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."
Saturday, June 9, 2007
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.
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Contacts:
Kim Jacque
9560 SW Nimbus Ave.
Beaverton, Oregon 97008
Phone Number: 503.624.9830
Fax Number: 503.639.0846
kjacque@acrymed.com
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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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