines in a combined "MMR" vaccine. The U.K., as did the U.S., categorized measles as "eliminated" over a decade ago, meaning it was no longer circulating from within its borders.

Child deaths from measles world-wide fell 71% to 158,000 in 2011 from 2000, says the Measles & Rubella Initiative, a partnership of global-health groups.

Most measles occurs in developing countries. But it is resurging in some of the very countries that have led global campaigns against it. France was close to eliminating it in 2007 before an outbreak infected more than 20,000 people between 2008 and 2011. Philosophical opposition to vaccines helped cause the outbreak, says the European Centre for Disease Prevention and Control.

The 117 U.S. cases reported so far this year are up from 54 in all of 2012 and could put the U.S. on track to match the 220 logged in 2011, the highest since 1996. England reported 1,168 cases in 2013 through May, up 64% from the year-earlier period and the highest recorded level since 1994.

"It's very galling we had measles eliminated and now we've got it again" in the U.K., says Paul Cosford, medical director of Public Health England, the government public-health agency.

The autism scare behind the Wales outbreaks tracks to the era of Dr. Wakefield, then a researcher at London's Royal Free Hospital, whose suggestion of a vaccine-autism link began to get press in 1997.

A paper Dr. Wakefield published in 1998 in the Lancet, a medical journal, described 12 "previously normal" children who developed gastrointestinal problems and developmental disorders including autism. His paper concluded that "in most cases, onset of symptoms was after measles, mumps, and rubella immunization. Further investigations are needed to examine this syndrome and its possible relation to this vaccine."

Medical experts immediately warned parents that they considered the research incomplete and speculative, and said there was no evidence of a link. Among other studies debunking his research, a 2004 review of epidemiological studies by the U.S. Institute of Medicine found no evidence MMR caused autism.



The Lancet retracted Dr. Wakefield's paper in 2010 after the U.K.'s General Medical Council concluded that his work was "irresponsible and dishonest." The council that year stripped him of his medical license, saying in a report that he had engaged in "serious professional misconduct."

Dr. Wakefield says he questioned MMR's safety but strongly urged parents to continue with a measles-only vaccine. "MMR doesn't protect against measles," he says. "Measles vaccine protects against measles." He says he stands by his work despite contrary conclusions by other scientists. He didn't respond to subsequent requests for comment on his license revocation.

His report helped spark backlash against MMR, especially in English-speaking countries, say health officials in the U.S., U.K., Australia and other countries. An estimated 2.1% of U.S. children who received other routine vaccines weren't immunized with MMR in 2000, up from 0.77% in 1995, according to a 2008 study published in Pediatrics that concluded the change was "associated with" Dr. Wakefield's study.

Dr. Wakefield says he rejects the idea that his research helped cause measles outbreaks, because he told parents to keep vaccinating with measles-only vaccine.

U.S. critics, including some who questioned vaccines in general, continued to campaign against the vaccine. Among them, former Playboy model and actress Jenny McCarthy, who has been named a co-host of ABC's "The View," became a leader of the anti-vaccine movement in the U.S. several years ago when in televised interviews she linked her son's autism to vaccinations. A publicist for Ms. McCarthy, who wrote the forward to a 2010 book by Dr. Wakefield, didn't respond to requests for comment.

Dr. Wakefield's work especially reverberated in the U.K. MMR vaccination rates among 2-year-olds in England fell to 80% in the 2004 fiscal year from about 92% in 1997.

But nowhere did the toxic mix of dubious science, sensational headlines and parental fear take a bigger toll than in southwest Wales. As Dr. Wakefield's concerns gathered steam in Britain's national media in 1997, a Port Talbot mother, Jackie Eckton, phoned the South Wales Evening Post to ask whether other parents had experienced problems with MMR.

In one 1997 article, Ms. Eckton told the Post the vaccine turned her 3-year-old, Daniel, who had been diagnosed with autism, into a "distant and silent recluse." She told the paper she wanted to form "some sort of action group so people can help each other fight this thing and what it does."

The Post instructed parents wanting to join her campaign to phone its news desk.

Within days, parents of 20 other children formed a group led by Ms. Eckton, and demanded an investigation into whether the shots—"jabs" in the U.K.—were faulty. The Post ran a headline: "Jab Mums Fear a Rogue Batch."
[image]

The health department told parents there was nothing wrong with the vaccine. The U.K.'s state-run health system encourages parents to vaccinate children but, unlike the U.S. system, doesn't require vaccinations for school enrollment.

Ms. Eckton's group grew, and stories about other children followed, with headlines like "Mum fears twins may be jab victims." After Dr. Wakefield's paper was published in February, 1998, the Post stepped up its coverage, with dozens of stories about worried parents.

Health experts in Wales say the Post's coverage was probably the main reason vaccination rates fell further here than elsewhere. By the third quarter of 1998, uptake of the vaccine in 2-year-olds fell by 14% in the newspaper's distribution area, compared with a 2.4% drop in the rest of Wales, according to a report in the Journal of Epidemiology & Community Health.

Doctors urged parents to vaccinate anyway, says Charlotte Jones, a general practitioner in Swansea, Wales. "We'd chase them up by letter, by telephone," she says, but many "weren't having it."

Ms. Jenkins's grandmother, Ms. Mugford, wasn't having it. "I got frightened—what if she ends up with autism? And I just let it go," she says of her decision not to vaccinate.

The backlash lingered for years. Hannah Williams, a 31-year-old mother of two boys, ages five and six, says she skipped their MMR vaccinations over autism fears. Her nephew had been vaccinated and developed autism, she says, so she and her husband "decided we weren't willing to take the risk."

Their pediatrician badgered them to vaccinate, she says, but "we'd just say no."

    “A Welsh mother urged a local paper to report vaccine fears after her son became a 'distant and silent recluse.”

It can take years for an outbreak to follow dropping vaccination rates. Doctors in Wales reported from 104 to 223 cases a year from 1999 to 2008. Reported cases rose to 567 in 2009 and fell to 117 in 2010.

Then, in November 2012, doctors started seeing a marked increase. There were dozens of new cases a week, and authorities declared an outbreak.

The outbreak especially hit children 10 to 18 years old who went unvaccinated during the autism scare.

About 10% of infected children in the outbreak area were admitted to the hospital, with complications including severe dehydration and pneumonia, says Sara Hayes, a director of public health in the outbreak area. Most of the infected have recovered. A 25-year-old man died of pneumonia related to the measles, according to Public Health Wales.

Ms. Jenkins in April joined thousands of other children who lined up for belated vaccinations. It was too late: She found the rash soon thereafter, she says. Ms. Jenkins, now 16, says her measles got so bad she had to visit the hospital. She recovered, as have most others.

"It took her getting measles for me to realize how dangerous it was," her grandmother says.

Dr. Wakefield rejects the idea that he helped cause the Welsh outbreak. The government's decision not to offer a measles-only vaccine, he says, "lays the blame fairly on their shoulders."

Measles-only vaccines weren't approved in Britain at the time, says Brendan Mason, an epidemiologist with Public Health Wales. Global health officials have long viewed single-disease vaccines as inferior to combination shots because they increase the likelihood children will miss some doses.

Dr. Wakefield in 2005 moved to Austin, Texas, where he helped found an autism research-and-treatment center. He resigned from the center in 2010 after the U.K. revoked his medical license and says he is now helping run an Austin-based video-production company.

Efforts to reach George Edwards, who edited the Post during the autism scare, were unsuccessful. In April, the BBC quoted him as saying that "at no time did the newspaper ever say to parents 'do not let your children have this jab.'"

The Post's current editor, Jonathan Roberts, wrote in an April editorial: "It is clear that there were genuine concerns in the mid-1990s about MMR and the Post gave them full and responsible coverage." Mr. Roberts says he doesn't have anything to add to his editorial.

Wales declared the outbreak over on July 3. But there may be other ripples from the late-1990s scare. U.K. health officials say the drop in MMR vaccination has contributed to a spike in mumps in the U.K. in recent years.

Public Health Wales warned in recent weeks that many people remain unvaccinated with MMR and leave Wales vulnerable to future outbreaks of measles and mumps.

And resistance persists: Even some Welsh parents who belatedly inoculated remain suspicious of MMR.

Ms. Williams, who had skipped her sons' vaccinations, took her boys to an emergency vaccination clinic during the outbreak. She says she isn't as worried about autism now that her children are older but still isn't convinced of MMR's safety.

Ms. Eckton, who started the parents' group, says she still believes MMR damaged her son, now 18, who she says is severely autistic.

"I'm only a parent who watched what happened to my son," says Ms. Eckton, 46. "When you feel guilt for that, that's quite hard."
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« Reply #83 on: July 20, 2013, 08:10:56 PM »


Some of the anti-vaccine hype in our culture is over-zealous (or misleading) on facts.  Polio vaccine succeeded on eliminating a horrible disease.  The alleged contamination of the virus occurred before the virus was discovered. From the link, the majority of the studies determined that virus did not cause cancer.  All of the current evidence indicates that polio vaccines have been free of SV40 since 1963.

It's good to do your homework ... and to always be skeptical of government, but - on this one - they did not show a reason to decline a vaccination, as one might think is implied by those sending this out.
« Last Edit: July 20, 2013, 08:15:35 PM by DougMacG » Logged
Crafty_Dog
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« Reply #84 on: July 30, 2013, 10:40:49 AM »

I made this point a few years ago here:

http://www.nytimes.com/2013/07/30/health/tracing-germs-through-the-aisles.html?nl=todaysheadlines&emc=edit_th_20130730

There is a vid-clip as part of the article.  Text follows here:
======================================================

 Twice a month for a year, Lance Price, a microbiologist at George Washington University, sent his researchers out to buy every brand of chicken, turkey and pork on sale in each of the major grocery stores in Flagstaff, Ariz. As scientists pushed carts heaped with meat through the aisles, curious shoppers sometimes asked if they were on the Atkins diet.



Lance Price, a microbiologist, is using genetic sequencing to try to match bacteria found in grocery meat to urinary infections in a study in Arizona.

In fact, Professor Price and his team are trying to answer worrisome questions about the spread of antibiotic-resistant germs to people from animals raised on industrial farms. Specifically, they are trying to figure out how many people in one American city are getting urinary infections from meat from the grocery store.

Professor Price describes himself as something of a hoarder. His own freezer is packed with a hodgepodge of samples swabbed from people’s sinuses and inner ears, and even water from a hookah pipe. But the thousands of containers of broth from the meat collected in Flagstaff, where his nonprofit research institute is based, are all neatly packed into freezers there, marked with bar codes to identify them.

He is now using the power of genetic sequencing in an ambitious attempt to precisely match germs in the meat with those in women with urinary infections. One recent day, he was down on his hands and knees in his university office in Washington, studying a family tree of germs from some of the meat samples, a printout of more than 25 pages that unfurled like a roll of paper towels. Its lines and numbers offered early clues to Professor Price’s central question: How many women in Flagstaff get urinary infections from grocery store meat? He expects preliminary answers this fall.

Researchers have been warning for years that antibiotics — miracle drugs that changed the course of human health in the 20th century — are losing their power. Some warn that if the trend isn’t halted, there could be a return to the time before antibiotics when people died from ordinary infections and children did not survive strep throat. Currently, drug resistant bacteria cause about 100,000 deaths a year, but mostly among patients with weakened immune systems, children and the elderly.

There is broad consensus that overuse of antibiotics has caused growing resistance to the medicines. Many scientists say evidence is mounting that heavy use of antibiotics to promote faster growth in farm animals is a major culprit, creating a reservoir of drug resistant bugs that are finding their way into communities. More than 70 percent of all the antibiotics used in the United States are given to animals.

Agribusiness groups disagree and say the main problem is overuse of antibiotic treatments for people. Bugs rarely migrate from animals to people, and even when they do, the risk they pose to human health is negligible, the industry contends.

Scientists say genetic sequencing will bring greater certainty to the debate. They will be able to trace germs in people to their origins, be it from a farm animal or other patients in a hospital. Representative Louise Slaughter, a Democrat from New York who has pushed for legislation to control antibiotic use on farms, said such evidence would be the “smoking gun” that would settle the issue.

Professor Price is seeking to quantify how extensively drug-resistant bugs in animals are infecting people. He is trying to do that by analyzing the full genetic makeup of germs collected from both grocery store meat and people in Flagstaff last year. The plummeting cost of genomic sequencing has made his research possible.

He is comparing the genetic sequences of E. coli germs resistant to multiple antibiotics found in the meat samples to the ones that have caused urinary tract infections in people (mostly women).

Urinary infections were chosen because they are so common. American women get more than eight million of them a year. In rare cases the infections enter the bloodstream and are fatal.

Resistant bacteria in meat are believed to cause only a fraction of such infections, but even that would account for infections in several hundred thousand people annually. The E. coli germ that Professor Price has chosen can be deadly, and is made even more dangerous by its tendency to resist antibiotics.

The infection happens when meat containing the germ is eaten, grows in the gut, and then is introduced into the urethra. Dr. Price said the germ could cause infection in other ways, such as through a cut while slicing raw meat. The bugs are promiscuous, so once they get into people, they can mutate and travel more easily among people. A new strain of the antibiotic-resistant bug MRSA, for example, was first detected in people in Holland in 2003, and now represents 40 percent of the MRSA infections in humans in that country, according to Jan Kluytmans, a Dutch researcher. That same strain was common in pigs on farms before it was found in people, scientists say. Dr. Price, 44, began his career testing anthrax for resistance to the Cipro antibiotic for biodefense research in the 1990s. His interest in public health led him to antibiotic resistance in the early 2000s. It seemed like a less theoretical threat.

First line antibiotics were no longer curing basic infections, and doctors were concerned. “I thought, ‘Wow this is so obviously crazy, I have to do something about this,’ ” he said. He has done his research on antibiotics at a nonprofit founded in 2002, the Translational Genomics Research Institute, in Phoenix. His lab in Flagstaff, an affiliate, is financed mostly by federal sources, including the National Institutes of Health and the Defense Department.

Dr. Price, trained in epidemiology and microbiology, has been sounding the alarm about antibiotic resistance for a number of years. He recently told a Congressional committee that evidence of the ill effects of antibiotics in farming was overwhelming.

He thinks the Food and Drug Administration’s efforts to limit antibiotic use on farms have been weak. In 1977, the F.D.A. said it would begin to ban some agricultural uses of antibiotics. But the House and Senate appropriations committees — dominated by agricultural interests — passed resolutions against the ban, and the agency retreated. More recently, the agency has limited the use of two important classes of antibiotics in animals. But advocates say it needs to go further and ban use of all antibiotics for growth promotion. Sweden and Denmark have already done so.

Ms. Slaughter said aggressive lobbying by agribusiness interests has played a major role in blocking passage of legislation. According to her staff, of the 225 lobbying disclosure reports filed during the last Congress on a bill she wrote on antibiotic use, nearly nine out of ten were filed by organizations opposed to the legislation.

But the economics of food presents perhaps the biggest obstacle. On large industrial farms, animals are raised in close contact with one another and with big concentrations of bacteria-laden feces and urine. Antibiotics keep infections at bay but also create drug resistance. Those same farms raise large volumes of cheap meat that Americans have become accustomed to.

Governments have begun to acknowledge the danger. The United States recently promised $40 million to a major drug company, GlaxoSmithKline, to help it develop medications to combat antibiotic resistance. But Dr. Price says that new drugs are only a partial solution.

“A lot of people say, ‘let’s innovate our way out of this,’ ” he said. “But if we don’t get a handle on the way we abuse antibiotics, we are just delaying the inevitable.”
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Crafty_Dog
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« Reply #85 on: September 05, 2013, 08:45:27 AM »

http://online.wsj.com/article/SB10001424127887323893004579055083617866454.html?mod=WSJ_hp_EditorsPicks
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« Reply #86 on: September 17, 2013, 10:51:47 AM »

http://www.nytimes.com/2013/09/17/health/cdc-report-finds-23000-deaths-a-year-from-antibiotic-resistant-infections.html?nl=todaysheadlines&emc=edit_th_20130917&_r=0
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« Reply #87 on: September 25, 2013, 09:28:59 PM »

 ELLEN KNICKMEYER
 
A World Health Organization emergency committee on Wednesday asked countries to step up monitoring for a lethal, year-old virus as Muslim pilgrims from around the world return home from the annual hajj in Saudi Arabia, home to most of the victims so far.  Many questions remain to be answered, but the most pressing is "we don't understand what kind of risk this poses for global spread," Keiji Fukuda, WHO assistant director-general, told reporters after the committee's third meeting on Middle East Respiratory Syndrome coronavirus, or MERS.  Nine European and Middle East countries have confirmed a total of 130 cases of the illness, with a 42% death rate, since the virus was identified in September 2012. More than 100 of the confirmed cases were in Saudi Arabia.  International disease experts convened Wednesday under the remit of the WHO concluded that the disease so far doesn't merit declaration of a health emergency, Dr. Fukuda said.  Members have asked to confer again after next month's hajj, he said. The world's largest annual gathering, the hajj draws more than 3 million pilgrims from dozens of countries for worship in the Muslim holy cities of Mecca and Medina.  The MERS committee is the second emergency panel created under WHO procedures established after the 2003 outbreak of SARS, a virus related to MERS that killed 750 people, mostly in China. The first WHO emergency committee addressed the H1N1 pandemic in 2009.  MERS committee members heard from health officials of Saudi Arabia and Qatar, another Gulf country that has confirmed MERS cases recently, Dr. Fukuda said. The United Arab Emirates, which also had recent confirmed cases, didn't make a representative available Wednesday, Dr. Fukuda said.

The experts expressed concern that many of the pilgrims will be returning to countries in sub-Saharan Africa and other developing regions that are unlikely to screen those who fall ill for MERS, the WHO official said.

Health officials have yet to determine how MERS, which typically causes respiratory infections, and sometimes kidney problems, infects humans. Studies on camels and bats as possible hosts have been inconclusive.  Newly concluded animal studies in Saudi Arabia by the U.N. Food and Agriculture Organization and others should provide new information soon, Dr. Fukuda said.  The emergency committee urged countries to do more MERS diagnostic testing and investigation. A committee statement emphasized "the importance of timely sharing of relevant information and of coordinating actions with WHO."

Dr. Fukuda declined to say whether Saudi Arabia was doing enough to investigate the disease. "We would like to have more information on the situation" from countries overall, he said.

One reason for the lingering uncertainty over the most basic facets of MERS is that the new virus has spread steadily, rather than in a surge of cases that yielded a corresponding surge of information, as SARS and other recent pandemics did, the WHO official said.
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« Reply #88 on: September 25, 2013, 09:44:07 PM »

second post



A Big Step in the Fight Against Superbugs

Our study zeroed in on an effective way to prevent deadly MRSA infections in hospitals. .
By JONATHAN B. PERLIN
 And RICHARD PLATT
 
In the U.S. and abroad, humans are at risk of increasingly weak antibiotics and increasingly strong superbugs. Before the discovery of penicillin in the early 20th century, a significant portion of people unlucky enough to contract a bacterial infection died. With increasing antibiotic resistance, we risk a post-antibiotic era every bit as frightening.

A report out this month from the Centers for Disease Control and Prevention highlights multidrug-resistant bacteria as one of the world's most serious and pressing health threats. "Antibiotic Resistance Threats in the United States, 2013" notes that drug resistance is often the result of poor stewardship, defined as the lack of careful use of antibiotics in humans and animals.

When antibiotics are used unnecessarily or inappropriately, we kill the most susceptible organisms and, in their void, create a more favorable environment for the selection of more-resistant bacteria. This has resulted in a scary alphabet soup of superbugs, including C. diff, CRE, MRSA, multidrug-resistant TB, and VRE, that can be deadly to those with suppressed immune systems and are threatening even the healthiest patients.

The CDC's strategies to address resistance include tracking resistant bacteria, improving uses of antibiotics, and developing new antibiotics and diagnostic tests for resistant bacteria. But success also means reducing the overuse of antibiotics and requires a commitment from more than health professionals. Patients need to change their expectations for receiving an antibiotic when an illness is likely viral—in which case it will never respond to an antibiotic—or self-limited, like a cold that will go away on its own. Doctors need to feel supported by patients, not pressured, when they exhibit prudent stewardship in prescribing only those medicines that will be effective.







Enlarge Image
image



imageAssociated Press
Plates of MRSA
.
Preventing infection is another critical piece of the CDC's national strategy, and we still have a lot to learn on that front. That is why Hospital Corporation of America, in partnership with researchers from the CDC, Harvard Pilgrim Health Care Institute and Harvard Medical School, University of California Irvine School of Medicine, Rush Medical College and Washington University, recently conducted a study known as Reduce MRSA (short for the Randomized Evaluation of Decolonization Versus Universal Clearance to Eliminate MRSA).

The study set out to address the question: What could hospitals do right now to dramatically reduce their infection rates? The answer turned out to be a surprisingly simple intervention to cleanse patients who potentially carry the virulent organism.

Methicillin-resistant Staphylococcus aureus, more commonly known as MRSA, was identified in the CDC report as a serious threat to human health. MRSA is a common organism, and individuals who have been exposed to it can become carriers. In the hospital, carriers are at particular risk of developing MRSA infections. MRSA may be transmitted to other patients and can cause bloodstream infections known as sepsis. There are some 80,000 cases of invasive MRSA infections per year, resulting in about 11,000 deaths annually. MRSA, and staphylococcus in general, account for approximately one-quarter of the 80,000 deaths from hospital-acquired infections in the U.S.

The Reduce MRSA trial, conducted across 74 intensive-care units at 43 hospitals, involved more than 74,000 patients over an 18-month period. Results show that hospitals urgently need to better define their standards for infection prevention.

Before this trial, the CDC didn't have enough information to determine which of three alternative approaches is truly best: Would it be most effective to screen patients for MRSA and, if they test positive, isolate them from other patients, or to screen patients for MRSA and, if they test positive, isolate them and apply the "decolonization," which means eradicating bacteria by using antimicrobial soap and nasal ointment to prevent bacteria from entering the bloodstream? Or would it be better to decolonize all patients immediately on admission to intensive-care units?

The third approach proved unequivocally best. Universal decolonization reduced all bloodstream infections, including those caused by MRSA, by 44%. The other approaches were not nearly as successful. There was negligible change in the reduction of bloodstream infections using the first approach; the second approach saw a 22% reduction.

While this study was notable for its outcome, it was also notable for its efficiency. It didn't take a single hospital dozens of years to amass the power of this study—it took 43 hospitals collaborating for 18 months. It didn't take a research team focused only on answering one question. The research was implemented by nurses and infection-prevention professionals during routine patient care, and not in a laboratory, but within the real-world environment of community hospitals. This suggests the prevention strategy can be implemented in hospitals everywhere, as it already has been by all HCA facilities.

The stakes are high. Breeding superbugs threatens a return to the vulnerability of the pre-antibiotic era, when untreatable bacterial diseases and TB were responsible for countless deaths. The Reduce MRSA study demonstrated that government, the private sector and academia, by conducting research collaboratively, can accelerate creating the best scientific evidence for practice. By using that evidence, we can change outcomes for patients, and maybe even the way history records our fate.

 Dr. Perlin is president, Clinical & Physician Services of Hospital Corporation of America. Dr. Platt, an infectious diseases specialist, is a professor at the Harvard Pilgrim Health Care Institute.
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bigdog
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« Reply #89 on: October 20, 2013, 07:42:27 PM »

http://www.pbs.org/wgbh/pages/frontline/hunting-the-nightmare-bacteria/

"Has the age of antibiotics come to an end? From a young girl thrust onto life support in Arizona to an uncontrollable outbreak at one of the nation’s most prestigious hospitals, FRONTLINE investigates the alarming rise of a deadly type of bacteria that our modern antibiotics can’t stop."
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« Reply #90 on: November 23, 2013, 01:51:22 AM »



https://medium.com/p/892b57499e77
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« Reply #91 on: December 12, 2013, 11:43:04 AM »

As this thread attests, I have been calling for action on this for quite some time:

http://www.nytimes.com/2013/12/12/health/fda-to-phase-out-use-of-some-antibiotics-in-animals-raised-for-meat.html?nl=todaysheadlines&emc=edit_th_20131212

F.D.A. Restricts Antibiotics Use for Livestock
By SABRINA TAVERNISE
Published: December 11, 2013 207 Comments


WASHINGTON — The Food and Drug Administration on Wednesday put in place a major new policy to phase out the indiscriminate use of antibiotics in cows, pigs and chickens raised for meat, a practice that experts say has endangered human health by fueling the growing epidemic of antibiotic resistance.


This is the agency’s first serious attempt in decades to curb what experts have long regarded as the systematic overuse of antibiotics in healthy farm animals, with the drugs typically added directly into their feed and water. The waning effectiveness of antibiotics — wonder drugs of the 20th century — has become a looming threat to public health. At least two million Americans fall sick every year and about 23,000 die from antibiotic-resistant infections.

“This is the first significant step in dealing with this important public health concern in 20 years,” said David Kessler, a former F.D.A. commissioner who has been critical of the agency’s track record on antibiotics. “No one should underestimate how big a lift this has been in changing widespread and long entrenched industry practices.”

The change, which is to take effect over the next three years, will effectively make it illegal for farmers and ranchers to use antibiotics to make animals grow bigger. The producers had found that feeding low doses of antibiotics to animals throughout their lives led them to grow plumper and larger. Scientists still debate why. Food producers will also have to get a prescription from a veterinarian to use the drugs to prevent disease in their animals.

Federal officials said the new policy would improve health in the United States by tightening the use of classes of antibiotics that save human lives, including penicillin, azithromycin and tetracycline. Food producers said they would abide by the new rules, but some public health advocates voiced concerns that loopholes could render the new policy toothless.

Health officials have warned since the 1970s that overuse of antibiotics in animals was leading to the development of infections resistant to treatment in humans. For years, modest efforts by federal officials to reduce the use of antibiotics in animals were thwarted by the powerful food industry and its substantial lobbying power in Congress. Pressure for federal action has mounted as the effectiveness of drugs important for human health has declined, and deaths from bugs resistant to antibiotics have soared.

Under the new policy, the agency is asking drug makers to change the labels that detail how a drug can be used so they would bar farmers from using the medicines to promote growth.

The changes, originally proposed in 2012, are voluntary for drug companies. But F.D.A. officials said they believed that the companies would comply, based on discussions during the public comment period. The two drug makers that represent a majority of such antibiotic products — Zoetis and Elanco — have already stated their intent to participate, F.D.A. officials said. Companies will have three months to tell the agency whether they will change the labels, and three years to carry out the new rules.

Additionally, the agency is requiring that licensed veterinarians supervise the use of antibiotics, effectively requiring farmers and ranchers to obtain prescriptions to use the drugs for their animals.

“It’s a big shift from the current situation, in which animal producers can go to a local feed store and buy these medicines over the counter and there is no oversight at all,” said Michael Taylor, the F.D.A.’s deputy commissioner for foods and veterinary medicine.

Some consumer health advocates were skeptical that the new rules would reduce the amount of antibiotics consumed by animals. They say that a loophole will allow animal producers to keep using the same low doses of antibiotics by contending they are needed to keep animals from getting sick, and evading the new ban on use for growth promotion.

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More meaningful, said Dr. Keeve Nachman, a scientist at the Johns Hopkins Center for a Livable Future, would be to ban the use of antibiotics for the prevention of disease, a step the F.D.A. so far has not taken. That would limit antibiotic uses to treatment of a specific sickness diagnosed by a veterinarian, a much narrower category, he said.

Another skeptic, Representative Louise M. Slaughter, a Democrat from New York, said that when the European Union tried to stop companies from using antibiotics to make farm animals bigger, companies continued to use antibiotics for disease prevention. She said antibiotic use only declined in countries like the Netherlands that instituted limits on total use and fines for noncompliance.

But another longtime critic of the F.D.A. on antibiotics, Dr. Stuart B. Levy, a professor of microbiology at Tufts University and the president of the Alliance for the Prudent Use of Antibiotics, praised the new rules. He was among the first to identify the problem in the 1970s. “I’m kind of happy,” he said. “For all of us who’ve been struggling with this issue, this is the biggest step that’s been taken in the last 30 years.”

Mr. Taylor, the agency official, said the F.D.A. had detailed what veterinarians needed to consider when they prescribed such drugs. For example, use has to be for animals at risk for developing a specific disease, with no reasonable alternatives to prevent it.

“It’s far from being a just-trust-them system,” he said. “Given the history of the issue, it’s not surprising that there are people who are skeptical.”

He added that some food producers had already curbed antibiotic use.

A spokeswoman for Zoetis, a major drug producer that said it would abide by the new rules, said the new policy was not expected to have a big effect on the revenues of the company because many of its drug products were also approved for therapeutic uses. (Dr. Nachman said that was an indication that overall use might not decline under the new rules.)

The Animal Health Institute, an association of pharmaceutical companies that make drugs for animals, said that it supported the policy and “will continue to work with the F.D.A. on its implementation.”

The National Pork Producers Council was less enthusiastic, saying, “We expect that hog farmers, and the federally inspected feed mills they purchase feed from, will follow the law.”

“It is part of our ethical responsibility to utilize antibiotics responsibly and part of our commitment to public health and animal health,” the council said in a statement.

The National Chicken Council said in a statement that its producers already worked closely with veterinarians, and that much of the antibiotics used in raising chickens were not used in human medicine.

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Crafty_Dog
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« Reply #92 on: December 17, 2013, 10:32:39 AM »

Antibiotics of the Future
Scientists hunt for new antibiotics amid a rise in resistant germs
By Shirley S. Wang
Dec. 16, 2013 7:06 p.m. ET

As bacteria continue to develop resistance to existing antibiotics, scientists are working on new strategies to combat bug-borne infections and diseases, Shirley Wang reports. Photo: AP.

Scientists are working to develop new strategies to combat the growing threat of germs that current antibiotics can't fight.

Some researchers are testing new substances, such as silver, to combine with antibiotics to boost their killing power. Other researchers are making use of genetic sequencing of bacteria to help develop killer drugs at a faster pace than medical science was capable of in the past.

Another strategy aims to render harmful bacteria incapable of infecting people, rather than killing the germs outright. One such technique would neutralize disease-causing toxins by disrupting the bacteria's internal mechanisms.

Antibiotic resistance is a growing threat to public health, medical officials say. Common germs such as Escherichia coli, or E. coli, which can cause urinary tract and other infections, and Neisseria gonorrhoeae, which causes gonorrhea, are becoming harder to treat because they increasingly don't respond to antibiotics. Some two million people in the U.S. are infected each year by antibiotic-resistant bacteria and 23,000 die as a result, according to the Centers for Disease Control and Prevention. The CDC says it doesn't have historical numbers.
View Graphics

One of the biggest threats is from Enterobacteriaceae, a family of germs that naturally lives in the gut and includes E. coli, the CDC says. There are about 9,000 cases a year of infections from the germs that can't be treated with usual antibiotics, resulting in 610 deaths. In 1998, there was just one case. Patients who don't respond to normal antibiotics are given older drugs that had been discontinued because of severe side effects, such as kidney damage, the CDC says.

Scientists say that Enterobacteriaceae are particularly hard to kill because of an outer cell wall that prevents many antibiotics from penetrating. James J. Collins, a professor of biomedical engineering at Boston University and Harvard University, and his colleagues recently discovered that adding trace amounts of silver—long known to have antimicrobial properties—allows the common antibiotic vancomycin to work against E. coli, whereas the antibiotic isn't effective against the microbe on its own. The silver appears to make the outer walls of the bacteria more permeable, allowing the antibiotic to get in and do its job, says Dr. Collins, who published the findings in the journal Science Translational Medicine in June.

(Some pharmaceutical companies are experimenting with other types of additives with the aim of short-circuiting bacteria's defenses.)


Researchers at Merck & Co., in Whitehouse Station, N.J., are targeting an enzyme called beta-lactamase that lives in certain bacteria and neutralizes antibiotics sent to destroy them. By adding an enzyme-inhibiting agent called MK-7655 to the antibiotic imipenem, researchers managed to kill about 97% of a type of antibiotic-resistant bacteria that causes urinary-tract infections and pneumonia, according to Nicholas Kartsonis, head of clinical development of antibacterial, antifungals and non-hepatology viruses at Merck Research Labs.

Synthetic Biologics Inc. is taking advantage of beta-lactamase's ability to neutralize antibiotics by adding a modified version of the enzyme to the drugs. The aim is to prompt the antibiotic to break down when it reaches the bowel, where side effects and drug resistance for bacteria called Clostridium difficile, or C. difficile, develops, but to leave the antibiotic intact in the bloodstream. The process should allow larger doses of antibiotics to be administered without the patient suffering typical side effects such as gastrointestinal problems, says John Monahan, who heads research and development for the Rockville, Md.-based company.

C. difficile, which causes life-threatening diarrhea and is blamed for 14,000 deaths a year, can spread rapidly in hospital patients on antibiotics. Although there are drugs to treat C. difficile, the bacteria are resistant to many antibiotics used to treat other types of infections.

Antibiotics naturally lose their effectiveness over time as bacteria populations build up resistance, and new drugs need to be continually developed to take their place. But antibiotic development by pharmaceutical companies slowed sharply after about 1990, in part because they are less profitable than other drugs used to treat chronic diseases. Compounding the problem has been an overuse of antibiotics in people and farm animals, which has accelerated the creation of antibiotic-resistant germs.

"Antibiotics have a finite lifetime because resistance is inevitable," says Michael Fischbach, a bioengineering and therapeutic sciences professor at the University of California, San Francisco. "Therefore, there's always a need to innovate."

Bacteria have ways of defending themselves against other bacteria, and most antibiotics are derived from the toxins they use. Identifying and developing new antibiotics is a long and slow process. Now, scientists are able to more efficiently scrutinize microbes for undiscovered antibiotics by sequencing their genomes and then using computer analysis to look for gene patterns that suggest a new antibiotic recipe. Typically, antibiotics are encoded by anywhere from 10 to 40 genes.

Sean Brady, head of the Laboratory of Genetically Encoded Small Molecules at Rockefeller University in New York, and his colleagues recently zeroed in on half a dozen gene sequences. The team found that the genes were encoded for toxins that appeared in lab testing to be active against pathogens resistant to the antibiotic vancomycin, which is commonly used to treat infections in the gut. The research was published in the Proceedings of the National Academy of Science in June.
2 million

The number of U.S. patients per year whose infections aren't treatable with the existing array of antibiotics

Whether the antibiotic will be useful in treating people remains to be seen, says Dr. Brady. The main problem with identifying new antibiotics isn't that they don't work, but that they cause severe side effects or toxicity, drug makers say.

Another group of researchers, headed by Dr. Fischbach at the University of California, has found a handful of new antibiotics that kill methicillin-resistant Staphylococcus aureus, or MRSA, by sequencing genomes of bacteria found in the environment. MRSA can cause a range of illnesses from skin infections to pneumonia and bloodstream infections.

An unusual strategy doesn't aim to kill bacteria at all, but rather to make them less harmful. Since bacteria only cause infections when their population has reached a certain threshold, called a quorum, researchers are looking for ways to disrupt the chemical signals the bugs use to communicate with each other. Another approach aims to neutralize toxins or disrupt other signaling molecules that are necessary for bacteria to be infectious.

"We don't challenge them to a duel but basically confuse them into not causing infection," says Gerry Wright, a professor of biochemistry and biomedical sciences at McMaster University in Hamilton, Ontario.

Dr. Brady and his team at Rockefeller University demonstrated that disrupting a cluster of genes reduced the virulence of a microbe that causes infection affecting the lungs, bones and joints. The researchers published the work late last year in the Journal of the American Chemical Society.
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« Reply #93 on: January 08, 2014, 04:02:35 PM »

http://www.pbs.org/wgbh/pages/frontline/health-science-technology/hunting-the-nightmare-bacteria/illinois-nightmare-bacteria-outbreak-raises-alarms/

The largest U.S. outbreak on record of one particular strain of a so-called “nightmare bacteria” is fueling alarm among public health officials about the spread of potentially lethal drug-resistant infections.

The outbreak, which has been traced to Advocate Lutheran General Hospital in suburban Chicago, has so far infected 44 people, according to the Centers for Disease Control and Prevention. Since 2009, just 97 cases of the infection have been reported to the agency.
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ccp
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« Reply #94 on: January 09, 2014, 09:21:45 AM »

Bigdog,

I haven't seen the CDC reports on this.  I am sure my ID colleagues have.  In NJ we are seeing ESBL infections.  These are the enterobacterioraceae that respond to "penem" and sometimes other antibiotics.   This one would be tough.
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bigdog
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« Reply #95 on: January 09, 2014, 01:22:38 PM »

Thanks for the follow up, ccp. If you see anything that adds or contradicts, I'd be interested.
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Crafty_Dog
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« Reply #96 on: May 10, 2014, 07:26:14 AM »

http://www.alternet.org/personal-health/antibiotic-resistance-6-diseases-may-come-back-haunt-us?1234
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Crafty_Dog
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« Reply #97 on: May 11, 2014, 01:41:33 PM »



The Rise of Antibiotic Resistance

By THE EDITORIAL BOARDMAY 10, 2014


The World Health Organization has surveyed the growth of antibiotic-resistant germs around the world — the first such survey it has ever conducted — and come up with disturbing findings. In a report issued late last month, the organization found that antimicrobial resistance in bacteria (the main focus of the report), fungi, viruses and parasites is an increasingly serious threat in every part of the world. “A problem so serious that it threatens the achievements of modern medicine,” the organization said. “A post-antibiotic era, in which common infections and minor injuries can kill, far from being an apocalyptic fantasy, is instead a very real possibility for the 21st century.”

The growth of antibiotic-resistant pathogens means that in ever more cases, standard treatments no longer work, infections are harder or impossible to control, the risk of spreading infections to others is increased, and illnesses and hospital stays are prolonged.

All of these drive up the costs of illnesses and the risk of death. The survey sought to determine the scope of the problem by asking countries to submit their most recent surveillance data (114 did so). Unfortunately, the data was glaringly incomplete because few countries track and monitor antibiotic resistance comprehensively, and there is no standard methodology for doing so.

Still, it is clear that major resistance problems have already developed, both for antibiotics that are used routinely and for those deemed “last resort” treatments to cure people when all else has failed.

Carbapenem antibiotics, a class of drugs used as a last resort to treat life-threatening infections caused by a common intestinal bacterium, have failed to work in more than half the people treated in some countries. The bacterium is a major cause of hospital-acquired infections such as pneumonia, bloodstream infections, and infections in newborns and intensive-care patients. Similarly, the failure of a last-resort treatment for gonorrhea has been confirmed in 10 countries, including many with advanced health care systems, such as Australia, Canada, France, Sweden and Britain. And resistance to a class of antibiotics that is routinely used to treat urinary tract infections caused by E. coli is widespread; in some countries the drugs are now ineffective in more than half of the patients treated. This sobering report is intended to kick-start a global campaign to develop tools and standards to track drug resistance, measure its health and economic impact, and design solutions.
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Big Pharma already gets plenty of money from the government for R&D. They only want to develop medicines that will make a huge profit....
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When you find a solution that doesn't hurt the PROFITS of any industry, then you'll get somewhere. So, basically, we're all in a lot of...
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The most urgent need is to minimize the overuse of antibiotics in medicine and agriculture, which accelerates the development of resistant strains. In the United States, the Food and Drug Administration has issued voluntary guidelines calling on drug companies, animal producers and veterinarians to stop indiscriminately using antibiotics that are important for treating humans on livestock; the drug companies have said they will comply. But the agency, shortsightedly, has appealed a court order requiring it to ban the use of penicillin and two forms of tetracycline by animal producers to promote growth unless they provide proof that it will not promote drug-resistant microbes.

The pharmaceutical industry needs to be encouraged to develop new antibiotics to supplement those that are losing their effectiveness. The Royal Pharmaceutical Society, which represents pharmacists in Britain, called this month for stronger financial incentives. It said that no new class of antibiotics has been discovered since 1987, largely because the financial returns for finding new classes of antibiotics are too low. Unlike lucrative drugs to treat chronic diseases like cancer and cardiovascular ailments, antibiotics are typically taken for a short period of time, and any new drug is apt to be used sparingly and held in reserve to treat patients resistant to existing drugs.

Antibiotics have transformed medicine and saved countless lives over the past seven decades. Now, rampant overuse and the lack of new drugs in the pipeline threatens to undermine their effectiveness.
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