21 Jun 2007
Deaths from previously treatable infections will become more common unless there is investment in the science needed to tackle antibiotic resistance Europe's leading scientists have warned in a report published today (21 June 2007).
The report(1), produced by European Academies Science Advisory Council (EASAC), of which the Royal Society is a member, highlights the ever growing problem of antibiotic resistance in pathogens such as MRSA, Clostridium difficile, E-coli and infectious diseases such as tuberculosis, pneumonia and meningitis.
Scientists from across Europe are calling for the EU and Member States to provide greater support for the development of simple and cheap means of identifying specific infections as early as possible and greater support for drug companies who are seeking to develop new treatments. The report also urges greater awareness and monitoring of the problem, more prudent use of antibiotics, more effective containment of the spread of resistance and greater cooperation and coordination across Europe.
Hospital acquired infections are believed to account for 175,000 deaths in Europe each year, many of which are attributable to antibiotic resistance.
Professor Volker ter Meulen, President of the Leopoldina Academy of Sciences, Germany and Chair the report's working group, said: "The problem of antibiotic resistance is growing. Our concern is that the European policy makers are not doing enough to stimulate the development of new antibacterial drugs and encourage the sharing of information between Member States. This is vital to identify patterns and tackle resistance.
"For example, research and development for new antibiotic drugs is not an attractive option for drug companies in comparison with treatments for long-term chronic illnesses which offer a better return on investment. Drug companies will need to be incentivised to continue valuable antibiotic R&D."
Antibiotic resistance is not just a problem for hospitals and patients but for everyone. Business will be hit, with employees off sick. There is also the danger that antibiotic resistant pathogens could enter the food chain via livestock.
Professor Richard Moxon, based at the University of Oxford and a member of the working group, said: "It is crucially important to rebuild European academic capability in microbiology and clinical infectious disease infrastructure. But antibiotic resistance is not just a medical issue. Social habits may lead to increased cases of resistance such as the over-prescribing of general antibiotics instead of ones designed to treat specific pathogens. In some EU states antibiotics can even be bought without prescriptions.
"All factors that could lead to antibiotic resistance or be affected by it need to be considered. EU institutions and Government departments in Member States responsible for public health, environment, industry and scientific research have to work together to take action to tackle this problem."
In monitoring the trend of drug resistance across Europe, the observation and recording of resistance is extremely valuable. The European Commission is responsible for coordinating this surveillance, and gathers information from Member States to plot the spread of infections. However the report found that data collected is of a variable standard making comparisons between countries difficult.
"Knowing where the problems are most common is extremely valuable to predict possible impacts on the economy, to bring about changes in healthcare practice and inform research funders throughout Europe on where research funding should be focused," added Professor ter Meulen
Friday, June 22, 2007
Tuesday, June 19, 2007
Kane Biotech Announces a Positive Independent Research Publication on Its DispersinB Technology
NEWS RELEASE
Jun 18, 2007 09:44 ET
WINNIPEG, MANITOBA--(Marketwire - June 18, 2007) - Kane Biotech Inc. (TSX VENTURE:KNE), a biotechnology company engaged in the development of products that prevent and disperse microbial biofilms, is pleased to announce an independent research publication on the Company's DispersinB technology, a patent pending anti-biofilm technology. The paper appeared in the recent edition of online scientific journal 'Antimicrobial Agents and Chemotherapy' published by American Society for Microbiology.
The research findings reported in the publication, entitled "Synergistic activity of dispersin B and cefamandole nafate in the inhibition of staphylococcal growth on polyurethanes" co-authored by Dr. Gianfranco Donelli from the Department of Health, Istituto Superiore di Santa, Rome, Italy, and Dr. Jeff Kaplan from the Department of Oral Microbiology, the University of Medicine and Dentistry of New Jersey (UMDNJ), demonstrates that DispersinB is not cytotoxic and that DispersinB treatment makes bacteria growing in biofilms more susceptible to an antibiotic such as cefamandole nafate.
"This research not only provides evidence that the DispersinB enzyme is non-toxic but also demonstrates that when DispersinB is combined with an antibiotic it enhances the activity of the antibiotic against biofilm-embedded bacteria such as Staphylococcus epidermidis" stated Dr. Kaplan, also the inventor of the technology. "These findings confirm that DispersinB-antibiotic combinations provide highly effective tools for preventing bacterial colonization of medical devices, including catheters."
"This study provides solid evidence that our technology is very effective in the fight against biofilms that attach to medical devices and also demonstrates that naturally occurring DispersinB is not cytotoxic." said Gord Froehlich, President and CEO of Kane Biotech. "Our database of scientific evidence continues to grow as we prepare this technology for commercialization."
DispersinB is a novel enzyme capable of both inhibiting and dispersing bacterial biofilms. Kane Biotech has a worldwide exclusive license to all human, animal and industrial applications of DispersinB from the UMDNJ. Kane Biotech is presently using dispersinB alone, and in combination with other antimicrobial agents to develop a proprietary medical device coating.
About Dr. Jeffrey Kaplan
Jeffrey Kaplan received a Bachelor of Science degree in Biology from the University of Illinois at Chicago in 1980 and a Ph.D. in Molecular Biology from the same institution in 1985. He received postdoctoral training in the Department of Microbiology at the Albert Einstein College of Medicine, Bronx, N.Y., and in the Department of Microbiology at Columbia University, College of Physicians and Surgeons, New York, N.Y. Dr. Kaplan worked for 10 years in the Oncology Department at Wyeth Pharmaceuticals, Pearl River, N.Y., before joining the Department of Oral Biology at New Jersey Dental School in 1999.
Dr. Kaplan's lab is studying the detachment and dispersal of bacterial cells from biofilms with an emphasis on the gram-negative periodontal pathogen Aggregatibacter actinomycetemcomitans. His research is funded by the several grant agencies, including the National Institute of Health (NIH), USA. His discovery of DispersinB supported by the NIH grant was listed in the "NIH Annual Performance Report of 2004" as one of the thirteen achievements of the year.
About Kane Biotech Inc.
Kane Biotech is a biotechnology company engaged in the development of products to prevent and disperse microbial biofilms. Biofilms develop when bacteria, and other microorganisms, form a protective matrix that acts as a shield against attack. When in a biofilm, bacteria become highly resistant to antibiotics, biocides, disinfectants, high temperatures and host immune responses. This resiliency contributes to human health problems such as recurrent urinary tract infections, medical device associated infections and tooth decay.
Kane Biotech Inc. uses a patent protected technology based on molecular mechanisms of biofilm formation and methods for finding compounds that inhibit or disrupt biofilms. The Company has evidence that this technology has a great potential to significantly improve the ability to prevent and/or destroy biofilms in several medical and industrial applications.
Caution Regarding Forward-Looking Information
Certain statements contained in this press release constitute forward-looking information within the meaning of applicable Canadian provincial securities legislation (collectively, "forward-looking statements"). These forward-looking statements relate to, among other things, our objectives, goals, targets, strategies, intentions, plans, beliefs, estimates and outlook, including, without limitation, our anticipated future operating results, and can, in some cases, be identified by the use of words such as "believe," "anticipate," "expect," "intend," "plan," "will," "may" and other similar expressions. In addition, any statements that refer to expectations, projections or other characterizations of future events or circumstances are forward-looking statements.
These statements reflect management's current beliefs and are based on information currently available to management. Certain material factors or assumptions are applied in making forward-looking statements, and actual results may differ materially from those expressed or implied in such statements. Important factors that could cause actual results to differ materially from these expectations include, among other things: Kane's early stage of development, lack of product revenues and history of operating losses, uncertainties related to clinical trials and product development, rapid technological change, uncertainties related to forecasts, competition, potential product liability, additional financing requirements and access to capital, unproven markets, supply of raw materials, income tax matters, management of growth, partnerships for development and commercialization of technology, effects of insurers' willingness to pay for products, system failures, dependence on key personnel, foreign currency risk, risks related to regulatory matters and risks related to intellectual property and other risks detailed from time to time in Kane's filings with Canadian securities regulatory authorities, as well as Kane's ability to anticipate and manage the risks associated with the foregoing. Kane cautions that the foregoing list of important factors that may affect future results is not exhaustive. When relying on Kane's forward-looking statements to make decisions with respect to Kane, investors and others should carefully consider the foregoing factors and other uncertainties and potential events.
These risks and uncertainties should be considered carefully and prospective investors should not place undue reliance on the forward-looking statements. Although the forward-looking statements contained in this press release are based upon what management believes to be reasonable assumptions, Kane cannot provide assurance that actual results will be consistent with these forward-looking statements. Kane undertakes no obligation to update or revise any forward-looking statement.
The TSX Venture Exchange does not accept responsibility for the adequacy or accuracy of this release.
For more information, please contact
Kane Biotech Inc.
Justin Gagnon
Investor Relations Professional
(204) 478-5602
(204) 453-1314 (FAX)
Email: jgagnon@kanebiotech.com
Website: www.kanebiotech.com
Jun 18, 2007 09:44 ET
WINNIPEG, MANITOBA--(Marketwire - June 18, 2007) - Kane Biotech Inc. (TSX VENTURE:KNE), a biotechnology company engaged in the development of products that prevent and disperse microbial biofilms, is pleased to announce an independent research publication on the Company's DispersinB technology, a patent pending anti-biofilm technology. The paper appeared in the recent edition of online scientific journal 'Antimicrobial Agents and Chemotherapy' published by American Society for Microbiology.
The research findings reported in the publication, entitled "Synergistic activity of dispersin B and cefamandole nafate in the inhibition of staphylococcal growth on polyurethanes" co-authored by Dr. Gianfranco Donelli from the Department of Health, Istituto Superiore di Santa, Rome, Italy, and Dr. Jeff Kaplan from the Department of Oral Microbiology, the University of Medicine and Dentistry of New Jersey (UMDNJ), demonstrates that DispersinB is not cytotoxic and that DispersinB treatment makes bacteria growing in biofilms more susceptible to an antibiotic such as cefamandole nafate.
"This research not only provides evidence that the DispersinB enzyme is non-toxic but also demonstrates that when DispersinB is combined with an antibiotic it enhances the activity of the antibiotic against biofilm-embedded bacteria such as Staphylococcus epidermidis" stated Dr. Kaplan, also the inventor of the technology. "These findings confirm that DispersinB-antibiotic combinations provide highly effective tools for preventing bacterial colonization of medical devices, including catheters."
"This study provides solid evidence that our technology is very effective in the fight against biofilms that attach to medical devices and also demonstrates that naturally occurring DispersinB is not cytotoxic." said Gord Froehlich, President and CEO of Kane Biotech. "Our database of scientific evidence continues to grow as we prepare this technology for commercialization."
DispersinB is a novel enzyme capable of both inhibiting and dispersing bacterial biofilms. Kane Biotech has a worldwide exclusive license to all human, animal and industrial applications of DispersinB from the UMDNJ. Kane Biotech is presently using dispersinB alone, and in combination with other antimicrobial agents to develop a proprietary medical device coating.
About Dr. Jeffrey Kaplan
Jeffrey Kaplan received a Bachelor of Science degree in Biology from the University of Illinois at Chicago in 1980 and a Ph.D. in Molecular Biology from the same institution in 1985. He received postdoctoral training in the Department of Microbiology at the Albert Einstein College of Medicine, Bronx, N.Y., and in the Department of Microbiology at Columbia University, College of Physicians and Surgeons, New York, N.Y. Dr. Kaplan worked for 10 years in the Oncology Department at Wyeth Pharmaceuticals, Pearl River, N.Y., before joining the Department of Oral Biology at New Jersey Dental School in 1999.
Dr. Kaplan's lab is studying the detachment and dispersal of bacterial cells from biofilms with an emphasis on the gram-negative periodontal pathogen Aggregatibacter actinomycetemcomitans. His research is funded by the several grant agencies, including the National Institute of Health (NIH), USA. His discovery of DispersinB supported by the NIH grant was listed in the "NIH Annual Performance Report of 2004" as one of the thirteen achievements of the year.
About Kane Biotech Inc.
Kane Biotech is a biotechnology company engaged in the development of products to prevent and disperse microbial biofilms. Biofilms develop when bacteria, and other microorganisms, form a protective matrix that acts as a shield against attack. When in a biofilm, bacteria become highly resistant to antibiotics, biocides, disinfectants, high temperatures and host immune responses. This resiliency contributes to human health problems such as recurrent urinary tract infections, medical device associated infections and tooth decay.
Kane Biotech Inc. uses a patent protected technology based on molecular mechanisms of biofilm formation and methods for finding compounds that inhibit or disrupt biofilms. The Company has evidence that this technology has a great potential to significantly improve the ability to prevent and/or destroy biofilms in several medical and industrial applications.
Caution Regarding Forward-Looking Information
Certain statements contained in this press release constitute forward-looking information within the meaning of applicable Canadian provincial securities legislation (collectively, "forward-looking statements"). These forward-looking statements relate to, among other things, our objectives, goals, targets, strategies, intentions, plans, beliefs, estimates and outlook, including, without limitation, our anticipated future operating results, and can, in some cases, be identified by the use of words such as "believe," "anticipate," "expect," "intend," "plan," "will," "may" and other similar expressions. In addition, any statements that refer to expectations, projections or other characterizations of future events or circumstances are forward-looking statements.
These statements reflect management's current beliefs and are based on information currently available to management. Certain material factors or assumptions are applied in making forward-looking statements, and actual results may differ materially from those expressed or implied in such statements. Important factors that could cause actual results to differ materially from these expectations include, among other things: Kane's early stage of development, lack of product revenues and history of operating losses, uncertainties related to clinical trials and product development, rapid technological change, uncertainties related to forecasts, competition, potential product liability, additional financing requirements and access to capital, unproven markets, supply of raw materials, income tax matters, management of growth, partnerships for development and commercialization of technology, effects of insurers' willingness to pay for products, system failures, dependence on key personnel, foreign currency risk, risks related to regulatory matters and risks related to intellectual property and other risks detailed from time to time in Kane's filings with Canadian securities regulatory authorities, as well as Kane's ability to anticipate and manage the risks associated with the foregoing. Kane cautions that the foregoing list of important factors that may affect future results is not exhaustive. When relying on Kane's forward-looking statements to make decisions with respect to Kane, investors and others should carefully consider the foregoing factors and other uncertainties and potential events.
These risks and uncertainties should be considered carefully and prospective investors should not place undue reliance on the forward-looking statements. Although the forward-looking statements contained in this press release are based upon what management believes to be reasonable assumptions, Kane cannot provide assurance that actual results will be consistent with these forward-looking statements. Kane undertakes no obligation to update or revise any forward-looking statement.
The TSX Venture Exchange does not accept responsibility for the adequacy or accuracy of this release.
For more information, please contact
Kane Biotech Inc.
Justin Gagnon
Investor Relations Professional
(204) 478-5602
(204) 453-1314 (FAX)
Email: jgagnon@kanebiotech.com
Website: www.kanebiotech.com
Monday, June 18, 2007
Antibiotics in failing health
By Karen Augé
Denver Post Staff Writer
The Denver Post
The last time a new tuberculosis drug was developed, Richard Nixon was in the White House and Dr. Michael Iseman was a young resident in a New York City hospital.
That drug, Rifampin, "was the biggest thing to hit TB in 30 years," said Iseman, now a doctor at National Jewish Medical and Research Center in Denver.
Since then, Iseman has become a recognized authority on TB and Rifampin has remained the centerpiece of TB treatment.
Now, however, a growing number of tuberculosis strains are not fazed by the drug - as in the highly publicized case of Andrew Speaker, who is being treated at National Jewish.
Tuberculosis isn't the only infection increasingly impervious to the antibiotics in medicine's arsenal.
In the past decade, federal agencies - such as the Centers for Disease Control and Prevention, the National Institutes of Health, and the Food and Drug Administration - have warned that antibiotic overuse has led to evolving drug-resistant bacteria.
At the same time, the agencies say, there is a dearth of research dollars for new antibiotics - creating a looming medical crisis.
"Infections that were once easily curable with antibiotics are becoming difficult, even impossible, to treat," the Infectious Disease Society of America warned in its report "Bad Bugs, No Drugs."
"The problem is dollars, not chemistry," said Christopher Spivey, a spokesman for the Boston-based Alliance for the Prudent Use of Antibiotics.
Antibiotics not as profitable
Antibiotic development requires huge investments of money, $400 million to $800 million, according to a study in the journal Clinical Infectious Diseases.
To provide as much income as drug companies get from the sale of one drug to a person who, for example, takes a weight-loss pill daily, a company would have to sell antibiotics to 200 to 500 people with an illness like pneumonia, Spivey said.
There are currently under development 50 drugs each for obesity, pain and Type II diabetes, according to PhRMA, a group representing the nation's leading drugmakers.
There are just nine new drugs in the works for tuberculosis and eight for malaria.
For staph infections and drug- resistant staph infections, PhRMA lists 23 drugs under development.
This isn't a new trend. FDA approval of new anti-bacterial drugs has dropped 56 percent in 20 years, according to a 2004 study by Brad Spellberg, a professor of medicine at the University of California, Los Angeles.
Work on new TB drugs has languished in part because of the widespread, mistaken belief that the disease was no longer a problem in this country, said Mel Spigelman, director of research and development for the Global Alliance for TB Drug Development.
Iseman said that on the world market drugmakers are discouraged from developing antibiotics.
"There is a tendency - in global use - for knock-offs," Iseman said. "Companies simply choose not to honor patent protections and it's done under the seemingly noble rubric of, 'we have patients dying of - whatever disease - in our country and we can't afford your drug, so we're going to make our own.' "
In its report, the infectious-disease society recommended incentives, such as tax breaks, for antibiotic research and development.
Difficult to draw attention
Still, drug companies don't get much public sympathy these days, which could make it politically tough for members of Congress to grant those tax breaks, Iseman said.
Antibiotic development "won't get on the radar until there is a really good killing plague," Spivey said.
In that respect, Speaker may have unintentionally done a favor for TB drug research by drawing attention to the disease, Spivey said.
Since 2000, interest in TB has picked up, said the TB Alliance's Spigelman.
While only a handful of new TB drugs are in the pipeline, even that is progress, Spigelman said.
"In 2000, we had zero," he said.
This year, the National Institutes of Health will spend $158 million on TB- drug research. The Bill and Melinda Gates Foundation has pledged $900 million over the next decade.
Four drug companies - Bayer, Novartis, AstraZeneca International and GlaxoSmithKline - now have units working on infectious diseases, including TB.
Bacteria, however, reproduce every 10 minutes or so, while it takes humans about 20 years to develop means to battle new strains, Iseman said.
"They have the ability to adapt to our drugs," he said. "So if you're in Vegas, you bet on the bugs."
Staff writer Karen Augé can be reached at 303-954-1733 or kauge@denverpost.com.
--------------------------------------------------------------------------------
A history of antibiotics and drug resistance
1920s-'50s: Scientists harness the power of living organisms to fight bacteria, ushering in the era of antibiotics.
1928: Scottish bacteriologist Alexander Fleming, above, accidentally discovers that a mold juice he names penicillin can kill staphylococcus bacteria.
1940: Oxford University pathologist Howard Florey isolates pure penicillin and demonstrates how it can cure a wide range of pathogens, including strep infections, gonorrhea and syphilis.
1943: Penicillin becomes the first antibiotic to be put in widespread use.
1944: Russian-born microbiologist Selman Waksman, working in the United States with soil microbiologist Albert Schatz, discovers streptomycin, a powerful antibiotic that proves effective against tuberculosis.
1958: American molecular geneticist Joshua Lederberg wins the Nobel Prize in medicine for demonstrating the way bacteria interact and exchange genetic material - a key concept behind drug resistance.
1967: The first penicillin-resistant pneumonococcal bacteria are reported in Papua New Guinea.
1968: Drug-resistant Shigella diarrhea kills 12,500 people in Guatemala.
1970-72: Penicillin-resistant gonorrhea spreads around the world, transmitted in part by U.S. servicemen, who contract the disease from prostitutes in Southeast Asia.
1976: Several weeks after attending an American Legion convention in Philadelphia, 34 people die from a mysterious form of pneumonia that thwarts available treatments and comes to be known as Legionnaires' disease.
1980s-'90s: The public-health effects of drug-resistant bacteria become clear, prompting new concerns about infectious diseases.
1986: The U.S. Food and Drug Administration, the Centers for Disease Control and Prevention, and the Department of Agriculture establish a national anti-
microbial-resistance monitoring system to track food-borne microbes.
1988-95: Studies in Finland, the Netherlands and other European countries find increased drug resistance in farm animals. Many of the livestock are fed antibiotics as growth-promoters.
1990: Puppeteer Jim Henson, creator of the Muppets, dies of toxic-shock syndrome induced by an aggressive strain of streptococcus that acts too quickly for antibiotics to work.
1992: An influx of immigrants sparks a tuberculosis epidemic in New York and other cities, forcing local officials to remobilize dormant TB prevention efforts. The federal government is spending just $55,000 a year monitoring drug resistance.
1995: A form of staph infection that is resistant to methicillin results in almost a half-billion dollars in direct medical costs and claims 1,409 lives in New York City hospitals.
1996: Japanese bacterial geneticists detect the world's first staph infection capable of resisting the powerful antibiotic vancomycin.
1997: Health officials report the percentage of antibiotic-resistant cases has surged from 2 percent in 1991 to 43 percent in 1997.
1998: The Institute of Medicine contends that overuse of antibiotics has brought about widespread drug resistance, estimating that as many as half of the prescriptions for the drugs given each year to outpatients are unnecessary. The U.S. Centers for Disease Control and Prevention spends more than $11 million a year monitoring drug resistance.
2000: The Food and Drug Administration approves one of the newest major new antibiotics, Bayer's ciprofloxacin hydrochloride, known as Cipro. Cipro makes news the following year as a treatment for a spate of unsolved anthrax poisonings.
Denver Post Staff Writer
The Denver Post
The last time a new tuberculosis drug was developed, Richard Nixon was in the White House and Dr. Michael Iseman was a young resident in a New York City hospital.
That drug, Rifampin, "was the biggest thing to hit TB in 30 years," said Iseman, now a doctor at National Jewish Medical and Research Center in Denver.
Since then, Iseman has become a recognized authority on TB and Rifampin has remained the centerpiece of TB treatment.
Now, however, a growing number of tuberculosis strains are not fazed by the drug - as in the highly publicized case of Andrew Speaker, who is being treated at National Jewish.
Tuberculosis isn't the only infection increasingly impervious to the antibiotics in medicine's arsenal.
In the past decade, federal agencies - such as the Centers for Disease Control and Prevention, the National Institutes of Health, and the Food and Drug Administration - have warned that antibiotic overuse has led to evolving drug-resistant bacteria.
At the same time, the agencies say, there is a dearth of research dollars for new antibiotics - creating a looming medical crisis.
"Infections that were once easily curable with antibiotics are becoming difficult, even impossible, to treat," the Infectious Disease Society of America warned in its report "Bad Bugs, No Drugs."
"The problem is dollars, not chemistry," said Christopher Spivey, a spokesman for the Boston-based Alliance for the Prudent Use of Antibiotics.
Antibiotics not as profitable
Antibiotic development requires huge investments of money, $400 million to $800 million, according to a study in the journal Clinical Infectious Diseases.
To provide as much income as drug companies get from the sale of one drug to a person who, for example, takes a weight-loss pill daily, a company would have to sell antibiotics to 200 to 500 people with an illness like pneumonia, Spivey said.
There are currently under development 50 drugs each for obesity, pain and Type II diabetes, according to PhRMA, a group representing the nation's leading drugmakers.
There are just nine new drugs in the works for tuberculosis and eight for malaria.
For staph infections and drug- resistant staph infections, PhRMA lists 23 drugs under development.
This isn't a new trend. FDA approval of new anti-bacterial drugs has dropped 56 percent in 20 years, according to a 2004 study by Brad Spellberg, a professor of medicine at the University of California, Los Angeles.
Work on new TB drugs has languished in part because of the widespread, mistaken belief that the disease was no longer a problem in this country, said Mel Spigelman, director of research and development for the Global Alliance for TB Drug Development.
Iseman said that on the world market drugmakers are discouraged from developing antibiotics.
"There is a tendency - in global use - for knock-offs," Iseman said. "Companies simply choose not to honor patent protections and it's done under the seemingly noble rubric of, 'we have patients dying of - whatever disease - in our country and we can't afford your drug, so we're going to make our own.' "
In its report, the infectious-disease society recommended incentives, such as tax breaks, for antibiotic research and development.
Difficult to draw attention
Still, drug companies don't get much public sympathy these days, which could make it politically tough for members of Congress to grant those tax breaks, Iseman said.
Antibiotic development "won't get on the radar until there is a really good killing plague," Spivey said.
In that respect, Speaker may have unintentionally done a favor for TB drug research by drawing attention to the disease, Spivey said.
Since 2000, interest in TB has picked up, said the TB Alliance's Spigelman.
While only a handful of new TB drugs are in the pipeline, even that is progress, Spigelman said.
"In 2000, we had zero," he said.
This year, the National Institutes of Health will spend $158 million on TB- drug research. The Bill and Melinda Gates Foundation has pledged $900 million over the next decade.
Four drug companies - Bayer, Novartis, AstraZeneca International and GlaxoSmithKline - now have units working on infectious diseases, including TB.
Bacteria, however, reproduce every 10 minutes or so, while it takes humans about 20 years to develop means to battle new strains, Iseman said.
"They have the ability to adapt to our drugs," he said. "So if you're in Vegas, you bet on the bugs."
Staff writer Karen Augé can be reached at 303-954-1733 or kauge@denverpost.com.
--------------------------------------------------------------------------------
A history of antibiotics and drug resistance
1920s-'50s: Scientists harness the power of living organisms to fight bacteria, ushering in the era of antibiotics.
1928: Scottish bacteriologist Alexander Fleming, above, accidentally discovers that a mold juice he names penicillin can kill staphylococcus bacteria.
1940: Oxford University pathologist Howard Florey isolates pure penicillin and demonstrates how it can cure a wide range of pathogens, including strep infections, gonorrhea and syphilis.
1943: Penicillin becomes the first antibiotic to be put in widespread use.
1944: Russian-born microbiologist Selman Waksman, working in the United States with soil microbiologist Albert Schatz, discovers streptomycin, a powerful antibiotic that proves effective against tuberculosis.
1958: American molecular geneticist Joshua Lederberg wins the Nobel Prize in medicine for demonstrating the way bacteria interact and exchange genetic material - a key concept behind drug resistance.
1967: The first penicillin-resistant pneumonococcal bacteria are reported in Papua New Guinea.
1968: Drug-resistant Shigella diarrhea kills 12,500 people in Guatemala.
1970-72: Penicillin-resistant gonorrhea spreads around the world, transmitted in part by U.S. servicemen, who contract the disease from prostitutes in Southeast Asia.
1976: Several weeks after attending an American Legion convention in Philadelphia, 34 people die from a mysterious form of pneumonia that thwarts available treatments and comes to be known as Legionnaires' disease.
1980s-'90s: The public-health effects of drug-resistant bacteria become clear, prompting new concerns about infectious diseases.
1986: The U.S. Food and Drug Administration, the Centers for Disease Control and Prevention, and the Department of Agriculture establish a national anti-
microbial-resistance monitoring system to track food-borne microbes.
1988-95: Studies in Finland, the Netherlands and other European countries find increased drug resistance in farm animals. Many of the livestock are fed antibiotics as growth-promoters.
1990: Puppeteer Jim Henson, creator of the Muppets, dies of toxic-shock syndrome induced by an aggressive strain of streptococcus that acts too quickly for antibiotics to work.
1992: An influx of immigrants sparks a tuberculosis epidemic in New York and other cities, forcing local officials to remobilize dormant TB prevention efforts. The federal government is spending just $55,000 a year monitoring drug resistance.
1995: A form of staph infection that is resistant to methicillin results in almost a half-billion dollars in direct medical costs and claims 1,409 lives in New York City hospitals.
1996: Japanese bacterial geneticists detect the world's first staph infection capable of resisting the powerful antibiotic vancomycin.
1997: Health officials report the percentage of antibiotic-resistant cases has surged from 2 percent in 1991 to 43 percent in 1997.
1998: The Institute of Medicine contends that overuse of antibiotics has brought about widespread drug resistance, estimating that as many as half of the prescriptions for the drugs given each year to outpatients are unnecessary. The U.S. Centers for Disease Control and Prevention spends more than $11 million a year monitoring drug resistance.
2000: The Food and Drug Administration approves one of the newest major new antibiotics, Bayer's ciprofloxacin hydrochloride, known as Cipro. Cipro makes news the following year as a treatment for a spate of unsolved anthrax poisonings.
Malta has third highest rate of antibiotic resistant infections in Europe
by Juan Ameen
A recently published European report has found that Malta has the third highest percentage of potentially deadly antibiotic-resistant hospital-acquired infections out of a list of 29 countries.
The report, which was compiled by the European Centre for Disease Prevention, found that Malta had an MRSA rate of around 55 per cent in 2005.
The study pointed out that, at present, the most important disease threat is from microorganisms that have become resistant to antibiotics. However, it went on to say that these are becoming a bigger problem outside hospitals because the microorganisms are also circulating within the community.
Romania had the highest rate of MRSA with almost 72 per cent, followed by Cyprus with around 65 per cent.
Malta came next with around 55 per cent, a slight reduction over last year’s figure of 57 per cent.
It estimated that around three million people in the EU catch a healthcare-associated infection that is fatal in around 50,000 cases.
It attributed the problem to the over-use or inappropriate use of antibiotic and anti-viral drugs, the spread of drug-resistant microbes, especially in hospitals, clinics and care centres, and a shortage of new antibiotic drugs.
“A key factor for the development of antimicrobial resistance is the amount of antibiotics used,” it said.
The study noted that detailed data on the use of antibiotics and its consumption patterns are difficult to obtain but pointed out that it is “difficult to understand why the amount of antibiotics consumed per inhabitant varies three-fold between member states.”
A recently published European report has found that Malta has the third highest percentage of potentially deadly antibiotic-resistant hospital-acquired infections out of a list of 29 countries.
The report, which was compiled by the European Centre for Disease Prevention, found that Malta had an MRSA rate of around 55 per cent in 2005.
The study pointed out that, at present, the most important disease threat is from microorganisms that have become resistant to antibiotics. However, it went on to say that these are becoming a bigger problem outside hospitals because the microorganisms are also circulating within the community.
Romania had the highest rate of MRSA with almost 72 per cent, followed by Cyprus with around 65 per cent.
Malta came next with around 55 per cent, a slight reduction over last year’s figure of 57 per cent.
It estimated that around three million people in the EU catch a healthcare-associated infection that is fatal in around 50,000 cases.
It attributed the problem to the over-use or inappropriate use of antibiotic and anti-viral drugs, the spread of drug-resistant microbes, especially in hospitals, clinics and care centres, and a shortage of new antibiotic drugs.
“A key factor for the development of antimicrobial resistance is the amount of antibiotics used,” it said.
The study noted that detailed data on the use of antibiotics and its consumption patterns are difficult to obtain but pointed out that it is “difficult to understand why the amount of antibiotics consumed per inhabitant varies three-fold between member states.”
Saturday, June 16, 2007
Study Finds Pomegranate Effective In Fighting Bacteria, Viruses
A Pace University Study has found that pure pomegranate juice and pomegranate liquid extract are effective in fighting viruses and bacteria. According to their findings, 100% Pomegranate juice and POMx liquid extract could significantly reduce microbes found in the mouth that commonly cause cavities, staph infections and food poisoning
If the answer to improved health through protection against common germs and pathogens was as simple as drinking pomegranate juice, it seems everyone would be a lot healthier.
Recent preliminary research by Milton Schiffenbauer, Ph.D., a biology professor at Pace University in New York, indicates it just might be that simple. The research revealed that 100% pomegranate juice and POMx liquid extract (pomegranate polyphenol extract), made from the Wonderful variety of pomegranate grown in California, have antiviral and antibiotic effects. His findings will be introduced May 22 at the American Society for Microbiology's annual meeting in Toronto in a presentation entitled: "The Inactivation of Virus and Destruction of Bacteria by Pomegranate Juice."
In this exploratory study, Schiffenbauer tested 100% pomegranate juice and POMx liquid extract and the effect each had on a bacterial virus T1 and several bacteria over various periods of time, in various conditions and with the addition of other ingredients. The titer of T1 virus,(a model system) which infects E.coli B decreased up to 100% within 10 minutes of the addition of 100% pomegranate juice or POMx liquid extract. The research was funded by Pace University and POM Wonderful LLC and was conducted using POM Wonderful pomegranate products.
Both were also found to be effective in the destruction of bacteria S. mutans, known to cause cavities, S. aureus, the most common cause of staph infections, and B. cereus, a common cause of food poisoning. Schiffenbauer's findings also indicate that 100% pomegranate juice and POMx liquid extract inhibit the spread of Methicillin-resistant Staphylococcus aureus (MRSA), having widespread implications in the treatment of these potentially pathogenic microorganisms.
The addition of the POM products to various oral agents, including toothpaste and mouthwash, gave these agents an antimicrobial effect.
This work comes on the heels of earlier studies conducted by Schiffenbauer that found that white tea and green tea extracts also have antimicrobial effects. According to Schiffenbauer, pomegranate has gotten even better results than the teas.
Source: postchronicle.com
If the answer to improved health through protection against common germs and pathogens was as simple as drinking pomegranate juice, it seems everyone would be a lot healthier.
Recent preliminary research by Milton Schiffenbauer, Ph.D., a biology professor at Pace University in New York, indicates it just might be that simple. The research revealed that 100% pomegranate juice and POMx liquid extract (pomegranate polyphenol extract), made from the Wonderful variety of pomegranate grown in California, have antiviral and antibiotic effects. His findings will be introduced May 22 at the American Society for Microbiology's annual meeting in Toronto in a presentation entitled: "The Inactivation of Virus and Destruction of Bacteria by Pomegranate Juice."
In this exploratory study, Schiffenbauer tested 100% pomegranate juice and POMx liquid extract and the effect each had on a bacterial virus T1 and several bacteria over various periods of time, in various conditions and with the addition of other ingredients. The titer of T1 virus,(a model system) which infects E.coli B decreased up to 100% within 10 minutes of the addition of 100% pomegranate juice or POMx liquid extract. The research was funded by Pace University and POM Wonderful LLC and was conducted using POM Wonderful pomegranate products.
Both were also found to be effective in the destruction of bacteria S. mutans, known to cause cavities, S. aureus, the most common cause of staph infections, and B. cereus, a common cause of food poisoning. Schiffenbauer's findings also indicate that 100% pomegranate juice and POMx liquid extract inhibit the spread of Methicillin-resistant Staphylococcus aureus (MRSA), having widespread implications in the treatment of these potentially pathogenic microorganisms.
The addition of the POM products to various oral agents, including toothpaste and mouthwash, gave these agents an antimicrobial effect.
This work comes on the heels of earlier studies conducted by Schiffenbauer that found that white tea and green tea extracts also have antimicrobial effects. According to Schiffenbauer, pomegranate has gotten even better results than the teas.
Source: postchronicle.com
Friday, June 15, 2007
USA: Milliken launches new antimicrobial-charged fabric technology
LAS VEGAS: The one of largest privately-held textile and chemical manufacturers in the world, Milliken® & Company has announced a new antimicrobial-charged fabric technology called BioSmart™ that harnesses the sanitising power of EPA-registered chlorine bleach and helps to reduce the spread of infection-causing bacteria and viruses, including emerging antibiotic-resistant microbes, said Travis Greer, senior technologist for Milliken’s Apparel and Specialty Fabrics division in a release.
The product made with BioSmart are key to effective infection prevention strategies and programs in the workplace, in community settings and at home and extends the capabilities of EPA-registered chlorine base sanitisers – proven hygienic agents that do not promote resistant microbes, to maintain an effective antimicrobial barrier against contamination.
The technology can be applied to synthetics, cotton and poly/cotton fabrics and are ideal for industries where bacterial contamination is a concern, including food processing and services, healthcare, public safety, hospitality, sports apparel, activewear and military.
BioSmart fabrics are non-irritating to the skin and have passed the ISO skin irritation and skin sensitivity tests an it is both durable and effective for the life of most garments as the fabric technology literally recharges after every washing, thus providing a longer shelf life and optimising value for manufacturers, laundries and consumers alike.
In addition, BioSmart fabrics are odorless, dry quickly and wick moisture and is currently available in butcher coats and other garments for the food safety and processing industries through G&K Services.
BioSmart is a patent-pending textile technology that binds chlorine molecules to the surface of fabrics.
Founded in 1865, Milliken & Company is a privately held textile and chemical company that employs approximately 10,000 associates worldwide and operates nearly 50 manufacturing facilities in the US and eight countries.
The product made with BioSmart are key to effective infection prevention strategies and programs in the workplace, in community settings and at home and extends the capabilities of EPA-registered chlorine base sanitisers – proven hygienic agents that do not promote resistant microbes, to maintain an effective antimicrobial barrier against contamination.
The technology can be applied to synthetics, cotton and poly/cotton fabrics and are ideal for industries where bacterial contamination is a concern, including food processing and services, healthcare, public safety, hospitality, sports apparel, activewear and military.
BioSmart fabrics are non-irritating to the skin and have passed the ISO skin irritation and skin sensitivity tests an it is both durable and effective for the life of most garments as the fabric technology literally recharges after every washing, thus providing a longer shelf life and optimising value for manufacturers, laundries and consumers alike.
In addition, BioSmart fabrics are odorless, dry quickly and wick moisture and is currently available in butcher coats and other garments for the food safety and processing industries through G&K Services.
BioSmart is a patent-pending textile technology that binds chlorine molecules to the surface of fabrics.
Founded in 1865, Milliken & Company is a privately held textile and chemical company that employs approximately 10,000 associates worldwide and operates nearly 50 manufacturing facilities in the US and eight countries.
Thursday, June 14, 2007
Too many antibiotics? Use could lead to resistant bacteria
By Matt Whetstone, Cadillac News
Philosophies about antibiotics are changing.
While antibiotics are great to treat disease, there is a drawback. In a nation where people have become increasingly reliant on antibiotics, bacteria have become increasingly resistant to the drugs.
In the medical community, beginning to change the way things are done truly begins by changing attitudes.
Oftentimes, patients enter a doctor’s office insistent on receiving antibiotics.
In a study performed using patients with strep throat, two groups were given antibiotics while a third was given a placebo. In the two groups given antibiotics, resistance levels rose by 50 percent.
The group given the placebo saw no increase in antibiotic resistance.
In Dr. Gerald Herring’s antibiotic toolbox, he has six options.
That’s six different chances to treat a bacterial infection in children.
“In general, the more antibiotics we use, the higher incidence of bacteria becoming resistant to antibiotics,” said Herring, a physician at Mackinaw Trail Pediatrics in Cadillac.
Another concern is that overusing antibiotics at a young age can cause children to become sensitized to a drug and result in allergic reactions, Herring said.
All of a sudden, six options could be cut in half.
The Centers for Disease Control calls antibiotic resistance one of the world’s most pressing public health problems. Overuse can mean longer-lasting illnesses, more doctor visits or extended hospital stays. Illnesses once easily treated could become much more difficult to remedy.
“A lot of patients still think they need antibiotics for colds,” Herring said. “There are a lot of misconceptions out there in the public.”
Take for example ear infections. It’s something Herring sees all the time as a pediatrician. When treating a child, Herring said he asks himself if the body can deal with an infection or if it needs some help.
Yet, 80 percent of ear infections heal on their own and in about the same time as if an antibiotic were used, Herring said.
It becomes more pressing to use antibiotics for an ear infection if a child has a high fever or if things are not improving after a few days. Not using antibiotics mean careful observation and treating the child’s symptoms.
For adults, doctors have more options when it comes to antibiotics but Herring said it’s the same situation.
“It’s a question of rethinking for physicians and re-educating of patients to teach them they don’t always need antibiotics,” he said.
Dr. James Wilson, Medical Director for District Health Department No. 10, said doctors weigh the risks versus the benefits when determining if an antibiotic is necessary. It means thinking short, intermediate and long term.
“Generally, it’s not good to be on antibiotics for a long time,” he said.
Like anything else, Wilson said microbes are constantly evolving and they will mutate if it can make them more resistant to antibiotics.
While there are many beneficial alternative treatment options, Wilson said there’s not always an incentive to use them under the U.S. medical system.
Likewise, alternative therapies are not regulated by the Food and Drug Administration, meaning it’s difficult to get information on the risks and benefits, he said.
Your local connection
What are bacteria and viruses?
Bacteria are single-celled organisms found everywhere. Many are not harmful but some can trigger illnesses, such as strep throat and some ear infections.
Viruses are smaller than bacteria and cause illnesses by invading healthy cells and reproducing.
What kinds of infections are caused by viruses and should not be treated with antibiotics?
Colds, flu, most coughs and bronchitis, sore throats (except those resulting from strep throat).
How do I know if an illness is caused by a viral or bacterial infection?
It is difficult, consult with a physician.
What is antibiotic resistance?
Antibiotic resistance occurs when bacteria change in a way that reduces or eliminates the effectiveness of antibiotics. These resistant bacteria survive and multiply, causing more harm, such as longer illness, more doctor visits and a need for more expensive and toxic antibiotics.
When do I need to take antibiotics?
Antibiotics should only be used when prescribed by a doctor to treat bacterial infections.
What can I do to avoid antibiotic resistant infections?
Talk to your doctor about antibiotic resistance. Ask if an antibiotic is likely to be effective in treating your illness.
Do not demand an antibiotic when a doctor determines one is not appropriate. Ask what else you can to do help relieve your symptoms.
How can a child be protected from antibiotic-resistant bacteria?
Use only if a doctor determines it will be effective. Antibiotics will not cure most colds, coughs, sore throats or runny noses. Children fight off colds on their own.
Source: Centers for Disease Control
Philosophies about antibiotics are changing.
While antibiotics are great to treat disease, there is a drawback. In a nation where people have become increasingly reliant on antibiotics, bacteria have become increasingly resistant to the drugs.
In the medical community, beginning to change the way things are done truly begins by changing attitudes.
Oftentimes, patients enter a doctor’s office insistent on receiving antibiotics.
In a study performed using patients with strep throat, two groups were given antibiotics while a third was given a placebo. In the two groups given antibiotics, resistance levels rose by 50 percent.
The group given the placebo saw no increase in antibiotic resistance.
In Dr. Gerald Herring’s antibiotic toolbox, he has six options.
That’s six different chances to treat a bacterial infection in children.
“In general, the more antibiotics we use, the higher incidence of bacteria becoming resistant to antibiotics,” said Herring, a physician at Mackinaw Trail Pediatrics in Cadillac.
Another concern is that overusing antibiotics at a young age can cause children to become sensitized to a drug and result in allergic reactions, Herring said.
All of a sudden, six options could be cut in half.
The Centers for Disease Control calls antibiotic resistance one of the world’s most pressing public health problems. Overuse can mean longer-lasting illnesses, more doctor visits or extended hospital stays. Illnesses once easily treated could become much more difficult to remedy.
“A lot of patients still think they need antibiotics for colds,” Herring said. “There are a lot of misconceptions out there in the public.”
Take for example ear infections. It’s something Herring sees all the time as a pediatrician. When treating a child, Herring said he asks himself if the body can deal with an infection or if it needs some help.
Yet, 80 percent of ear infections heal on their own and in about the same time as if an antibiotic were used, Herring said.
It becomes more pressing to use antibiotics for an ear infection if a child has a high fever or if things are not improving after a few days. Not using antibiotics mean careful observation and treating the child’s symptoms.
For adults, doctors have more options when it comes to antibiotics but Herring said it’s the same situation.
“It’s a question of rethinking for physicians and re-educating of patients to teach them they don’t always need antibiotics,” he said.
Dr. James Wilson, Medical Director for District Health Department No. 10, said doctors weigh the risks versus the benefits when determining if an antibiotic is necessary. It means thinking short, intermediate and long term.
“Generally, it’s not good to be on antibiotics for a long time,” he said.
Like anything else, Wilson said microbes are constantly evolving and they will mutate if it can make them more resistant to antibiotics.
While there are many beneficial alternative treatment options, Wilson said there’s not always an incentive to use them under the U.S. medical system.
Likewise, alternative therapies are not regulated by the Food and Drug Administration, meaning it’s difficult to get information on the risks and benefits, he said.
Your local connection
What are bacteria and viruses?
Bacteria are single-celled organisms found everywhere. Many are not harmful but some can trigger illnesses, such as strep throat and some ear infections.
Viruses are smaller than bacteria and cause illnesses by invading healthy cells and reproducing.
What kinds of infections are caused by viruses and should not be treated with antibiotics?
Colds, flu, most coughs and bronchitis, sore throats (except those resulting from strep throat).
How do I know if an illness is caused by a viral or bacterial infection?
It is difficult, consult with a physician.
What is antibiotic resistance?
Antibiotic resistance occurs when bacteria change in a way that reduces or eliminates the effectiveness of antibiotics. These resistant bacteria survive and multiply, causing more harm, such as longer illness, more doctor visits and a need for more expensive and toxic antibiotics.
When do I need to take antibiotics?
Antibiotics should only be used when prescribed by a doctor to treat bacterial infections.
What can I do to avoid antibiotic resistant infections?
Talk to your doctor about antibiotic resistance. Ask if an antibiotic is likely to be effective in treating your illness.
Do not demand an antibiotic when a doctor determines one is not appropriate. Ask what else you can to do help relieve your symptoms.
How can a child be protected from antibiotic-resistant bacteria?
Use only if a doctor determines it will be effective. Antibiotics will not cure most colds, coughs, sore throats or runny noses. Children fight off colds on their own.
Source: Centers for Disease Control
Tuesday, June 12, 2007
Return of the White Plague
By Howard Markel
Sunday, June 10, 2007; Page B01
Andrew Speaker, the 31-year-old Atlanta lawyer with a bad case of wanderlust and a worse case of tuberculosis, isn't just a media sensation. He's also the personification of a time machine, returning us to a not-so-distant era when diseases that we now casually assume are treatable claimed thousands of lives. And that grim part of our past could become our future.
Speaker got plenty of press as he was ordered into federal quarantine, having crisscrossed the Atlantic on commercial flights while infected with extensively drug-resistant tuberculosis (XDR-TB). But what hasn't garnered nearly enough attention is a sober consideration of just how deadly tuberculosis can be. The rising worldwide number of XDR-TB cases like Speaker's may herald the end of a glorious 60-year holiday from many common and highly contagious diseases -- such as polio, measles and cholera -- that once routinely ravaged vast swaths of humanity.
For those of you who consider tuberculosis a thing of the distant past, let me tell you a story. As a young man in 1913, Eugene O'Neill, the future playwright and winner of the Nobel and Pulitzer prizes, was confined for five months to a TB sanatorium. His family considered the initial diagnosis practically a death sentence. They had a point: Tuberculosis was then the leading cause of death for Americans ages 20 to 45. But by living under an enforced regimen of rest, fresh air and exercise, and by eating a diet rich in fat and protein, O'Neill recovered. A young woman he met and fell in love with in the sanatorium was not nearly so fortunate. Emaciated, pale and weak, she entered her last bloody round of violent coughing 18 months later. Writing about her death, O'Neill described tuberculosis as a cruel game of drawing straws, with more short straws than long ones.
The ancient Greeks had a wonderful word to describe tuberculosis's ravages: phthisis, which describes a living body that shrivels with intense heat as if placed on a flame. Later, the Romans applied the Latin word "consumere" -- to eat up or devour -- to the malady. Indeed, when O'Neill's TB was diagnosed, the disease was still referred to as "consumption." This is precisely what untreated (or untreatable) tuberculosis does. It consumes with a passionate and incisive energy; it slowly, inexorably devours the very structure of the lungs and other critical organs, with the single goal of conquering its host -- but not until its progeny have had the opportunity to travel to and settle in the lungs of another human, to start the horrific process all over again.
Ironically, there has long been a disturbing tendency to romanticize the white plague, as tuberculosis is also known. It is, after all, the malady that carried away the poet John Keats and the scribbling Bronte sisters; the illness that rang down the final curtain on Moliere, Voltaire and Chekhov. And, of course, there are those operas by Verdi and Puccini featuring heroines struck down in their prime by tuberculosis. When reflecting on this artistic history, the late literary critic Susan Sontag once called tuberculosis an "aphrodisiac," a disease with "extraordinary power of seduction."
But in real life, tuberculosis is a messy, agonizing and debilitating ordeal. Once the tubercle bacilli gain the momentum to proceed unchecked through the body, there is no romance to be found. The actual experience of tuberculosis is one of exhaustion, not literary inspiration; drenching bouts of sweating, not hypersexual allure; groaning, not arias; a cough punctuated by uncontrollable spurts of blood, not the lover's kiss. This is the nightmarish reality of tuberculosis that O'Neill and his peers understood all too well -- and the one we so easily forget.
As doctors have long known, and as the rest of the world is beginning to appreciate, TB is very much alive and well. It began to rise again in developed nations in the 1980s, largely as a result of funding cuts for TB prevention and treatment programs and the emergence of the AIDS pandemic. The reemergence of tuberculosis has been most devastating, however, in impoverished nations, particularly ones where HIV/AIDS is prevalent, because AIDS significantly increases a person's susceptibility to tuberculosis. As TB cases have multiplied, so have the numbers of people either inadequately or incompletely treated -- which, in turn, has led to the emergence of drug-resistant strains of the microbe that causes the disease.
Our understanding of the prevalence of XDR-TB is somewhat sketchy. Nevertheless, the transformation of a once treatable disease into an infectious foe as deadly as it was when Eugene O'Neill was confined to his 1913 sanatorium is the worst nightmare of those charged with protecting public health. XDR-TB has appeared 49 times in the United States between 1993 and 2006 and is of particular concern in Eastern Europe, South Africa and Asia.
In the fall of 2006, the World Health Organization declared XDR-TB to be a global emergency and beseeched the wealthiest nations to contribute $95 million by the end of this year to contain it. But many billions more are needed to thoroughly treat the millions of cases of drug-sensitive tuberculosis so that those patients don't become resistant to standard antibiotics.
Today, more than one-third of the world's more than 6 billion people have been exposed to the tuberculosis germ. Five to 10 percent of them, or at least 100 million, will develop symptomatic TB. Each will infect 10 to 20 people before they are either successfully treated or they die. Last year, active -- and contagious -- tuberculosis was diagnosed in more than 8.8 million people. Approximately 420,000, or 5 percent, of them have a drug-resistant strain that requires several more medications than drug-sensitive cases do; about 30,000 of these 420,000 cases are even more difficult and expensive to treat, the highly lethal XDR-TB.
TB is not the only disease once close to eradication that is experiencing a scary renaissance. Drug-resistant strains of syphilis have reportedly been on the rise; and strains of once-conquered germs such as staph and strep have developed powerful and broad resistance to just about every antibiotic known and, as a result, wreak havoc on unsuspecting hospital patients. In the never-ending dance between humans and microbes, we have been leading for only about half a century. These deadly germs are evolving, mutating and revising their structure to reclaim the upper hand in their powers of infection.
We live in a risky world menaced by war, terrorism, economic inequities and global warming, to name a few major threats. But ask any doctor what keeps him awake at night, and he will probably tell you about emerging and reemerging infectious diseases such as XDR-TB. Which brings me back to Andrew Speaker's not so excellent adventure.
Aside from the disagreements over which health officer said what, arguments about the loopholes between federal, state and local health regulations, or the media ruckus over whether Speaker was just a guy trying to have a nice wedding or a modern-day Typhoid Mary with a law degree, one obvious point demands our attention. Tuberculosis is a bad disease, and it's contagious. International air travel poses real risks in the spread of tuberculosis. Coughing, sneezing, singing, yelling and even laughing can spread TB germs. People contract tuberculosis after prolonged exposure (eight hours or more) to someone with the illness. This is the same length of time as most transoceanic flights, where passengers breathe re-circulated air for hours on end.
Those infected have a moral imperative not to put others in harm's way, even though it may mean postponing a wedding and a honeymoon. This has been a truism since Roman times. Salus populi suprema lex esto, went their saying: Let the public's health be the supreme law.
So, if you're confronted with the slightest chance of spreading a terrible infection (and with tuberculosis, that determination can take many weeks), assume that you are contagious until proven otherwise. Failure to follow that simple rule eats away at the foundation of public health surveillance and modern medical care. One only wishes that before Speaker embarked upon the first of many flights last month, he had recalled an admonition he must have heard from his mother or kindergarten teacher: If you are sick, stay home.
Someone's life may depend on it.
howard@umich.edu
Howard Markel, a professor of communicable diseases and the history of medicine at the University of Michigan, is the author of "When Germs Travel."
Sunday, June 10, 2007; Page B01
Andrew Speaker, the 31-year-old Atlanta lawyer with a bad case of wanderlust and a worse case of tuberculosis, isn't just a media sensation. He's also the personification of a time machine, returning us to a not-so-distant era when diseases that we now casually assume are treatable claimed thousands of lives. And that grim part of our past could become our future.
Speaker got plenty of press as he was ordered into federal quarantine, having crisscrossed the Atlantic on commercial flights while infected with extensively drug-resistant tuberculosis (XDR-TB). But what hasn't garnered nearly enough attention is a sober consideration of just how deadly tuberculosis can be. The rising worldwide number of XDR-TB cases like Speaker's may herald the end of a glorious 60-year holiday from many common and highly contagious diseases -- such as polio, measles and cholera -- that once routinely ravaged vast swaths of humanity.
For those of you who consider tuberculosis a thing of the distant past, let me tell you a story. As a young man in 1913, Eugene O'Neill, the future playwright and winner of the Nobel and Pulitzer prizes, was confined for five months to a TB sanatorium. His family considered the initial diagnosis practically a death sentence. They had a point: Tuberculosis was then the leading cause of death for Americans ages 20 to 45. But by living under an enforced regimen of rest, fresh air and exercise, and by eating a diet rich in fat and protein, O'Neill recovered. A young woman he met and fell in love with in the sanatorium was not nearly so fortunate. Emaciated, pale and weak, she entered her last bloody round of violent coughing 18 months later. Writing about her death, O'Neill described tuberculosis as a cruel game of drawing straws, with more short straws than long ones.
The ancient Greeks had a wonderful word to describe tuberculosis's ravages: phthisis, which describes a living body that shrivels with intense heat as if placed on a flame. Later, the Romans applied the Latin word "consumere" -- to eat up or devour -- to the malady. Indeed, when O'Neill's TB was diagnosed, the disease was still referred to as "consumption." This is precisely what untreated (or untreatable) tuberculosis does. It consumes with a passionate and incisive energy; it slowly, inexorably devours the very structure of the lungs and other critical organs, with the single goal of conquering its host -- but not until its progeny have had the opportunity to travel to and settle in the lungs of another human, to start the horrific process all over again.
Ironically, there has long been a disturbing tendency to romanticize the white plague, as tuberculosis is also known. It is, after all, the malady that carried away the poet John Keats and the scribbling Bronte sisters; the illness that rang down the final curtain on Moliere, Voltaire and Chekhov. And, of course, there are those operas by Verdi and Puccini featuring heroines struck down in their prime by tuberculosis. When reflecting on this artistic history, the late literary critic Susan Sontag once called tuberculosis an "aphrodisiac," a disease with "extraordinary power of seduction."
But in real life, tuberculosis is a messy, agonizing and debilitating ordeal. Once the tubercle bacilli gain the momentum to proceed unchecked through the body, there is no romance to be found. The actual experience of tuberculosis is one of exhaustion, not literary inspiration; drenching bouts of sweating, not hypersexual allure; groaning, not arias; a cough punctuated by uncontrollable spurts of blood, not the lover's kiss. This is the nightmarish reality of tuberculosis that O'Neill and his peers understood all too well -- and the one we so easily forget.
As doctors have long known, and as the rest of the world is beginning to appreciate, TB is very much alive and well. It began to rise again in developed nations in the 1980s, largely as a result of funding cuts for TB prevention and treatment programs and the emergence of the AIDS pandemic. The reemergence of tuberculosis has been most devastating, however, in impoverished nations, particularly ones where HIV/AIDS is prevalent, because AIDS significantly increases a person's susceptibility to tuberculosis. As TB cases have multiplied, so have the numbers of people either inadequately or incompletely treated -- which, in turn, has led to the emergence of drug-resistant strains of the microbe that causes the disease.
Our understanding of the prevalence of XDR-TB is somewhat sketchy. Nevertheless, the transformation of a once treatable disease into an infectious foe as deadly as it was when Eugene O'Neill was confined to his 1913 sanatorium is the worst nightmare of those charged with protecting public health. XDR-TB has appeared 49 times in the United States between 1993 and 2006 and is of particular concern in Eastern Europe, South Africa and Asia.
In the fall of 2006, the World Health Organization declared XDR-TB to be a global emergency and beseeched the wealthiest nations to contribute $95 million by the end of this year to contain it. But many billions more are needed to thoroughly treat the millions of cases of drug-sensitive tuberculosis so that those patients don't become resistant to standard antibiotics.
Today, more than one-third of the world's more than 6 billion people have been exposed to the tuberculosis germ. Five to 10 percent of them, or at least 100 million, will develop symptomatic TB. Each will infect 10 to 20 people before they are either successfully treated or they die. Last year, active -- and contagious -- tuberculosis was diagnosed in more than 8.8 million people. Approximately 420,000, or 5 percent, of them have a drug-resistant strain that requires several more medications than drug-sensitive cases do; about 30,000 of these 420,000 cases are even more difficult and expensive to treat, the highly lethal XDR-TB.
TB is not the only disease once close to eradication that is experiencing a scary renaissance. Drug-resistant strains of syphilis have reportedly been on the rise; and strains of once-conquered germs such as staph and strep have developed powerful and broad resistance to just about every antibiotic known and, as a result, wreak havoc on unsuspecting hospital patients. In the never-ending dance between humans and microbes, we have been leading for only about half a century. These deadly germs are evolving, mutating and revising their structure to reclaim the upper hand in their powers of infection.
We live in a risky world menaced by war, terrorism, economic inequities and global warming, to name a few major threats. But ask any doctor what keeps him awake at night, and he will probably tell you about emerging and reemerging infectious diseases such as XDR-TB. Which brings me back to Andrew Speaker's not so excellent adventure.
Aside from the disagreements over which health officer said what, arguments about the loopholes between federal, state and local health regulations, or the media ruckus over whether Speaker was just a guy trying to have a nice wedding or a modern-day Typhoid Mary with a law degree, one obvious point demands our attention. Tuberculosis is a bad disease, and it's contagious. International air travel poses real risks in the spread of tuberculosis. Coughing, sneezing, singing, yelling and even laughing can spread TB germs. People contract tuberculosis after prolonged exposure (eight hours or more) to someone with the illness. This is the same length of time as most transoceanic flights, where passengers breathe re-circulated air for hours on end.
Those infected have a moral imperative not to put others in harm's way, even though it may mean postponing a wedding and a honeymoon. This has been a truism since Roman times. Salus populi suprema lex esto, went their saying: Let the public's health be the supreme law.
So, if you're confronted with the slightest chance of spreading a terrible infection (and with tuberculosis, that determination can take many weeks), assume that you are contagious until proven otherwise. Failure to follow that simple rule eats away at the foundation of public health surveillance and modern medical care. One only wishes that before Speaker embarked upon the first of many flights last month, he had recalled an admonition he must have heard from his mother or kindergarten teacher: If you are sick, stay home.
Someone's life may depend on it.
howard@umich.edu
Howard Markel, a professor of communicable diseases and the history of medicine at the University of Michigan, is the author of "When Germs Travel."
We're near top of killer bug table
By Anne-Marie Walsh
Saturday June 09 2007
Irish hospitals come seventh in a league table of incidents of the deadly infection across 29 countries, according to new EU figures.
The research confirms that patients are highly exposed to the hospital-based bacteria and the rate of infection has not improved since 2001.
Only six other countries, Romania, Cyprus, Malta, Portugal, the UK and Greece (in that order), have a higher rate of the antibiotic-resistant infection.
However, a spokesperson for the ECDC pointed out that the Irish figures could be misleading.
"One of the reasons that Ireland and the UK have relatively high levels of MRSA is that they are quite active in monitoring it," he said.
"Some other EU countries may not be looking as hard or monitoring it as well."
But he added: "Compared with Ireland, the Netherlands and Scandinavia have been quite successful in preventing MRSA.
The level of MRSA in Ireland has risen in the last 10 years and has levelled off."
The investigation by the EU Centre for Disease Prevention and Control (ECDC) shows that the rate of MRSA went up by 1pc in the latest available year's data.
It is at the same level it was at in 2001, and 3pc higher than the 1999 rate of 39pc, suggesting that Government initiativeson eradication have had little impact.
The ECDC warned last night that the spread of hospital-acquired infections was now the main disease threat in Europe.
It said that, if the present "rapid negative development" was not halted, mankind would soon lose one of its most important weapons against infectious disease - antibiotics.
MRSA (methicillin-resistant staphylococcus aureus) is one of the bugs in the staphylococcus aureus family of bacteria that cannot be treated with drugs.
It made up 42pc of the 1,360 detected infections in this family of bacteria in Ireland in 2005.
This represented 571 people, according to the authors of the pioneering report from the ECDC.
The rest of the cases infected with the staphylococcus aureus bacteria could be treated with drugs.
MRSA is among the forms of superbugs from the staphylococcus aureus family of bacteria that are resistant to antibiotics.
They can live on the skin and in the nose and cause a variety of illnesses including meningitis and septicaemia.
If the bacteria enters the bloodstream, it can be extremely dangerous and is potentially fatal if it belongs to the variety that is resistant to antibiotics.
The ECDC report on infectious diseases ranked countries based on the proportion of S-aureus infections found to be antibiotic-resistant.
Romania topped the table with the highest proportion of the superbug, at over 60pc.
Every year, around 3m people in the EU catch a healthcare-associated infection, of whom around 50,000 die.
One in every 10 patients admitted to hospital in the EU will catch an infection there.
"One of the biggest challenges we face is the emergence of new microbes against which our defences are weak, or even non-existent," said Markos Kyprianou, European Commissioner for Health.
"Pandemic preparedness is, and must remain, a priority for the EU."
- Anne-Marie Walsh
Saturday June 09 2007
Irish hospitals come seventh in a league table of incidents of the deadly infection across 29 countries, according to new EU figures.
The research confirms that patients are highly exposed to the hospital-based bacteria and the rate of infection has not improved since 2001.
Only six other countries, Romania, Cyprus, Malta, Portugal, the UK and Greece (in that order), have a higher rate of the antibiotic-resistant infection.
However, a spokesperson for the ECDC pointed out that the Irish figures could be misleading.
"One of the reasons that Ireland and the UK have relatively high levels of MRSA is that they are quite active in monitoring it," he said.
"Some other EU countries may not be looking as hard or monitoring it as well."
But he added: "Compared with Ireland, the Netherlands and Scandinavia have been quite successful in preventing MRSA.
The level of MRSA in Ireland has risen in the last 10 years and has levelled off."
The investigation by the EU Centre for Disease Prevention and Control (ECDC) shows that the rate of MRSA went up by 1pc in the latest available year's data.
It is at the same level it was at in 2001, and 3pc higher than the 1999 rate of 39pc, suggesting that Government initiativeson eradication have had little impact.
The ECDC warned last night that the spread of hospital-acquired infections was now the main disease threat in Europe.
It said that, if the present "rapid negative development" was not halted, mankind would soon lose one of its most important weapons against infectious disease - antibiotics.
MRSA (methicillin-resistant staphylococcus aureus) is one of the bugs in the staphylococcus aureus family of bacteria that cannot be treated with drugs.
It made up 42pc of the 1,360 detected infections in this family of bacteria in Ireland in 2005.
This represented 571 people, according to the authors of the pioneering report from the ECDC.
The rest of the cases infected with the staphylococcus aureus bacteria could be treated with drugs.
MRSA is among the forms of superbugs from the staphylococcus aureus family of bacteria that are resistant to antibiotics.
They can live on the skin and in the nose and cause a variety of illnesses including meningitis and septicaemia.
If the bacteria enters the bloodstream, it can be extremely dangerous and is potentially fatal if it belongs to the variety that is resistant to antibiotics.
The ECDC report on infectious diseases ranked countries based on the proportion of S-aureus infections found to be antibiotic-resistant.
Romania topped the table with the highest proportion of the superbug, at over 60pc.
Every year, around 3m people in the EU catch a healthcare-associated infection, of whom around 50,000 die.
One in every 10 patients admitted to hospital in the EU will catch an infection there.
"One of the biggest challenges we face is the emergence of new microbes against which our defences are weak, or even non-existent," said Markos Kyprianou, European Commissioner for Health.
"Pandemic preparedness is, and must remain, a priority for the EU."
- Anne-Marie Walsh
Saturday, June 9, 2007
Biofilms -- slimy layers of bacteria that antibiotics don't fully kill -- are found in hospitals, kitchens, even your mouth. Scientists are on the att
WHETHER on a contact lens or a catheter, in your lungs or in your ears, a few bacterial invaders can set up a slimy fortress that can prove almost impossible to demolish. All it takes is a wet surface and a few days.
The sticky mess is called a biofilm, a slick layer of bacteria that is one of the biggest problems facing medicine today. Biofilms are forcing scientists to reevaluate their view of bacteria as free-floating bugs to one of sophisticated communities stuck on surfaces.
The National Institutes of Health estimates that more than 80% of microbial infections in the human body are caused by biofilms, many of them creating chronic and reoccurring problems. Two of the most serious: The layer of Pseudomonas aeruginosa that forms in the trachea of cystic fibrosis patients and the hospital-acquired infections resulting from biofilm formation on implanted medical devices.
Even the healthiest among us deals with biofilms on a daily basis in the form of dental plaque. And biofilms containing a pathogenic strain of E. coli were behind the spinach recall in October.
The problem with biofilms is that, because of their tightknit structure, they are resistant to traditional disinfectants and antibiotics. New research is aimed at finding ways to battle these goo-covered conglomerates. By understanding how biofilms thrive, scientists are devising new strategies for defeating them.
Biofilms form in a series of steps that scientists are just starting to understand. Step one occurs when a few bacteria attach to a surface. They activate certain genes within their genomes and inactivate others, starting their transformation from free-floaters to biofilm.
The bacteria begin to secrete polymers that hold aggregates of cells together. Then, as the biofilm grows, it becomes more complex and even starts to act like a multicellular organism.
Structures arise — such as channels to bring in nutrients and take away wastes.
Bacteria in different areas of the biofilm take on different roles. Some cells secrete enzymes, while others continue to make sticky matrix proteins. Some bacteria continue to rapidly divide, while others enter a dormant state.
The heterogeneity of biofilms is part of what makes them so robust, says Phil Stewart, director of the Center for Biofilm Engineering at Montana State University in Bozeman. A drug that can kill some of the bacteria in the biofilm might be useless against some of their neighbors.
The final step in the biofilm life cycle is dispersion. As conditions get crowded and resources become scarce, groups of cells detach and float away — potentially setting up new biofilms if they happen to land in a good spot.
"It's a little bit like seeds," Stewart says.
In many chronic and recurring infections — such as ear infections, prostatitis in men, urinary tract infections and endocarditis — these biofilm seeds set off the immune system and cause symptoms such as fever and inflammation that signal to doctor and patient that something's amiss.
When antibiotics are administered, the free-floating bacteria are killed. But the original biofilm remains unscathed. Although the infection appears to be cured, it is only a matter of time before another chunk of biofilm is set free and the symptoms return.
There are no good ways to fight biofilms because an awareness of their importance has only emerged in the last decade, Stewart says. Before that, research on bacteria focused on homogeneous cultures of fast-growing cells in flasks. Tools that fight these kinds of bacteria are great for acute infections in which bacteria are freely floating in the body. But they are almost useless against biofilms.
The Center for Biofilm Engineering is trying to change this by developing standardized methods for working with biofilms that the whole research community can use. A few companies and academic scientists are already exploring new avenues in treating and preventing biofilms.
One of the problems with today's antibiotics is that many only attack bacteria that are actively growing. This means that the dormant cells in a biofilm will escape treatment and be left behind to regrow the biofilm. So one approach to fighting biofilms is to come up with drugs that can kill all the biofilm residents.
Cubist Pharmaceuticals in Lexington, Mass., developed an antibiotic called daptomycin (marketed as Cubicin) that is able to do just that, enabling doctors to eradicate a biofilm with drug treatment.
But even if you could use antibiotics to kill all the bacteria in a biofilm, that might not be the best idea, says Wenyuan Shi, professor of oral biology and medicine at UCLA's School of Dentistry.
"Think of a lawn infested with dandelions," he says. "If you kill everything, the dandelions will come back first. But if you use a dandelion-specific killer and the grass fills in the lawn, the dandelions won't come back."
Many biofilms are composed of both good and bad bacteria. Shi's lab has developed a "smart bomb" that targets the harmful bacteria in a biofilm. A short antimicrobial peptide is attached to another one that mimics a pheromone used by bacteria to communicate. This hybrid bacteria-fighting molecule attaches to certain bacteria and makes sure only the targeted bugs are killed.
Shi has formed a Los Angeles-based company, C3Jian, to develop this technique for use in dental hygiene products. The company recently received the go-ahead for a clinical pilot study of a dental varnish that incorporates its peptides. It expects to have a product on the market in about three years.
Another approach to fighting biofilms is to try to break up their slimy coating and return them to the free-floating state that scientists are used to dealing with. Once released from the biofilm, the bacteria can be killed with antibiotics.
Kane Biotech, a company based in Winnipeg, Canada, is developing treatments and preventives based on an enzyme called Dispersin B, which was discovered in the bacterial species Actinobacillus actinomycetemcomitans but is now mass produced by the company using E. coli bacteria. Dispersin B breaks up the sugary bonds in the slime of biofilms, separating the bacteria from one another.
In animal studies, the company has reported that a combination of Dispersin B and broad-spectrum antibiotics can effectively prevent biofilm buildup in central venous catheters. (Such catheters, which are inserted into large veins in the neck, chest or groin, frequently become colonized by biofilms when bacteria make their way in from the patients' skin or from contact with healthcare workers.) Kane is also working on ways to incorporate Dispersin B into treatments for chronic wounds such as diabetic foot ulcers, which are thought to be slow-healing because of infections by biofilms.
David Davies, assistant professor of biological sciences at Binghamton University in New York, also is taking the divide-and-conquer approach. But instead of attacking biofilm slime from the outside with an enzyme, his lab is working with a chemical messenger derived from biofilms themselves.
This messenger — its name is proprietary — is common to many species of biofilm bacteria and is responsible for the dispersion effect that is a normal part of their life cycle. Davies' group intends to tweak this messenger so that it could be used as a medicine that would trick biofilms into thinking it was time to break up. Once they do so, it would make the bacteria susceptible to classical antibiotic treatments.
Biosignal, an Australian biotech company, is trying to prevent biofilms from forming on medical devices in the first place. Its product is derived from a type of seaweed called Delisea pulchra that is found off the Australian coast. Although many surfaces in the ocean are covered with biofilm, the leaves of this plant are not. That's because they produce chemicals called furanones that prevent biofilm formation.
Furanones don't kill bacteria. According to Stewart, this is ideal. By not exposing the bacteria to poisons, there is less pressure for the selection of resistant strains — a problem that has become widespread with the increased use of antibiotics.
Peter Steinberg, a professor of biological sciences at the University of New South Wales in Australia and the head of research and development at Biosignal, says that the company has found a way to produce refined versions of furanones in the lab. The company is using them to make coatings for contact lenses. A small clinical trial in Australia involving 10 patients wearing the coated contact lenses overnight showed that the furanone coating is safe and well-tolerated.
The firm is working toward larger, longer trials and is in the early stages of developing furanone coatings for medical devices such as catheters.
A group in Israel led by Gad Lavie, an assistant professor at Sheba Medical Center, is taking a more physical approach to the biological problem of biofilms on medical devices. Working with NanoVibronix, an Israeli company, Lavie has found that when scientists attach a small acoustic-wave-producing device to the outside portion of a urinary catheter, biofilm formation is prevented.
The acoustic waves cause vibrations in the catheter that are imperceptible to patients but apparently repulsive to bacteria. In a small clinical trial conducted last year in Germany, six of seven patients fitted with nonvibrating catheters in their urethras developed biofilms in them. None of the vibrating catheters showed any signs of biofilm formation.
"It was really amazing," Lavie says. These results are significant, he adds, because patients who are catheterized for long periods of time must have their catheters changed every four to five days because of biofilm buildup. He expects that vibrating catheters might not need to be replaced for months.
Biofilm research is still an emerging field. Although many approaches for dealing with biofilms in health and industrial settings have been thought up, most are still in the development stage. For now, the surest way to proceed in treating biofilms is to remove them when possible.
In hospitals, this means replacing catheters every few days. In the kitchen, it means really scrubbing produce clean. And, of course, Stewart says, "tooth brushing is a good idea."
Breeding grounds
Biofilms are not just in the human body. They can occur on any moist surface.
Fresh produce: The moist, nutrient-rich surfaces of fruits and vegetables are prime for biofilms. They can be hard to remove even with washing. This is not usually a problem unless a pathogenic bacterium, such as the strain of E. coli that was involved in the spinach recall, becomes part of the mix. Eco-Safe Systems USA is marketing a product that dissolves ozone gas in water, producing an antibacterial wash that can kill bacteria instantly, even when it is hiding in a biofilm. The ozone then breaks down to oxygen. The USDA allows produce washed with ozonated water to be labeled organic.
Industrial pipes: Biofilms can set up residence inside pipes and cause devastating corrosion. They were behind the breach found in the Alaska Pipeline last summer. Sixteen miles of pipe had to be replaced.
Household pipes: Biofilms can also build up in water pipes and air-conditioning ducts. If they grow in the pipes feeding the hot tubs, chunks of bacteria can break off, enter the hot tub and become aerosolized, leading to an infection known as "hot tub lung."
— Erin Cline
The sticky mess is called a biofilm, a slick layer of bacteria that is one of the biggest problems facing medicine today. Biofilms are forcing scientists to reevaluate their view of bacteria as free-floating bugs to one of sophisticated communities stuck on surfaces.
The National Institutes of Health estimates that more than 80% of microbial infections in the human body are caused by biofilms, many of them creating chronic and reoccurring problems. Two of the most serious: The layer of Pseudomonas aeruginosa that forms in the trachea of cystic fibrosis patients and the hospital-acquired infections resulting from biofilm formation on implanted medical devices.
Even the healthiest among us deals with biofilms on a daily basis in the form of dental plaque. And biofilms containing a pathogenic strain of E. coli were behind the spinach recall in October.
The problem with biofilms is that, because of their tightknit structure, they are resistant to traditional disinfectants and antibiotics. New research is aimed at finding ways to battle these goo-covered conglomerates. By understanding how biofilms thrive, scientists are devising new strategies for defeating them.
Biofilms form in a series of steps that scientists are just starting to understand. Step one occurs when a few bacteria attach to a surface. They activate certain genes within their genomes and inactivate others, starting their transformation from free-floaters to biofilm.
The bacteria begin to secrete polymers that hold aggregates of cells together. Then, as the biofilm grows, it becomes more complex and even starts to act like a multicellular organism.
Structures arise — such as channels to bring in nutrients and take away wastes.
Bacteria in different areas of the biofilm take on different roles. Some cells secrete enzymes, while others continue to make sticky matrix proteins. Some bacteria continue to rapidly divide, while others enter a dormant state.
The heterogeneity of biofilms is part of what makes them so robust, says Phil Stewart, director of the Center for Biofilm Engineering at Montana State University in Bozeman. A drug that can kill some of the bacteria in the biofilm might be useless against some of their neighbors.
The final step in the biofilm life cycle is dispersion. As conditions get crowded and resources become scarce, groups of cells detach and float away — potentially setting up new biofilms if they happen to land in a good spot.
"It's a little bit like seeds," Stewart says.
In many chronic and recurring infections — such as ear infections, prostatitis in men, urinary tract infections and endocarditis — these biofilm seeds set off the immune system and cause symptoms such as fever and inflammation that signal to doctor and patient that something's amiss.
When antibiotics are administered, the free-floating bacteria are killed. But the original biofilm remains unscathed. Although the infection appears to be cured, it is only a matter of time before another chunk of biofilm is set free and the symptoms return.
There are no good ways to fight biofilms because an awareness of their importance has only emerged in the last decade, Stewart says. Before that, research on bacteria focused on homogeneous cultures of fast-growing cells in flasks. Tools that fight these kinds of bacteria are great for acute infections in which bacteria are freely floating in the body. But they are almost useless against biofilms.
The Center for Biofilm Engineering is trying to change this by developing standardized methods for working with biofilms that the whole research community can use. A few companies and academic scientists are already exploring new avenues in treating and preventing biofilms.
One of the problems with today's antibiotics is that many only attack bacteria that are actively growing. This means that the dormant cells in a biofilm will escape treatment and be left behind to regrow the biofilm. So one approach to fighting biofilms is to come up with drugs that can kill all the biofilm residents.
Cubist Pharmaceuticals in Lexington, Mass., developed an antibiotic called daptomycin (marketed as Cubicin) that is able to do just that, enabling doctors to eradicate a biofilm with drug treatment.
But even if you could use antibiotics to kill all the bacteria in a biofilm, that might not be the best idea, says Wenyuan Shi, professor of oral biology and medicine at UCLA's School of Dentistry.
"Think of a lawn infested with dandelions," he says. "If you kill everything, the dandelions will come back first. But if you use a dandelion-specific killer and the grass fills in the lawn, the dandelions won't come back."
Many biofilms are composed of both good and bad bacteria. Shi's lab has developed a "smart bomb" that targets the harmful bacteria in a biofilm. A short antimicrobial peptide is attached to another one that mimics a pheromone used by bacteria to communicate. This hybrid bacteria-fighting molecule attaches to certain bacteria and makes sure only the targeted bugs are killed.
Shi has formed a Los Angeles-based company, C3Jian, to develop this technique for use in dental hygiene products. The company recently received the go-ahead for a clinical pilot study of a dental varnish that incorporates its peptides. It expects to have a product on the market in about three years.
Another approach to fighting biofilms is to try to break up their slimy coating and return them to the free-floating state that scientists are used to dealing with. Once released from the biofilm, the bacteria can be killed with antibiotics.
Kane Biotech, a company based in Winnipeg, Canada, is developing treatments and preventives based on an enzyme called Dispersin B, which was discovered in the bacterial species Actinobacillus actinomycetemcomitans but is now mass produced by the company using E. coli bacteria. Dispersin B breaks up the sugary bonds in the slime of biofilms, separating the bacteria from one another.
In animal studies, the company has reported that a combination of Dispersin B and broad-spectrum antibiotics can effectively prevent biofilm buildup in central venous catheters. (Such catheters, which are inserted into large veins in the neck, chest or groin, frequently become colonized by biofilms when bacteria make their way in from the patients' skin or from contact with healthcare workers.) Kane is also working on ways to incorporate Dispersin B into treatments for chronic wounds such as diabetic foot ulcers, which are thought to be slow-healing because of infections by biofilms.
David Davies, assistant professor of biological sciences at Binghamton University in New York, also is taking the divide-and-conquer approach. But instead of attacking biofilm slime from the outside with an enzyme, his lab is working with a chemical messenger derived from biofilms themselves.
This messenger — its name is proprietary — is common to many species of biofilm bacteria and is responsible for the dispersion effect that is a normal part of their life cycle. Davies' group intends to tweak this messenger so that it could be used as a medicine that would trick biofilms into thinking it was time to break up. Once they do so, it would make the bacteria susceptible to classical antibiotic treatments.
Biosignal, an Australian biotech company, is trying to prevent biofilms from forming on medical devices in the first place. Its product is derived from a type of seaweed called Delisea pulchra that is found off the Australian coast. Although many surfaces in the ocean are covered with biofilm, the leaves of this plant are not. That's because they produce chemicals called furanones that prevent biofilm formation.
Furanones don't kill bacteria. According to Stewart, this is ideal. By not exposing the bacteria to poisons, there is less pressure for the selection of resistant strains — a problem that has become widespread with the increased use of antibiotics.
Peter Steinberg, a professor of biological sciences at the University of New South Wales in Australia and the head of research and development at Biosignal, says that the company has found a way to produce refined versions of furanones in the lab. The company is using them to make coatings for contact lenses. A small clinical trial in Australia involving 10 patients wearing the coated contact lenses overnight showed that the furanone coating is safe and well-tolerated.
The firm is working toward larger, longer trials and is in the early stages of developing furanone coatings for medical devices such as catheters.
A group in Israel led by Gad Lavie, an assistant professor at Sheba Medical Center, is taking a more physical approach to the biological problem of biofilms on medical devices. Working with NanoVibronix, an Israeli company, Lavie has found that when scientists attach a small acoustic-wave-producing device to the outside portion of a urinary catheter, biofilm formation is prevented.
The acoustic waves cause vibrations in the catheter that are imperceptible to patients but apparently repulsive to bacteria. In a small clinical trial conducted last year in Germany, six of seven patients fitted with nonvibrating catheters in their urethras developed biofilms in them. None of the vibrating catheters showed any signs of biofilm formation.
"It was really amazing," Lavie says. These results are significant, he adds, because patients who are catheterized for long periods of time must have their catheters changed every four to five days because of biofilm buildup. He expects that vibrating catheters might not need to be replaced for months.
Biofilm research is still an emerging field. Although many approaches for dealing with biofilms in health and industrial settings have been thought up, most are still in the development stage. For now, the surest way to proceed in treating biofilms is to remove them when possible.
In hospitals, this means replacing catheters every few days. In the kitchen, it means really scrubbing produce clean. And, of course, Stewart says, "tooth brushing is a good idea."
Breeding grounds
Biofilms are not just in the human body. They can occur on any moist surface.
Fresh produce: The moist, nutrient-rich surfaces of fruits and vegetables are prime for biofilms. They can be hard to remove even with washing. This is not usually a problem unless a pathogenic bacterium, such as the strain of E. coli that was involved in the spinach recall, becomes part of the mix. Eco-Safe Systems USA is marketing a product that dissolves ozone gas in water, producing an antibacterial wash that can kill bacteria instantly, even when it is hiding in a biofilm. The ozone then breaks down to oxygen. The USDA allows produce washed with ozonated water to be labeled organic.
Industrial pipes: Biofilms can set up residence inside pipes and cause devastating corrosion. They were behind the breach found in the Alaska Pipeline last summer. Sixteen miles of pipe had to be replaced.
Household pipes: Biofilms can also build up in water pipes and air-conditioning ducts. If they grow in the pipes feeding the hot tubs, chunks of bacteria can break off, enter the hot tub and become aerosolized, leading to an infection known as "hot tub lung."
— Erin Cline
Evolution at Work: Watching Bacteria Grow Drug Resistant
Day by day, the doctors unwittingly helped the bacteria infecting their young heart patient to evolve. The more intensively they treated his affliction with antibiotics, the more the microbes resisted the therapy.
In a strict medical sense, the young man, identified only as Patient X, died of complications from a congenital heart ailment and a Staphylococcus aureus infection.
More broadly, evolution killed him.
The life-and-death struggle inside his infected heart was driven by the same evolutionary forces of natural selection and adaptation that are causing a pandemic of drug-resistant diseases world-wide. The emergence of such immunity among infectious diseases is one of the most well-documented problems in modern public health. Until now, however, researchers knew little about how bacteria multiplying inside the human body overcome the drugs designed to control them.
Patient X died in October 2000 after a 12-week hospital stay. His case comes to light now because researchers only recently developed the computational techniques needed to sequence generations of bacteria. The hospital, which also wasn't identified, gave the patient's Staph samples to the Rockefeller team for research purposes. The techniques still are too slow and expensive for clinical use.
When Patient X was admitted to the hospital, he was already suffering from a Staphylococcus aureus infection, but it was still vulnerable to antibiotics. During treatment, however, the bacteria quickly developed stronger resistance to four antibiotics, including vancomycin, the drug of last resort for intractable infections, the scientists reported. As living bacteria, the Staph were driven to survive.
Every time the patient took his medicine, the antibiotics killed the weakest bacteria in his bloodstream. Any cell that had developed a protective mutation to defend itself against the drug survived, passing on its special trait to descendants. With every round of treatment, the cells refined their defenses through the trial and error of survival. "It means that during a normal course of treatment there is an evolutionary revolution going on in your body," said Stanford University biologist Stephen Plaumbi, author of "The Evolution Explosion: How Humans Cause Rapid Evolutionary Change."
These resistant microbes, all disease-producing organisms spawned by the original infection, quickly accumulated 35 useful mutations. Each one altered a molecular sensor or production of a protein.
Researchers then matched these gradual genetic changes to increasing levels of drug resistance, shocked that it took so little to undermine the foundation of modern infectious-disease control. "We have now really looked into the belly of the beast and seen the mechanism," said Rockefeller microbiologist Alexander Tomasz.
Nearly two million people catch bacterial infections in U.S. hospitals every year and 90,000 of them die -- seven times as high as a decade ago as germs become immune to almost every antibiotic developed during the past 60 years. The most common is the Staphylococcus bacteria. World-wide, some two billion people carry these bacteria; up to 53 million people are thought to harbor antibiotic-resistant forms.
On average, people who contract Staph infections stay in the hospital three times as long and face five times the risk of dying. But these infections are becoming more prevalent outside hospitals. Antibiotic-resistant Staph infections increased almost sevenfold from 2001 to 2005, researchers reported last week in the Archives of Internal Medicine. Contagions such as tuberculosis, pneumonia and bubonic plague also are becoming immune to the drugs that once kept them at bay.
The death of Patient X highlights the speed of natural selection in fostering antibiotic resistance. "When you talk about the evolution of an arm or an eye or a species, you might be talking about millions of years. You can get bacteria resistant in a week," Dr. Mwangi said.
The Rockefeller researchers believe that a better understanding of evolution will lead to better antibiotic treatments. They want to disable the genes that allow these disease bacteria to mutate and adapt. The Staph bacteria that evolved inside Patient X now have such strong defenses that, in recent tests, they easily withstood even the next generation of clinical antibiotics. For the time being, the microbes are keeping one step ahead.
In a strict medical sense, the young man, identified only as Patient X, died of complications from a congenital heart ailment and a Staphylococcus aureus infection.
More broadly, evolution killed him.
The life-and-death struggle inside his infected heart was driven by the same evolutionary forces of natural selection and adaptation that are causing a pandemic of drug-resistant diseases world-wide. The emergence of such immunity among infectious diseases is one of the most well-documented problems in modern public health. Until now, however, researchers knew little about how bacteria multiplying inside the human body overcome the drugs designed to control them.
Patient X died in October 2000 after a 12-week hospital stay. His case comes to light now because researchers only recently developed the computational techniques needed to sequence generations of bacteria. The hospital, which also wasn't identified, gave the patient's Staph samples to the Rockefeller team for research purposes. The techniques still are too slow and expensive for clinical use.
When Patient X was admitted to the hospital, he was already suffering from a Staphylococcus aureus infection, but it was still vulnerable to antibiotics. During treatment, however, the bacteria quickly developed stronger resistance to four antibiotics, including vancomycin, the drug of last resort for intractable infections, the scientists reported. As living bacteria, the Staph were driven to survive.
Every time the patient took his medicine, the antibiotics killed the weakest bacteria in his bloodstream. Any cell that had developed a protective mutation to defend itself against the drug survived, passing on its special trait to descendants. With every round of treatment, the cells refined their defenses through the trial and error of survival. "It means that during a normal course of treatment there is an evolutionary revolution going on in your body," said Stanford University biologist Stephen Plaumbi, author of "The Evolution Explosion: How Humans Cause Rapid Evolutionary Change."
These resistant microbes, all disease-producing organisms spawned by the original infection, quickly accumulated 35 useful mutations. Each one altered a molecular sensor or production of a protein.
Researchers then matched these gradual genetic changes to increasing levels of drug resistance, shocked that it took so little to undermine the foundation of modern infectious-disease control. "We have now really looked into the belly of the beast and seen the mechanism," said Rockefeller microbiologist Alexander Tomasz.
Nearly two million people catch bacterial infections in U.S. hospitals every year and 90,000 of them die -- seven times as high as a decade ago as germs become immune to almost every antibiotic developed during the past 60 years. The most common is the Staphylococcus bacteria. World-wide, some two billion people carry these bacteria; up to 53 million people are thought to harbor antibiotic-resistant forms.
On average, people who contract Staph infections stay in the hospital three times as long and face five times the risk of dying. But these infections are becoming more prevalent outside hospitals. Antibiotic-resistant Staph infections increased almost sevenfold from 2001 to 2005, researchers reported last week in the Archives of Internal Medicine. Contagions such as tuberculosis, pneumonia and bubonic plague also are becoming immune to the drugs that once kept them at bay.
The death of Patient X highlights the speed of natural selection in fostering antibiotic resistance. "When you talk about the evolution of an arm or an eye or a species, you might be talking about millions of years. You can get bacteria resistant in a week," Dr. Mwangi said.
The Rockefeller researchers believe that a better understanding of evolution will lead to better antibiotic treatments. They want to disable the genes that allow these disease bacteria to mutate and adapt. The Staph bacteria that evolved inside Patient X now have such strong defenses that, in recent tests, they easily withstood even the next generation of clinical antibiotics. For the time being, the microbes are keeping one step ahead.
British hospitals 'among worst for superbugs'
British hospitals are among the worst in Europe for superbugs, according to figures published yesterday.
Britain was found to be the fifth worst country for superbug resistance
In a league table of 29 countries only Portugal, Malta, Cyprus and Romania have higher proportions of potentially deadly antibiotic-resistant hospital-acquired infections.
Only some forms of superbugs are resistant to antibiotics - including those known as MRSA. They are part of the staphylococcus aureus family of bacteria that can live on the skin or in the nose and can cause a range of illnesses and symptoms from boils and abscesses to life-threatening diseases such as meningitis and septicaemia.
By Bruno Waterfield and Nic Fleming
The bacteria become dangerous to patients once they enter the bloodstream and those that are resistant to antibiotics pose the greatest threat.
The European Union's Centre for Disease Prevention and Control (ECDC) report on communicable diseases ranked countries based on the proportion of S aureus infections found to be antibiotic-resistant.
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With an MRSA rate of 44 per cent, Britain was found to be the fifth worst for superbug resistance, behind countries including Greece, Slovakia, Hungary, Poland and the Czech Republic.
The ECDC study compiled data showing the trend in superbug antibiotic resistance in recent years for each country.
The amount of MRSA as a proportion of all staphylococcus aureus infections in British hospitals was unchanged between 2002 and 2005.
In contrast it fell in other countries including Slovenia, Greece and in France.
Doctors fear the spread of resistance to antibiotics could lead to problems in treating other illnesses such as pneumonia.
The ECDC says the spread of hospital-acquired infections is now the main disease threat in Europe, despite continuing concerns over tuberculosis and HIV.
The report states: "If the present rapid negative development is not halted, mankind will soon lose one of its most important weapons against infectious diseases.
"The most important threat in Europe is posed by micro-organisms that have become resistant to antibiotics."
Figures released by the Office of National Statistics in February showed the number of death certificates in England and Wales that mentioned MRSA rose 39 per cent to 1,629 between 2004 and 2005.
This is widely seen as an underestimate because other causes are often listed when MRSA could have contributed to or been the primary cause deaths. Health officials privately concede they are unlikely to hit the Government target of halving the number of MRSA cases by April.
Andrew Lansley, the shadow health secretary, said: "With 7,000 nursing posts and 9,000 beds lost in the last year, it is little wonder that we are amongst the worst countries in Europe for rates of MRSA infections."
A spokesman for the Department of Health said: "The report does not show that the UK has one of the worst infection rates in Europe.
"The table only refers to the proportion of staphylococcus aureus blood stream infections that are caused by MRSA.
"Available information indicates that the prevalence of hospital-acquired infections in the UK is similar to those of other European countries and the United States."
Britain was found to be the fifth worst country for superbug resistance
In a league table of 29 countries only Portugal, Malta, Cyprus and Romania have higher proportions of potentially deadly antibiotic-resistant hospital-acquired infections.
Only some forms of superbugs are resistant to antibiotics - including those known as MRSA. They are part of the staphylococcus aureus family of bacteria that can live on the skin or in the nose and can cause a range of illnesses and symptoms from boils and abscesses to life-threatening diseases such as meningitis and septicaemia.
By Bruno Waterfield and Nic Fleming
The bacteria become dangerous to patients once they enter the bloodstream and those that are resistant to antibiotics pose the greatest threat.
The European Union's Centre for Disease Prevention and Control (ECDC) report on communicable diseases ranked countries based on the proportion of S aureus infections found to be antibiotic-resistant.
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With an MRSA rate of 44 per cent, Britain was found to be the fifth worst for superbug resistance, behind countries including Greece, Slovakia, Hungary, Poland and the Czech Republic.
The ECDC study compiled data showing the trend in superbug antibiotic resistance in recent years for each country.
The amount of MRSA as a proportion of all staphylococcus aureus infections in British hospitals was unchanged between 2002 and 2005.
In contrast it fell in other countries including Slovenia, Greece and in France.
Doctors fear the spread of resistance to antibiotics could lead to problems in treating other illnesses such as pneumonia.
The ECDC says the spread of hospital-acquired infections is now the main disease threat in Europe, despite continuing concerns over tuberculosis and HIV.
The report states: "If the present rapid negative development is not halted, mankind will soon lose one of its most important weapons against infectious diseases.
"The most important threat in Europe is posed by micro-organisms that have become resistant to antibiotics."
Figures released by the Office of National Statistics in February showed the number of death certificates in England and Wales that mentioned MRSA rose 39 per cent to 1,629 between 2004 and 2005.
This is widely seen as an underestimate because other causes are often listed when MRSA could have contributed to or been the primary cause deaths. Health officials privately concede they are unlikely to hit the Government target of halving the number of MRSA cases by April.
Andrew Lansley, the shadow health secretary, said: "With 7,000 nursing posts and 9,000 beds lost in the last year, it is little wonder that we are amongst the worst countries in Europe for rates of MRSA infections."
A spokesman for the Department of Health said: "The report does not show that the UK has one of the worst infection rates in Europe.
"The table only refers to the proportion of staphylococcus aureus blood stream infections that are caused by MRSA.
"Available information indicates that the prevalence of hospital-acquired infections in the UK is similar to those of other European countries and the United States."
NEWS RELEASE-FDA Science Board to Meet on June 14
News Release
FOR IMMEDIATE RELEASE
P07-100
June 8, 2007
Media Inquiries:
301-827-6242
Consumer Inquiries:
888-INFO-FDA
The U.S. Food and Drug Administration's (FDA) Science Board will hold a public meeting on June 14, 2007. The board, an advisory committee to the FDA, provides the agency with expert outside advice on specific technical issues, as well as emerging issues within the scientific community, industry, and academia. Members counsel the agency on regulatory science, the formulation of an appropriate research agenda, and on upgrading FDA's scientific and research facilities.
"Science provides the foundation for FDA's regulatory decisions," said Janet Woodcock, M.D., FDA's deputy commissioner and chief medical officer. "Science and technology are creating products with enormous promise and, frequently, considerable challenges. This in-depth review of our scientific capacity is critical to assuring that FDA will continue to meet the regulatory challenges of the future."
Members of the board will address food protection, the agency's interim safety/risk assessment of melamine, a report on the Antimicrobial Resistance Monitoring System (NARMS), and an agency-wide review of FDA science. For a complete agenda, briefing documents, and a list of subject matters experts that serve as advisors to the subcommittee and their affiliations, please see: www.fda.gov/ohrms/dockets/ac/oc07.htm#ScienceBoard.
The board, chaired by Kenneth Shine, M.D., University of Texas System, Austin, is composed of nine members. Other members include: Gail H. Cassell, Ph.D., Eli Lilly and Company, Indianapolis; Susan Kay Harlander, Ph.D., BT Safety, LLC, Eden Prairie; Lonnie King, D.V.M., Centers for Disease Control and Prevention, Atlanta; Barbara J. McNeil, M.D., Ph.D., Harvard Medical School, Boston; David R. Parkinson, M.D., Biogen Idec, San Diego, Calif.; F. Xavier Pi-Sunyer, M.D., St. Luke's-Roosevelt Hospital Center, New York; Allen D. Roses, M.D., GlaxoSmithKline, Research Triangle Park, N.C.; and Larry D. Sasich, Pharm.D., consumer representative, Erie, Pa.
Last year, the board established the Subcommittee for the Review of FDA Science to determine whether the FDA's current science portfolio is properly positioned to deal new regulatory challenges stemming from developments in science and technology.
During the daylong meeting, the Subcommittee will provide an update on the progress of their review. The subcommittee, chaired by Gail H. Cassell, Ph.D., of Eli Lilly and Company, will submit a draft written report of its preliminary findings to the board this summer. The subcommittee has asked 28 scientific subject-matter experts, drawn from government, industry and academia, to contribute to the report.
The Science Board meeting is scheduled for June 14 from 8 a.m. to 4:30 p.m. at the Holiday Inn, 2 Montgomery Village Ave., Gaithersburg, Md.
Public comments can be submitted; please see the Federal Register notice for this meeting for more information: www.fda.gov/OHRMS/DOCKETS/98fr/E7-9737.htm.
####
FOR IMMEDIATE RELEASE
P07-100
June 8, 2007
Media Inquiries:
301-827-6242
Consumer Inquiries:
888-INFO-FDA
The U.S. Food and Drug Administration's (FDA) Science Board will hold a public meeting on June 14, 2007. The board, an advisory committee to the FDA, provides the agency with expert outside advice on specific technical issues, as well as emerging issues within the scientific community, industry, and academia. Members counsel the agency on regulatory science, the formulation of an appropriate research agenda, and on upgrading FDA's scientific and research facilities.
"Science provides the foundation for FDA's regulatory decisions," said Janet Woodcock, M.D., FDA's deputy commissioner and chief medical officer. "Science and technology are creating products with enormous promise and, frequently, considerable challenges. This in-depth review of our scientific capacity is critical to assuring that FDA will continue to meet the regulatory challenges of the future."
Members of the board will address food protection, the agency's interim safety/risk assessment of melamine, a report on the Antimicrobial Resistance Monitoring System (NARMS), and an agency-wide review of FDA science. For a complete agenda, briefing documents, and a list of subject matters experts that serve as advisors to the subcommittee and their affiliations, please see: www.fda.gov/ohrms/dockets/ac/oc07.htm#ScienceBoard.
The board, chaired by Kenneth Shine, M.D., University of Texas System, Austin, is composed of nine members. Other members include: Gail H. Cassell, Ph.D., Eli Lilly and Company, Indianapolis; Susan Kay Harlander, Ph.D., BT Safety, LLC, Eden Prairie; Lonnie King, D.V.M., Centers for Disease Control and Prevention, Atlanta; Barbara J. McNeil, M.D., Ph.D., Harvard Medical School, Boston; David R. Parkinson, M.D., Biogen Idec, San Diego, Calif.; F. Xavier Pi-Sunyer, M.D., St. Luke's-Roosevelt Hospital Center, New York; Allen D. Roses, M.D., GlaxoSmithKline, Research Triangle Park, N.C.; and Larry D. Sasich, Pharm.D., consumer representative, Erie, Pa.
Last year, the board established the Subcommittee for the Review of FDA Science to determine whether the FDA's current science portfolio is properly positioned to deal new regulatory challenges stemming from developments in science and technology.
During the daylong meeting, the Subcommittee will provide an update on the progress of their review. The subcommittee, chaired by Gail H. Cassell, Ph.D., of Eli Lilly and Company, will submit a draft written report of its preliminary findings to the board this summer. The subcommittee has asked 28 scientific subject-matter experts, drawn from government, industry and academia, to contribute to the report.
The Science Board meeting is scheduled for June 14 from 8 a.m. to 4:30 p.m. at the Holiday Inn, 2 Montgomery Village Ave., Gaithersburg, Md.
Public comments can be submitted; please see the Federal Register notice for this meeting for more information: www.fda.gov/OHRMS/DOCKETS/98fr/E7-9737.htm.
####
Friday, June 8, 2007
Strange but True: Antibacterial Products May Do More Harm Than Good
Antibacterial soaps and other cleaners may actually be aiding in the development of superbacteria.
By Coco Ballantyne
Tuberculosis, food poisoning, cholera, pneumonia, strep throat and meningitis: these are just a few of the unsavory diseases caused by bacteria. Hygiene—keeping both home and body clean—is one of the best ways to curb the spread of bacterial infections, but lately consumers are getting the message that washing with regular soap is insufficient. Antibacterial products have never been so popular. Body soaps, household cleaners, sponges, even mattresses and lip glosses are now packing bacteria-killing ingredients, and scientists question what place, if any, these chemicals have in the daily routines of healthy people.
Traditionally, people washed bacteria from their bodies and homes using soap and hot water, alcohol, chlorine bleach or hydrogen peroxide. These substances act nonspecifically, meaning they wipe out almost every type of microbe in sight—fungi, bacteria and some viruses—rather than singling out a particular variety.
Soap works by loosening and lifting dirt, oil and microbes from surfaces so they can be easily rinsed away with water, whereas general cleaners such as alcohol inflict sweeping damage to cells by demolishing key structures, then evaporate. "They do their job and are quickly dissipated into the environment," explains microbiologist Stuart Levy of Tufts University School of Medicine.
Unlike these traditional cleaners, antibacterial products leave surface residues, creating conditions that may foster the development of resistant bacteria, Levy notes. For example, after spraying and wiping an antibacterial cleaner over a kitchen counter, active chemicals linger behind and continue to kill bacteria, but not necessarily all of them.
When a bacterial population is placed under a stressor—such as an antibacterial chemical—a small subpopulation armed with special defense mechanisms can develop. These lineages survive and reproduce as their weaker relatives perish. "What doesn't kill you makes you stronger" is the governing maxim here, as antibacterial chemicals select for bacteria that endure their presence.
As bacteria develop a tolerance for these compounds there is potential for also developing a tolerance for certain antibiotics. This phenomenon, called cross-resistance, has already been demonstrated in several laboratory studies using triclosan, one of the most common chemicals found in antibacterial hand cleaners, dishwashing liquids and other wash products. "Triclosan has a specific inhibitory target in bacteria similar to some antibiotics," says epidemiologist Allison Aiello at the University of Michigan School of Public Health.
When bacteria are exposed to triclosan for long periods of time, genetic mutations can arise. Some of these mutations endow the bacteria with resistance to isoniazid, an antibiotic used for treating tuberculosis, whereas other microbes can supercharge their efflux pumps—protein machines in the cell membrane that can spit out several types of antibiotics, Aiello explains. These effects have been demonstrated only in the laboratory, not in households and other real world environments, but Aiello believes that the few household studies may not have been long enough. "It's very possible that the emergence of resistant species takes quite some time to occur…; the potential is there," she says.
Apart from the potential emergence of drug-resistant bacteria in communities, scientists have other concerns about antibacterial compounds. Both triclosan and its close chemical relative triclocarban (also widely used as an antibacterial), are present in 60 percent of America's streams and rivers, says environmental scientist Rolf Halden, co-founder of the Center for Water and Health at Johns Hopkins Bloomberg School of Public Health. Both chemicals are efficiently removed from wastewater in treatment plants but end up getting sequestered in the municipal sludge, which is used as fertilizer for crops, thereby opening a potential pathway for contamination of the food we eat, Halden explains. "We have to realize that the concentrations in agricultural soil are very high," and this, "along with the presence of pathogens from sewage, could be a recipe for breeding antimicrobial resistance" in the environment, he says.
Triclosan has also been found in human breast milk, although not in concentrations considered dangerous to babies, as well as in human blood plasma. There is no evidence showing that current concentrations of triclosan in the human body are harmful, but recent studies suggest that it acts as an endocrine disrupter in bullfrogs and rats.
Further, an expert panel convened by the Food and Drug Administration determined that there is insufficient evidence for a benefit from consumer products containing antibacterial additives over similar ones not containing them.
"What is this stuff doing in households when we have soaps?" asks molecular biologist John Gustafson of New Mexico State University in Las Cruces. These substances really belong in hospitals and clinics, not in the homes of healthy people, Gustafson says.
Of course, antibacterial products do have their place. Millions of Americans suffer from weakened immune systems, including pregnant women and people with immunodeficiency diseases, points out Eugene Cole, an infectious disease specialist at Brigham Young University. For these people, targeted use of antibacterial products, such as triclosan, may be appropriate in the home, he says.
In general, however, good, long-term hygiene means using regular soaps rather than new, antibacterial ones, experts say. "The main way to keep from getting sick," Gustafson says, "is to wash your hands three times a day and don't touch mucous membranes."
By Coco Ballantyne
Tuberculosis, food poisoning, cholera, pneumonia, strep throat and meningitis: these are just a few of the unsavory diseases caused by bacteria. Hygiene—keeping both home and body clean—is one of the best ways to curb the spread of bacterial infections, but lately consumers are getting the message that washing with regular soap is insufficient. Antibacterial products have never been so popular. Body soaps, household cleaners, sponges, even mattresses and lip glosses are now packing bacteria-killing ingredients, and scientists question what place, if any, these chemicals have in the daily routines of healthy people.
Traditionally, people washed bacteria from their bodies and homes using soap and hot water, alcohol, chlorine bleach or hydrogen peroxide. These substances act nonspecifically, meaning they wipe out almost every type of microbe in sight—fungi, bacteria and some viruses—rather than singling out a particular variety.
Soap works by loosening and lifting dirt, oil and microbes from surfaces so they can be easily rinsed away with water, whereas general cleaners such as alcohol inflict sweeping damage to cells by demolishing key structures, then evaporate. "They do their job and are quickly dissipated into the environment," explains microbiologist Stuart Levy of Tufts University School of Medicine.
Unlike these traditional cleaners, antibacterial products leave surface residues, creating conditions that may foster the development of resistant bacteria, Levy notes. For example, after spraying and wiping an antibacterial cleaner over a kitchen counter, active chemicals linger behind and continue to kill bacteria, but not necessarily all of them.
When a bacterial population is placed under a stressor—such as an antibacterial chemical—a small subpopulation armed with special defense mechanisms can develop. These lineages survive and reproduce as their weaker relatives perish. "What doesn't kill you makes you stronger" is the governing maxim here, as antibacterial chemicals select for bacteria that endure their presence.
As bacteria develop a tolerance for these compounds there is potential for also developing a tolerance for certain antibiotics. This phenomenon, called cross-resistance, has already been demonstrated in several laboratory studies using triclosan, one of the most common chemicals found in antibacterial hand cleaners, dishwashing liquids and other wash products. "Triclosan has a specific inhibitory target in bacteria similar to some antibiotics," says epidemiologist Allison Aiello at the University of Michigan School of Public Health.
When bacteria are exposed to triclosan for long periods of time, genetic mutations can arise. Some of these mutations endow the bacteria with resistance to isoniazid, an antibiotic used for treating tuberculosis, whereas other microbes can supercharge their efflux pumps—protein machines in the cell membrane that can spit out several types of antibiotics, Aiello explains. These effects have been demonstrated only in the laboratory, not in households and other real world environments, but Aiello believes that the few household studies may not have been long enough. "It's very possible that the emergence of resistant species takes quite some time to occur…; the potential is there," she says.
Apart from the potential emergence of drug-resistant bacteria in communities, scientists have other concerns about antibacterial compounds. Both triclosan and its close chemical relative triclocarban (also widely used as an antibacterial), are present in 60 percent of America's streams and rivers, says environmental scientist Rolf Halden, co-founder of the Center for Water and Health at Johns Hopkins Bloomberg School of Public Health. Both chemicals are efficiently removed from wastewater in treatment plants but end up getting sequestered in the municipal sludge, which is used as fertilizer for crops, thereby opening a potential pathway for contamination of the food we eat, Halden explains. "We have to realize that the concentrations in agricultural soil are very high," and this, "along with the presence of pathogens from sewage, could be a recipe for breeding antimicrobial resistance" in the environment, he says.
Triclosan has also been found in human breast milk, although not in concentrations considered dangerous to babies, as well as in human blood plasma. There is no evidence showing that current concentrations of triclosan in the human body are harmful, but recent studies suggest that it acts as an endocrine disrupter in bullfrogs and rats.
Further, an expert panel convened by the Food and Drug Administration determined that there is insufficient evidence for a benefit from consumer products containing antibacterial additives over similar ones not containing them.
"What is this stuff doing in households when we have soaps?" asks molecular biologist John Gustafson of New Mexico State University in Las Cruces. These substances really belong in hospitals and clinics, not in the homes of healthy people, Gustafson says.
Of course, antibacterial products do have their place. Millions of Americans suffer from weakened immune systems, including pregnant women and people with immunodeficiency diseases, points out Eugene Cole, an infectious disease specialist at Brigham Young University. For these people, targeted use of antibacterial products, such as triclosan, may be appropriate in the home, he says.
In general, however, good, long-term hygiene means using regular soaps rather than new, antibacterial ones, experts say. "The main way to keep from getting sick," Gustafson says, "is to wash your hands three times a day and don't touch mucous membranes."
Battle-Hardened Bacteria
When Andrew Speaker boarded an Air France flight for Paris last month carrying a form of extensively drug-resistant tuberculosis, he became a global pariah--both for the lethal bug in his system and for the folly of exposing other people to it. But while Speaker may have been reckless, the blame for the emergence of drug-resistant bugs like the one he is incubating falls partly on the rest of us. For years public-health officials have been raising the alarm about how our overreliance on antibiotics is breeding a generation of superbugs, increasingly resistant to the medicines designed to kill them. The problem has only gotten worse as antibiotic use has expanded to agriculture, where cattle, chicken and fish are routinely treated with the drugs to keep infectious diseases in check.
According to the Centers for Disease Control and Prevention, more than 70% of the bacteria that cause infections in hospitals are resistant to at least one antibiotic. Methicillin-resistant Staphylococcus aureus (MRSA), which causes boils or pimples on the skin, is only the latest superbug to make the rounds and has appeared in dozens of high school and college athletic locker rooms, as well as in three NFL locker rooms. Drug-resistant tuberculosis cases, including those of the variety affecting Speaker, have risen along with peaks in AIDS cases, as people with weakened immune systems are especially vulnerable to infection with multiple bugs.
The only way to thwart the bacteria, say public-health officials, is to curb the use of antibiotics. That's not likely to happen, with antibacterial hand sanitizers now in handy pocket packs and few folks willing to tough out a throat or ear infection without pharmaceutical help. The more the bugs come into contact with such agents, the faster bacteria find ways to mutate around them.
And that points to a fundamental weakness of current antibiotics. All exploit the fact that the best agents to kill bacteria come from other bacteria. Each species makes toxins that can either kill other species or arrest their growth, and existing antibiotics are modified versions of these natural defenses. But that is just the kind of biological arms race that microbes and other living things excel at adapting to. So researchers working on the next generation of antibiotics are taking advantage of new knowledge about bacterial genetics and a better understanding of the resistance process to stay one step ahead of the ever changing bugs.
One way to do this is to confuse the bacteria, hitting them with not just one natural toxin but two. At Vertex Pharmaceuticals in Cambridge, Mass., scientists are developing a new class of antibiotics that targets a pair of enzymes the microbes depend on to copy their genes and reproduce. Adapting in two directions at once slows down the bacteria enough to give the drug time to work. "Mathematically, it becomes much harder for the bacteria to develop resistance to different targets at the same time," says Dr. John Alam, the company's chief medical officer.
Another strategy is to ambush the bacteria with an unlikely ally: viruses. Vincent Fischetti at Rockefeller University is enlisting the help of bacteriophages, viruses that infect only bacterial cells, leaving human ones alone. They hijack the bacterium's genetic machinery and within minutes start to pump out hundreds of copies of themselves. When enough progeny build up inside the cell, the phages produce an enzyme that chews through the cell wall, causing it to explode with the force of a popping champagne cork and spew out the viral intruders.
Treating humans with live viruses--even ones that shouldn't harm us--is always risky, so Fischetti decided to isolate just the bacteria-puncturing enzyme and use it to kill bacteria from the outside. So far, he has developed compounds against pneumococcus, streptococcus and anthrax and hopes to eventually treat infected patients by squirting the enzymes in nasal-spray form weekly.
None of these agents are quite ready for the pharmacy yet, and until they are, researchers are focusing on new ways to maximize the power of drugs we do have. By studying bacterial DNA, scientists at the Naval Research Laboratory are decoding the genetic battle plans that the bugs use to develop resistance. These secrets can help doctors prescribe antibiotics more effectively by knowing which strains are most susceptible to which drugs.
As the TB scare reminded us, that's important in a world in which superbugs can quickly go global. Bacteria may be resourceful things, but science, while slower, can be smarter. It's just a matter of knowing your enemy--and packing the right weapons. [This article contains a complex diagram. Please see hardcopy or pdf.] USING A VIRUS TO ATTACK BACTERIA 1 A bacteriophage is a virus that infects bacteria but not human cells
Bacteriophage
Genes
2 It inserts its genetic material into a bacterial cell
Bacterium
Viral genes
3 The bacterium is hijacked into producing new viruses
4 After about 45 minutes, the viruses produce a lytic enzyme, which causes the bacterial cell wall to burst
5 The enzyme can be purified from these viruses or manufactured to be used as an antibiotic-like agent to kill bacteria
Lytic enzyme
Ruptured bacterial cell wall
Source: Vincent Fischetti, Ph.D., Rockefeller University
TIME Diagram by Joe Lertola
According to the Centers for Disease Control and Prevention, more than 70% of the bacteria that cause infections in hospitals are resistant to at least one antibiotic. Methicillin-resistant Staphylococcus aureus (MRSA), which causes boils or pimples on the skin, is only the latest superbug to make the rounds and has appeared in dozens of high school and college athletic locker rooms, as well as in three NFL locker rooms. Drug-resistant tuberculosis cases, including those of the variety affecting Speaker, have risen along with peaks in AIDS cases, as people with weakened immune systems are especially vulnerable to infection with multiple bugs.
The only way to thwart the bacteria, say public-health officials, is to curb the use of antibiotics. That's not likely to happen, with antibacterial hand sanitizers now in handy pocket packs and few folks willing to tough out a throat or ear infection without pharmaceutical help. The more the bugs come into contact with such agents, the faster bacteria find ways to mutate around them.
And that points to a fundamental weakness of current antibiotics. All exploit the fact that the best agents to kill bacteria come from other bacteria. Each species makes toxins that can either kill other species or arrest their growth, and existing antibiotics are modified versions of these natural defenses. But that is just the kind of biological arms race that microbes and other living things excel at adapting to. So researchers working on the next generation of antibiotics are taking advantage of new knowledge about bacterial genetics and a better understanding of the resistance process to stay one step ahead of the ever changing bugs.
One way to do this is to confuse the bacteria, hitting them with not just one natural toxin but two. At Vertex Pharmaceuticals in Cambridge, Mass., scientists are developing a new class of antibiotics that targets a pair of enzymes the microbes depend on to copy their genes and reproduce. Adapting in two directions at once slows down the bacteria enough to give the drug time to work. "Mathematically, it becomes much harder for the bacteria to develop resistance to different targets at the same time," says Dr. John Alam, the company's chief medical officer.
Another strategy is to ambush the bacteria with an unlikely ally: viruses. Vincent Fischetti at Rockefeller University is enlisting the help of bacteriophages, viruses that infect only bacterial cells, leaving human ones alone. They hijack the bacterium's genetic machinery and within minutes start to pump out hundreds of copies of themselves. When enough progeny build up inside the cell, the phages produce an enzyme that chews through the cell wall, causing it to explode with the force of a popping champagne cork and spew out the viral intruders.
Treating humans with live viruses--even ones that shouldn't harm us--is always risky, so Fischetti decided to isolate just the bacteria-puncturing enzyme and use it to kill bacteria from the outside. So far, he has developed compounds against pneumococcus, streptococcus and anthrax and hopes to eventually treat infected patients by squirting the enzymes in nasal-spray form weekly.
None of these agents are quite ready for the pharmacy yet, and until they are, researchers are focusing on new ways to maximize the power of drugs we do have. By studying bacterial DNA, scientists at the Naval Research Laboratory are decoding the genetic battle plans that the bugs use to develop resistance. These secrets can help doctors prescribe antibiotics more effectively by knowing which strains are most susceptible to which drugs.
As the TB scare reminded us, that's important in a world in which superbugs can quickly go global. Bacteria may be resourceful things, but science, while slower, can be smarter. It's just a matter of knowing your enemy--and packing the right weapons. [This article contains a complex diagram. Please see hardcopy or pdf.] USING A VIRUS TO ATTACK BACTERIA 1 A bacteriophage is a virus that infects bacteria but not human cells
Bacteriophage
Genes
2 It inserts its genetic material into a bacterial cell
Bacterium
Viral genes
3 The bacterium is hijacked into producing new viruses
4 After about 45 minutes, the viruses produce a lytic enzyme, which causes the bacterial cell wall to burst
5 The enzyme can be purified from these viruses or manufactured to be used as an antibiotic-like agent to kill bacteria
Lytic enzyme
Ruptured bacterial cell wall
Source: Vincent Fischetti, Ph.D., Rockefeller University
TIME Diagram by Joe Lertola
Thursday, June 7, 2007
Interest in Breakthrough Antimicrobial Technology for Medical Devices Results in Growth for AcryMed
Abstract:
Strong industry interest in SilvaGard, a breakthrough antimicrobial nanotechnology, has resulted in significant growth for AcryMed, the company that developed and now licenses the technology. Built on years of research in developing silver antimicrobial wound treatments, SilvaGard addresses a still un-met clinical need, preventing the spread of deadly medical device-related infections. By harnessing the advantages of nanotechnology with the broad-spectrum infection-fighting ability of Ionic silver, SilvaGard provides a safe and effective solution to render medical devices impervious to infection causing biofilms.
Press Release
Interest in Breakthrough Antimicrobial Technology for Medical Devices Results in Growth for AcryMed
Portland, OR | Posted on June 5th, 2007
To accommodate the increased demand for its patented technologies, AcryMed has recently doubled the size of its laboratory facilities and hired new scientific and technical staff. According to AcryMed, the company has received inquiries that span a large number of medical device markets.
"The spread of hospital acquired infections is a significant problem that unnecessarily effect millions of U.S. patients each year and adds more than 28 billion dollars to our nation's healthcare costs," said Jack McMaken, president of AcryMed. "Since a large portion of harmful bacteria is harbored on medical devices such as indwelling catheters and implants, manufacturers are extremely interested in finding ways to curtail the role their products play in spreading infections. SilvaGard represents the first significant breakthrough in this area in quite some time."
SilvaGard prevents the spread of device-related infections by depositing antimicrobial silver nanoparticles onto the surfaces of medical devices and thus providing a protective barrier. Studies have shown that SilvaGard is not only safe for use, but also highly effective against a wide spectrum of infection-causing bacteria including MRSA and other antibiotic-resistant "superbugs."
The initial FDA market clearance of SilvaGard antimicrobial technology was given to I-Flow Corporation for marketing the company's ON-Q® SilverSoaker™ regional anesthesia delivery catheters. In recent findings presented at the Surgical Infection Society (SIS) meeting, I-Flow's ON-Q SilverSoaker antimicrobial catheter demonstrated a significantly lower risk of developing a surgical site infection in an on-going prospective study of patients undergoing colorectal surgery. The preliminary results captured the outcomes of 120 patients, randomized to either treatment with continuous local anesthetic using the antimicrobial treated ON-Q catheter or to the control treatment employing traditional pain relief. At 30-days post surgery, patients who received treatment with the antimicrobial ON-Q device had a significantly lower incidence of site infections at 0%, as compared to the control group at 22.9%. The study is scheduled to be complete by year-end. To learn more about the benefits of the ON-Q, visit www.AskYourSurgeon.com or www.IFLO.com.
Through collaborative development efforts, AcryMed and its medical device company partners expect to announce new product applications, leveraging SilvaGard-technology in the coming months.
####
About AcryMed
cryMed is a pioneering innovator at the forefront of innovations in the fields of infection control and wound healing. The company's SilvaSorb® products for advanced wound care and SilvaGard nanoparticle surface treatment for medical devices are among the breakthrough technologies that have distinguished AcryMed as an industry leader. AcryMed maintains on-site GMP manufacturing and lab facilities at its Portland, Oregon-based headquarters. The company is ISO certified and operates under ISO 13485 and EN 93/42/EEC. For more information on AcryMed, SilvaSorb, SilvaGard or other wound care and infection control technologies developed by AcryMed, visit their web site at http://www.acrymed.com or call 503-624-9830.
For more information, please click here
Contacts:
Kim Jacque
9560 SW Nimbus Ave.
Beaverton, Oregon 97008
Phone Number: 503.624.9830
Fax Number: 503.639.0846
kjacque@acrymed.com
Copyright © PRWeb™
Strong industry interest in SilvaGard, a breakthrough antimicrobial nanotechnology, has resulted in significant growth for AcryMed, the company that developed and now licenses the technology. Built on years of research in developing silver antimicrobial wound treatments, SilvaGard addresses a still un-met clinical need, preventing the spread of deadly medical device-related infections. By harnessing the advantages of nanotechnology with the broad-spectrum infection-fighting ability of Ionic silver, SilvaGard provides a safe and effective solution to render medical devices impervious to infection causing biofilms.
Press Release
Interest in Breakthrough Antimicrobial Technology for Medical Devices Results in Growth for AcryMed
Portland, OR | Posted on June 5th, 2007
To accommodate the increased demand for its patented technologies, AcryMed has recently doubled the size of its laboratory facilities and hired new scientific and technical staff. According to AcryMed, the company has received inquiries that span a large number of medical device markets.
"The spread of hospital acquired infections is a significant problem that unnecessarily effect millions of U.S. patients each year and adds more than 28 billion dollars to our nation's healthcare costs," said Jack McMaken, president of AcryMed. "Since a large portion of harmful bacteria is harbored on medical devices such as indwelling catheters and implants, manufacturers are extremely interested in finding ways to curtail the role their products play in spreading infections. SilvaGard represents the first significant breakthrough in this area in quite some time."
SilvaGard prevents the spread of device-related infections by depositing antimicrobial silver nanoparticles onto the surfaces of medical devices and thus providing a protective barrier. Studies have shown that SilvaGard is not only safe for use, but also highly effective against a wide spectrum of infection-causing bacteria including MRSA and other antibiotic-resistant "superbugs."
The initial FDA market clearance of SilvaGard antimicrobial technology was given to I-Flow Corporation for marketing the company's ON-Q® SilverSoaker™ regional anesthesia delivery catheters. In recent findings presented at the Surgical Infection Society (SIS) meeting, I-Flow's ON-Q SilverSoaker antimicrobial catheter demonstrated a significantly lower risk of developing a surgical site infection in an on-going prospective study of patients undergoing colorectal surgery. The preliminary results captured the outcomes of 120 patients, randomized to either treatment with continuous local anesthetic using the antimicrobial treated ON-Q catheter or to the control treatment employing traditional pain relief. At 30-days post surgery, patients who received treatment with the antimicrobial ON-Q device had a significantly lower incidence of site infections at 0%, as compared to the control group at 22.9%. The study is scheduled to be complete by year-end. To learn more about the benefits of the ON-Q, visit www.AskYourSurgeon.com or www.IFLO.com.
Through collaborative development efforts, AcryMed and its medical device company partners expect to announce new product applications, leveraging SilvaGard-technology in the coming months.
####
About AcryMed
cryMed is a pioneering innovator at the forefront of innovations in the fields of infection control and wound healing. The company's SilvaSorb® products for advanced wound care and SilvaGard nanoparticle surface treatment for medical devices are among the breakthrough technologies that have distinguished AcryMed as an industry leader. AcryMed maintains on-site GMP manufacturing and lab facilities at its Portland, Oregon-based headquarters. The company is ISO certified and operates under ISO 13485 and EN 93/42/EEC. For more information on AcryMed, SilvaSorb, SilvaGard or other wound care and infection control technologies developed by AcryMed, visit their web site at http://www.acrymed.com or call 503-624-9830.
For more information, please click here
Contacts:
Kim Jacque
9560 SW Nimbus Ave.
Beaverton, Oregon 97008
Phone Number: 503.624.9830
Fax Number: 503.639.0846
kjacque@acrymed.com
Copyright © PRWeb™
DFG approves 11 new Collaborative Research Centers
News Release
5-Jun-2007
Changes to the program simplify the funding of independent junior research groups
The Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) will establish eleven new Collaborative Research Centres (SFBs) on 1 July 2007. They will receive a total of 75.5 million euros in funding over the next four years. Research conducted in the centres will include work on the reconstruction of biological body functions using versatile “molecular switches” and innovative optical technology. Four of the new SFBs will be Transregional Collaborative Research Centres, which are located at multiple sites.
As well as establishing the newly approved Collaborative Research Centres, the committee also approved the continuation of 19 Collaborative Research Centres for another funding period, bringing the total number of Collaborative Research Centres financed by the DFG to 270 as of 1 July 2007. The total funding volume for 2007 will amount to approximately 388 million euros.
The committee also amended the funding programme: the “SFB independent junior research groups” component will become part of the Emmy Noether Programme, in order to bring more balance and simplicity to the funding offered by the DFG for young scientists and researchers who already hold a doctorate. In addition, as of 2008 the DFG will largely do away with the earmarking of certain funds that has existed up to now (for example funding specifically for inviting visiting researchers and scientists), in order to boost the individual responsibility of the Collaborative Research Centres and to simplify the utilisation of the funding granted to them. In the future, it will also be possible for Collaborative Research Centres to submit proposals for projects that will enable them to gather, generate, process and store the data relating to their projects in a more structured manner, using state-of-the-art computer data storage methods.
The new Collaborative Research Centres:
In Transregional Collaborative Research Centre 37 “Micro- and Nanosystems in Medicine – Reconstruction of Biologic Functions”, researchers from the fields of medicine, material science and the natural sciences will investigate the development of new technologies and methods of treatment in regenerative medicine using nano and laser technology. The centre will be based in Hannover, Aachen and Rostock. (Host university: Hannover Medical School (MHH), Coordinator: Axel Haverich)
Transregional Collaborative Research Centre 38 will deal with “Structures and Processes of the Initial Development of an Ecosystem in an Artificial Water Catchment Area”. Researchers from Cottbus, Munich and Zurich will work on the assumption that the early stages of an ecosystem have a decisive impact on its development and subsequent conditions. (Host university: Brandenburg Technical University, Cottbus, Coordinator: Reinhard F. Hüttl)
Transregional Collaborative Research Centre 45 will study the “Periods, Moduli Spaces and Arithmetic of Algebraic Varieties”. Researchers from the universities of Mainz, Bonn and Duisburg-Essen seek to combine various methodological approaches, ranging from the fields of algebraic and complex geometry to arithmetic geometry. (Host university: Johannes Gutenberg University, Mainz, Coordinator: Stefan Müller-Stach)
In Transregional Collaborative Research Centre 49 “Condensed Matter Systems with Variable Many-Body Interactions”, scientists and researchers from Frankfurt/Main, Kaiserslautern and Mainz will be investigating the collective behaviour of interacting many-body systems. This will serve to extend cooperation between quantum optics, solid state physics and chemistry. This centre will also include the first integrated Research Training Group, taking advantage of the recently introduced programme element designed to improve the qualification path for doctoral students participating in Collaborative Research Centres. (Host university: Johann Wolfgang Goethe University, Frankfurt am Main, Coordinator: Michael Lang)
Switchable molecules are able to change their properties reversibly in response to external stimulation, for example by light or magnetic field, a peculiarity that SFB 677 “Switch Functions” will investigate in greater depth. One of the objectives of their work will be to develop autonomous molecular switches suitable for use in medical or technical applications. (Host university: Christian Albrechts University, Kiel, Coordinator: Rainer Herges)
Researchers involved in SFB 728 “Environmental-Induced Aging Processes” will look at the mechanisms of aging at the molecular level and study their importance for the aging process of whole organs using models. In doing so, it may be possible to develop pharmacological prevention and treatment concepts. (Host university: Heinrich Heine University of Düsseldorf, Coordinator: Jean Krutmann)
The rejection of transplanted organs and the shortage of donated organs continue to pose challenges to transplantation medicine as a whole. This is the motivation for SFB 738 “Optimising Conventional and Innovative Transplantation”. (Host university: Hannover Medical School (MHH), Coordinator: Michael P. Manns)
The dynamic, i.e. temporally variable, parameters of molecules and biomolecules in chemical reactions are the topic that SFB 749 “Dynamic and Intermediate Molecular Transformations” will address. The structural analyses that are planned will be made possible by combining chemistry and biochemistry with theoretical chemistry and physics, as well as the application of state-of-the-art ultra-fast methods and high-precision theoretical procedures. (Host university: Ludwig-Maximilians University of Munich, Coordinator: Thomas Carell)
The SFB 755 “Nanoscale Photonic Imaging” plans to investigate complex systems such as macromolecular fluids and living cells. Innovative optical techniques, which allow exceptionally high spatial or temporal resolution to be achieved or which use X-rays, are being developed for this study. (Host university: Georg-August University of Göttingen, Coordinator: Tim Salditt)
Identifying a route to rapid and targeted development of a new class of structural materials is the overall objective of SFB 761 “Steel – ab initio. Designing Novel Ferric Materials Using Quantum Mechanics”. Researchers aim to do this using ab initio methods and other numerical processes, validated by experiment. (Host university: RWTH Technical University of Aachen, Coordinator: Wolfgang Bleck)
Researchers in SFB 766 “The Bacterial Cell Envelope: Structure, Function and Infection Interface” aim to develop molecular knowledge of the cell envelope of bacteria, which is currently limited, in order to be able to influence undesirable bacterial processes such as infections and the formation of biofilms, and potentially develop new antimicrobial agents. (Host university: Eberhard Karls University, Tübingen, Coordinator: Wolfgang Wohlleben)
Contact: Dr. Eva-Maria Streier
em.streier@dfg.de
49-228-885-2250
Deutsche Forschungsgemeinschaft
###
Further information is available from the coordinators of the respective Collaborative Research Centres.
At the DFG’s Head Office, please contact Klaus Wehrberger, Head, Research Centres Division, Tel. +49 (0)228 885-2355, e-mail: Klaus.Wehrberger@dfg.de.
Additional information on Collaborative Research Centres can be found at http://www.dfg.de/sfb/en.
5-Jun-2007
Changes to the program simplify the funding of independent junior research groups
The Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) will establish eleven new Collaborative Research Centres (SFBs) on 1 July 2007. They will receive a total of 75.5 million euros in funding over the next four years. Research conducted in the centres will include work on the reconstruction of biological body functions using versatile “molecular switches” and innovative optical technology. Four of the new SFBs will be Transregional Collaborative Research Centres, which are located at multiple sites.
As well as establishing the newly approved Collaborative Research Centres, the committee also approved the continuation of 19 Collaborative Research Centres for another funding period, bringing the total number of Collaborative Research Centres financed by the DFG to 270 as of 1 July 2007. The total funding volume for 2007 will amount to approximately 388 million euros.
The committee also amended the funding programme: the “SFB independent junior research groups” component will become part of the Emmy Noether Programme, in order to bring more balance and simplicity to the funding offered by the DFG for young scientists and researchers who already hold a doctorate. In addition, as of 2008 the DFG will largely do away with the earmarking of certain funds that has existed up to now (for example funding specifically for inviting visiting researchers and scientists), in order to boost the individual responsibility of the Collaborative Research Centres and to simplify the utilisation of the funding granted to them. In the future, it will also be possible for Collaborative Research Centres to submit proposals for projects that will enable them to gather, generate, process and store the data relating to their projects in a more structured manner, using state-of-the-art computer data storage methods.
The new Collaborative Research Centres:
In Transregional Collaborative Research Centre 37 “Micro- and Nanosystems in Medicine – Reconstruction of Biologic Functions”, researchers from the fields of medicine, material science and the natural sciences will investigate the development of new technologies and methods of treatment in regenerative medicine using nano and laser technology. The centre will be based in Hannover, Aachen and Rostock. (Host university: Hannover Medical School (MHH), Coordinator: Axel Haverich)
Transregional Collaborative Research Centre 38 will deal with “Structures and Processes of the Initial Development of an Ecosystem in an Artificial Water Catchment Area”. Researchers from Cottbus, Munich and Zurich will work on the assumption that the early stages of an ecosystem have a decisive impact on its development and subsequent conditions. (Host university: Brandenburg Technical University, Cottbus, Coordinator: Reinhard F. Hüttl)
Transregional Collaborative Research Centre 45 will study the “Periods, Moduli Spaces and Arithmetic of Algebraic Varieties”. Researchers from the universities of Mainz, Bonn and Duisburg-Essen seek to combine various methodological approaches, ranging from the fields of algebraic and complex geometry to arithmetic geometry. (Host university: Johannes Gutenberg University, Mainz, Coordinator: Stefan Müller-Stach)
In Transregional Collaborative Research Centre 49 “Condensed Matter Systems with Variable Many-Body Interactions”, scientists and researchers from Frankfurt/Main, Kaiserslautern and Mainz will be investigating the collective behaviour of interacting many-body systems. This will serve to extend cooperation between quantum optics, solid state physics and chemistry. This centre will also include the first integrated Research Training Group, taking advantage of the recently introduced programme element designed to improve the qualification path for doctoral students participating in Collaborative Research Centres. (Host university: Johann Wolfgang Goethe University, Frankfurt am Main, Coordinator: Michael Lang)
Switchable molecules are able to change their properties reversibly in response to external stimulation, for example by light or magnetic field, a peculiarity that SFB 677 “Switch Functions” will investigate in greater depth. One of the objectives of their work will be to develop autonomous molecular switches suitable for use in medical or technical applications. (Host university: Christian Albrechts University, Kiel, Coordinator: Rainer Herges)
Researchers involved in SFB 728 “Environmental-Induced Aging Processes” will look at the mechanisms of aging at the molecular level and study their importance for the aging process of whole organs using models. In doing so, it may be possible to develop pharmacological prevention and treatment concepts. (Host university: Heinrich Heine University of Düsseldorf, Coordinator: Jean Krutmann)
The rejection of transplanted organs and the shortage of donated organs continue to pose challenges to transplantation medicine as a whole. This is the motivation for SFB 738 “Optimising Conventional and Innovative Transplantation”. (Host university: Hannover Medical School (MHH), Coordinator: Michael P. Manns)
The dynamic, i.e. temporally variable, parameters of molecules and biomolecules in chemical reactions are the topic that SFB 749 “Dynamic and Intermediate Molecular Transformations” will address. The structural analyses that are planned will be made possible by combining chemistry and biochemistry with theoretical chemistry and physics, as well as the application of state-of-the-art ultra-fast methods and high-precision theoretical procedures. (Host university: Ludwig-Maximilians University of Munich, Coordinator: Thomas Carell)
The SFB 755 “Nanoscale Photonic Imaging” plans to investigate complex systems such as macromolecular fluids and living cells. Innovative optical techniques, which allow exceptionally high spatial or temporal resolution to be achieved or which use X-rays, are being developed for this study. (Host university: Georg-August University of Göttingen, Coordinator: Tim Salditt)
Identifying a route to rapid and targeted development of a new class of structural materials is the overall objective of SFB 761 “Steel – ab initio. Designing Novel Ferric Materials Using Quantum Mechanics”. Researchers aim to do this using ab initio methods and other numerical processes, validated by experiment. (Host university: RWTH Technical University of Aachen, Coordinator: Wolfgang Bleck)
Researchers in SFB 766 “The Bacterial Cell Envelope: Structure, Function and Infection Interface” aim to develop molecular knowledge of the cell envelope of bacteria, which is currently limited, in order to be able to influence undesirable bacterial processes such as infections and the formation of biofilms, and potentially develop new antimicrobial agents. (Host university: Eberhard Karls University, Tübingen, Coordinator: Wolfgang Wohlleben)
Contact: Dr. Eva-Maria Streier
em.streier@dfg.de
49-228-885-2250
Deutsche Forschungsgemeinschaft
###
Further information is available from the coordinators of the respective Collaborative Research Centres.
At the DFG’s Head Office, please contact Klaus Wehrberger, Head, Research Centres Division, Tel. +49 (0)228 885-2355, e-mail: Klaus.Wehrberger@dfg.de.
Additional information on Collaborative Research Centres can be found at http://www.dfg.de/sfb/en.
Tuesday, June 5, 2007
Study of staph shows how bacteria evolve resistance
Antibacterial resistance doesn’t happen overnight. But until recently nobody knew exactly how long it took — or how it happened at all. Now, by studying blood taken from a single patient over a period of months, Rockefeller University researchers have been able to trace how a common strain of bacteria adapted its genes to counteract the antibiotics used to try to kill it, until it finally emerged into the kind of fully resistant microbe that is wreaking havoc in hospitals worldwide. Total elapsed time: 90 days.
This is the first time that such a process has been observed “within” a patient, and the results, published in the May 21 issue of the Proceedings of the National Academy of Sciences sheds light on how such resistance occurs through selective pressure, says the study’s lead investigator, Alexander Tomasz, head of the Laboratory of Microbiology at Rockefeller University.
“What is thrilling is that we got as close as one can to the birthplace of antibiotic resistance in a patient, and now we can study which of the genetic mutations we found are really essential for resistance,” Tomasz says. If the genetic alterations they discovered are common to all known mutated strains of the bacteria — which Tomasz suspects is true — then knowing these genes may help clinicians design ways to block multidrug resistance, he says.
The microbe they isolated is Staphylococcus aureus, which is one of the most frequent causes of a wide range of hospital- and community-acquired infections, and is best known as the cause of toxic shock syndrome. The pathogen has acquired resistance to the majority of available antibiotics, including, recently, vancomycin, which was believed to be the only major agent that could treat it. “It has fantastic adaptive capabilities which have led to the worldwide spread of resistant lineages that are posing serious limits to clinical treatment,” Tomasz says.
But no one has known how such resistance occurs — whether it happens within individual patients, or whether patients with wounds pick up resistant microbes that have somehow infiltrated hospitals.
In this study, Tomasz, along with first author Michael Mwangi, a postdoc in the Tomasz lab, Eric Siggia, head of the Laboratory of Theoretical Condensed Matter Physics, and collaborators from Rockefeller, the Howard Hughes Medical Institute, the U.S. Department of Energy and Cornell University, obtained access to the blood of a patient with congenital heart disease who was treated extensively, but unsuccessfully, with several antibiotics including vancomycin. The team isolated the bacteria from the blood, and then used the whole-genome “shotgun” sequencing method to work out the entire genetic structure of S. aureus as it changed. They sequenced both the initial isolate and the later drug-resistant bacterium. The comparison of the two sequences showed that the resistant bacterium carried 35 mutations in 33 places on its genome and also showed that the mutations showed up in the intermediate isolates in a sequential order in parallel with the gradually increasing resistance to vancomycin. Although initially sensitive to vancomycin, some of the bacteria were probably able to “hide” from the antibiotic in the tissue of the patient’s heart valve, Tomasz says. “The bacteria can bury themselves there and form a wall made of fibrin and platelets, and in that way, microbes in this abscess can selectively adapt to antibiotics in the bloodstream.”
The researchers discovered that as the bacteria acquired resistance to vancomycin, they also became resistant to a new antibiotic, daptomycin, which was thought to be able to treat multidrug-resistant S. aureus. “This is more than we bargained for,” Tomasz says. “The patient wasn’t even exposed to daptomycin, yet the bacteria acquired a resistance to it.” Further testing revealed that one of the mutated loci associated with decreasing vancomycin susceptibility resembled that found from isolates recovered in different regions of the world, raising hopes that these findings will indeed offer a representative model of resistant S. aureus, and may someday lead to new mechanisms for fighting drug-resistant staph.
Proceedings of the National Academy of Sciences 104(22): 9451-9456 (May 29, 2007)
This is the first time that such a process has been observed “within” a patient, and the results, published in the May 21 issue of the Proceedings of the National Academy of Sciences sheds light on how such resistance occurs through selective pressure, says the study’s lead investigator, Alexander Tomasz, head of the Laboratory of Microbiology at Rockefeller University.
“What is thrilling is that we got as close as one can to the birthplace of antibiotic resistance in a patient, and now we can study which of the genetic mutations we found are really essential for resistance,” Tomasz says. If the genetic alterations they discovered are common to all known mutated strains of the bacteria — which Tomasz suspects is true — then knowing these genes may help clinicians design ways to block multidrug resistance, he says.
The microbe they isolated is Staphylococcus aureus, which is one of the most frequent causes of a wide range of hospital- and community-acquired infections, and is best known as the cause of toxic shock syndrome. The pathogen has acquired resistance to the majority of available antibiotics, including, recently, vancomycin, which was believed to be the only major agent that could treat it. “It has fantastic adaptive capabilities which have led to the worldwide spread of resistant lineages that are posing serious limits to clinical treatment,” Tomasz says.
But no one has known how such resistance occurs — whether it happens within individual patients, or whether patients with wounds pick up resistant microbes that have somehow infiltrated hospitals.
In this study, Tomasz, along with first author Michael Mwangi, a postdoc in the Tomasz lab, Eric Siggia, head of the Laboratory of Theoretical Condensed Matter Physics, and collaborators from Rockefeller, the Howard Hughes Medical Institute, the U.S. Department of Energy and Cornell University, obtained access to the blood of a patient with congenital heart disease who was treated extensively, but unsuccessfully, with several antibiotics including vancomycin. The team isolated the bacteria from the blood, and then used the whole-genome “shotgun” sequencing method to work out the entire genetic structure of S. aureus as it changed. They sequenced both the initial isolate and the later drug-resistant bacterium. The comparison of the two sequences showed that the resistant bacterium carried 35 mutations in 33 places on its genome and also showed that the mutations showed up in the intermediate isolates in a sequential order in parallel with the gradually increasing resistance to vancomycin. Although initially sensitive to vancomycin, some of the bacteria were probably able to “hide” from the antibiotic in the tissue of the patient’s heart valve, Tomasz says. “The bacteria can bury themselves there and form a wall made of fibrin and platelets, and in that way, microbes in this abscess can selectively adapt to antibiotics in the bloodstream.”
The researchers discovered that as the bacteria acquired resistance to vancomycin, they also became resistant to a new antibiotic, daptomycin, which was thought to be able to treat multidrug-resistant S. aureus. “This is more than we bargained for,” Tomasz says. “The patient wasn’t even exposed to daptomycin, yet the bacteria acquired a resistance to it.” Further testing revealed that one of the mutated loci associated with decreasing vancomycin susceptibility resembled that found from isolates recovered in different regions of the world, raising hopes that these findings will indeed offer a representative model of resistant S. aureus, and may someday lead to new mechanisms for fighting drug-resistant staph.
Proceedings of the National Academy of Sciences 104(22): 9451-9456 (May 29, 2007)
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