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
Saturday, June 16, 2007
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.
Subscribe to:
Posts (Atom)
