In New Theory, Swine Flu Started in Asia, Not Mexico

June 24, 2009

By DONALD G. McNEIL Jr.  newyorktimes.com

Contrary to the popular assumption that the new swine flu pandemic arose on factory farms in Mexico, federal agriculture officials now believe that it most likely emerged in pigs in Asia, but then traveled to North America in a human.  But they emphasized that there was no way to prove their theory and only sketchy data underpinning it.  There is no evidence that this new virus, which combines Eurasian and North American genes, has ever circulated in North American pigs, while there is tantalizing evidence that a closely related “sister virus” has circulated in Asia.  American breeding pigs, possibly carrying North American swine flu, are frequently exported to Asia, where the flu could have combined with Asian strains. But because of disease quarantines that make it hard to import Asian pigs, experts said, it is unlikely that a pig brought the new strain back West.

“The most likely scenario is that it came over in the mammalian species that moves most freely around the world,” said Dr. Amy L. Vincent, a swine flu specialist at the Agriculture Department’s laboratory in Ames, Iowa, referring, of course, to people.  The first person to carry the flu to North America from Asia, assuming that is what happened, has never been found and never will be, because people stop carrying the virus when they get better.  Moreover, the officials said, the chances of proving their theory are diminishing as the virus infects more people globally. It has now reached more than 90 countries, according to the World Health Organization. Since some of those people will inevitably spread it to pigs, its history will become impossible to trace.  “To tell whether a pig is newly infected by a human or had the virus before the human epidemic began really can’t be done,” said Dr. Kelly M. Lager, another Agriculture Department swine disease expert.  The highly unusual virus — which includes genetic bits of North American human, avian and swine flus and Eurasian swine flu — has not been detected in any pigs except those in a single herd in Canada that was found infected in late April.

A carpenter who worked on the farm after visiting Mexico had been thought to have infected the herd. But in mid-June, Canadian health agencies said he was not to blame. The whole herd was culled, and the virus has not been found elsewhere in Canada, as it would have been if it were endemic, since American and Canadian laboratories test thousands of flu samples to help the pork industry develop vaccines.  But a sample taken from a pig in Hong Kong in 2004 was recently found to have a virus nearly matching the new flu. That flu, which had seven of the new flu’s eight genome sequences, was noted in an article in Nature magazine on June 11, which called it a “sister virus.”  Scientists tracking the virus’s lineage have complained that there is far too little global surveillance of flu in swine. Public databases have 10 times as many human and avian flu sequences as they do porcine ones, said Dr. Michael W. Shaw, a scientist in the flu division of the Centers for Disease Control and Prevention, and there are far fewer pig flu sequences from Asia than from North America and Europe, and virtually none from South America or Africa. “Something could have been going on there for a long time and we wouldn’t know,” Dr. Shaw said.

But national veterinary officials said they knew of no close relatives of the new virus in the large private North American databases, either. That makes it most likely, they said, that it has been circulating in Asia.  The new virus was first isolated in late April by American and Canadian laboratories from samples taken from people with flu in Mexico, Southern California and Texas. Soon the earliest known human case was traced to a 5-year-old boy in La Gloria, Mexico, a rural town in Veracruz.  Because that area is home to hog-fattening operations with thousands of pigs in crowded barns near lagoons of manure, opponents of factory farming were quick to blame the industry.  In May, the Mexican government said it had tested pigs on the Veracruz farms and found them free of the virus. Smithfield Foods, an owner of the farms, and the National Pork Producers Council, the industry’s lobbying arm, were quick to publicize that announcement.  But outside veterinary experts still disagree on whether those tests proved anything.  According to Smithfield, Mexican government veterinarians tested snout swabs taken on April 30 and blood samples stored since January.  But since the human outbreak in Veracruz is believed to have started in February, many veterinary experts said testing pig snouts for live virus in April proved nothing. Any pig sick in February would have long since recovered and, since hogs are usually slaughtered at 6 months old, many of those alive in early February would be bacon by April.  But Dr. Greg Stevenson, an expert in swine diagnostics at Iowa State University, said that since flu could persist in a large herd for months, “if it had been there in February, it would probably still be there at the end of April.”

The blood tests — in which scientists look for antibodies formed in response to a previous infection — present a different set of problems. Antibodies are much harder to tell apart from one another than viruses are.  A pig that had the new H1N1 flu would come up positive on an antibody test. But so would a pig that had the regular H1N1 swine flu that has circulated since 1930, or even a pig that had been vaccinated against the earlier H1N1 flu — and all the Smithfield pigs routinely get flu shots.  The company said vaccinated pigs could be distinguished from previously ill pigs because illness produced more antibodies.  But outside experts were skeptical. An antibody test specific enough to identify only the new flu strain “would take months to develop, at a minimum, and would require considerable R & D expertise and technology,” said Dr. Christopher W. Olsen, a swine flu expert at the University of Wisconsin’s veterinary medical school.  The governor of Veracruz has asked the National Autonomous University of Mexico to do its own investigation of industrial hog farming in his state; the work is expected to take months. Carlos Arias, the biochemist leading the team, said he hoped to test all the swab and tissue samples stored by the farms and the national veterinary laboratory.




How the Food Makers Captured Our Brains

June 23, 2009

By TARA PARKER-POPE

newyorktime.com


As head of the Food and Drug Administration, Dr. David A. Kessler served two presidents and battled Congress and Big Tobacco. But the Harvard-educated pediatrician discovered he was helpless against the forces of a chocolate chip cookie.  In an experiment of one, Dr. Kessler tested his willpower by buying two gooey chocolate chip cookies that he didn’t plan to eat. At home, he found himself staring at the cookies, and even distracted by memories of the chocolate chunks and doughy peaks as he left the room. He left the house, and the cookies remained uneaten. Feeling triumphant, he stopped for coffee, saw cookies on the counter and gobbled one down.  “Why does that chocolate chip cookie have such power over me?” Dr. Kessler asked in an interview. “Is it the cookie, the representation of the cookie in my brain? I spent seven years trying to figure out the answer.”  The result of Dr. Kessler’s quest is a fascinating new book, “The End of Overeating: Taking Control of the Insatiable American Appetite” (Rodale).  During his time at the Food and Drug Administration, Dr. Kessler maintained a high profile, streamlining the agency, pushing for faster approval of drugs and overseeing the creation of the standardized nutrition label on food packaging.


 But Dr. Kessler is perhaps best known for his efforts to investigate and regulate the tobacco industry, and his accusation that cigarette makers intentionally manipulated nicotine content to make their products more addictive.  In “The End of Overeating,” Dr. Kessler finds some similarities in the food industry, which has combined and created foods in a way that taps into our brain circuitry and stimulates our desire for more.  When it comes to stimulating our brains, Dr. Kessler noted, individual ingredients aren’t particularly potent. But by combining fats, sugar and salt in innumerable ways, food makers have essentially tapped into the brain’s reward system, creating a feedback loop that stimulates our desire to eat and leaves us wanting more and more even when we’re full.  Dr. Kessler isn’t convinced that food makers fully understand the neuroscience of the forces they have unleashed, but food companies certainly understand human behavior, taste preferences and desire. In fact, he offers descriptions of how restaurants and food makers manipulate ingredients to reach the aptly named “bliss point.” Foods that contain too little or too much sugar, fat or salt are either bland or overwhelming. But food scientists work hard to reach the precise point at which we derive the greatest pleasure from fat, sugar and salt.


The result is that chain restaurants like Chili’s cook up “hyper-palatable food that requires little chewing and goes down easily,” he notes. And Dr. Kessler reports that the Snickers bar, for instance, is “extraordinarily well engineered.” As we chew it, the sugar dissolves, the fat melts and the caramel traps the peanuts so the entire combination of flavors is blissfully experienced in the mouth at the same time.  Foods rich in sugar and fat are relatively recent arrivals on the food landscape, Dr. Kessler noted. But today, foods are more than just a combination of ingredients. They are highly complex creations, loaded up with layer upon layer of stimulating tastes that result in a multisensory experience for the brain. Food companies “design food for irresistibility,” Dr. Kessler noted. “It’s been part of their business plans.”  But this book is less an exposé about the food industry and more an exploration of us. “My real goal is, How do you explain to people what’s going on with them?” Dr. Kessler said. “Nobody has ever explained to people how their brains have been captured.”  The book, a New York Times best seller, includes Dr. Kessler’s own candid admission that he struggles with overeating.  “I wouldn’t have been as interested in the question of why we can’t resist food if I didn’t have it myself,” he said. “I gained and lost my body weight several times over. I have suits in every size.”


This is not a diet book, but Dr. Kessler devotes a sizable section to “food rehab,” offering practical advice for using the science of overeating to our advantage, so that we begin to think differently about food and take back control of our eating habits.  One of his main messages is that overeating is not due to an absence of willpower, but a biological challenge made more difficult by the overstimulating food environment that surrounds us. “Conditioned hypereating” is a chronic problem that is made worse by dieting and needs to be managed rather than cured, he said. And while lapses are inevitable, Dr. Kessler outlines several strategies that address the behavioral, cognitive and nutritional factors that fuel overeating.  Planned and structured eating and understanding your personal food triggers are essential. In addition, educating yourself about food can help alter your perceptions about what types of food are desirable. Just as many of us now find cigarettes repulsive, Dr. Kessler argues that we can also undergo similar “perceptual shifts” about large portion sizes and processed foods. For instance, he notes that when people who once loved to eat steak become vegetarians, they typically begin to view animal protein as disgusting.  The advice is certainly not a quick fix or a guarantee, but Dr. Kessler said that educating himself in the course of writing the book had helped him gain control over his eating.  “For the first time in my life, I can keep my weight relatively stable,” he said. “Now, if you stress me and fatigue me and put me in an airport and the plane is seven hours late — I’m still going to grab those chocolate-covered pretzels. The old circuitry will still show its head.”


Mexican swine flu victims were young, some healthy
Mon Jun 29, 2009 5:07pm
By Maggie Fox, Health and Science Editor

WASHINGTON (Reuters) - Swine flu patients in Mexico were young and many were healthy before developing severe infections, doctors reported on Monday. The first detailed studies of the outbreak of a new strain of H1N1 influenza show the epidemic in Mexico resembled the early stages of other pandemics, and showed there is no way yet to predict who will become severely ill from the virus. The World Health Organization has confirmed 70,893 cases in the new H1N1 swine flu pandemic, with 311 deaths. However, U.S. health officials last week said there were likely at least a million cases there alone. Iraq, Lithuania, Monaco and Nepal all confirmed their first cases on Monday. Dr. Rogelio Perez-Padilla of the National Institute of Respiratory Diseases in Mexico City and colleagues studied 18 H1N1 cases in March and April, more than half of them aged 13 to 47.

Only eight had pre-existing medical conditions that might worsen their flu infection, they wrote -- including high blood pressure, diabetes, asthma and sleep apnea. Seven died -- all of multiple organ failure. The doctors said 90 percent of the seriously ill patients were under 50 -- in contrast to seasonal influenza, which causes mostly mild illness in people under the age of 65. "Most of our patients were young to middle-aged and had previously been healthy," they wrote in their report, published in the New England Journal of Medicine. "One contributing factor for death in our patients may have been delayed admission and delayed initiation of oseltamivir." Oseltamivir, sold by Roche AG under the brand name Tamiflu, can treat influenza, although Denmark reported the first case on Monday of swine flu resisting the drug's effects. "We did not find a factor that, before the onset of illness, predicted a worse outcome or death among our patients," Perez-Padilla's team wrote.

HEALTHCARE WORKERS
In addition, 22 of 190 healthcare workers who came close to the patients themselves got flu-like illness but were treated with Tamiflu and none got seriously ill. Dr. Stefano Bertozzi of the National Institute of Public Health in Mexico and colleagues studied the cases of 2,155 people who developed severe pneumonia from H1N1 infection in March and April, 821 who had detailed hospital records and 100 who died. They found that 87 percent of those who died were aged 5 to 59, and 71 percent of severe cases were among people 5 to 59, compared to a usual average of 32 percent for seasonal flu. "This wave of pneumonia is reminiscent of the initial phase of pandemics from the last century," they wrote. Health experts have speculated that people over the age of 52 have some protection from the new virus because it may resemble a strain of H1N1 flu that circulated before 1957. "Influenza A H1N1 abruptly disappeared from humans in 1957 and was replaced by a new reassortant virus that combined genes from the H1N1 strain and an avian virus," Dr. Shanta Zimmer and Dr. Donald Burke of the University of Pittsburgh wrote in a second report in the same journal. Flu viruses frequently swap genes in a process called reassortment.
(Editing by Vicki Allen)


* H5N1 circulates freely in Indonesia
* Flu viruses cause more deaths in poorer countries

By Olivia RondonuwuMon Jun 29, 2009 4:14pm Reuters.com

JAKARTA (Reuters) - Indonesia's first cases of the new H1N1 flu have raised concerns that if the virus spreads it could combine with the entrenched and deadly H5N1 avian influenza to create a more lethal strain of flu. Even if this worst-case scenario did not occur, experts say populous, developing countries such as Indonesia, India or Egypt, where healthcare systems can be rudimentary, will suffer more deaths from the new virus. Indonesian Health Minister Siti Fadillah Supari, who confirmed six new H1N1 cases on Sunday, said she was concerned about H1N1, widely known as swine flu, "marrying" with H5N1 avian flu. Influenza viruses not only mutate quickly and unpredictably, but they can swap genes, especially if a person or animal becomes infected with two strains at once. The new H1N1 strain is itself a mixture of various strains, genetic tests show. H5N1 bird flu has been circulating in Asia for years and has hit Indonesia harder than any other country. Although it only rarely infects people, it has killed 262 out of 433 infected globally since 2003, with 141 of those cases in Indonesia.

"We are scared because we are the warehouse of the world's most virulent H5N1," Supari said. "I am worried if the viruses encounter each other in the field," C.A. Nidom, the head of the Avian Influenza lab at Airlangga University in Surabaya, said. The World Health Organization declared a pandemic of H1N1 swine flu earlier this month and said the virus causes a moderately severe flu, spreading very easily from person to person. H5N1 spreads mostly from a bird to a person and stops there, but is far deadlier. The mortality rate for H1N1 is 0.2 percent, according to a study in the New England Journal of Medicine, while for H5N1 it is just over 60 percent.

SERIOUS THREAT
Scientists say usually as a virus becomes more transmissible from one human to another it also becomes less deadly, although this is not guaranteed. But Kamaruddin Zarkasie of Indonesia's Bogor Agriculture University said he felt the risk the two viruses might combine was only a random possibility. Even if they do not, H1N1 may be a serious threat, other experts said. Ben Cowling, public health expert at the University of Hong Kong, said people with serious infections who would be admitted to hospitals in developed countries and survive might die in poorer countries.

"It would be reasonable to say the mortality rate in underdeveloped settings is likely to be more comparable to the ICU (admission) rate in developed settings, or five times higher than the mortality rate in developed settings," Cowling said. "In poorer parts of India and China ... people are nutritionally less able to fight infection and they don't have the drugs that we have in major cities," said Robert Booy, head of clinical research at the University of Sydney's National Center for Immunization Research & Surveillance. H1N1 has killed more than 300 people and there have been at least 67,000 confirmed cases worldwide.(Additional reporting by Karima Anjani and Tan Ee Lyn in Hong Kong; Editing by Ed Davies and Maggie Fox)




We will wash water, and warm fire, and cool ice, and underprop the earth. We will teach birds to fly, and fishes to swim, and ruminants to chew the cud. It is time we had looked into these things.




Henry David Thoreau




Swine flu 'shows drug resistance'






Experts have reported the first case of swine flu that is resistant to tamiflu - the main drug being used to fight the pandemic.Roche Holding AG confirmed a patient with H1N1 influenza in Denmark showed resistance to the antiviral drug. David Reddy, company executive, said it was not unexpected given that common seasonal flu could do the same. The news comes as a nine-year-old girl has become the third to die in the UK with swine flu. It is understood from her doctors at Birmingham Children's Hospital that she had underlying health conditions. It is not yet known whether swine flu contributed to her death. Meanwhile, the Department of Health has announced a big jump in the number of patients in England confirmed with swine flu - up 1,604 since Friday, taking the UK total so far to 5,937. Routine sampling in the UK has shown that there is currently no resistance to oseltamivir or zanamivir. Experts have been using tamiflu, also known as oseltamivir, in a bid to stop the H1N1 spreading in communities.



If taken early, it ensures that symptoms are mild and reduces the chance of a victim giving the illness to someone else. This first reported case of resistance developed in a swine flu patient taking Tamiflu. Mr Reddy stressed that there were no signs of a tamiflu-resistant strain of H1N1 circulating in the community. This is in contrast to seasonal H1N1 flu where a Tamiflu resistant strain emerged last year and is now widely circulating.



Experts fear if this were to happen, it could render tamiflu ineffective. Another antiviral drug, called zanamivir or Relenza, made by GlaxoSmithKline, is also effective against swine flu. The UK government has been stockpiling these antiviral drugs and currently has enough to treat half of the population, with a contract to bring that up to 80% as soon as possible. Supplies of flu vaccine have also been ordered and the first doses could be administered in the autumn. A spokeswoman for the Health Protection Agency said: "The Health Protection Agency continues to watch for antiviral resistance and will be carrying out regular sample testing throughout this outbreak. "We have been monitoring antiviral drug resistance since the beginning of this outbreak. Routine sampling in the UK has shown that there is currently no resistance to oseltamivir or zanamivir." Virologist Professor John Oxford said: "I'm not surprised about this finding. The question is whether it is going to spread. We will soon know the answer."





Wakey wakey rise and shine

It's on again, off again, on again

Watch me fall like dominoes

In pretty patterns

Fingers in the blackbird pie

I'm tingling, tingling, tingling

It's what you feel not what you ought to

What you ought to, what you ought to

Reasonable and sensible

Dead from the neck up

I guess I'm stuffed Stuffed Stuffed

We thought you had it in you

But not

Not

Not

For no real reason

Squeeze the tubes and empty bottles

I take a bow, take a bow, take a bow

It's what you feel not what you ought to

What you ought to, what you ought to

The elephant that's in the room

Is tumbling tumbling tumbling

In duplicate and triplicate

Plastic bags

In duplicate and triplicate

Dead from the neck up

I guess I'm stuffed

Stuffed

Stuffed

We thought you had it in you

But not

Not

Not

Exactly where do you get off?

Is enough

Is enough

I love you but enough is enough,

Enough of that stuff

There's no real reason


Relatives grieve for pregnant Texas woman with swine flu who died

May 6th, 2009

Associated Press writers Alicia A. Caldwell in El Paso and Jamie Stengle in Dallas contributed to this report.


HARLINGEN, Texas — This week should have been a joyous time for Judy Trunnell, a 33-year-old teacher who had just given birth to a healthy baby girl. But the friends and relatives whose cars lined the quiet street in front of her home in a quiet subdivision Tuesday instead were mourning her, the first American citizen with swine flu to die. Trunnell died after being hospitalized for two weeks. She slipped into a coma, and her baby was delivered by Cesarean section, said a cousin, Mario Zamora.

“There are a number of health conditions that put people in a higher risk group where they are more likely to develop serious complications should they get any type of influenza,” McBride said. “Pregnancy is not a chronic condition.” Trunnell died early Tuesday after being hospitalized since April 19, said Leonel Lopez, Cameron County epidemiologist. She was extremely ill when she was hospitalized, said Dr. Joseph McCormick, regional dean of the University of Texas School of Public Health’s Brownsville campus.

Trunnell taught in the Mercedes Independent School District about 15 miles west of her hometown of Harlingen, a city of about 63,000 near the U.S.-Mexico border. Mercedes school Superintendent Walter Watson said he was told early Tuesday that Trunnell died after being taken off life support. “It brings tears to my eyes to my eyes to know she won’t be with our children or hers,” he said. “You just don’t replace people like that,” Watson said.

Trunnell was first seen by a physician April 14. Doctors knew she had flu but did not know what kind, Lopez said. The area is undergoing a Type A influenza epidemic and swine flu is one variety of that, he said. She was confirmed to have swine flu shortly before she died, he said.

U.S. health officials on Tuesday withdrew their recommendation that schools with suspected swine flu cases shut down for two weeks. Mercedes school district officials said the district would close its schools until Monday. The only other swine flu death in the U.S. was that of a Mexico City toddler who also had other health problems and had been visiting relatives in Brownsville, near Harlingen. He died last week at a Houston children’s hospital.


Regular flu viruses strike each winter and also can be deadly. They kill about 36,000

TUE., APR 28, 2009 - 7:40 AM

By DAVID WAHLBERG

Wisconsin State Journal

dwahlberg@madison.com

 Americans and hospitalize 200,000 annually, according to the CDC. The swine flu virus, which contains genes from pigs, birds and humans, is something of a mystery. Just 50 cases of swine flu were reported worldwide in people from 1958 to 2005, said Christopher Olsen, a flu researcher at UW-Madison, who published a study on those cases in 2007.

Another 12 cases have been reported since 2005, not including the current outbreak, according to the CDC. Unlike the current outbreak, almost all of those cases involved direct contact with infected pigs, Olsen said. Of the 50 cases he studied, seven people died — including a 32-year-old pregnant woman in Wisconsin who died in 1988 after having contact with pigs at a county fair in the southeast part of the state; her baby was delivered and survived. Her husband and three health-care workers who treated her also were sickened, and 19 pig exhibitors at the fair were found to have been infected without becoming ill.

In 1976, a solider died and a dozen were sickened by swine flu at Fort Dix in New Jersey. With the current outbreak, it’s too early to tell how much people previously infected with regular flu viruses may be immune to swine flu, said Yoshihiro Kawaoka, another flu researcher at UW-Madison. "It’s very difficult to predict if the virus will take off or not because we don’t know how transmissible the virus is," Kawaoka said. Still, the outbreak is "a major concern," he said. "It could have a major impact on the economy."



Putting the pieces together

May 28th 2009 | NEW YORK
From
The Economist print edition

A better understanding of how the new strain of influenza arose

YOU are now officially permitted to blame the pigs. When a strain of influenza with pandemic potential struck in April, it was generally referred to as “swine flu” because it seemed similar to an existing group of strains, known as A/H1N1, which are commonly found in pigs. But when it became clear that the new bug was being spread by people, not porkers, the pig-breeding industry complained that it was being unfairly maligned. It also became apparent that the new virus contains bits and pieces derived from avian and human strains of influenza, as well as porcine ones, further muddying its origins.

A new study, however, suggests pigs really were to blame. Several dozen researchers, led by Rebecca Garten of America’s Centres for Disease Control and Prevention (CDC), sequenced full or partial genomes of 76 samples of the new virus, which has afflicted almost 13,000 people around the world so far. In a paper published in Science, they confirm that the closest genetic relatives of the new virus are swine-flu strains from both North America and Eurasia. The virus is made of eight gene segments of known provenance but which have not previously been seen in this combination. The genetic material in them is indeed a hotchpotch derived from avian, human and swine sources, but all eight segments come most recently from pigs.


On the positive side, the researchers discovered that the antigens (proteins that provoke an immune response) found in different samples have remained similar to each other. That, according to Derek Smith of Cambridge University, one of the paper’s authors, may make it easier to design a vaccine against the new virus. The World Health Organisation and a number of European governments are now talking to manufacturers about expediting the development of such a vaccine and, on May 22nd, American officials announced a $1 billion scheme with the same goal.

The worrying news is that the study found the genetic material in the new influenza is significantly different from that in its known close relatives. This, they conclude, means the bug was circulating and evolving undetected in swine for quite some time before the first people were infected. In other words, the early-warning systems did not work.

Another cause for concern is that Canadian officials recently confirmed that the new strain has hopped from humans back into pigs in Alberta. Because swine are natural mixing vessels for influenza strains from different species (hence the hotchpotch found by Dr Garten and her colleagues), the fear is that a deadlier form could emerge and jump back into humans.

This new study does not answer the big questions of how, exactly, the virus crossed over to humans and why it kills some people and not others—in particular, why it hits the young (and thus, presumably, healthy) harder than the elderly. A different study by the CDC has found that nearly two-thirds of swine-flu infections in America have been in people aged between five and 24, whereas only 1% of cases affected those over 65. This is the reverse of the pattern seen in seasonal flu, which kills thousands of old people every winter. One possible explanation, according to Anne Schuchat of the CDC, is that “older adults might have been in contact a long time ago with a virus similar to the one we see now.” That, she surmises, might give them an immunity to this new menace that young people lack.

Two million Americans face heightened cancer risks from air pollution, EPA says

June 24, 2009

Robin Bravender


Two million Americans face increased cancer risks of greater than 100 in a million from exposure to toxic air pollution, according to a U.S. EPA report released today. EPA estimates that all 285 million U.S. residents have an increased cancer risk of greater than 10 in a million from exposure to air toxics. The average cancer risk, based on 2002 pollution levels, is 36 in a million. The agency has asserted that levels above a 100-in-a-million risk level are generally unacceptable.


The data comes from a county-by-county analysis of toxic air pollution released today in a survey known as the National Air Toxics Assessment (NATA). The report covers 181 air toxics and diesel particulate matter and estimates risks from exposure to emissions from industrial sources and mobile sources such as cars and trucks. "The implication for me is we still have a long way to go to reduce toxic air pollution to protect the public," said John Walke, a senior attorney at the Natural Resources Defense Council. "It still shows an unacceptable number of Americans being exposed to cancer risk solely attributed to air pollution on top of all the other risks from smoking and indoor air pollution and other risks." Mobile emissions account for about 30 percent of the overall cancer risk, the study found. The majority of that risk comes from benzene, a carcinogen that is released into the air by burning coal and oil. Gasoline service stations and motor vehicle exhaust also release benzene.


Other contributors to cancer risks include local industry emissions, which make up about 25 percent of the average overall risk, and "background" pollutants with no known emission sources. Those "background" toxics, including carbon tetrachloride, account for the remaining 45 percent of overall cancer risk. The study is based on 2002 data and is the first such document released by EPA since 2006, when the agency analyzed 1999 data. The new report does not account for changes in air quality since 2002. The agency has already begun work on the next such analysis that will focus on 2005 emissions inventory data.


EPA study site

The Sky

by Charles Baudelaire

 

Where'er he be, on water or on land,
Under pale suns or climes that flames enfold;
One of Christ's own, or of Cythera's band,
Shadowy beggar or Crœsus rich with gold;
 
Citizen, peasant, student, tramp; whate'er
His little brain may be, alive or dead;
Man knows the fear of mystery everywhere,
And peeps, with trembling glances, overhead.
 
The heaven above? A strangling cavern wall;
The lighted ceiling of a music-hall
Where every actor treads a bloody soil--
 
The hermit's hope; the terror of the sot;
The sky: the black lid of the mighty pot
Where the vast human generations boil!

vis medicatrix naturae

Closing the Farm to Plate Knowledge Gap
by Rob Smart
Published on Friday, June 19, 2009 by Civil Eats


In the battle for the hearts and minds (and pocket books) of everyday Americans, the large corporate players in today's industrial food system must be pleased. Consumer advocates for sustainable, healthy food are fighting with farmers, not because either picked a fight with the other, but because the knowledge gap between them has grown so expansive that is understandings rule the day. Credit the gap to industrial specialization and consumer marketing, which I will return to in a moment. Often times, these misunderstandings turn personal, further driving apart two groups that have much to gain by working together. How this benefits the industrial food players may not be obvious, but by fighting amongst ourselves, we are paying less attention to the mechanized system generating massive amounts of unhealthy, environmentally unfriendly food and unprecedented concentrations of profits.

For the average consumer, and likely many farmers, the "black box" of industrial food is a mystery. There is little to no transparency, except through increasingly common investigative journalism and documentaries, which industrialists and their associations quickly line up to discredit. Keeping us in the dark allows industrial food processors and large food retailers to paint an idyllic picture of grassy fields and red barns backed annually by an estimated $33 billion1 spent on advertising to reinforce a desired, yet highly inaccurate image of where our food comes from. Unfortunately, they have most of us fooled, which is why it is critical that we - consumers and farmers alike - find a shared set of priorities to unite our voices in securing safe, healthy, tasty food for generations to come. Let us abandon overused stereotypes and language that divides us, and instead concentrate on educating consumers about where the food they eat comes from, including industrial and "alternative" food systems. Closing the farm-to-plate knowledge gap won't be easy. With the earliest advances in agriculture resulting in food surpluses, people, no longer physically needed on the farm, moved to urban centers to pursue non-agricultural careers. As the years passed and the complexity of the food system increased, people came to rely, exclusively in most cases today, on food processors and retailers to provide for them. In effect, we traded knowledge for convenient, cheap food.

On the surface, this seems like a great tradeoff, and for most of agriculture's history it has been. Civilizations prospered. Farmers made a decent living. Consumers readily found fresh produce, meats, and other ingredients to prepare wholesome, nutritious, tasty meals. But things started to change. Industrialization intensified. Corporate consolidation accelerated. Seeds became intellectual property (protected by patents). High-paid lobbyists proliferated. Politicians bowed. And, most important, people stopped paying attention. Take a snap shot of today's food system. Study the details. What you find are a number of increasingly dramatic side effects that most people are not aware of, most of which are getting worse. Today's average farmer makes about 55 percent less money for the food they grow than they did 50 years ago. According to the USDA [1], farmers' share of consumer food expenditures dropped from about $0.40 per dollar in 1950 to around $0.19 in 2006. The balance of consumer expenditures, termed the Marketing Bill, goes to "value-add" (i.e., industrial food companies) While farmers' financial situations have deteriorated, food manufacturers' fortunes have skyrocketed to the tune of $3.1 trillion in revenues per year with above average profit margins. Judging by the fact [2] that the Top 50 Food Processors and Top 50 Supermarket & Grocery Chains all have over $1.0 billion in annual sales, with Wal-Mart topping the list at nearly $100 billion, increasing concentrations of power are clear. One billion people are obese, thanks in part to value-add convenience foods (e.g., fast food, prepared meals, snacks, sodas), massive advertising campaigns, and time-constrained lifestyles (e.g., two income households with kids). This, while another one billion people go hungry, bypassed because they are unable to provide profit margins required by industrial food.
According to the U.S. Centers for Disease Control, obesity (one of the "western diseases" attributed to diet) accounted for $75 billion [3] in extra medical costs in 2003.

The Journal of the American Medical Association attributed some 112,000 premature deaths in 2000 to obesity. These additional health care costs, half of which are paid for by taxpayers, have all but erased the cost-of-living savings claimed by the makers of cheap, convenient food. And it's going to get worse before it gets better. Analysis by the United Nations' Food and Agriculture Organization reports that agriculture contributes 14% of human-released greenhouse gases each year, through methane from livestock and rice paddies, nitrous oxide from fertilizers, and fossil fuel use during production. In an era where controlling carbon emissions is critical, the industrialized food system must change or give up market share to environmentally friendly alternatives. We have turned our food over to a system that doesn't have our best interests in mind, despite what billions of dollars of advertising tell us. Power is concentrated, not by farms or consumers, but by multi-national corporations. Increasing complexity rules the day, making it harder for even those in industry to keep food safe. And the halls of Congress are jammed with food system lobbyists fighting for more power, or, at a minimum, maintaining the status quo. It's up to us - farmers and consumers - to take back control of the food we eat. At a minimum, we need to fight for the checks and balances needed to ensure safe, affordable, and environmentally-friendly food for generations to come. It won't be easy given the stacked deck industry is playing with. But by thoughtfully considering each other's perspectives, while separating ourselves from the complex, concentrated, industrial food system, we will find the common ground necessary to drive the change we seek.

© 2009 Civil EatsRob Smart is a food entrepreneur focusing on regional food systems and consumer retail experiences. He blogs on alternative food systems at Every Kitchen Table [4] and micro-blogs on Twitter as Jambutter

'When Adam dalf, and Eve span, who was thanne a gentilman? From the beginning all men were created equal by nature, and that servitude had been introduced by the unjust and evil oppression of men, against the will of God, who, if it had pleased Him to create serfs, surely in the beginning of the world would have appointed who should be a serf and who a lord'
-- John Ball, 14th century martyr --


New Strain Of H1N1 Swine Flu Virus Identified In Brazil

17 Jun 2009


Scientists in Brazil say they have isolated and identified a new strain of the A(H1N1) swine flu virus from a patient who was hospitalized in São Paulo in April and who has since made a complete recovery. The scientists don't know if the new strain causes more severe infections. The new strain came from a sample isolated from a 26-year old São Paulo man who started to have symptoms of flu shortly after returning from Mexico. He was hospitalized on 24 April and has since made a full recovery. While in hospital the patient gave a sample for analysis. A team at the Instituto Adolfo Lutz in São Paulo, led by virologist Dr Terezinha Maria de Paiva, isolated the new strain, A/São Paulo/1454/H1N1, from this sample at the end of April.
Using electron microscopes, another team at Instituto Adolfo Lutz, led by Cecília Luiza Simões, looked at nucleotide sequences in the new strain. They looked in particular at segments number 4 and 7. Segment 4 codes for the protein Hemagglutinin (HA) which is responsible for virus infectivity and triggers the production of antibodies in the human immune system. Segment 7 codes for the matrix proteins (MP) M1 and M2, which help the virus to develop and maintain its structure. When they compared segment 4 and segment 7 of the new A/São Paulo/1454/H1N1 strain against the novel swine flu reference strain A/Califórnia/04/H1N1 they found that segment 7 appeared to be "completely conserved" while segment 4 showed a number of discrete alterations in nucleotide and amino acid sequences.


The complete nucleotide sequences for these HA and MP segments have been published in GenBank, the American open access gene sequence database, under access numbers GQ247724 (for the HA gene) and GQ250156 (for the MP). News of the new strain, together with the newly reported deaths of two people in Argentina to the swine flu virus, have added to fears that South America is heading for a tough winter dominated by the flu pandemic. Together with the two new deaths in Argentina, there are two in Chile, and another in Colombia, bringing the total number of officially recorded deaths to swine flu in South America to 5. On Tuesday, Chile's reported total of lab confirmed cases leapt from 2,355 to 3,125. Argentina has reported 733 cases, Peru 113, Brazil 69, Ecuador 84 and four other South American countries have reported nearly 120 between them, according to AFP news agency.


The Southern Hemisphere is entering the flu season now, whereas production for the swine flu virus vaccine is still months away from completion, so southern countries will have to face the pandemic without them. While the current strain appears to cause mostly mild infections with few deaths compared to the number of cases, there are fears that it will mutate to a more severe form. And the worry is, that the more "hosts" that are present in a population without immunity, the bigger the chance that it will mutate. The last time this happened with a pandemic strain was the 1918 Spanish flu which killed millions of people worldwide. It started as a mild version, mutated to a much deadlier form and then returned in a second wave. And like this new strain of H1N1 swine flu, the group most severely affected was healthy young adults, unlike the seasonal flu which mostly strikes the sick and the elderly.
-- GenBank
Sources: AFP, Instituto Adolfo Lutz.written by: Catharine Paddock, PhD Copyright: Medical News TodayNot to be reproduced without permission of Medical News Today


World hunger 'hits one billion'
22:29 GMT, Friday, 19 June 2009 23:29 UK

One billion people throughout the world suffer from hunger, a figure which has increased by 100 million because of the global financial crisis, says the UN. The UN's Food and Agriculture Organisation (FAO) said the figure was a record high. Persistently high food prices have also contributed to the hunger crisis. The director general of the FAO said the level of hunger, one-sixth of the world's population, posed a "serious risk" to world peace and security. The UN said almost all of the world's undernourished live in developing countries, with the most, some 642 million people, living in the Asia-Pacific region. In sub-Saharan Africa, the next worst-hit region, the figure stands at 265 million. Just 15 million people are left hungry in the developed world. "The silent hunger crisis - affecting one-sixth of all of humanity - poses a serious risk for world peace and security," said Jacques Diouf. "We urgently need to forge a broad consensus on the total and rapid eradication of hunger in the world and to take the necessary actions."

'Contradiction'
The increase in the number of hungry people was blamed on lower incomes and increased unemployment, which in turn reduced access to food by the poor, the UN agency said. But it contrasted sharply with evidence that much of the developed world is richer than ever before.

WORLD HUNGER

Asia-Pacific: 642m
Sub-Saharan Africa: 265m
Latin America and Caribbean: 53m
Middle East and North Africa: 42m
Developed world: 15m
Source: United Nations Food and Agriculture Organization

"It's the first time in human history that we have so many hungry people in the world," said FAO spokesman Kostas Stamoulis, director of the organisation's development department. "And that's a contradiction, because a lot of the world is very rich despite the economic crisis." Mr Diouf urged governments to provide development and economic assistance to boost agriculture, particularly by smallholder farmers. "Investment in agriculture must be increased because for the majority of poor countries a healthy agricultural sector is essential to overcome poverty and hunger and is a pre-requisite for overall economic growth," he said.

Urban suffering
The UK's international development ministry (Dfid) said the figures were "a scandal" and said it was helping some of the poorest farmers in the world to boost the amount of food they produce. "In the last year we have pledged more than £900 million to lift millions out of hunger to help farmers boost agriculture production," a Dfid spokesman said. The UN warns that poor people living in cities will probably face the most severe problems in coping with the global recession, because lower export demand and reduced foreign investment are likely to hit urban jobs harder. Many migrants to urban areas would be likely to return to rural areas, it added, transferring the burden. Incomes have also dropped "substantially" in some developing countries where families depend on remittances from relatives working abroad. With the financial crisis hitting all parts of the world more or less simultaneously, developing countries have less room to adjust, the UN agency says.
Food prices

Among the pressures is the reality that borrowing from international capital markets is "more limited" in a global crisis, the FAO said. Food costs in developing countries now seem more expensive, despite prices in world markets declining during the food and fuel crisis of 2006-08, it added. They remained on average 24% higher in real terms by the end of 2008 compared to 2006. "For poor consumers, who spend up to 60% of their incomes on staple foods, this means a strong reduction in their effective purchasing power," the FAO said.


Animal farm: pig in the middle
The 2009 flu pandemic highlights the urgent need for an independent international body for research into human diseases that originate in animals.
Nature 459, 889 (18 June 2009) doi:10.1038/459889a; Published online 17 June 2009

When animal pathogens make the leap into humans — as has happened with the 2009 pandemic virus that originated in swine — animal-health scientists can find themselves in an awkward position. Unlike their colleagues in public health, who focus their energies on protecting the planet's 6.8 billion humans, animal-health specialists tend to work through government agencies, whose primary mission is to promote and protect national and international livestock and meat trade. This focus on commerce can sometimes lead to conflicts of interest, as well as some policy positions that border on denial. Since the first outbreaks of the 2009 pandemic virus in the United States and Mexico, for example, the Paris-based World Organisation for Animal Health (OIE) has expended considerable energy trying to keep people from calling the virus 'swine flu'. The OIE's quite legitimate concern is that this nomenclature might adversely affect trade, with countries taking unnecessary measures such as culling herds, or invoking trade bans on pigs and pork. From a strictly scientific point of view, however, there is abundant genetic evidence that the name is appropriate. It is a reassorted swine influenza virus that has jumped from pigs to humans.

The OIE has also played down the possibility that the 2009 pandemic flu might be spreading in pigs, noting that it has not been found in any animals outside of one farm in Canada. But how vigorous has the search been? There is no requirement that the authorities be notified of flu in pigs, as the animals generally recover, and farmers have little incentive to report an outbreak in their herds given the potential repercussions. Furthermore, little funding has been available for extensive surveillance. A case in point is the European Surveillance Network for Influenza in Pigs, whose paltry 100,000 (US$139,000) in annual funding expired in March, just a month before the pandemic strain was first detected. Yet public-health researchers say that if the virus is circulating in pigs, and moving back and forth between pigs and humans, it increases the risk that the virus will genetically reassort into a more dangerous pathogen (see page 894).

The human–animal disease interface is fraught with such competing agendas. But to the OIE's credit, it has had a key role in creating a body that could be a model for a credible, honest broker. Founded jointly with the United Nations' Food and Agriculture Organization (FAO) in 2005, the OIE/FAO Network of Expertise on Animal Influenza (OFFLU) has been bringing together labs working on surveillance and research of human infectious diseases that have arisen in animals. OFFLU has also been outspoken on the need for countries to share virus samples and sequences for research (see Nature 440, 255–256; 2006) and has built important bridges with the World Health Organization (WHO) and other public-health agencies. Surveillance of human diseases that originate in animals remains in the nineteenth century. What is needed now is international support for a greatly expanded OFFLU-like network that has enough funding to do its own research and to coordinate global surveillance efforts on influenza and other diseases emerging from animals. The WHO and other public-health organizations should also be made an integral part of the network. The 2009 pandemic has forced scientists to confront the elephant — or pig — in the room, which is that surveillance of human diseases that originate in animals remains in the nineteenth century (see Nature 440, 6–7; 2006), and is chronically underfunded. Animal- and public-health bodies must now step up and fund a serious joint initiative in this area.


FDA Warns Web Sites against Marketing Fraudulent H1N1 Flu Virus Claims


June 15, 2009 -- Media Inquiries: Christopher Kelly, 301-796-4676, christopher.kelly@fda.hhs.govConsumer Inquiries: 888-INFO-FDA


The U.S. Food and Drug Administration is enforcing the laws that protect consumers from illegal products marketed through the Internet that claim to diagnose, prevent, mitigate, treat or cure the 2009 H1N1 flu virus. On May 1, 2009, the FDA warned consumers regarding products related to the 2009 H1N1 flu virus offered on the Internet. The products involved are those that are promoted and marketed to diagnose, mitigate, prevent, treat, or cure the 2009 H1N1 flu virus but are not approved, cleared, or authorized by the FDA. The agency advised operators of offending Web sites that they must take immediate action to ensure that they are not marketing products intended to diagnose, mitigate, prevent, treat, or cure the 2009 H1N1 flu virus that have not been cleared, approved, or authorized by the FDA. Since then, the FDA has issued more than 50 warning letters to offending Web sites and as a result, more than 66 percent of these Web sites have removed the offending claims and/or products. “We are committed to aggressively pursuing those who attempt to take advantage of a public health emergency by promoting and marketing unapproved, uncleared, or unauthorized products,” said Margaret A. Hamburg, M.D., Commissioner of Food and Drugs. “We have achieved some success and will remain vigilant in our efforts to protect consumers from these fraudulent, potentially dangerous products.” Examples of unapproved, uncleared, or unauthorized products targeted by the FDA include:


--A shampoo that claimed to protect against the H1N1 flu virus;


--A dietary supplement that claimed to protect infants and young children from contracting the H1N1 flu virus;


--A “new” supplement that claimed to cure H1N1 flu infection within four to eight hours;


--A spray that claimed to leave a layer of ionic silver on one’s hands that killed the virus;--Several tests that have not been approved to detect the H1N1 flu virus;


--An electronic instrument costing thousands of dollars that claimed to utilize “photobiotic energy” and “deeply penetrating mega-frequency life-force energy waves” to strengthen the immune system and prevent symptoms associated with H1N1 viral infection.



The FDA’s warning letters are consistent with an aggressive strategy the agency put into place to protect consumers from individuals or businesses that promote fraudulent claims for products in an attempt to take advantage of the public’s concerns about the 2009 H1N1 flu virus. Unapproved, uncleared, or unauthorized products that claim to diagnose, mitigate, prevent, treat or cure the 2009 H1N1 flu are illegal and a potentially significant threat to the public health. These warning letters were the result of daily Internet surfs conducted by the FDA’s Office of Enforcement, Office of Criminal Investigations, and staff from the Center for Devices and Radiological Health, the Center for Drug Evaluation and Research, and the Center for Food Safety and Applied Nutrition. The warning letters issued by e-mail and the FDA requested a response within 48 hours. In addition, the FDA posted the offending Web sites and products on the agency’s Web site. “Taking swift action to inform unsuspecting consumers about products that could be dangerous to their health is a major priority for the FDA,” said Hamburg. The FDA will consider further civil or criminal enforcement action against those Web sites that fail to resolve the violations cited in warning letters. Actions could include seizure, injunction, and criminal prosecution.

Guidance for pregnancy in wake of the novel influenza (h1n1)
courtesy of the Center for Disease Control

May 7th, 2009

Human infections with a novel influenza A (H1N1) virus that is easily transmissible among humans were first identified in April 2009. The epidemiology and clinical presentations of these infections are currently under investigation. There are insufficient data available at this point to determine who at higher risk for complications of novel influenza A (H1N1) virus infection. However, it’s reasonable to assume that the same age and risk groups who are at higher risk for seasonal influenza complications also should be considered at higher risk for novel influenza A (H1N1) complications. Evidence that influenza can be more severe in pregnant women comes from observations during previous pandemics and from studies among pregnant women who had seasonal influenza. An excess of influenza-associated excess deaths among pregnant women were reported during the pandemics of 1918–1919 and 1957–1958. Adverse pregnancy outcomes have been reported following previous influenza pandemics, with increased rates of spontaneous abortion and preterm birth reported, especially among women with pneumonia. Case reports and several epidemiologic studies conducted during interpandemic periods also indicate that pregnancy increases the risk for influenza complications for the mother and might increase the risk for adverse perinatal outcomes or delivery complications.

Pregnant women with novel influenza A (H1N1) virus would be expected to present with typical acute respiratory illness (e.g., cough, sore throat, rhinorrhea) and fever or feverishness. Many pregnant women will go on to have a typical course of uncomplicated influenza. However, for some pregnant women, illness might progress rapidly, and might be complicated by secondary bacterial infections including pneumonia. Fetal distress associated with severe maternal illness can occur. Pregnant women who have suspected novel influenza A (H1N1) virus infection should be tested, and specimens from women who have unsubtypeable influenza A virus infections should have specimens sent to the state public health laboratory for additional testing to identify novel influenza A (H1N1).




Flu (Influenza) Antigenic Shift

courtesy of the National Institute of Allergy and Infectious Diseases

The genetic change that enables a flu strain to jump from one animal species to another, including humans, is called antigenic shift. Antigenic shift can happen in three ways:

Antigenic Shift 1 - A duck or other aquatic bird passes a bird strain of influenza A to an intermediate host such as a chicken or pig. A person passes a human strain of influenza A to the same chicken or pig. When the viruses infect the same cell, the genes from the bird strain mix with genes from the human strain to yield a new strain. The new strain can spread from the intermediate host to humans.


Antigenic Shift 2- Without undergoing genetic change, a bird strain of influenza A can jump directly from a duck or other aquatic bird to humans.


Antigenic Shift 3- Without undergoing genetic change, a bird strain of influenza A can jump directly from a duck or other aquatic bird to an intermediate animal host and then to humans. The new strain may further evolve to spread from person to person. If so, a flu pandemic could arise.

Overactive Immune Response Key Contributor to Lethality
Mouse Study Reveals New Clues about Virulence of 1918 Influenza Virus

The first comprehensive analysis of an animal’s immune response to the 1918 influenza virus provides new insights into the killer flu, report federally supported scientists in an article appearing online today in the journal Nature. Key among these insights, they found that the 1918 virus triggers a hyperactive immune response that may contribute to the lethality of the virus. Furthermore, their results suggest that it is the combination of all eight of the 1918 flu virus genes interacting synergistically that accounts for the exceptional virulence of this virus. Michael G. Katze, Ph.D., of the University of Washington School of Medicine, Seattle, a grantee of the National Institute of Allergy and Infectious Diseases (NIAID), one of the National Institutes of Health (NIH), led the research team with University of Washington’s John Kash, Ph.D. The work with the fully reconstructed 1918 virus was conducted by coauthor Terrence Tumpey, Ph.D., in a biosafety level 3-enhanced laboratory at the U.S. Centers for Disease Control and Prevention in Atlanta.

Triple-Reassortant Swine Influenza A (H1) in Humans in the United States, 2005–2009

Published at www.nejm.org May 7, 2009 (10.1056/NEJMoa0903812)

Triple-reassortant swine influenza A (H1) viruses — containing genes from avian, human, and swine influenza viruses — emerged and became enzootic among pig herds in North America during the late 1990s. Methods We report the clinical features of the first 11 sporadic cases of infection of humans with triple-reassortant swine influenza A (H1) viruses, occurring from December 2005 through February 2009, until just before the current epidemic of swine-origin influenza A (H1N1) among humans. These data were obtained from routine national influenza surveillance reports and from joint case investigations by public and animal health agencies.

Results The median age of the 11 patients was 10 years (range, 16 months to 48 years), and 4 had underlying health conditions. Nine of the patients had had exposure to pigs, five through direct contact and four through visits to a location where pigs were present but without contact. In another patient, human-to-human transmission was suspected. The range of the incubation period, from the last known exposure to the onset of symptoms, was 3 to 9 days. Among the 10 patients with known clinical symptoms, symptoms included fever (in 90%), cough (in 100%), headache (in 60%), and diarrhea (in 30%). Complete blood counts were available for four patients, revealing leukopenia in two, lymphopenia in one, and thrombocytopenia in another. Four patients were hospitalized, two of whom underwent invasive mechanical ventilation. Four patients received oseltamivir, and all 11 recovered from their illness.

Conclusions From December 2005 until just before the current human epidemic of swine-origin influenza viruses, there was sporadic infection with triple-reassortant swine influenza A (H1) viruses in persons with exposure to pigs in the United States. Although all the patients recovered, severe illness of the lower respiratory tract and unusual influenza signs such as diarrhea were observed in some patients, including those who had been previously healthy.

Reconstruction of the 1918 Influenza Pandemic Virus


CDC researchers and their colleagues have successfully reconstructed the influenza virus that caused the 1918-19 flu pandemic, which killed as many as 50 million people worldwide. A report of their work, "Characterization of the Reconstructed 1918 Spanish Influenza Pandemic Virus," was published in the October 7 issue of Science. The work is a collaboration among scientists from CDC , Mount Sinai School of Medicine , the Armed Forces Institute of Pathology , and Southeast Poultry Research Laboratory. The following questions and answers describe this important research and related issues.


Early Pandemic Flu Wave May Protect Against Worse One LaterEvidence Shows Spring Outbreak in 1918 May Have Immunized Against Deadlier Second Wave

New evidence about the worldwide influenza pandemic of 1918-1919 indicates that getting the flu early protected many people against a second deadlier wave, an article co-authored by an NIH epidemiologist concludes. American soldiers, British sailors and a group of British civilians who were afflicted by the first mild wave of influenza in early 1918 apparently were more immune than others to the severe clinical effects of a more virulent strain later in the year, according to the paper published in the Nov. 15 issue of the Journal of Infectious Diseasesby medical historian John Barry, staff scientist Cécile Viboud, Ph.D., of the NIH’s Fogarty International Center and epidemiologist Lone Simonson, Ph.D., of The George Washington University.

Interregional spread of influenza through United States described by virus type, size of population and commuting rates and distance

Researchers at the National Institutes of Health (NIH) conclude that the regional spread of annual influenza epidemics throughout the United States is more closely connected with rates of movement of people to and from work than with geographical distance or air travels. They also found that epidemics spread faster between more populous locations. This valuable study highlights new approaches to using historical data sources and statistical analysis to create epidemiological models. These models not only help us understand the transmission of influenza but also could guide policy for its control" said Dr. Elias A. Zerhouni, NIH Director.

Bacterial Pneumonia Caused Most Deaths in 1918 Influenza PandemicImplications for Future Pandemic Planning

For Immediate ReleaseTuesday, August 19, 2008
Anne A. Oplinger

Bacterial Pneumonia Caused Most Deaths in 1918 Influenza PandemicImplications for Future Pandemic Planning

The majority of deaths during the influenza pandemic of 1918-1919 were not caused by the influenza virus acting alone, report researchers from the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health. Instead, most victims succumbed to bacterial pneumonia following influenza virus infection. The pneumonia was caused when bacteria that normally inhabit the nose and throat invaded the lungs along a pathway created when the virus destroyed the cells that line the bronchial tubes and lungs.
A future influenza pandemic may unfold in a similar manner, say the NIAID authors, whose paper in the Oct. 1 issue of The Journal of Infectious Diseases is now available online. Therefore, the authors conclude, comprehensive pandemic preparations should include not only efforts to produce new or improved influenza vaccines and antiviral drugs but also provisions to stockpile antibiotics and bacterial vaccines as well. The work presents complementary lines of evidence from the fields of pathology and history of medicine to support this conclusion. "The weight of evidence we examined from both historical and modern analyses of the 1918 influenza pandemic favors a scenario in which viral damage followed by bacterial pneumonia led to the vast majority of deaths," says co-author NIAID Director Anthony S. Fauci, M.D. "In essence, the virus landed the first blow while bacteria delivered the knockout punch."

NIAID co-author and pathologist Jeffery Taubenberger, M.D., Ph.D., examined lung tissue samples from 58 soldiers who died of influenza at various U. S. military bases in 1918 and 1919. The samples, preserved in paraffin blocks, were re-cut and stained to allow microscopic evaluation. Examination revealed a spectrum of tissue damage "ranging from changes characteristic of the primary viral pneumonia and evidence of tissue repair to evidence of severe, acute, secondary bacterial pneumonia," says Dr. Taubenberger. In most cases, he adds, the predominant disease at the time of death appeared to have been bacterial pneumonia. There also was evidence that the virus destroyed the cells lining the bronchial tubes, including cells with protective hair-like projections, or cilia. This loss made other kinds of cells throughout the entire respiratory tract — including cells deep in the lungs — vulnerable to attack by bacteria that migrated down the newly created pathway from the nose and throat. In a quest to obtain all scientific publications reporting on the pathology and bacteriology of the 1918-1919 influenza pandemic, Dr. Taubenberger and NIAID co-author David Morens, M.D., searched bibliography sources for papers in any language. They also reviewed scientific and medical journals published in English, French and German, and located all papers reporting on autopsies conducted on influenza victims. From a pool of more than 2,000 publications that appeared between 1919 and 1929, the researchers identified 118 key autopsy series reports. In total, the autopsy series they reviewed represented 8,398 individual autopsies conducted in 15 countries.

The published reports "clearly and consistently implicated secondary bacterial pneumonia caused by common upper respiratory flora in most influenza fatalities," says Dr. Morens. Pathologists of the time, he adds, were nearly unanimous in the conviction that deaths were not caused directly by the then-unidentified influenza virus, but rather resulted from severe secondary pneumonia caused by various bacteria. Absent the secondary bacterial infections, many patients might have survived, experts at the time believed. Indeed, the availability of antibiotics during the other influenza pandemics of the 20th century, specifically those of 1957 and 1968, was probably a key factor in the lower number of worldwide deaths during those outbreaks, notes Dr. Morens. The cause and timing of the next influenza pandemic cannot be predicted with certainty, the authors acknowledge, nor can the virulence of the pandemic influenza virus strain. However, it is possible that — as in 1918 — a similar pattern of viral damage followed by bacterial invasion could unfold, say the authors. Preparations for diagnosing, treating and preventing bacterial pneumonia should be among highest priorities in influenza pandemic planning, they write. "We are encouraged by the fact that pandemic planners are already considering and implementing some of these actions," says Dr. Fauci.
Visit http://www.PandemicFlu.gov for one-stop access to U.S. Government information on avian and pandemic flu. NIAID conducts and supports research — at NIH, throughout the United States, and worldwide — to study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID Web site at http://www.niaid.nih.gov. The National Institutes of Health (NIH) — The Nation's Medical Research Agency — includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.
--------------------------------------------------------------------------------Reference: DM Morens et al. Predominant role of bacterial pneumonia as a cause of death in pandemic influenza: Implications for pandemic influenza preparedness. The Journal of Infectious Diseases DOI: 10.1086/591708 (2008).


CDC Telebriefing on Investigation of Human Cases of H1N1 Flu

May 15, 2009, 1:30 p.m. ET


Highlights


Operator: The next is from Helen Branswell, The Canadian Press.  Your line is up.


Helen Branswell: Hi, thank you very much for taking my question.  I was just looking at flu watch for this week, or FluView, excuse me.  And it′s really kind of interesting to see there seems to be quite a spike in activity not just for the new H1N1 but for a bunch of different types of flu.  Is that an artifact of the fact that more testing is being done now than woo normally be done this time of the year, or is something weird going on? 


Dan Jernigan: I can with great certainty say that that is a reflection of the amount of testing that′s going on.  For those of you that follow this kind of thing, if you′re looking at the curves, you will see that there′s a nice bell shape to our season from last year -- from this past season, rather.  And that significant increase at the end of the season, that significant increase is a reflection of this profound amount of testing that has gone on in the last few weeks.  The interesting thing, as you point out is that when we start testing everyone that looks like they have flu, we find a number of them that do have flu and what we′re find is only about half of those have the h 1 -- the new h1 virus.  The others have the circulating seasonal kinds of viruses.  And so what that means is that there is even at this end of the usual season, the regular season, a fair amount of regular viruses that are circulating in addition to these from h1.  But I think the important message is that we would be expecting to see the season to be slowing down or almost completely stopped from the kinds of surveillance systems that we normally monitor.  But what we′re seeing is that there are some areas that actually have reports of the amounts of respiratory disease that are coming into their clinics that are equivalent to peak influenza season, and so that′s an indicator to us that there′s something going on with the amount of influenza disease out there.  But in terms of us enumerating that, we′re not able to do that at this point.


Operator: The next is from John Cohen, Science Magazine.  Your line is open.


John Cohen: I did.  You′re saying there′s increased activity from normal surveillance but it′s confusing given that there′s so much more surveillance, how do you factor out whether it′s the increased surveillance that′s leading to this abnormal activity when 50 percent of what you′re seeing is seasonal flu? 


Dan Jernigan: Right.  I think it′s a difference between the types of surveillance systems.  So one of them is the -- what we call viral logic surveillance.  It′s where we actually collect the viruses and enumerate them, characterize them, et cetera.  And so that′s one that is completely dependent upon people sending in specimens where they can be appropriated tested and characterized.  And that′s where you see that tremendous increase at the end of this season.  The other is an influenza illness network of 4,500 clinicians and other providers that tell us how many people are coming into their clinics for all causes and also tell us how many of those people are coming in with fever and influenza-like illness symptoms.  And so that one is going to be less affected by media and by other factors and is not one that we stimulate through any kind of public health activity but would be in part, perhaps, reflective of some media interest.  But even in the time that the interest has waned, we see that those folks are still coming in.  And what we also see is that those upticks in certain regions are consistent with anecdotal reports and other reports we get of school closures and of increased illness in communities. 


Operator: The next is from David Brown, Washington Post.  Your line is open.


David Brown: Yes, Hi, thanks.  There′s a report that there is a -- yet another new H1N1 virus that has been found in the states of Durango, Zack teakous and halisco in Mexico that is distinct from both this -- this swine H1N1 and the seasonal Brisbane H1N1.  Have you heard of this?  And can you tell us anything about this? 


Dan Jernigan: We′ve heard of some reports about that, but I have not had any direct information about the specifics of that case.  So there′s ongoing dialogue between us and the folks that are in Mexico and so as we know more about that, we will be able to let people know.


Operator: The next is from Kate Trainor, aghp.  Your line is open.


Kate Trainor: Hi.  Thank you for taking my question.  I know the CDC has said you′re going to be looking very closely at the southern hemisphere for what develops down there.  So I was wondering if you can tell us what specific signs you might be looking for that SEVERE disease might or might not be coming this way in the fall.  And sort of on the other side of that, how do you weigh that information against the fact that the harder you look, the more stuff you′re going to find, kind of similar to what′s going on here as far as finding both the seasonal and new H1N1 flu in the northern hemisphere? 


Dan Jernigan: Over the last few years, the CDC and other public health agencies have been working with folks notice southern hemisphere and in tropical areas to try to characterize with the baseline what the amount of influenza is through their seasons.  For many countries in the southern hemisphere, their seasons are just now starting and will peak in the next month to two.  So we want to be able to work there to identify a couple of things in particular.  We want to look at severity and we want to look at the spread of infection.  So there are different ways to do that.  We work with the laboratories down there to characterize the viruses that are circulating.  That will tell us if virus that′s we have chosen for a vaccine are still good or the right ones that are likely to come back.  It will also tell us if there′s changes in the virus and also if there′s development of antiviral resistance.  The next thing we would want to look at is people who are admitted for SEVERE acute respiratory illness, so there are protocols and process that′s have been worked out over the last few years that will be implemented through our partners in this regions to try to characterize that.  And then finally there are estimates of the amount of influenza-like illness in the community, that we welcome working with them as well.


Operator: The next is from Kafi Drexel, New York 1.  Your line is open.


Kafi Drexel: Hi, how are you?  Earlier today in New York City′s press conference regarding the latest cluster of H1N1 at an intermediate school here, the question was posed kind of by, why has this been happening in schools?  And our outgoing health commissioner himself commented that it′s a little surprising to them because they usually don′t see this in a regular flu season where there are situations where 20 or 30 kids at a time come in with high fever on a single day.  Also, it doesn′t seem like this is impacting as many older adults as usual at this point.  So do you have any further insight as to why some of these clusters may be happening more in school environments?  Are you looking at whether or not H1N1 is acting differently in younger people?  And then also, regarding the vaccine, if you could talk a little bit more specifically on where the CDC is as far as what′s happening with that and what the thinking is as far as going ahead and developing that for fall.  Looking ahead. 


Dan Jernigan: Yes.  I think you′re pointing out an important feature of influenza, and that is that younger people are often more affected.  If we look at who gets influenza each year, the predominance, if you want to call it reservoir of influenza is in the school-aged children′ so, therefore, schools are where a younger place can congregate and share their influenza viruses amongst themselves and that often then allows for other folks to become infected as well.  For this particular H1N1, it′s following along seasonal flu in that sense.  But when we look at the blood of people who have -- that we have collected over the past few years, we′re able to see that the older you are, the more likely you might have some evidence that you could respond somewhat to the H1N1 novel virus that′s circulating.  And so what that suggests to us is that not only are skids as usual affected more, there is a chance that they may be completely naive or immune, not have any immunity to the virus.  So that suggests that we want to do something to make sure that we protect them.  And so while in the usual season, we may not close schools.  Now it may make sense to do that.  My understanding is in New York City these school closures have occurred because of the staffing issues and the number of peoples affected, and I believe that was their decision.  In terms of the vaccine, as you know, there′s many steps involved with producing a flu sax seen.   Vaccine.  And we′re working with under HHS agencies and vaccine manufacturers to go through those steps as fast as possible.