Fryderyk Chopin was born in Warsaw 200 years ago. By the time of his death from tuberculosis in 1849, the virtuoso and composer seemed to float gracefully above his troubled age. He came to resemble a musical "angel", "too fine, too exquisite, too perfect" for this crude world, as his great love, and great torment, the feminist novelist George Sand, once expressed it.
http://www.independent.co.uk/arts-entertainment/books/reviews/chopin-prince-of-the-romantics-by-adam-zamoyski-1937419.html
Thursday, 8 April 2010
Tbc in London
HEALTH in Haringey is among the worst in London, statistics published last week reveal.
Out of the 32 separate indicators, the borough was considered worse than the London average in 15 of them.
Worst areas included drug misuse, new cases in Tuberculosis, diabetes and male life expectancy which sits at 76.
But 35 in every 1000 residents are claiming incapacity benefit because of mental illness, according to the Department of Health report. That equals 1 in 29.
http://www.haringeyindependent.co.uk/news/7990036.Health_in_Haringey_among_worst_in_London/
Out of the 32 separate indicators, the borough was considered worse than the London average in 15 of them.
Worst areas included drug misuse, new cases in Tuberculosis, diabetes and male life expectancy which sits at 76.
But 35 in every 1000 residents are claiming incapacity benefit because of mental illness, according to the Department of Health report. That equals 1 in 29.
http://www.haringeyindependent.co.uk/news/7990036.Health_in_Haringey_among_worst_in_London/
India's Tuberculosis Program Provides Hope to Millions
April 7, 2010
India has one of the most severe burdens of tuberculosis in the world, accounting for one-fifth of the global incidence. TB is India's leading cause of adult illness and death from a communicable disease. Most of those infected are 15- to 59-year-old adults, the most economically productive segment of society.
In 1993, the Indian Government began to treat tuberculosis patients with the World Health Organization-recommended Directly Observed Treatment Short-course (DOTS). Left on their own, many TB patients fail to take the entire regimen of medication, contributing to the spread of drug-resistant TB for which treatment is long, difficult and expensive. Under DOTS, healthcare workers observe patients as they take their medicine.
More than one billion people covered by DOTS Strategy
In 1997 the Government formally launched the DOTS strategy nationwide. The first World Bank credit (1997- 2005) allowed rapid expansion of the DOTS strategy throughout the country. By providing free diagnostic and treatment services through public or non-public institutions, the project ensured the availability of TB diagnosis and treatment to all citizens regardless of their economic status. Full nationwide coverage of the DOTS strategy was achieved in March 2006, covering over one billion people.
"In the earlier TB control program, patients were good with collecting medicines, but we could not ensure that they took them. Now these medicines are administered at the clinic and its several satellite centers, thus ensuring that patients actually do take their medicines," said Dr. Ravinder Verma, Medical Officer In-charge, at a government Chest Clinic and HIV Center in New Delhi.
Detection and cure rates increased dramatically
The results have been dramatic. Diagnosis is far more accurate. While x-rays were used to detect the disease earlier, the sputum analysis test has increased detection levels from 30% to 70% at the national level, achieving global targets. Between 1997 and 2008, more than 9.5 million people suffering from TB were diagnosed and placed on treatment, thus saving more than 1.7 million additional lives.
Cure rates for those placed on treatment have also increased dramatically - tripling from 25% in 1997 to 86% in 2009, exceeding the global target. As a result, deaths from the disease were cut sevenfold - from 29% in 1997 to 4% in 2008.
Another key reason for the success is that the entire DOTS program is decentralized. Diagnosis done in the villages rather than in district hospitals. Quality-assured diagnostic facilities are available through more than 12,000 microscopy centers.
Moreover, more than 300,000 local health workers or trained community volunteers ensure that patients adhere to their drug regimen. Associations of medical professionals are promoting international standards for TB care. Also participating are over 250 medical colleges and some 2,500 NGOs.
http://www.reliefweb.int/rw/rwb.nsf/db900SID/SMAR-84A9DH?OpenDocument
India has one of the most severe burdens of tuberculosis in the world, accounting for one-fifth of the global incidence. TB is India's leading cause of adult illness and death from a communicable disease. Most of those infected are 15- to 59-year-old adults, the most economically productive segment of society.
In 1993, the Indian Government began to treat tuberculosis patients with the World Health Organization-recommended Directly Observed Treatment Short-course (DOTS). Left on their own, many TB patients fail to take the entire regimen of medication, contributing to the spread of drug-resistant TB for which treatment is long, difficult and expensive. Under DOTS, healthcare workers observe patients as they take their medicine.
More than one billion people covered by DOTS Strategy
In 1997 the Government formally launched the DOTS strategy nationwide. The first World Bank credit (1997- 2005) allowed rapid expansion of the DOTS strategy throughout the country. By providing free diagnostic and treatment services through public or non-public institutions, the project ensured the availability of TB diagnosis and treatment to all citizens regardless of their economic status. Full nationwide coverage of the DOTS strategy was achieved in March 2006, covering over one billion people.
"In the earlier TB control program, patients were good with collecting medicines, but we could not ensure that they took them. Now these medicines are administered at the clinic and its several satellite centers, thus ensuring that patients actually do take their medicines," said Dr. Ravinder Verma, Medical Officer In-charge, at a government Chest Clinic and HIV Center in New Delhi.
Detection and cure rates increased dramatically
The results have been dramatic. Diagnosis is far more accurate. While x-rays were used to detect the disease earlier, the sputum analysis test has increased detection levels from 30% to 70% at the national level, achieving global targets. Between 1997 and 2008, more than 9.5 million people suffering from TB were diagnosed and placed on treatment, thus saving more than 1.7 million additional lives.
Cure rates for those placed on treatment have also increased dramatically - tripling from 25% in 1997 to 86% in 2009, exceeding the global target. As a result, deaths from the disease were cut sevenfold - from 29% in 1997 to 4% in 2008.
Another key reason for the success is that the entire DOTS program is decentralized. Diagnosis done in the villages rather than in district hospitals. Quality-assured diagnostic facilities are available through more than 12,000 microscopy centers.
Moreover, more than 300,000 local health workers or trained community volunteers ensure that patients adhere to their drug regimen. Associations of medical professionals are promoting international standards for TB care. Also participating are over 250 medical colleges and some 2,500 NGOs.
http://www.reliefweb.int/rw/rwb.nsf/db900SID/SMAR-84A9DH?OpenDocument
Slum Life and Tbc -- USAID intentions
Statement from USAID Administrator Rajiv Shah on the Occasion of World Health Day
WASHINGTON, April 7 /PRNewswire-USNewswire/ -- This year the focus of World Health Day is on the world's growing urban population. The theme, "1000 cities, 1000 lives" provides an opportunity to highlight the work that is being done to improve health in urban settings. The unprecedented rate of urban growth has far outstripped the ability of these cities to provide infrastructure for new residents. This lack of infrastructure will lead to an estimated 2 billion people living in slums over the next 20 years.
The growth of slums, which results from poorly managed urban growth, can give rise to the spread of both chronic and infectious diseases. Poor air quality, lack of access to potable water, limited sanitation, and poverty can lead to higher rates of infant and child mortality, higher rates of infectious diseases such as tuberculosis, and poor nutrition.
The U.S. Agency for International Development (USAID) is working to meet the challenges of urbanization and health through our "Making Cities Work" strategy. This strategy targets the needs of the urban poor and other vulnerable people by driving economic growth and improving access to health care and quality education. The United States has also made a bold commitment to invest in healthy and productive lives as part of President Obama's Global Health Initiative. Finally, USAID's Urban Programs Team engages local governments, citizens, non-governmental organizations and the private sector to develop sustainable solutions to urban challenges.
USAID is committed to working with our partners to promote health, development and a better quality of life for people in cities around the world.
http://www.prnewswire.com/news-releases/statement-from-usaid-administrator-rajiv-shah-on-the-occasion-of-world-health-day-90094377.html
WASHINGTON, April 7 /PRNewswire-USNewswire/ -- This year the focus of World Health Day is on the world's growing urban population. The theme, "1000 cities, 1000 lives" provides an opportunity to highlight the work that is being done to improve health in urban settings. The unprecedented rate of urban growth has far outstripped the ability of these cities to provide infrastructure for new residents. This lack of infrastructure will lead to an estimated 2 billion people living in slums over the next 20 years.
The growth of slums, which results from poorly managed urban growth, can give rise to the spread of both chronic and infectious diseases. Poor air quality, lack of access to potable water, limited sanitation, and poverty can lead to higher rates of infant and child mortality, higher rates of infectious diseases such as tuberculosis, and poor nutrition.
The U.S. Agency for International Development (USAID) is working to meet the challenges of urbanization and health through our "Making Cities Work" strategy. This strategy targets the needs of the urban poor and other vulnerable people by driving economic growth and improving access to health care and quality education. The United States has also made a bold commitment to invest in healthy and productive lives as part of President Obama's Global Health Initiative. Finally, USAID's Urban Programs Team engages local governments, citizens, non-governmental organizations and the private sector to develop sustainable solutions to urban challenges.
USAID is committed to working with our partners to promote health, development and a better quality of life for people in cities around the world.
http://www.prnewswire.com/news-releases/statement-from-usaid-administrator-rajiv-shah-on-the-occasion-of-world-health-day-90094377.html
Regulation of antigen presentation by Mycobacterium tuberculosis: a role for Toll-like receptors
Regulation of antigen presentation by Mycobacterium tuberculosis: a role for Toll-like receptors
Clifford V. Harding & W. Henry Boom
Mycobacterium tuberculosis survives in antigen-presenting cells (APCs) such as macrophages and dendritic cells. APCs present antigens in association with major histocompatibility complex (MHC) class II molecules to stimulate CD4+ T cells, and this process is essential to contain M. tuberculosis infection. Immune evasion allows M. tuberculosis to establish persistent or latent infection in macrophages and results in Toll-like receptor 2 (TLR2)-dependent inhibition of MHC class II transactivator expression, MHC class II molecule expression and antigen presentation. This reduction of antigen presentation might reflect a general mechanism of negative-feedback regulation that prevents excessive T cell-mediated inflammation and that M. tuberculosis has subverted to create a niche for survival in infected macrophages and evasion of recognition by CD4+ T cells.
http://www.nature.com/nrmicro/journal/v8/n4/abs/nrmicro2321.html
Clifford V. Harding & W. Henry Boom
Mycobacterium tuberculosis survives in antigen-presenting cells (APCs) such as macrophages and dendritic cells. APCs present antigens in association with major histocompatibility complex (MHC) class II molecules to stimulate CD4+ T cells, and this process is essential to contain M. tuberculosis infection. Immune evasion allows M. tuberculosis to establish persistent or latent infection in macrophages and results in Toll-like receptor 2 (TLR2)-dependent inhibition of MHC class II transactivator expression, MHC class II molecule expression and antigen presentation. This reduction of antigen presentation might reflect a general mechanism of negative-feedback regulation that prevents excessive T cell-mediated inflammation and that M. tuberculosis has subverted to create a niche for survival in infected macrophages and evasion of recognition by CD4+ T cells.
http://www.nature.com/nrmicro/journal/v8/n4/abs/nrmicro2321.html
MicuRx Pharmaceuticals and Cumencor Pharmaceuticals
Biotechnology companies MicuRx Pharmaceuticals and Cumencor Pharmaceuticals said Wednesday they are collaborating with Pfizer Inc. to develop antibiotics for drug-resistant tuberculosis in China.
Under the deal, New York-based Pfizer will provide an upfront payment, funding for the discovery and preclinical development of antibiotics, and payments linked to the development and commercialization of any antibiotics developed through the partnership.
Financial details of the deal were not disclosed.
Cumencor Pharmaceuticals, based in China, is applying MicuRx's technology to develop antibiotics. MicuRx is based in Hayward, Calif.
http://www.businessweek.com/ap/financialnews/D9EUBI3O0.htm
Under the deal, New York-based Pfizer will provide an upfront payment, funding for the discovery and preclinical development of antibiotics, and payments linked to the development and commercialization of any antibiotics developed through the partnership.
Financial details of the deal were not disclosed.
Cumencor Pharmaceuticals, based in China, is applying MicuRx's technology to develop antibiotics. MicuRx is based in Hayward, Calif.
http://www.businessweek.com/ap/financialnews/D9EUBI3O0.htm
Wednesday, 7 April 2010
Bovine TB in Nebraska
LINCOLN – Nebraska Agriculture Director Greg Ibach today provided information on the status of bovine tuberculosis (TB) testing in the state. The update included details to wrap up the investigation into the June 2009 finding of two TB positive beef cows in a Rock County herd. Ibach also offered information in follow-up to a January announcement regarding NDA’s cooperation with South Dakota officials on the finding of a TB-positive beef cow in that state.“We are extremely pleased that after extensive testing, we did not find any additional positive cases of TB in association with the Rock County investigation,” Ibach said. “Unfortunately the disease has been found in association with another investigation.“I don’t believe this new case is indicative of a TB problem in our state,” he said. “I think it is representative of the vast scope of agriculture in Nebraska and the regionalization of the livestock industry. We are a major processor of red meat, and we are one of the largest cattle feeding states. Those factors mean NDA must exercise due diligence regarding disease surveillance and investigations.”
http://www.cattlenetwork.com/NDA-Director-Provides-Update-On-Bovine-Tuberculosis-In-Nebraska/2010-04-07/Article_Latest_News.aspx?oid=1037314&fid=CN-LATEST_NEWS_&aid=760
http://www.cattlenetwork.com/NDA-Director-Provides-Update-On-Bovine-Tuberculosis-In-Nebraska/2010-04-07/Article_Latest_News.aspx?oid=1037314&fid=CN-LATEST_NEWS_&aid=760
Tuesday, 6 April 2010
Evidence to Policy Initiative
New global health initiative will help bridge gap between knowledge, action
Sir Richard Feachem
UCSF and SEEK Development, a global health and development consulting group based in Berlin, Germany, have launched an international partnership that aims to improve global health by helping to turn scientific evidence into policy and action. The Evidence-to-Policy Initiative, or E2Pi, officially launches this week in San Francisco and Berlin, Germany. “For many of the world’s major health challenges – including HIV, tuberculosis, malaria, and maternal and child deaths – a failure to translate evidence on what works into practical health policies is costing lives,” said Sir Richard Feachem, director of the UCSF Global Health Group, which is leading the collaboration. E2Pi aims to help address some of these challenges by closing the gap between what is known and what gets done in practice. “The gap between available scientific knowledge and its application in solving global health problems is one of the reasons why poor countries suffer such a high burden of disease and premature death,” said Feachem, who was formerly the founding executive director of the Global Fund to Fight AIDS, Tuberculosis and Malaria. “E2Pi will help to address this issue by conducting rigorous and independent analyses of the available research evidence leading to specific, action-oriented recommendations to policy- and decision-makers.” Funding for the initiative’s first three years is provided by a $3.2 million grant from the Bill & Melinda Gates Foundation. E2Pi has already produced a series of briefings summarizing evidence of progress in tackling eight global health priorities (HIV/AIDS, tuberculosis, malaria, polio, immunization, maternal and child health, nutrition, and neglected tropical diseases). These briefings supported the launch of the Living Proof Project, an advocacy campaign spearheaded by the Bill & Melinda Gates Foundation that aims to sustain and increase investments in global health (www.livingproofproject.org).
Sir Richard Feachem
UCSF and SEEK Development, a global health and development consulting group based in Berlin, Germany, have launched an international partnership that aims to improve global health by helping to turn scientific evidence into policy and action. The Evidence-to-Policy Initiative, or E2Pi, officially launches this week in San Francisco and Berlin, Germany. “For many of the world’s major health challenges – including HIV, tuberculosis, malaria, and maternal and child deaths – a failure to translate evidence on what works into practical health policies is costing lives,” said Sir Richard Feachem, director of the UCSF Global Health Group, which is leading the collaboration. E2Pi aims to help address some of these challenges by closing the gap between what is known and what gets done in practice. “The gap between available scientific knowledge and its application in solving global health problems is one of the reasons why poor countries suffer such a high burden of disease and premature death,” said Feachem, who was formerly the founding executive director of the Global Fund to Fight AIDS, Tuberculosis and Malaria. “E2Pi will help to address this issue by conducting rigorous and independent analyses of the available research evidence leading to specific, action-oriented recommendations to policy- and decision-makers.” Funding for the initiative’s first three years is provided by a $3.2 million grant from the Bill & Melinda Gates Foundation. E2Pi has already produced a series of briefings summarizing evidence of progress in tackling eight global health priorities (HIV/AIDS, tuberculosis, malaria, polio, immunization, maternal and child health, nutrition, and neglected tropical diseases). These briefings supported the launch of the Living Proof Project, an advocacy campaign spearheaded by the Bill & Melinda Gates Foundation that aims to sustain and increase investments in global health (www.livingproofproject.org).
Tuberculosis World Wide
Tuberculosis kills more than 1.7 million people around the world each year, and this figure is growing as over-crowded conditions in poverty stricken areas can elevate transmission rates. The World Health Organization’s (WHO) recently published report, entitled “Multidrug and extensively drug-resistant TB (M/XDR-TB): 2010 Global Report on Surveillance and Response” outlines the prevalence of the disease and its potential global impact. In it, data from 114 countries around the world are examined to determine the extent of this “serious threat to global health.”
No retreat on TB
The following editorial appeared in the Miami Herald on Wednesday, March 31 2010:
A new report by the World Health Organization details how drug-resistant strains of tuberculosis are raising the stakes to combat this contagious disease worldwide.
A global epidemic -- and security threat -- is in the making if this airborne disease is not attacked swiftly and with precision. For South Florida, an international hub for tourists and immigrants, the threat is real.
Unfortunately, President Obama's budget proposal this year would cut $50 million from a $4 billion, five-year plan to fight TB globally and flatlines money for domestic TB-fighting programs. That's a turnaround from the Bush administration, which pushed through record levels of support to the global fund to fight AIDS, tuberculosis and malaria in 2008. This is no time to retreat.
On average, the global fund saves 3,600 lives a day, but, still, 1.7 million people die each year from TB because it goes untreated.
U.S. statistics show the number of TB cases decreased in this country by 11.4 percent in 2009, according to the Centers for Disease Control, but the rate for immigrants continues to be higher. Rates in parts of Russia, in African countries like Lesotho and in our hemisphere -- Haiti, Mexico and the Dominican Republic -- are spiking, particularly in rural regions. They need more labs to conduct TB tests and ensure the right antibiotics are tackling ever tougher strains.
Urgency matters now because new antibiotic-resistant strains of TB are emerging. New types of drugs need to be developed that can treat extensively drug-resistant tuberculosis, known as XDR-TB. So far, 58 nations have reported XDR-TB cases, and, more troublesome, there are another 79 countries that didn't track cases, so it's anyone's guess. Whether rich or poor, TB strikes indiscriminately. This is a global battle, and the United States should be leading the way -- not retreating from this menace.
A new report by the World Health Organization details how drug-resistant strains of tuberculosis are raising the stakes to combat this contagious disease worldwide.
A global epidemic -- and security threat -- is in the making if this airborne disease is not attacked swiftly and with precision. For South Florida, an international hub for tourists and immigrants, the threat is real.
Unfortunately, President Obama's budget proposal this year would cut $50 million from a $4 billion, five-year plan to fight TB globally and flatlines money for domestic TB-fighting programs. That's a turnaround from the Bush administration, which pushed through record levels of support to the global fund to fight AIDS, tuberculosis and malaria in 2008. This is no time to retreat.
On average, the global fund saves 3,600 lives a day, but, still, 1.7 million people die each year from TB because it goes untreated.
U.S. statistics show the number of TB cases decreased in this country by 11.4 percent in 2009, according to the Centers for Disease Control, but the rate for immigrants continues to be higher. Rates in parts of Russia, in African countries like Lesotho and in our hemisphere -- Haiti, Mexico and the Dominican Republic -- are spiking, particularly in rural regions. They need more labs to conduct TB tests and ensure the right antibiotics are tackling ever tougher strains.
Urgency matters now because new antibiotic-resistant strains of TB are emerging. New types of drugs need to be developed that can treat extensively drug-resistant tuberculosis, known as XDR-TB. So far, 58 nations have reported XDR-TB cases, and, more troublesome, there are another 79 countries that didn't track cases, so it's anyone's guess. Whether rich or poor, TB strikes indiscriminately. This is a global battle, and the United States should be leading the way -- not retreating from this menace.
Monday, 5 April 2010
NAME CHANGE
Today. 2010, April 5th, I've expanded the interest to add the fields of Malnutrition and Malaria, very much the problems of Africa and Asia, in a second blog.
Thursday, 28 August 2008
VACCINE AGAINST TB
http://www.bizjournals.com/seattle/stories/2008/08/25/daily19.html?ana=from_rss
The Infectious Disease Research Institute (IDRI) said it’s been awarded a $6.3 million federal grant to study a new tuberculosis vaccine.The four-year grant is from the National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health. Tuberculosis vaccines haven’t changed much in many years, according to researchers at the Seattle nonprofit.“The currently available vaccine, Bacillus Calmette-Guerin (BCG), was developed in 1921 and fails to protect most people beyond childhood,” said Rhea Coler of IDRI, said in a statement.IDRI is focusing on the making of adjuvants — an essential ingredient in several vaccines — that it believes can target specific immune pathways and improve vaccine protection
The Infectious Disease Research Institute (IDRI) said it’s been awarded a $6.3 million federal grant to study a new tuberculosis vaccine.The four-year grant is from the National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health. Tuberculosis vaccines haven’t changed much in many years, according to researchers at the Seattle nonprofit.“The currently available vaccine, Bacillus Calmette-Guerin (BCG), was developed in 1921 and fails to protect most people beyond childhood,” said Rhea Coler of IDRI, said in a statement.IDRI is focusing on the making of adjuvants — an essential ingredient in several vaccines — that it believes can target specific immune pathways and improve vaccine protection
Wednesday, 27 August 2008
TB in SIBERIA
TOMSK, RUSSIA—Prisoners in western Siberia who contract tuberculosis (TB) get sent to a forbidding complex in the heart of this provincial city. Armed guards with dogs patrol the nearby streets. Barbed wire covers the top of the outer walls. Iron bars clang shut when anyone enters. TB can keep you out of a remote Siberian prison camp, but it doesn't keep you out of jail.
And a decade ago, passing through this prison hospital's portals also posed a significant risk of premature death. Between 1991 and 2001 the incidence of TB in Russia's prisons reached a staggering 7,000 cases per 100,000 inmates, according to one estimate. Prisoners made up 25 percent of all new cases in the nation. In this oil-rich province the size of New Mexico with just over a million inhabitants, the prison TB rate reached the equivalent of 4,000 cases per 100,000 inmates, with nearly one of every 11 cases proving fatal.
The massive economic dislocation that accompanied the collapse of the Soviet Union turned Russia into an ideal breeding ground for a TB epidemic. Unemployment and alcoholism skyrocketed. Health and social services collapsed. As petty theft and violent crime soared, the prison population swelled to more than a million, with millions more moving in and out of incarceration. Many developed TB either because their immune systems, weakened by drugs, alcohol and poor nutrition, could no longer keep latent TB in check (an estimated one third of the world's population has latent TB) or they caught it from other prisoners.
The prisons in turn became an "epidemiological pump" for spreading the disease throughout the general population. Ex-prisoners, often with improperly treated TB that had mutated into the multidrug resistant form of the disease, moved back into cramped apartment blocs where, during the long, cold Siberian winters, hallways and unventilated apartments provided ideal conditions for airborne transmission to unwary neighbors, friends and family members। The annual rate of new TB cases among the general population in Russia more than doubled in the 1990s to 88 cases per 100,000 inhabitants. In Siberia the rate soared to over 130 new cases per 100,000 souls. For a comparison, the U.S. had around 10 cases per 100,000 residents per year during the same period, and currently has about four cases per 100,000 annually.
http://www.sciam.com/article.cfm?id=prison-plague-post-soviet-russia
And a decade ago, passing through this prison hospital's portals also posed a significant risk of premature death. Between 1991 and 2001 the incidence of TB in Russia's prisons reached a staggering 7,000 cases per 100,000 inmates, according to one estimate. Prisoners made up 25 percent of all new cases in the nation. In this oil-rich province the size of New Mexico with just over a million inhabitants, the prison TB rate reached the equivalent of 4,000 cases per 100,000 inmates, with nearly one of every 11 cases proving fatal.
The massive economic dislocation that accompanied the collapse of the Soviet Union turned Russia into an ideal breeding ground for a TB epidemic. Unemployment and alcoholism skyrocketed. Health and social services collapsed. As petty theft and violent crime soared, the prison population swelled to more than a million, with millions more moving in and out of incarceration. Many developed TB either because their immune systems, weakened by drugs, alcohol and poor nutrition, could no longer keep latent TB in check (an estimated one third of the world's population has latent TB) or they caught it from other prisoners.
The prisons in turn became an "epidemiological pump" for spreading the disease throughout the general population. Ex-prisoners, often with improperly treated TB that had mutated into the multidrug resistant form of the disease, moved back into cramped apartment blocs where, during the long, cold Siberian winters, hallways and unventilated apartments provided ideal conditions for airborne transmission to unwary neighbors, friends and family members। The annual rate of new TB cases among the general population in Russia more than doubled in the 1990s to 88 cases per 100,000 inhabitants. In Siberia the rate soared to over 130 new cases per 100,000 souls. For a comparison, the U.S. had around 10 cases per 100,000 residents per year during the same period, and currently has about four cases per 100,000 annually.
http://www.sciam.com/article.cfm?id=prison-plague-post-soviet-russia
Friday, 22 August 2008
OPTIONS FOR SCREENING AND TREATMENT OF TUBERCULOSIS REVIEWED
Screening for M tuberculosis infection should be targeted to persons at high risk for infection or progression to active disease. Risk factors for tuberculosis include birth in an endemic country, economically disadvantaged status, and immunosuppressive conditions. Although the TST is the standard test for diagnosis of M tuberculosis, antigen-specific interferon-gamma release assays are useful, particularly in persons with previous bacille Calmette-Guérin vaccination or possible nontuberculous mycobacteria.
The treatment of choice for most patients with latent tuberculosis infection is isoniazid monotherapy, except for those in whom primary drug-resistant tuberculosis is suspected. Directly observed combination therapy with isoniazid, rifampin, pyrazinamide, and ethambutol should be promptly started once active tuberculosis is diagnosed. Combination therapy should be administered for a 2-month "intensive phase" and should, in most cases, be followed by treatment with isoniazid and a rifamycin product for a 4- to 7-month "continuation phase."
http://www.medscape.com/viewarticle/579389
The treatment of choice for most patients with latent tuberculosis infection is isoniazid monotherapy, except for those in whom primary drug-resistant tuberculosis is suspected. Directly observed combination therapy with isoniazid, rifampin, pyrazinamide, and ethambutol should be promptly started once active tuberculosis is diagnosed. Combination therapy should be administered for a 2-month "intensive phase" and should, in most cases, be followed by treatment with isoniazid and a rifamycin product for a 4- to 7-month "continuation phase."
http://www.medscape.com/viewarticle/579389
Thursday, 21 August 2008
ACTION OF RIFAMYCIN ANTIBIOTICS
http://newswire.rockefeller.edu/?page=engine&id=799
Rifamycin antibiotics attack tuberculosis bacteria with walls, not signals
Amid concerns about the rising number of new tuberculosis cases worldwide, researchers led by Rockefeller University’s Seth A. Darst have reexamined and disproved a theory that describes how a potent class of antibiotics kills a deadly form of bacteria. The findings, which will appear in this week’s online issue of the Proceedings of the National Academy of Sciences, not only bring scientists closer to understanding how these antibiotics work but also how the bacteria become resistant to their effects.The class of antibiotics, called rifamycins, was developed in the 1950s to combat tuberculosis-causing bacteria. The problem, however, was that the bacteria fought back, quickly developing resistance. And the rate of decline for new tuberculosis cases has begun to slow during the past decade, with more than nine million people across the globe currently afflicted.
Rifamycins kill their prey by binding to RNA polymerase, the enzyme that kicks off gene expression by transcribing DNA to messenger RNA. However, the exact mechanism by which rifamycins interfere with the process had long remained unknown. A breakthrough came in 2001, when Elizabeth Campbell, a research associate in Darst’s Laboratory of Molecular Biophysics, and her colleagues showed that rifamycins bind next to RNA polymerase’s active center such that the rifamycin acts like a wall, physically blocking RNA from elongating. These results supported a steric-occlusion model for rifamycin action that explained — and continues to explain — past findings.But the newer model, proposed three years ago, describes a very different mechanism. Called the allosteric model, it proposes that rifamycins do, indeed, bind to the enzyme next to the enzyme’s active center, but instead of blocking the elongating RNA molecule, rifamycins transmit a signal to the enzyme’s active center, decreasing a magnesium ion’s ability to bind. Without the magnesium ion, Mg2+, RNA cannot be transcribed.“It was a beautiful model, but there were parts of it that didn’t add up and those parts directly conflicted with the model published in 2001,” says lead researcher Andrey Feklistov, a postdoc in the Darst lab who conducted the research along with several colleagues at Rockefeller, the Waksman Institute of Microbiology at Rutger’s University and The Public Health Research Institute of New Jersey Medical School.The steric-occlusion model suggested that the stronger the rifamycin binds — that is, the sturdier the wall — the better it would work to halt transcription. But according to the allosteric model proposed by a team from The Ohio State University, that wasn’t necessarily the case. Even if rifamycins bind strongly, the enzyme could still be rifamycin-resistant due to a blip along the long signaling pathway. “So we did what scientists do,” says Feklistov. “We took another look.”By testing the same two mutant strains of RNA polymerase that the Ohio team used, ones that had mutations along the proposed signaling pathway, the Darst team found that the mutants were resistant to rifamycin precisely because the antibiotic could not bind tightly to the enzyme. “This suggests that the steric-occlusion model best explains the available biochemical and structural evidence that has been published,” says Feklistov. Moreover, the Darst team found that rifamycins have no effect on metal ion binding to the active center, in direct contradiction to the allosteric model.Understanding the mechanism by which rifamycins kill bacteria allows scientists to better understand how the tuberculosis-causing bacteria develop resistance to the antibiotics — and develop drugs to combat this effect. “At this stage,” says Feklistov, “any evidence, positive or negative, will help focus our attention toward this goal.”
Rifamycin antibiotics attack tuberculosis bacteria with walls, not signals
Amid concerns about the rising number of new tuberculosis cases worldwide, researchers led by Rockefeller University’s Seth A. Darst have reexamined and disproved a theory that describes how a potent class of antibiotics kills a deadly form of bacteria. The findings, which will appear in this week’s online issue of the Proceedings of the National Academy of Sciences, not only bring scientists closer to understanding how these antibiotics work but also how the bacteria become resistant to their effects.The class of antibiotics, called rifamycins, was developed in the 1950s to combat tuberculosis-causing bacteria. The problem, however, was that the bacteria fought back, quickly developing resistance. And the rate of decline for new tuberculosis cases has begun to slow during the past decade, with more than nine million people across the globe currently afflicted.
Rifamycins kill their prey by binding to RNA polymerase, the enzyme that kicks off gene expression by transcribing DNA to messenger RNA. However, the exact mechanism by which rifamycins interfere with the process had long remained unknown. A breakthrough came in 2001, when Elizabeth Campbell, a research associate in Darst’s Laboratory of Molecular Biophysics, and her colleagues showed that rifamycins bind next to RNA polymerase’s active center such that the rifamycin acts like a wall, physically blocking RNA from elongating. These results supported a steric-occlusion model for rifamycin action that explained — and continues to explain — past findings.But the newer model, proposed three years ago, describes a very different mechanism. Called the allosteric model, it proposes that rifamycins do, indeed, bind to the enzyme next to the enzyme’s active center, but instead of blocking the elongating RNA molecule, rifamycins transmit a signal to the enzyme’s active center, decreasing a magnesium ion’s ability to bind. Without the magnesium ion, Mg2+, RNA cannot be transcribed.“It was a beautiful model, but there were parts of it that didn’t add up and those parts directly conflicted with the model published in 2001,” says lead researcher Andrey Feklistov, a postdoc in the Darst lab who conducted the research along with several colleagues at Rockefeller, the Waksman Institute of Microbiology at Rutger’s University and The Public Health Research Institute of New Jersey Medical School.The steric-occlusion model suggested that the stronger the rifamycin binds — that is, the sturdier the wall — the better it would work to halt transcription. But according to the allosteric model proposed by a team from The Ohio State University, that wasn’t necessarily the case. Even if rifamycins bind strongly, the enzyme could still be rifamycin-resistant due to a blip along the long signaling pathway. “So we did what scientists do,” says Feklistov. “We took another look.”By testing the same two mutant strains of RNA polymerase that the Ohio team used, ones that had mutations along the proposed signaling pathway, the Darst team found that the mutants were resistant to rifamycin precisely because the antibiotic could not bind tightly to the enzyme. “This suggests that the steric-occlusion model best explains the available biochemical and structural evidence that has been published,” says Feklistov. Moreover, the Darst team found that rifamycins have no effect on metal ion binding to the active center, in direct contradiction to the allosteric model.Understanding the mechanism by which rifamycins kill bacteria allows scientists to better understand how the tuberculosis-causing bacteria develop resistance to the antibiotics — and develop drugs to combat this effect. “At this stage,” says Feklistov, “any evidence, positive or negative, will help focus our attention toward this goal.”
TUBERCULOSIS IN CHILDREN
http://www.medindia.net/news/Tuberculosis-Control-Efforts-Must-Include-Kids-40822-1.htm
William Burman from the Denver Public Health and the University of Colorado Health Sciences Center, Denver, USA, and colleagues said that kids are an often ignored but important part of tuberculosis control efforts. In high-burden settings, children make up as much as 20 percent of new cases of active tuberculosis. Young children are also at high risk of having severe, rapidly progressive forms of tuberculosis. However, nearly 40 years after the development of short-course treatments in adults, there are still major uncertainties about dosing for children of common TB drugs. "Only in recent years has there been a substantial effort to manufacture child-friendly formulations of first-line tuberculosis drugs (such as crushable mini-pills, granules, oral suspensions)," the researchers said. "And in the past 15 years, children have been included in only one study of new agents for tuberculosis: a large Phase 3 trial evaluating once-weekly rifapentine + isoniazid for treatment of latent tuberculosis," they added. The researchers said that including children in drug development is especially critical, as the two main threats to tuberculosis control, HIV-related immunodeficiency and drug-resistant tuberculosis, challenge our ability to develop effective drug regimens. Burman and colleagues outline several traditional barriers to the involvement of children in tuberculosis drug development such as difficulty confirming TB diagnosis, concern about side effects, and regulatory requirements.
William Burman from the Denver Public Health and the University of Colorado Health Sciences Center, Denver, USA, and colleagues said that kids are an often ignored but important part of tuberculosis control efforts. In high-burden settings, children make up as much as 20 percent of new cases of active tuberculosis. Young children are also at high risk of having severe, rapidly progressive forms of tuberculosis. However, nearly 40 years after the development of short-course treatments in adults, there are still major uncertainties about dosing for children of common TB drugs. "Only in recent years has there been a substantial effort to manufacture child-friendly formulations of first-line tuberculosis drugs (such as crushable mini-pills, granules, oral suspensions)," the researchers said. "And in the past 15 years, children have been included in only one study of new agents for tuberculosis: a large Phase 3 trial evaluating once-weekly rifapentine + isoniazid for treatment of latent tuberculosis," they added. The researchers said that including children in drug development is especially critical, as the two main threats to tuberculosis control, HIV-related immunodeficiency and drug-resistant tuberculosis, challenge our ability to develop effective drug regimens. Burman and colleagues outline several traditional barriers to the involvement of children in tuberculosis drug development such as difficulty confirming TB diagnosis, concern about side effects, and regulatory requirements.
Tuesday, 11 December 2007
US statistics
Arch Intern Med. 2007;167(22):2443-2452.
Trends in Tuberculosis/Human Immunodeficiency Virus Comorbidity, United States, 1993-2004
Rachel Albalak, PhD; Richard J. O’Brien, MD; et al.
Background To our knowledge, this is the first assessment of trends in tuberculosis (TB)/human immunodeficiency virus (HIV) comorbidity in the United States based on national TB surveillance data.
Methods We analyzed all incident TB cases reported to the Centers for Disease Control and Prevention national TB surveillance system from all 50 states and the District of Columbia from 1993 through 2004. Trends in TB/HIV cases were examined according to selected demographic and clinical characteristics.
Results Cases of TB/HIV decreased from 3681 (15% of 25 108 TB cases) in 1993 to 1187 (8% of 14 515 TB cases) in 2004, accounting for 23% of the overall decrease in TB cases during this period. The TB/HIV case rate decreased from 1.4/100 000 in 1993 to 0.4/100 000 in 2004. The highest TB/HIV comorbidity rates persisted in persons aged 25 to 44 years (13.8%), males (9.7%), US-born persons (10.7%), non-Hispanic blacks (17.8%), and persons from the Northeast (11.0%) and the South (10.1%). Propensity stratification, used to account for the unequal probability of patients with TB being tested for HIV during the study period, did not show important differences in TB/HIV comorbidity trends.
Conclusions Comorbidity due to TB/HIV decreased substantially between 1993 and 2004, primarily in US-born persons in states that experienced a TB resurgence between 1985 and 1992. These decreases coincide with improvements in TB control and advances in HIV treatment and diagnosis. The overall decreases obscure the wide variation in comorbidity that exists among some demographic groups and the recent slowing in the decline over the past 3 years.
Trends in Tuberculosis/Human Immunodeficiency Virus Comorbidity, United States, 1993-2004
Rachel Albalak, PhD; Richard J. O’Brien, MD; et al.
Background To our knowledge, this is the first assessment of trends in tuberculosis (TB)/human immunodeficiency virus (HIV) comorbidity in the United States based on national TB surveillance data.
Methods We analyzed all incident TB cases reported to the Centers for Disease Control and Prevention national TB surveillance system from all 50 states and the District of Columbia from 1993 through 2004. Trends in TB/HIV cases were examined according to selected demographic and clinical characteristics.
Results Cases of TB/HIV decreased from 3681 (15% of 25 108 TB cases) in 1993 to 1187 (8% of 14 515 TB cases) in 2004, accounting for 23% of the overall decrease in TB cases during this period. The TB/HIV case rate decreased from 1.4/100 000 in 1993 to 0.4/100 000 in 2004. The highest TB/HIV comorbidity rates persisted in persons aged 25 to 44 years (13.8%), males (9.7%), US-born persons (10.7%), non-Hispanic blacks (17.8%), and persons from the Northeast (11.0%) and the South (10.1%). Propensity stratification, used to account for the unequal probability of patients with TB being tested for HIV during the study period, did not show important differences in TB/HIV comorbidity trends.
Conclusions Comorbidity due to TB/HIV decreased substantially between 1993 and 2004, primarily in US-born persons in states that experienced a TB resurgence between 1985 and 1992. These decreases coincide with improvements in TB control and advances in HIV treatment and diagnosis. The overall decreases obscure the wide variation in comorbidity that exists among some demographic groups and the recent slowing in the decline over the past 3 years.
Sunday, 9 December 2007
More recent history -- Christmas seals
This year the American Lung Association is celebrating 100 years of Christmas Seals® by launching a new Christmas Seals(R) website, http://www.christmasseals.org. "Most Americans alive today have no vivid memories of how widespread deadly tuberculosis was before the 1950s, but it claimed entire families in this country, struck down people from all walks of life, often in their prime."
Jacob Riis, a journalist best known as the author of How the Other Half Lives, pleaded in a newspaper article for someone in America to develop a stamp or seal like the ones he saw being sold in Denmark as a method of raising funds to provide treatment to those without means. Emily Bissell, an American Red Cross volunteer from a prominent Delaware family, took up Riis' challenge. She designed the first Christmas Seal using the American Red Cross proprietary cross and sold them in her local post office. While not a substitute for official U.S. postage, she encouraged people to buy and affix these seals to holiday packages to demonstrate commitment to helping treat tuberculosis. Sales, however, were slow. Leigh Mitchell Hodges, a columnist for the Philadelphia Inquirer, came to the rescue, convincing his editor to run a picture of the seal every day leading up to Christmas and to publish stories about tuberculosis. Buoyed by this publicity, Ms. Bissell succeeded beyond her wildest dreams, and the American Lung Association, then known as the National Tuberculosis Society, gained a means of raising funds.
Jacob Riis, a journalist best known as the author of How the Other Half Lives, pleaded in a newspaper article for someone in America to develop a stamp or seal like the ones he saw being sold in Denmark as a method of raising funds to provide treatment to those without means. Emily Bissell, an American Red Cross volunteer from a prominent Delaware family, took up Riis' challenge. She designed the first Christmas Seal using the American Red Cross proprietary cross and sold them in her local post office. While not a substitute for official U.S. postage, she encouraged people to buy and affix these seals to holiday packages to demonstrate commitment to helping treat tuberculosis. Sales, however, were slow. Leigh Mitchell Hodges, a columnist for the Philadelphia Inquirer, came to the rescue, convincing his editor to run a picture of the seal every day leading up to Christmas and to publish stories about tuberculosis. Buoyed by this publicity, Ms. Bissell succeeded beyond her wildest dreams, and the American Lung Association, then known as the National Tuberculosis Society, gained a means of raising funds.
Saturday, 8 December 2007
BCG Disease
A vaccine meant to protect against tuberculosis is jeopardising the lives of HIV-infected infants, warn experts in a major new report. They call for improvements to vaccination programmes to avoid increasing the health risks for children whose immune systems are weakened by HIV.
The report focuses on how the “global epidemics of HIV and tuberculosis has exploded to create a deadly co-epidemic”, that is rapidly spreading in sub-Saharan Africa. It warns that about a third of the world’s 40 million people with HIV/AIDS are co-infected with TB, and that the mortality rate these people is five times higher than that for tuberculosis alone.
It also notes that the use of the Bacille Calmette-Guérin (BCG) vaccine against TB in babies with HIV may actually be making the situation worse.
Veronica Miller, a co-author of the report and director of the Washington, DC-based Forum for Collaborative HIV Research, said that there is an "urgent" need for changes to vaccination programmes in sub-Saharan Africa, including improved testing to know whether infants have HIV before vaccinating them against TB.
Live strain
The growing threat of TB and the drug-resistant forms of this bacterial infection that commonly attacks the lungs has increased the need for widespread vaccination, experts say.
Unfortunately, there is a lack of new vaccines against TB, which kills nearly 2 million people each year. For this reason, doctors must rely on the BCG vaccine, developed almost a century ago from a usually non-pathogenic, live strain of Mycobacterium bovis – the cow form of the bacterium that causes TB.
Physicians routinely administer this vaccine to newborns in regions where TB has re-emerged as a threat. This means that millions of infants in developing nations in Africa and Asia receive the vaccine in their first few hours of life.
Unfortunately, though, many of these infants are born with HIV, and subsequently have a weakened immune system. This weakened condition makes them vulnerable to “BCG disease”, a serious illness caused by the M. bovis of the BCG vaccine, which would otherwise not pose a threat.
BCG disease
One recent study conducted in South Africa and published in the journal Clinical Infectious Diseases found that six out of the eight children that became severely ill from the BCG vaccine ultimately died from the M. bovis infection (vol 15, p 559-61). The majority of these children were found to have had HIV.
Miller says that an estimated 600,000 children are born with HIV each year and hundreds are at risk of dying as a consequence of BCG vaccination.
The World Health Organization (WHO) had previously recommended that the BCG vaccine be given to all healthy infants as soon as possible after birth. However, the WHO revised its position and stated in a May 2007 report that "recent evidence shows that children who were HIV-infected when vaccinated with BCG at birth, and who later developed AIDS, were at increased risk of developing BCG disease."
The report adds that, "among these children, the benefits of potentially preventing severe TB are outweighed by the risks associated with the use of BCG vaccine."
Sophisticated tests
The challenge is to develop more sophisticated HIV tests for newborns, says Miller, who also conducts research at George Washington University in Washington, DC, US. But this will take a bigger financial commitment from governments and aid organisations, she adds.
She explains that the types of HIV tests commonly used in the developing world cannot distinguish the HIV status of infants until they reach about six months of age.
The search for more effective tuberculosis vaccines could produce novel options that avoid the problem of BCG-related illness, says Lewellys Barker at the Aeras Global TB Vaccine Foundation in Rockville, Maryland, US.
He notes that scientists are designing TB vaccines that involve the injection of proteins, as opposed to live bacteria, which would not pose as great a threat to children with HIV.
Journal reference: HIV-TB Co-Infection: Meeting the Challenge (pdf)
The report focuses on how the “global epidemics of HIV and tuberculosis has exploded to create a deadly co-epidemic”, that is rapidly spreading in sub-Saharan Africa. It warns that about a third of the world’s 40 million people with HIV/AIDS are co-infected with TB, and that the mortality rate these people is five times higher than that for tuberculosis alone.
It also notes that the use of the Bacille Calmette-Guérin (BCG) vaccine against TB in babies with HIV may actually be making the situation worse.
Veronica Miller, a co-author of the report and director of the Washington, DC-based Forum for Collaborative HIV Research, said that there is an "urgent" need for changes to vaccination programmes in sub-Saharan Africa, including improved testing to know whether infants have HIV before vaccinating them against TB.
Live strain
The growing threat of TB and the drug-resistant forms of this bacterial infection that commonly attacks the lungs has increased the need for widespread vaccination, experts say.
Unfortunately, there is a lack of new vaccines against TB, which kills nearly 2 million people each year. For this reason, doctors must rely on the BCG vaccine, developed almost a century ago from a usually non-pathogenic, live strain of Mycobacterium bovis – the cow form of the bacterium that causes TB.
Physicians routinely administer this vaccine to newborns in regions where TB has re-emerged as a threat. This means that millions of infants in developing nations in Africa and Asia receive the vaccine in their first few hours of life.
Unfortunately, though, many of these infants are born with HIV, and subsequently have a weakened immune system. This weakened condition makes them vulnerable to “BCG disease”, a serious illness caused by the M. bovis of the BCG vaccine, which would otherwise not pose a threat.
BCG disease
One recent study conducted in South Africa and published in the journal Clinical Infectious Diseases found that six out of the eight children that became severely ill from the BCG vaccine ultimately died from the M. bovis infection (vol 15, p 559-61). The majority of these children were found to have had HIV.
Miller says that an estimated 600,000 children are born with HIV each year and hundreds are at risk of dying as a consequence of BCG vaccination.
The World Health Organization (WHO) had previously recommended that the BCG vaccine be given to all healthy infants as soon as possible after birth. However, the WHO revised its position and stated in a May 2007 report that "recent evidence shows that children who were HIV-infected when vaccinated with BCG at birth, and who later developed AIDS, were at increased risk of developing BCG disease."
The report adds that, "among these children, the benefits of potentially preventing severe TB are outweighed by the risks associated with the use of BCG vaccine."
Sophisticated tests
The challenge is to develop more sophisticated HIV tests for newborns, says Miller, who also conducts research at George Washington University in Washington, DC, US. But this will take a bigger financial commitment from governments and aid organisations, she adds.
She explains that the types of HIV tests commonly used in the developing world cannot distinguish the HIV status of infants until they reach about six months of age.
The search for more effective tuberculosis vaccines could produce novel options that avoid the problem of BCG-related illness, says Lewellys Barker at the Aeras Global TB Vaccine Foundation in Rockville, Maryland, US.
He notes that scientists are designing TB vaccines that involve the injection of proteins, as opposed to live bacteria, which would not pose as great a threat to children with HIV.
Journal reference: HIV-TB Co-Infection: Meeting the Challenge (pdf)
Half a million years
ScienceDaily (Dec. 8, 2007) — Although most scientists believe tuberculosis emerged only several thousand years ago, new research from The University of Texas at Austin reveals the most ancient evidence of the disease has been found in a 500,000-year-old human fossil from Turkey.
The discovery of the new specimen of the human species, Homo erectus, suggests support for the theory that dark-skinned people who migrate northward from low, tropical latitudes produce less vitamin D, which can adversely affect the immune system as well as the skeleton.
Prior to this discovery in western Turkey, which helps scientists fill a temporal and geographical gap in human evolution, the oldest evidence of tuberculosis in humans was found in mummies from Egypt and Peru that date to several thousand years ago.
Paleontologists spent decades prospecting in Turkey for remains of Homo erectus, widely believed to be the first human species to migrate out of Africa. After moving north, the species had to adapt to increasingly seasonal climates.
The researchers identified this specimen of Homo erectus as a young male based on aspects of the cranial suture closure, sinus formation and the size of the ridges of the brow. They also found a series of small lesions etched into the bone of the cranium whose shape and location are characteristic of the Leptomeningitis tuberculosa, a form of tuberculosis that attacks the meninges of the brain.
After reviewing the medical literature on the disease that has reemerged as a global killer, the researchers found that some groups of people demonstrate a higher than average rate of infection, including Gujarati Indians who live in London, and Senegalese conscripts who served with the French army during World War I.
The research team identified two shared characteristics in the communities: a path of migration from low, tropical latitudes to northern temperate regions and darker skin color.
People with dark skin produce less vitamin D because the skin pigment melanin blocks ultraviolet light. And, when they live in areas with lower ultraviolet radiation such as Europe, their immune systems can be compromised.
John Kappelman, professor of anthropology at The University of Texas at Austin, is part of an international team of researchers from the United States, Turkey and Germany who have published their findings in the Dec. 7 issue of the American Journal of Physical Anthropology.
It is likely that Homo erectus had dark skin because it evolved in the tropics, Kappelman explained. After the species moved north, it had to adapt to more seasonal climates. The researchers hypothesize the young male's body produced less vitamin D and this deficiency weakened his immune system, opening the door to tuberculosis.
"Skin color represents one of biology's most elegant adaptations," Kappelman said. "The production of vitamin D in the skin serves as one of the body's first lines of defenses against a whole host of infections and diseases. Vitamin D deficiencies are implicated in hypertension, multiple sclerosis, cardiovascular disease and cancer."
Before antibiotics were invented, doctors typically treated tuberculosis by sending patients to sanatoria where they were prescribed plenty of sunshine and fresh air.
"No one knew why sunshine was integral to the treatment, but it worked," Kappelman said. "Recent research suggests the flush of ultraviolet radiation jump-started the patients' immune systems by increasing the production of vitamin D, which helped to cure the disease."
The Leakey Foundation and the Scientific and Technical Research Council of Turkey funded the research.
Adapted from materials provided by University of Texas at Austin.
The discovery of the new specimen of the human species, Homo erectus, suggests support for the theory that dark-skinned people who migrate northward from low, tropical latitudes produce less vitamin D, which can adversely affect the immune system as well as the skeleton.
Prior to this discovery in western Turkey, which helps scientists fill a temporal and geographical gap in human evolution, the oldest evidence of tuberculosis in humans was found in mummies from Egypt and Peru that date to several thousand years ago.
Paleontologists spent decades prospecting in Turkey for remains of Homo erectus, widely believed to be the first human species to migrate out of Africa. After moving north, the species had to adapt to increasingly seasonal climates.
The researchers identified this specimen of Homo erectus as a young male based on aspects of the cranial suture closure, sinus formation and the size of the ridges of the brow. They also found a series of small lesions etched into the bone of the cranium whose shape and location are characteristic of the Leptomeningitis tuberculosa, a form of tuberculosis that attacks the meninges of the brain.
After reviewing the medical literature on the disease that has reemerged as a global killer, the researchers found that some groups of people demonstrate a higher than average rate of infection, including Gujarati Indians who live in London, and Senegalese conscripts who served with the French army during World War I.
The research team identified two shared characteristics in the communities: a path of migration from low, tropical latitudes to northern temperate regions and darker skin color.
People with dark skin produce less vitamin D because the skin pigment melanin blocks ultraviolet light. And, when they live in areas with lower ultraviolet radiation such as Europe, their immune systems can be compromised.
John Kappelman, professor of anthropology at The University of Texas at Austin, is part of an international team of researchers from the United States, Turkey and Germany who have published their findings in the Dec. 7 issue of the American Journal of Physical Anthropology.
It is likely that Homo erectus had dark skin because it evolved in the tropics, Kappelman explained. After the species moved north, it had to adapt to more seasonal climates. The researchers hypothesize the young male's body produced less vitamin D and this deficiency weakened his immune system, opening the door to tuberculosis.
"Skin color represents one of biology's most elegant adaptations," Kappelman said. "The production of vitamin D in the skin serves as one of the body's first lines of defenses against a whole host of infections and diseases. Vitamin D deficiencies are implicated in hypertension, multiple sclerosis, cardiovascular disease and cancer."
Before antibiotics were invented, doctors typically treated tuberculosis by sending patients to sanatoria where they were prescribed plenty of sunshine and fresh air.
"No one knew why sunshine was integral to the treatment, but it worked," Kappelman said. "Recent research suggests the flush of ultraviolet radiation jump-started the patients' immune systems by increasing the production of vitamin D, which helped to cure the disease."
The Leakey Foundation and the Scientific and Technical Research Council of Turkey funded the research.
Adapted from materials provided by University of Texas at Austin.
Subscribe to:
Posts (Atom)
