Health Department Offers Tips To Avoid Norovirus Infection

With outbreaks of viral gastroenteritis, or "stomach flu," continuing to be reported across the commonwealth and nation, the Pennsylvania Department of Health is reminding the general public about ways they can help to avoid norovirus infection -- a common cause of the illness.

"Norovirus infection is very common this time of year and it's very contagious," said state Health Secretary Dr. Calvin B. Johnson. "If you have symptoms of norovirus, such as vomiting and diarrhea, you should try to stay home and practice good hygiene, like washing your hands frequently and thoroughly to avoid spreading the illness to others."

Norovirus symptoms often begin suddenly and can include nausea, stomach cramping, vomiting and diarrhea. Norovirus illness can be a difficult experience for those affected, but it is normally short-lived and people recover within 12 to 60 hours.

The spread of norovirus can be prevented by following some simple guidelines:

-- Frequently wash your hands, especially after using the bathroom and changing diapers, and before eating or preparing food.

-- Anyone ill with diarrhea should not prepare food for other people. In particular, people with diarrhea should not work in restaurants, day care centers, or medical settings unless they are cleared to do so by their doctor or the local health department.

-- Carefully wash fruits and vegetables, and steam oysters before eating them.

-- Thoroughly clean and disinfect contaminated surfaces immediately after an episode of diarrhea or vomiting by using a bleach-based household cleaner.

-- Immediately remove and wash clothing or linens that may be contaminated with virus after an episode of diarrhea or vomiting (use hot water and soap).

-- Flush or discard any vomit and/or stool in the toilet and make sure that the surrounding area is kept clean.

Because norovirus is very contagious, sudden outbreaks can result when people bring the infection into facilities such as hospitals, residential and nursing homes and schools. No one who has suffered from vomiting and diarrhea should visit or work in crowded places until they have been completely free from symptoms for at least 48 hours.

For most healthy individuals, drinking plenty of fluids and resting at home is sufficient to recover from a norovirus infection and there is no need for hospital treatment. However, the elderly or very young can sometimes get more severe infection and they, or anyone else who is concerned about their medical condition, should talk to their doctor for advice.

For more information about norovirus, visit the Centers for Disease Control and Prevention Web site at http://www.cdc.gov/ncidod/dvrd/revb/gastro/norovirus.htm.

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Study Uncovers A Lethal Secret Of 1918 Influenza Virus

In a study of non-human primates infected with the influenza virus that killed 50 million people in 1918, an international team of scientists has found a critical clue to how the virus killed so quickly and efficiently.

Writing this week (Jan. 18, 2007) in the journal Nature, a team led by University of Wisconsin-Madison virologist Yoshihiro Kawaoka reveals how the 1918 virus - modern history's most savage influenza strain - unleashes an immune response that destroys the lungs in a matter of days, leading to death.

The finding is important because it provides insight into how the virus that swept the world in the closing days of World War I was so efficiently deadly, claiming many of its victims people in the prime of life. The work suggests that it may be possible in future outbreaks of highly pathogenic flu to stem the tide of death through early intervention.

The study "proves the 1918 virus was indeed different from all of the other flu viruses we know of," says Kawaoka, a professor in the UW-Madison School of Veterinary Medicine and at the University of Tokyo.

The new study, conducted at the Public Health Agency of Canada's National Microbiology Laboratory in Winnipeg, Manitoba, utilized the 1918 flu virus, which has been reconstructed by researchers using genes obtained from the tissues of victims of the great pandemic in a reverse genetics process that enables scientists to make fully functioning viruses.

"In 1918, the existence of viruses had barely been recognized. In fact, the influenza virus wasn't identified until 1933. Thanks to recent technological advancements, we are now able to study this virus and how it wreaked havoc around the globe," explains Darwyn Kobasa, research scientist with the Public Health Agency of Canada and lead author of the new study. "This research provides an important piece in the puzzle of the 1918 virus, helping us to better understand influenza viruses and their potential to cause pandemics."

By infecting monkeys with the virus, the team was able to show that the 1918 virus prompted a deadly respiratory infection that echoed historical accounts of how the disease claimed its victims.

Importantly, the new work shows that infection with the virus prompted an immune response that seems to derail the body's typical reaction to viral infection and instead unleashes an attack by the immune system on the lungs. As immune cells attack the respiratory system, the lungs fill with fluid and victims, in essence, drown. The mechanisms that contribute to the lethality of the virus were uncovered by University of Washington researchers using functional genomics, a technique in which researchers analyze the gene functions and interactions. Learning more about the virulence mechanisms of the 1918 flu virus may help researchers understand how to keep the virus from causing such a severe immune response.

"This study in macaques, combined with our earlier research showing the host response in mice infected with the 1918 flu, suggests that the host immune response is out of control in animals infected with the virus," said Michael G. Katze, professor of microbiology at the University of Washington in Seattle, who led the functional genomics portion of the new study and led the previous mouse-based study. "Our analysis revealed potential mechanisms of virulence, which we hope will help us develop novel antiviral strategies to both outwit the virus and moderate the host immune response."

The same excessive immune reaction is characteristic of the deadly complications of H5N1 avian influenza, the strain of bird flu present in Asia and which has claimed nearly 150 human lives but has not yet shown a capacity to spread easily among people.

"What we see with the 1918 virus in infected monkeys is also what we see with H5N1 viruses," Kawaoka says, suggesting that the ability to modulate immune response may be a shared feature of the most virulent influenza viruses.

In the new study, conducted in a high-level biosafety laboratory (BSL 4) at the Public Health Agency of Canada's National Microbiology Laboratory, seven primates were infected with the reconstructed 1918 virus. Clinical signs of disease were apparent within 24 hours of infection and within eight days euthanization was necessary. The rapid course of the disease mirrors how quickly the disease ran its course in its human victims in 1918.

Upon infection, the virus grew rapidly in the infected animals, suggesting the agent somehow sets the stage for virulent infection: "Somehow, early in infection, this virus does something to the host that allows it to grow really well," says Kawaoka. "But we don't know what that is."

Knowing that the virus does something early in infection to trigger such a devastating immune response may provide biomedical researchers with clues about how to intervene and stop or mitigate the virus' potentially lethal effects, Kawaoka says.

"Things may be happening at an early time point (in infection), but we may be able to step in and stop that reaction."

###

In addition to Kawaoka, authors of the new Nature paper include Darwyn Kobasa, Steven M. Jones, Hideki Ebihara, Friederike Feldman, Judie B. Alimonti, Lisa Fernando, Yan Li and Heinz Feldman of Canada's National Microbiology Laboratory; Kyoko Shinya of Japan's Tottori University; John C. Kash and Michael G. Katze of the University of Washington; John Copps of the Canadian Food Inspection Agency's National Centre for Foreign Animal Disease; and Yasuko Hatta, Jin Hyun Kim, Peter Halfmann and Masato Hatta of UW-Madison.

The new study was supported by the Public Health Agency of Canada, the Japanese Ministries of Education, Culture, Sports, Science and Technology, and private grants to Kawaoka. - Terry Devitt.

Contact: Yoshihiro Kawaoka
University of Wisconsin-Madison

Built-in Molecular Brakes Curb The Sniffles

Researchers at Johns Hopkins have discovered how our anti-infection machinery turns itself down and limits the sniffles, congestion and fevers that are a side effect of the campaign against invading viruses. The discovery seems to solve part of the mystery of why the misery of the common cold lasts only so long.

The key to curbing any excess activity by the immune system apparently rests with Carabin, a newly discovered protein made by the specialized white blood cells that march in when a virus attacks.

Results of a study published online this week at Nature show that Carabin "acts like an internal brake to dial down the speed and intensity of an immune response so that it doesn't go too fast or too far, or careen out of control and attack healthy cells," says Jun O. Liu, Ph.D., professor of pharmacology, neuroscience and oncology at Hopkins.

Searching for proteins that control immunity, Liu and his team homed in on those that latch on to parts of cells that are active during an infection. "Carabin popped out," says Liu.

To see what Carabin could do, the research team added it to white blood cells already primed and ready for anti-infection action. The more Carabin in the cells, the less active the cells became.

When people are infected with a cold virus, for example, the virus enters cells and hijacks its works so that the cells become viral factories. The immune system's white blood cells go after these infected cells not only by fielding chemicals that kill them directly, but also by turning on genes that help out. When Liu and his group added Carabin to cells and then studied such genes, they discovered that Carabin disabled the "on" switches, keeping the genes off.

"By now we were pretty convinced that Carabin can turn down the immune system, so the next question was, 'what controls Carabin?'" Liu noted.

Tracking Carabin to its origins, the researchers said they were surprised to learn that viral infection not only turns on the immune system machinery, but also triggers the making of Carabin, which in turn shuts off the immune response.

"It's like having a built-in timer to keep the immune system in check," says Liu.

If Carabin turns out, after further study, to be a keystone natural inhibitor of immune responses, Liu added, it may prove useful in stopping such unwanted immune reactions as the rejection of transplanted organs.

###

The research was funded by the Department of Pharmacology at the Johns Hopkins School of Medicine and the Keck Foundation.

Authors on the paper are Fan Pan, Luo Sun, David Kardian, Katharine Whartenby, Drew Pardoll and Liu, all of Hopkins.

On the Web:

http://www.hopkinsmedicine.org/pharmacology/research/liu.html

http://www.hopkinsmedicine.org/pharmacology/index.html

http://www.nature.com/

Contact: Audrey Huang
Johns Hopkins Medical Institutions

Association Of Tuberculosis With Smoking And Indoor Air Pollution

All works published in PLoS Medicine are open access. Everything is immediately available without cost to anyone, anywhere to read, download, redistribute, include in databases, and otherwise use subject only to the condition that the original authorship is properly attributed. Copyright is retained by the authors. The Public Library of Science uses the Creative Commons Attribution License.

Association of Tuberculosis with smoking and indoor air pollution

Smokers have an increased risk of tuberculosis (TB) infection, TB disease, and of dying from TB compared to people who do not smoke.

A new study from Hsien-Ho Lin and colleagues at Harvard School of Public Health reviewed the published evidence for an association between tobacco smoking, passive smoking, and indoor air pollution from fuels such as wood and charcoal and the risk of infection, disease, and death from TB. Among hundreds of reports from electronic databases, the authors reviewed 33 eligible papers on tobacco smoking and TB, five papers on passive smoking and TB, and five on indoor air pollution and TB.

The researchers separately assessed different aspects of TB risk: TB infection as measured by a positive tuberculin skin test, TB disease, and mortality from TB. They found an approximately 2-fold increase in risk of TB infection among smokers as compared with nonsmokers. The great majority of studies evaluating the link between active smoking and TB disease or TB mortality also showed an association, but these data could not be combined together because of wide potential differences between the studies. In addition, there was some association of TB with passive smoking, and also with indoor air pollution, though the evidence for these associations was more limited, and will need to be confirmed by further work.

The authors conclude that "TB control programs might benefit from a focus on interventions aimed at reducing tobacco and indoor air pollution exposures, especially among those at high risk for exposure to TB".

Citation: Lin H, Ezzati M, Murray M (2007) Tobacco smoke, indoor air pollution and tuberculosis: A systematic review and meta-analysis. PLoS Med 4(1): e20.

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New Proteomic Method To Detect Inflammation In Amniotic Fluid

All works published in PLoS Medicine are open access. Everything is immediately available without cost to anyone, anywhere to read, download, redistribute, include in databases, and otherwise use subject only to the condition that the original authorship is properly attributed. Copyright is retained by the authors. The Public Library of Science uses the Creative Commons Attribution License.

New proteomic method to detect inflammation in amniotic fluid

A score that measures the proteomic profile of amniotic fluid may predict inflammation before delivery. Researchers from Yale University, led by Catalin Buhimschi, have previously identified a set of four protein markers that were closely associated with inflammation in the amniotic fluid, and developed a score based on these proteins В­the "Mass Restricted" (MR) score. This score has been shown to be able to identify women at risk of preterm delivery. In the current study, the researchers assessed whether MR scores were associated with the outcome of pregnancy; the presence of infection in the placenta, and severe infection in the newborn baby.

169 women recruited into the study had a sample of amniotic fluid taken as part of their routine clinical management from which the protein MR score was calculated, and evidence of bacterial infection was sought. These results were then related to length of time until delivery, presence of placental inflammation after birth, and whether there was evidence of infection in the babies. In line with findings from their previous studies, women with a higher MR score gave birth sooner. There was also agreement between the MR score and evidence of inflammation in the placenta, and mothers with a high MR score were more likely to give birth to babies with suspected or confirmed sepsis.

In this group of women, the MR score seemed to be the most accurate in predicting inflammation when compared with other tests for inflammation such as white cell count, and may therefore provide a useful test for recognizing women at risk of preterm delivery and babies at risk of poor outcome. However, although promising, a further evaluation of the test in different populations will be needed before it could become a standard procedure in the clinic.

Citation: Buhimschi CS, Bhandari V, Hamar BD, Bahtiyar MO, Zhao G, et al. (2007) Proteomic profiling of the amniotic fluid to detect inflammation, infection, and neonatal sepsis. PLoS Med 4(1): e18.

About the PUBLIC LIBRARY OF SCIENCE

PLoS is a nonprofit organization of scientists whose aim is to make the world's scientific and medical research literature a public resource. We are funded by a grant from the Gordon and Betty Moore Foundation to develop a publishing program based on the Open Access business model, whereby the costs of publication are paid upfront so that anyone with an internet connection can have access to the content, in a free and unrestricted manner. Our immediate goal is to launch two top-tier journals - PLoS Biology (in October, 2003) and PLoS Medicine (in 2004).

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Billions Of Dollars Saved In U.S. By Polio Vaccination

A new study by researchers at the Harvard School of Public Health (HSPH) finds that polio vaccination in the United States has resulted in a net savings of over $180 billion, even without including the large, intangible benefits associated with avoided fear and suffering. This first study to retrospectively demonstrate the enormous benefits of polio vaccination appears as part of a special issue on polio in the December 2006 issue of Risk Analysis.

The history of polio vaccination in the U.S. spans over 50 years and includes different phases of the disease, multiple vaccines, and a sustained significant commitment of financial resources. Lead author of the study, Kimberly Thompson, associate professor of risk analysis and decision science at HSPH, emphasized that this study "should help people understand and better appreciate the huge economic savings that can come from investments in public health interventions."

The researchers, Professor Thompson and Dr. Radboud Duintjer Tebbens, a research associate at HSPH, estimated the costs and the effectiveness of historical polio vaccination strategies. They found that the U.S. invested over $35 billion between 1955 and 2005 and will continue to invest billions into the future to pay for polio vaccination. They estimated that these historical and future investments translate into over 1.7 billion vaccinations that prevent approximately 1.1 million cases of paralytic polio and over 160,000 deaths, thus saving Americans hundreds of billions of dollars in treatment costs.

Dr. Stephen Cochi, U.S. Centers for Disease Control and Prevention Global Immunization Division Senior Advisor and an expert on polio said, "This study documents the extraordinary power of vaccines not only as highly effective tools to prevent disease, disability, and death, but to provide enormous economic savings to society."

Although the last case of paralytic polio from wild poliovirus occurred in the U.S. in 1979, poliovirus outbreaks currently still occur around the world and American children continue to receive polio vaccinations. Dr. Bruce Aylward, Director of the Global Polio Eradication Initiative at the World Health Organization, stated that, "as we stand on the brink of eliminating wild polioviruses around the world, these results provide a glimpse of the massive economic benefits of global polio eradication." To date, the Global Polio Eradication Initiative has succeeded in reducing the annual cases of paralytic polio from an estimated 350,000 cases in 1988 to less than 2,000 cases in 2006. The only remaining areas of the world that have not yet disrupted transmission include regions in four countries (Afghanistan, India, Nigeria, and Pakistan). Thompson and Duintjer Tebbens also co-authored several other articles in the same issue that characterize the risks and costs of future options for polio risk management, the costs and value of global surveillance, and the trade-offs associated with different choices related to outbreak response.

Support for this study was provided by the Harvard Kids Risk Project. http://www.kidsrisk.harvard.edu/. Support for other studies by the authors in the special issue was provided by the U.S. Centers for Disease Control and Prevention.

Harvard School of Public Health is dedicated to advancing the public's health through learning, discovery, and communication. More than 300 faculty members are engaged in teaching and training the 900-plus student body in a broad spectrum of disciplines crucial to the health and well being of individuals and populations around the world. Programs and projects range from the molecular biology of AIDS vaccines to the epidemiology of cancer; from risk analysis to violence prevention; from maternal and children's health to quality of care measurement; from health care management to international health and human rights. For more information on the school visit: http://www.hsph.harvard.edu/.

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Informing Partners Can Help Cut Sexually Transmitted Infections

Doctors should encourage patients with sexually transmitted infections to tell their partners to seek treatment and, in some cases, provide home testing kits or drugs to help reduce infection rates, says a new study on bmj.com.

Partner notification is an important part of managing most curable sexually transmitted infections, but the stigma attached to sexually transmitted infections often makes this difficult.

Researchers analysed 14 studies involving 12,389 women and men diagnosed with a common sexually transmitted infection, including chlamydia, gonorrhoea, and non-specific urethritis.

Three new strategies were used in these studies that made it easier for patients to share responsibility for the care of their sexual partners: patient delivered partner therapy (where a patient is given drugs or a prescription for their partners), home sampling for partners, and providing additional information for partners.

All three strategies were more effective than simple patient referral (where a patient is simply encouraged to tell their partners to seek treatment).

However, the team found that simple patient referral, with extra information about the infection and its treatment that the patient can give to their partners, seemed to be as effective as patient delivered partner therapy.

Involving patients with sexually transmitted infections in shared responsibility for the care of their sexual partners improves outcomes, say the authors. Health professionals should consider these three strategies for the management of individual patients.

Click here to view paper: http://press.psprings.co.uk/bmj/january/partners.pdf.

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Bacteria In Staph Infections Can Cause Necrotizing Pneumonia

Researchers at the Texas A&M Health Science Center Institute of Biosciences and Technology at Houston have discovered a toxin present in the bacteria responsible for the current nationwide outbreak of staph infections also has a role in an aggressive pneumonia that is often fatal within 72 hours.

Their study is available online in Science Express and in an upcoming issue of the journal Science.

"The virulence of CA-MRSA (community-associated methicillin-resistant Staphylococcus aureus) strains that produce the PVL (Panton Valentine leukocidin) toxin presents a nightmare scenario," said M. Gabriela Bowden, Ph.D., research assistant professor at HSC-IBT and co-senior author. "If the community-acquired strain establishes itself in the hospital setting, it will be difficult to contain."

The most common cause of staph infections, S. aureus is a bacteria found on the skin or in the nose of about 25-30 percent of people. It also can be the culprit in minor skin infections like pimples and boils, as well as major diseases like meningitis, endocarditis, toxic shock syndrome and pneumonia.

In their study, Dr. Bowden and her colleagues at the HSC-IBT Center for Extracellular Matrix Biology used mice to analyze S. aureus Panton Valentine leukocidin (PVL), a pore-forming toxin secreted by bacterial strains associated with both the current outbreak of CA-MRSA and necrotizing pneumonia.

CA-MRSA causes serious skin and soft tissue infections in healthy persons who have not been recently hospitalized or undergone invasive medical procedures, while necrotizing pneumonia destroys healthy lung tissue and can be fatal within 72 hours. With the PVL toxin, the bacterium also attacks infection-fighting white blood cells (leukocytes).

In the 1940s, the high mortality rate from S. aureus was abated by penicillin, but the bacteria soon developed a resistance. Methicillin provided new treatment options for infections in the late 1950s, but as of the late 1990s, it has become resistant.

In December, the United Kingdom had its first documented report of fatal necrotizing pneumonia cases caused by PVL-positive CA-MRSA. Eight hospitalized patients developed infections from CA-MRSA, and two died. It was previously believed the hospitals were free of these virulent strains of CA-MRSA.

Testing several bacterial strains, the HSC-IBT researchers learned PVL itself has an enhanced ability to disrupt cells in the body, and PVL-positive S. aureus has a greater capacity to attach to and colonize the lung, the latter resulting in necrotizing pneumonia.

"Our research shows in vivo that PVL is sufficient to cause pneumonia," Dr. Bowden said. "PVL-producing S. aureus overexpress other factors that enhance inflammation and bacterial attachment to the lung. These combined effects result in a vicious cycle of tissue destruction and inflammation, explaining the rapid onset and lethal outcome of this type of pneumonia."

Using these findings, the next step is additional studies to identify targets for potential development of therapies to treat S. aureus infections, including the PVL-positive strain.

"The present study underscores the aggressiveness of these strains and the urgent need to develop new strategies to battle these infections," Dr. Bowden said.

Other Science Express study contributors from the Center for Extracellular Matrix Biology were Magnus Höök, Ph.D., director and professor; Eric Brown, Ph.D., assistant professor (now at The University of Texas School of Public Health at Houston); Maria Labanderia-Rey, postdoctoral fellow; Vanessa Vazquez, graduate student; and Elena Barbu, graduate student. Florence Couzon, Sandrine Boisset, Michele Bes, Yvonne Benito, Jerome Etienne and François Vandenesch from the University of Lyon and Hospices Civils de Lyon (France) also contributed.

Grants from the HSC, French Ministry of Research, National Institutes of Health, and Neva and Wesley West and Hamill Foundations supported this research.

The Texas A&M Health Science Center provides the state with health education, outreach and research. Its six components located in communities throughout Texas are Baylor College of Dentistry, the College of Medicine, the Graduate School of Biomedical Sciences, the Institute of Biosciences and Technology, the Irma Lerma Rangel College of Pharmacy, and the School of Rural Public Health.

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Americans In The Dark About Shingles

Thought you were done with the chickenpox as a kid? Think again. Shingles, a disease caused by the same virus as chickenpox, affects roughly one million Americans each year. As people age, their risk of getting shingles increases but despite its incidence many people are completely unaware of the disease.
"People don't really know about shingles unless they know someone who has had shingles, or they develop it themselves," said Stephen Tyring M.D., professor of medicine at the University of Texas Health Science Center in Houston.

The results of a recent national survey by the American Pain Foundation support Trying's position. The survey revealed that many older adults were not aware of their risk for the disease. More than half of the respondents who reported having heard of shingles were not sure of the risk factors. And many respondents were unaware of the relationship between chickenpox and shingles.

After a person gets the chickenpox, most often during childhood, the inactivated virus can live on in certain nerve cells in the body. In healthy people, the body's immune system usually keeps the virus at bay. As people age or their immune system becomes compromised, the virus can reactivate and result in shingles.

The risk of shingles increases with age. "With each decade, a person's immunity weakens, so that by 60 years of age, the likelihood of shingles significantly increases," says Tyring. "In fact, one out of two people who live to the age of 85 will have had shingles." And although seniors are at higher risk, shingles can affect people of all ages.

The first signs of shingles may not be visually noticeable. People often experience tingling, burning, itching or pain. During the first few days of symptoms, fluid-filled blisters will break out in a rash, usually on one side of the body or face. The rash is often painful and will heal in two to four weeks, in most people. However, some people experience post-herpetic neuralgia, or long-term nerve pain which can persist for months or even years after the initial rash. Long-term nerve pain caused by shingles can vary and has been described as burning, throbbing, stabbing or shooting. The older a person gets, the more he or she is at risk for long-term nerve pain.

Men and women are affected equally by shingles. "I have seen, however, in my practice that women come into the doctor's office sooner, while men tend to wait," Tyring said. Shingles patients, both men and women, are often given analgesics along with antiviral medications for treatment. "Antiviral medicines for shingles may help speed up healing and reduce pain in some patients, but if possible, treatment should begin within 72 hours of the onset of symptoms," according to Tyring.

Although the disease affects the sexes equally, its greater impact on older adults should capture the attention of women.

"Women make up more than 60 percent of population 85 years and older, so any condition that is prone to strike older people is of special concern to women," said Phyllis Greenberger, MSW, president and CEO of the Society for Women's Health Research. "Older Americans should talk to their health care providers about their risk for shingles."

To raise awareness about shingles and complications that can arise from the disease, the American Pain Foundation is sponsoring a national education program called "Spotlight on Shingles" that features a Web site and a toll-free number that people can call to receive a free informational brochure about shingles. For more information, visit http://www.spotlightonshingles.com.

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Highly Pathogenic Bird Flu Case Confirmed In South Korea

South Korean authorities have just confirmed that breeding chickens in Chonan, 55 miles south of the capital Seoul, were infected with the highly pathogenic H5N1 bird flu virus strain. This is the fifth outbreak in the country during the last three months.

Preparations are underway to cull over one-quarter of a million birds within half-a-kilometer of the farm, say officials from the Ministry of Agriculture. Measures to stem the spread of the virus also include a total restriction in the movement of birds and eggs within a 10 kilometer radius of the infected area.

Experts were surprised at this latest outbreak. Recently there had been an outbreak at Iksan, to the south of Chonan, where tens of thousands of birds had been culled. Emergency measures at Iksan had been thoroughly carried out. During the last three years over 1.2 million heads of poultry have been culled in South Korea.

Lab tests have revealed a virulent strain of the bird flu virus in bird droppings found at a reservoir about 13 miles from the infected farm in Chonan. Further tests will tell us whether it is the virulent H5N1 strain. If so, we could be looking at migratory birds as the source of the H5N1 bird flu spread.

-- Ministry of Agriculture and Forestry, Rep. of Korea (in English)
-- Ministry of Agriculture and Forestry, Rep. of Korea (in Korean)

Written by: Christian Nordqvist
Editor: Medical News Today