Aside from avoiding contact with possibly contaminated birds and poultry, here are other ways to avoid getting infected:
- check for the latest travel advise from the Centers for Disease Control and Prevention website or call their hotline at 1-888-246-2675 when traveling especially when it is an international trip
- when traveling to countries that are known to have bird flu outbreaks, avoid poultry farms and bird markets, and avoid contact with any surfaces that may have poultry feces or secretions
- wash hands frequently, or use alcohol based hand sanitizers
- make sure poultry dishes are cooked thoroughly, as the virus can be destroyed in high temperatures
I am often asked, “where did Bird flu come from.” There really isn’t a definitive answer, a variation of bird flu has probably been around since the dawn of humankind in one form or another. The first known avian influenza virus was identified in Italy in 1878 as a “serious disease of chickens”.
In Hong Kong 1997, the H5N1 strain of avian influenza virus was first documented, when it caused severe respiratory problems in 18 humans, of whom six died. A total culling of all chickens and removal of chicken meat from all markets in the area was supposed to put a stop to the virus, however less then 6 years later in February of 2003 another outbreak of H5N1 killed 1 person and sickened another in Hong Kong.
Recent research suggests that the Spanish flu of 1918 was a mutated form of the H1N1 virus, the name associated with the then current Bird Flu mutation. Two teams of scientists conducted this research.
One led by Sir John Skehel, director of the National Institute for Medical Research in London and another by Professor Ian Wilson of the Scripps Research Institute in San Diego.
They used a sample of lung tissue collected from the remains of an Inuit woman, in Alaska, who died during the 1918 Spanish flu and DNA samples from the remains of solders who died during world war two of the disease.
The two teams analyzed the structure of the gene and discovered how subtle alterations to the shape of a protein molecule had allowed it to move from birds to humans with such devastating effects.
Since the Hong Kong strain of the bird flu in 1997 was reported, tens of millions of birds have died of H5N1 influenza and hundreds of millions of birds were culled (slaughtered and disposed of).
All evidence suggests that if in fact the H5N1 virus were to mutate into a human transmittable disease, somewhere around 150,000,000 human deaths directly due to H5N1 infection (or two to three percent of the world’s human population) would occur.
The question seemed straight forward.
“In human medicine, most people would agree that a person gets sick with a cold or with the flu when their immune system is suppressed. Has anyone considered what is suppressing the immune system of the people and chickens in Vietnam, making them more susceptible to deadly effects of H5N1? Has anyone investigated what is suppressing the immune system of migratory birds?” The question was posed to Dr. Alex Thiermann, President of the OIE, the World Organization for Animal Health at the First Bird Flu Summit held in Washington, DC, February 27-28, 2006. His response, “No one is looking at this, in fact, no one has even thought about it” was echoed by the reporters and scientists during the ensuing coffee break.
An investigation into the immunosuppressive effects of environmental chemicals–with a particular focus on dioxin–may shed light into the seemingly scattered and disconnected outbreaks of bird flu around globe. The association between dioxin and influenza may even explain the increased number of deaths in China, Vietnam, and in particular, Indonesia.
Dioxin: The most toxic chemical on earth
Dioxin is a general term that describes a complex family of more than 400 chemicals. An unintentional waste product, dioxin is formed during industrial processes which combine chlorine with an organic substance, such as wood, pulp or paper, in the presence of heat. Production facilities that manufacture pesticides smelt copper and bleach paper all release of dioxins as by-products. Additionally, dioxin can enter the environment through the incineration of plastics, particularly those that burn municipal and medical waste.
A highly persistent chemical, dioxin can take more than 15 years to degrade to half its original concentration. If released into the local water supplies–for example, ponds and rivers–it can accumulate in fish. If not immediately absorbed by aquatic life, the remaining dioxin is rapidly deposited into the sediment. It will remain there, virtually forever, unless it moves up the food chain through grasses and frogs, becoming particularly toxic to humans and waterfowl.
Dioxin has been shown to disrupt the immune system at exposures as low as 1.0 ppt. This is the equivalent of a single drop of liquid placed in the center car a ten-kilometer (6.2 miles) long cargo train.(1) Because chemicals are usually a mixture of toxic and non-toxic compounds, a score for each chemical is developed called its Toxic Equivalency (TEQ). The TEQ of any chemical is established by comparing it to TCDD, the most toxic form dioxin in the world.
Dioxin combined with influenza viruses: Serious consequences
A definite link exists between dioxin exposure and the effect of influenza viruses on the immune system, a connection that has been studied using laboratory mice.
Research has clearly demonstrated that two types of white blood cells, Natural Killer (NK) and CD8+ cells, are exquisitely sensitive to extremely small concentrations of TCDD. Studies have shown that if mice are subjected to 100-1,000 ppt of TCDD prior to being exposed to common influenza A viruses, the number of mice that died was significantly higher than the number of control mice that were not pre-exposed to this dioxin.(2) In another study, when mice were subjected to a mere 10 ppt of TCDD one week before they were exposed to influenza A viruses, the mortality rate among the mice doubled. Researchers noted that this was the “smallest toxic dose of dioxin ever demonstrated” to inhibit the ability of the immune system to ward off the flu.(3)
In a third study, fluid extracted directly from the lungs of deceased mice demonstrated that the increased mortality seen in TCDD-exposed mice was due to the intense inflammatory action of dioxin. Death was not due to viral infection alone.(4) In other words, the combination of influenza viruses and dioxin caused so much inflammation in the lungs–due to a massive cytokine storm–that normal lung tissue was destroyed, leading to death of most of the mice.
Dioxin in Vietnam
The volume of herbicides sprayed during the U.S. conflict in Vietnam between 1961 and 1971 has been estimated that more than 19 million liters. The highest concentrations were deposited over the Mekong Delta in what is now southern Vietnam. The containers with dioxin were known as Agent Orange, identified by orange striped barrels. More than 30 years later, this persistent chemical remains in the soil and food of local residents, continuing to cause serious health problems.
Absent ongoing aerial spraying, dioxin’s primary route for entering the body is through food grown on toxic soils. Canadian researchers found that dioxin levels in soil samples throughout different regions of southern Vietnam to be as high as 898 ppt. The most extreme levels of contamination-in the area of Bien Hung Lake-were measured to be greater than 1.1 million ppt.(5)
In 2002, levels of dioxin were measured in 16 different food samples were collected from local markets around the Bien Hung Lake in southern Vietnam. The preliminary results were startling. Three of the specimens contained dioxin levels that were so extraordinarily high they were sent to a second, independent laboratory for additional analysis. The second lab confirmed the disturbing results. In the final report, chemical contaminants and large concentrations dioxin, up to 536 ppt, were detected in all 16 food samples. To put these elevated levels in perspective, the usual dioxin level found in food is less than 0.1 ppt.(6)
Dioxin, influenza and humans: a connection?
In May 2006, Indonesia reported a cluster of human bird flu cases that involved eight family members, seven of whom died. All but one person in the family appeared to have contracted the virus from another family member. This became the first reported incidence of H5N1 spreading from one person to another, and then another. Alarmed officials feared that the bird flu virus had acquired characteristics that would soon allow easy passage from human-to-human.
The members of the deceased family lived in a small village in Karo district located in the Indonesian province of North Sumatra. The Karo highland borders on Lake Toba, the world’s largest volcanic lake. The largest lake in Southeast Asia, Toba has been deteriorating since 1998, defenseless against Indorayon, a paper, pulp and rayon manufacturer owned by multinational companies and funded by the World Bank. Untill it was shut down, Indorayon was the largest polluter of Lake Toba in the past decade, dumping tons of chlorine and dioxin into the waters.
Interestingly, hundreds, perhaps thousands, of individuals with H5N1 influenza have not been sick enough to require medical care, as confirmed by Dick Thompson, spokesperson for the WHO in March, 2005.(7) However, between 2003 and April, 11, 2007, there have been 291 cases and 171 deaths, with 61% of the deaths in Vietnam and Indonesia. An investigation, perhaps including a fat biopsy, should be undertaken to determine if those who died had significantly higher concentrations of dioxin in their body than those who have been exposed to H5N1 and remained well or fully recovered.
What can be done?
A global pandemic is brewing, but not because a virus may “jump species” and rapidly circumnavigate the globe, wiping out everyone in its wake. It appears that only those most at risk will be affected. But critically important information is missing: What is each person’s individual level of risk? Beyond spending billions on global bureaucratic preparedness, true prevention is in order through developing tests and detoxification methods for humans.
Instead of funding the development a vaccine that as a marginal chance of being effective, billions of dollars would be better spent funding international environmental clean up programs. Legislative initiatives that put enforcement teeth into international treaties that are already on the books may be the best way of aborting disaster.
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(1) Quynh, Hoang Trong, MD, et al. “Long-term consequences of Vietnam War,” Nordic News Network, Report to the Environmental Conference on Cambodia, Laos and Vietnam.
(2) Burleson, G. R., et al. “Effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on influenza virus host resistance in mice,” Toxicological Sciences, 29 (1996): 40-47
(3) Burleson, G. R., et al. “Effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on influenza virus host resistance in mice,” Toxicological Sciences, 29 (1996): 40-47.
(4) Luebke, R. W, et al. “Mortality in dioxin-exposed mice infected with influenza: mitochondrial toxicity (Reye’s-like syndrome) versus enhanced inflammation as the mode of action,” Toxicological Sciences 69 (2002): 109-116.
(5) Schecter, A., Quynh, H. T., Pavuk, M., Papke, O., Malisch, R., Constable, J. D. “Food as a source of dioxin exposure in the residents of Bien Hoa City, Vietnam,” Journal of Occupational and Environmental Medicine 45 (2003): 781-788. PMID: 12915779.
(6) Schecter A., et al. “Food as a source of dioxin exposure in the residents of Bien Hoa City, Vietnam,” Journal of Occupational and Environmental Medicine 45 (2003): 781-788. PMID: 12915779.
(7) 23 Roos, Robert. “Relatives of avian flu patients have asymptomatic cases,” CIDRAP News, 9 March 2005.
The World Health Organization (WHO) makes reports and updates regarding new human cases of infection with bird flu. The only subtype that can cause severe illness to people is Influenza A /H5N1 virus, initially it affects chickens, ducks and other birds by the process of mutation they can become highly pathogenic. Because highly pathogenic viruses can survive for long periods in tissue, water and in the environment, especially when temperatures are low is transmitted very easily in chickens and other birds through direct contact with feces and secretions from infected birds, eggs, feed, water, cages equipment, vehicles and clothing. Public health authorities monitor human illnesses associated with avian influenza. In Hong-Kong occured for the first time infection both in humans and poultry and were killed about 1.5 million chickens.
In China and Hong-Kong avian influenza A (H9N2) virus infection affected two children who recovered. The source was unknown, but suspected the poultry.
In Virginia, 2002 an outbreak of H7N2 among poultry was descovered but,with no human victims. Canada, 2004: human infections among poultry workers with H7N3.
Thailand and Vietnam human infections with H5N1. Azerbaijan, Cambodia, China, Djibouti, Egypt, Indonesia, Iraq, Thailand, Turkey, 2006: Human infections with H5N1 occurred as a result of contact with infected poultry and with infected death swangs. Cambodia, China, Indonesia, Thailand and Vietnam, 2005 two persons have been infected with H5N1 as result of consuming uncooked duck blood. China two cases of patogenic infections with avian influenza A (H5N1) have been confirmed in a family travelling through China. Netherlands, 2003 were reported outbreaks of influenza A (H7N7) in several farms, after which in pigs and people, 90 people were confrmed with bird flu virus H7N7 in association with cases of eye conjunctivitis, one death occured at a veterinarian with acute respiratory distress syndrome and other complications after having direct contact with infected poultry. In New York, 2003 there has been registered one case a patient with respiratory symptoms which recovered in few weeks and tests confirmed it had been avian influenza A (H7N2) virus. Signs and symptoms of bird flu in humans are similar to other influenza viruses: sore throat and cough, fever, muscle weakness and/or pain, eye infections, with life-threatening complications such as: severe viral pneumonia, respiratory distress syndrome, multi- organ failure.
U.S. Food and Drug Administration suggests the following antiviral agents supposed to prevent and treat avian influenza: amantadine, rimantadine, oseltamivir, and zanamivir. They may be not always effective it has been demonstrated that viruses are resistent to amantadine and rimantadine. In the United States they are not in use any more for the treatment or prevention (prophylaxis) of influenza A. Specialists are monitoring the resistence of avian influenza A viruses to influenza antiviral medications.