As part of a national movement to provide health-care consumers with more information, the Georgia Hospital Association has launched a Web site that allows patients to check out the cost and quality of common medical procedures at the state's 141 acute care hospitals.
In fact, the site — www.gahospitalpricecheck.com — is chock-full of so many facts and figures it can be hard to navigate.
"It's a gold mine of material," said Bill Vaughan, a health care analyst for Consumers Union, the not-for-profit organization that publishes Consumer Reports magazine, "but mining is difficult work."
Once they get the hang of the site, Georgians can learn how quickly they may receive an antibiotic for pneumonia at various hospitals or whether a stop-smoking program will be part of their treatment for a heart condition. They can compare hospitals to see which performs a procedure the most often, or charges less for it.
Among the things they won't find are hospitals' specific numbers on patient mortality, infections or the rate of patient readmissions. Those factors are combined into a single "quality index score" on the site from the Partnership for Health and Accountability, a collaborative statewide program that includes the hospital association.
While the site now shows hospitals' listed prices for various procedures, patients with insurance probably won't pay that amount. The Hospital Association plans to add information from insurance carriers so patients can calculate their actual out-of-pocket costs.
Specialty-care hospitals are not included on the site, but plans are in place to add psychiatric and rehabilitation centers. Ambulatory care, long-term institutions and pharmacies are not addressed.
The Web page "is not the be-all end-all yet," said Vi Naylor, the Georgia Hospital Association's executive vice president, "but we're certainly poised to be." Institutions provide their own information, but "it goes through all sorts of checks related to accuracy and completeness," Naylor said. "I hang my hat on that information."
Agencies that review the material include the Joint Commission on Accreditation of Healthcare Organizations, which looks at outcomes from treatment as part of the accreditation process. The commission prescribes the methods for gathering data.
Patients are "hungry for help in making decisions" about their care, said Bill Bornstein, chief quality officer for Emory Healthcare, the hospital system affiliated with Emory University. But, he said, patients shouldn't make determinations based on numbers alone.
"It's very difficult to account for differences in patient population, degrees of illness, medical education and how all those things factor together," Bornstein said. "Georgia, like everywhere else, has a spectrum of hospitals that range from small rural hospitals to major academic medical centers like Emory. . . . Trying to incorporate all that into a single quality index is difficult."
Wayne Oliver, the Right to Know project director of the Center for Health Transformation founded by former U.S. House Speaker Newt Gingrich (R-Ga.), said the Web site could make hospitals better.
"Just having the information published on the Web site makes health care providers compete not only on price and quality, but also on providing the kind of care patients need to receive," he said.
The Georgia Hospital Association put together the site in response to state and national pushes for transparency in health care, Naylor said.
Consumer groups have called for years for more information about the cost and quality of health care. In August, President Bush directed the agencies that administer federal health insurance programs to share price and quality information about health care providers. Gov. Sonny Perdue followed with an order creating an advisory board to examine how to provide consumers with more health care information.
The association prepared the Web site last year, based on a model from Wisconsin that has been used by at least 10 other states, Naylor said.
Georgia's new site may save taxpayers money, Naylor said, since its cost is borne by the hospital association. "That's one less thing the state has to do," she said.
The hospital association will continue refining the site based on user feedback, said spokesman Kevin Bloye. "We want to make sure this site is as consumer friendly as possible," he said.
HOW TO USE THE WEB SITE
1. Basic or advanced search
Selecting a basic search allows users to check charges and information for 64 types of medical conditions.
An advanced search offers users the ability to obtain information about all types of hospital stays throughout the state.
2. AGE, AREA AND HOSPITAL
A simple pulldown menu asks for age, county, city/town and the regional or statewide facility.
3. What's your problem?
The basic search gives you general categories such as childbirth, psychiatric, bones, joints and muscles and several more. Each one shows a subcategory when you scroll over with the mouse.
The advanced search asks for specific categories such as diseases of the eye, respiratory system, mental disorders, etc. Subsequent menus narrow down the focus of your medical needs.
An easy-to-read tab chart gives comparisons on lengths of stay, the number of cases (of your specified medical need) and average prices.
As part of a national movement to provide health-care consumers with more information, the Georgia Hospital Association has launched a Web site that allows patients to check out the cost and quality of common medical procedures at the state's 141 acute care hospitals.
A chemical compound found in crabs and shrimp that has long been known to have certain medicinal value also can act like a "bed of nails," fending off microbes seeking to colonize wound dressings, catheters and other implantable medical devices, according to Montana State University researchers. Using the compound to coat these medical devices, they say, could help prevent thousands of bacterial and yeast infections annually.
The preliminary finding, by Philip Stewart, Ph.D., director of MSU's Center for Biofilm Engineering, and Ross Carlson, Ph.D., assistant professor of chemical engineering, was described today at the 232nd national meeting of the American Chemical Society, the world's largest scientific society.
In their laboratory studies, chitosan - a sugar in the cells of crabs and shrimp - repelled bacteria and yeast, effectively preventing these microbes from forming slimy, glue-like layers of infectious cells, known as biofilms, Stewart said. These biofilms account for up to 65 percent of the bacterial infections in the United States, according to the Centers for Disease Control and Prevention.
The researchers say that while chitosan is well known for its antimicrobial activity, this is the first time its anti-biofilm activity has been described.
"Coating chitosan onto a surface seems to stop bacteria and yeast from colonizing that surface," Stewart said. "Chitosan almost acts like a bed of nails. If a microbe alights on it, the chitosan skewers it or causes it to leak. That might not kill microbes outright, but it certainly discourages them from establishing a foothold."
Biofilms are considered the leading cause of up to 400,000 cases of catheter-related, bloodstream infections each year, Stewart said. In addition, biofilms can arise on virtually any device implanted in the body, including mechanical heart valves, contact lens, artificial hips and knees, and breast implants. Once a biofilm-induced infection takes hold, it can be difficult to treat and often requires the surgical removal of the affected device, he said.
If further testing in animals and humans proves successful, coating these devices with chitosan could become an important first line of defense, according to Stewart. "I don't want to claim we've fully solved the problem here," he said, "but … I think over the next 10 years we're going to be seeing new technologies in the form of coatings that will prevent or at least reduce the incidence of infection."
Chitosan is derived from chitin, the main component of crustacean shells. It is sold commercially as a nutritional supplement and is an FDA-approved material for staunching blood loss. Chitosan also is used in biomaterials, as a thickener in cosmetics and a flocculating agent in water treatment. As a biomaterial, chitosan has a track record for its non-toxicity, biocompatibility, ability to promote healing and its inherent antimicrobial properties.
Reprinted from www.IHI.org
Institute for Healthcare Improvement Vice President and patient safety expert, Carol Haraden, PhD, comments on the power and popularity of “bundles” in improvement initiatives. While the allure of this tool is undeniable, says Haraden, quality teams should resist the impulse to label any list of good changes a bundle. She clarifies what a bundle is and is not, and suggests tips for using bundles most effectively to get results.
Q: What is a bundle?
A: IHI developed the concept of “bundles” to help health care providers more reliably deliver the best possible care for patients undergoing particular treatments with inherent risks. A bundle is a structured way of improving the processes of care and patient outcomes: a small, straightforward set of practices — generally three to five — that, when performed collectively and reliably, have been proven to improve patient outcomes.
Q: What makes a bundle so special?
A: The power of a bundle comes from the body of science behind it and the method of execution: with complete consistency. It’s not that the changes in a bundle are new; they’re well established best practices, but they’re often not performed uniformly, making treatment unreliable, at times idiosyncratic. A bundle ties the changes together into a package of interventions that people know must be followed for every patient, every single time.
Q: So a bundle is a list of the right things to do for a given patient?
A: It resembles a list, but a bundle is more than that. A bundle has specific elements that make it unique.
The changes are all necessary and all sufficient, so if you’ve got four changes in the bundle and you remove any one of them, you wouldn’t get the same results — meaning: the patient won’t have as high a chance of getting better. It’s a cohesive unit of steps that must all be completed to succeed. The changes are all based on randomized controlled trials, what we call Level 1 evidence. They’ve been proven in scientific tests and are accepted, well-established. There should be no controversy involved, no debate or discussion of bundle elements. A bundle focuses on how to deliver the best care — not what the care should be. We want providers to get right to work on the how: on completing steps x, y, and z for every patient.
The changes in a bundle are clear-cut and straightforward; they involve all-or-nothing measurement. Successfully completing each step is a simple and straightforward process. It’s a “yes” or “no” answer: “Yes, I did this step and that one; no, I did not yet do this last one.” Successfully implementing a bundle is clear-cut: “Yes, I completed the ENTIRE bundle, or no, I did not complete the ENTIRE bundle.” There is no in between; no partial “credit” for doing some of the steps some of the time. Bundle changes also occur in the same time and space continuum: at a specific time and in a specific place, no matter what. This might be during morning rounds every day or every six hours at the patient’s bedside, for instance.
Q: Can you give an example?
A: The 100,000 Lives Campaign has several bundles as “planks” or interventions. This initiative is likely a big factor in the popularity of the bundle — thousands of people in hospitals across the country have learned about bundles by applying them as part of their participation in the Campaign. There are three bundles in the Campaign that have been incredibly effective helping hospitals reduce to nearly zero the incidence of deadly infections that used to be so common they were accepted as unavoidable.
Central Line Bundle: This is a set of five steps to help prevent “catheter-related blood stream infections,” deadly bacterial infections that can be introduced through an IV in a patient’s vein supplying food, medications, blood or fluid. The steps are simple, common sense tasks: using proper hygiene and sterile contact barriers; properly cleaning the patient’s skin; finding the best vein possible for the IV; checking every day for infection; and removing or changing the line only when needed.
Surgical Site Infection Bundle: Any surgical procedure brings the risk of infection that can extend a patient’s hospital stay or cause more serious problems. The Campaign’s Surgical Site Infection Bundle involves appropriate use of antibiotics before and after surgery, stopping the practice of using razors — which cause nicks that invite infection — to remove a patient’s hair before surgery, keeping the patient warm during surgery, and monitoring the patient’s blood sugar after surgery.
Ventilator Bundle: Ventilator-associated pneumonia (VAP) is a serious lung infection that can happen to patients on a ventilator. The Ventilator Bundle has four care steps: raising the head of the patient’s bed between 30 and 40 degrees; giving the patient medication to prevent stomach ulcers; preventing blood clots when patients are inactive; and seeing if patients can breathe on their own without a ventilator.
Q: What’s the problem with how people use bundles?
A: The concept of a bundle has such traction that people are trying to use them more often and in more ways than they really should. There’s a tendency to want to call everything a bundle, any checklist involving patient care procedures, for example. But a bundle isn’t a checklist, and just taking an ineffective checklist and calling it a bundle won’t make it any better. The goal is to make a process more reliable, and you do that by improving habits and processes. The magic of the bundle comes from the guidelines I’ve laid out here; the way the work is organized. People need to ask themselves: why will calling it a bundle make it better?
Q: What’s the difference between a bundle and a checklist?
A: A checklist can be very helpful and an important vehicle for ensuring safe and reliable care. The elements in a checklist are often a mixture of nice-to-do tasks or processes (useful and important but not evidence-based changes) and have-to-do processes (proven by randomized control trials). A checklist may also have many, many elements.
A bundle is a small but critical set of processes all determined by Level 1 evidence. And it needs to meet all the criteria I described previously. Because some elements of a checklist are nice to do but not required, when they are not completed, there may be no effect on the patient. When a bundle element is missed, the patient is at much greater risk for serious complications.
There’s also a level of accountability tied to a bundle that you don’t always have with a checklist. An identified person or team owns it. A checklist might be owned by everybody on a floor or on a team, but we know that, in reality, when it’s owned by everyone — nobody owns it! Things don’t always get done. So maybe the pharmacist does one thing in a checklist, a nurse another, the doctor something else, but really it’s no one person’s job at the end of the day. A bundle is a person or a team’s responsibility — period. And it’s their job at a certain point and time — during rounds every single day, possibly. So it isn’t the kind of thing where people say: “You check that, I’ll check this.” No. It’s very clear who has to do what and when, within a specific time frame. The accountability and focus give a bundle a lot of its power.
Q: Can you give an example?
A: Let’s take a discharge planning list. It’s a reminder list of things people on a team should be doing throughout the patient’s stay to help move the treatment process along toward discharge. People look at it often but no one typically “owns” it and there aren’t clearly delineated dates and times attached to each element. It’s so easy for incredibly busy nurses, aides, therapists, and doctors to assume that the next person will pick up where they left off.
Q: You’re not saying don’t bother with checklists, are you?
A: No, not at all. I don’t mean to diminish the importance of a checklist. They can be really helpful; sometimes essential. When you get on a plane, you should be grateful to know that the pilot won’t take off until going through every single task in the “pre-flight checklist.” It’s an incredibly important list; in fact, when you talk to a pilot, they don’t call it a “checklist,” they call it “pre-flight procedures.” It’s practically written in stone — revered and followed religiously with every flight. It’s more than a list: it’s a codified set of procedures.
Q: Is that the only problem with how bundles are used?
A: We’re also seeing a trend where people keep adding changes to an existing bundle, a valid bundle they’ve adopted. It gets bigger and bigger — ultimately to the point where it’s unworkable, impossible to follow and not effective anymore. If you do add changes to a bundle, the chance of success is much higher if you use the bundle criteria I’ve described here as a check for the appropriateness of inclusion.
Q: So, your final message about bundles is what?
A: A bundle is a specific tool with clear parameters. It has a small number of elements that are all scientifically robust, that when taken together create much improved outcomes. Don’t feel compelled to convert helpful checklists into overloaded bundles. If the concept of a bundle becomes so broad and loose in meaning, its power will start to diminish. We don’t want that to happen.
Taking a single course of a certain type of antibiotics gives rise to high levels of antibiotic resistant bacteria in the mouth, an effect that lasts for at least half a year, a new study has found.
The extraordinary persistence of the effect startled the scientists who discovered it and others in the field as well – and underscores the need for judicious use of these precious drugs, experts said.
Senior author Dr. Herman Goossens said he and his co-authors assumed that if they followed the subjects in their study for six months they would see the rates of resistant bacteria in their mouths return to normal levels. But that didn't happen.
"We were pretty staggered by these data," said Goossens, a microbiologist at the University of Antwerp, in Belgium. "We never expected this." Goossens said the findings suggest that even after a single – and short – course of antibiotics, a person could spread resistant strains of bacteria to close contacts within a household or a hospital for months.
The findings, reported Thursday in the journal The Lancet, are a sharp reminder of the power of antibiotics, suggested Eric Brown, a biochemist at McMaster University in Hamilton. "So a quick course of antibiotics and a half a year later, you're still carrying resistant organisms. That's a little bit terrifying," said Brown, whose laboratory is working on alternative ways to kill bacteria, because of the rising problem of antibiotic resistance.
It also suggests doctors treating patients for bacterial infections should carefully consider which antibiotics they prescribe if those patients have taken antibiotics within the past year – the period Goossens thinks it might take for resistance levels to subside to normal after antibiotic use.
"If you're a doc who's about to treat a patient who has been treated before, it should have an impact on the decisions you make about what to give that patient," Brown said.
The study, which was partially funded by drug maker Abbott Laboratories, is the first to definitively show that antibiotic use is the major factor in the emergence of antibiotic resistance, Goossens said.
It seems a bit like proving the known.
Plenty of research has shown that as antibiotic use rises in a population, the rate of antibiotic-resistant infections rises as well. Based on those findings, infection control experts have been campaigning for years to get doctors to cut back on antibiotic use out of a fear that resistance is threatening the continued efficacy of these important drugs.
But because those studies looked across populations, they couldn't rule out other factors that might have been involved and therefore could only draw a link between antibiotics and antibiotic resistance.
Proving antibiotic use causes antibiotic resistance requires studying individuals – and that's what Goossens and his colleagues did.
A group of 224 healthy volunteers were randomly selected to receive either azithromycin or clarithromycin – both drugs from the macrolides class of antibiotics – or a fake treatment. Neither the volunteers nor the researchers knew who received which.
The back of the mouth of each participant was swabbed at the start of the study and then at regular intervals after the subject had completed the course of antibiotics. The swabs were tested to determine whether the streptococci in the mouths were susceptible or resistant to the antibiotics.
Surprisingly, the researchers found that roughly 28 per cent of the streptococci in the mouths of all subjects were resistant from the start. But whereas that level didn't change for participants who received a placebo, the proportion of antibiotic-resistant bacteria in the mouths of treated participants spiked to about 90 per cent shortly after treatment.
At six weeks out, the resistant bugs still made up about 60 per cent of streptococci and at six months, 50 per cent.
Should people in this position become infected with streptococci – which cause respiratory and other ailments – those infections might not respond to antibiotics. Furthermore it's known that bacteria can pass along resistance to other types of bacteria, again making affected people more vulnerable to resistant infections.
"It . . . should serve as a wake-up call for individual prescribing physicians, nurse practitioners, midwives, dentists and others that inappropriate use of antibiotics does have consequences," said Dr. John Conly, former chair of the Canadian Committee on Antibiotic Resistance and head of the department of medicine at Foothills Medical Centre in Calgary.
And those consequences are felt at a variety of levels, said a commentary that accompanied the research.
"The key message is that antibiotic prescribing affects the patient, their environment and all the people that come into contact with that patient or with their environment," wrote Stephanie Dancer, of the department of microbiology at Glasgow's Southern General Hospital.
"Clearly we're overusing antibiotics," said Goossens. "We've done this for decades."
Feb 08, 2007
Helen Branswell, Canadian Press
(Excerpted from CBS News)
Two years ago, Bobbie Mackeon got a paper cut. She thought it was no big deal. But it got infected. Bobbie, a nurse practitioner, spoke with the doctors at her hospital, and they all figured an antibiotic would take care of it. It didn’t. Nor did the next two antibiotics she tried. “The bug that was in there was eating these antibiotics for breakfast,” she says.
With her infection still raging, Bobbie turned to an intravenous antibiotic, which finally did help. But complications then led to potentially fatal blood clots. “The blood clot was about four inches across and it had little bubbles around it, which told us it was infected,” she says.
The clots were so severe that her life now depends on high doses of blood thinners, which created new problems. Any injury can now be life threatening, because it is difficult to stop her body from bleeding. Now, instead of running as she used to, she works out, carefully, in her garage.
That a tiny infection could spiral into a life-threatening condition doesn’t surprise Michael Shnayerson or Mark Plotkin. In their new book, “The Killers Within,” they explore why antibiotics don’t work the way they used to. Susan Spencer reports.
“The bad news is the bad bugs are getting badder faster. They’re getting stronger faster,” says Plotkin. “We no longer live in a time when antibiotics work 100 percent of the time and in fact there are some bugs resistant to all the antibiotics used against them. And people are dying,” says Shnayerson. Even common staph infections, once easily cured, now can kill. The superbugs, which first showed up in hospitals, are everywhere.
The culprit: overuse of antibiotics. Like all living things, bacteria adapt to the environment. Faced with an antibiotic, a few hearty bugs survive. Those superbugs then multiply, creating a new strain that the old antibiotic can’t touch.
The more antibiotics used, the more the bacteria evolve. After five decades, Americans have been using and now overusing these "wonder drugs."
“Too many doctors still feel that antibiotics basically do no harm. And that i'ts better to give them than not,” says Shnayerson.
Patients demand them even for colds - viral infections against which antibiotics are useless. Adding to overuse is agriculture. Farmers use antibiotics in feed, mostly to make the animals grow a little faster. According to Plotkin, a recent study estimates that farms use 70 percent of all antibiotics in the U.S.
“I think were looking at the end of the antibiotic era if we don’t start changing our behavior,” says Mackeon’s colleague, Dr. David Witt, an infectious disease specialist at Kaiser Permanente in California.
Most chilling, Witt says, is the rising rate of resistance in one very common bug, pneumococcus, which causes most cases of pneumonia, ear infection, and sinusitis. “Everybody gets them. All of your kids have had them,” Witt says.
When Gail Mullin’s 3-week-old daughter, Hollie, got her first ear infection, Gail, like many mothers, asked for antibiotics. But more infections followed. And the antibiotics kept coming: amoxicillin, augmentin, zithromax, receptin - 17 different courses in one year. By the time Hollie was 18 months old, she contracted a bacteria that was resistant to every oral antibiotic available.
Her only hope was a drug called vancomycin, a potent antibiotic given intravenously. The doctor told her it was the last option.
Hollie was lucky. Vancomycin did work. Her parents learned a lesson. “By giving Holllie as many antibiotics as we did by the time she was a year old we created a superbug,” says her mother.
Vancomycin saved Mackeon as well. But now she struggles with the blood clots. Despite efforts to regain her health, Bobbie has been unable to work for much of the past two years.
“Bobbie is a good example of the worst-case scenario,” says Witt. He expects to see many more such cases, which is why he carefully checks and rechecks every antibiotic ordered at the hospital.
“I don’t want to give you the wrong impression. I love antibiotics. They are life-saving, they are miracles. And I want to save them for when we need them,” he says.
There is some good news. A new study finds that doctors are ordering fewer antibiotics for children. But experts estimate that there’s still are tens of millions of unnecessary prescriptions being written each year.
Now even Vancomycin is losing its punch. This prospect is “chilling,” Witt says.
Nosocomial etiologies in BLOODSTREAM INFECTIONS include the following:
Coagulase-negative staphylococci, 40%
Staphylococcus aureus, 9.3%
Enterobacter species, 6.2%
Acinetobacter baumannii with substantial antimicrobial resistance is reported with increasing frequency.
JAMA says that, looking back, the year 2003 will probably be recognized as the year that methicillin-resistant Staphylococcus aureus (MRSA) really started to take off in the community. Rather than be confined to the institutionalized, MRSA appeared to now attack those in the prime of life, even the most athletic among us. These investigators from the Minnesota Department of Health (Minneapolis), French Reference Centre for Staphylococci (Lyon), and the Centers for Disease Control and Prevention (Atlanta) performed a prospective study of MRSA cases in Minnesota during calendar year 2000.
Using 12 laboratories, they were able to identify sufficient numbers of community-associated cases (CA) to make valid demographic, clinical, and microbiological comparisons with healthcare-associated cases (HCA).
The 12 referring laboratories were dispersed throughout the state and serviced representative populations. They identified MRSA cases from clinical cultures rather than systematic survey. Facility infection control personnel then performed chart review to gather appropriate demographic and clinical information in order to determine whether the case was CA or HCA. HCA was prospectively defined by conventional criteria. CA was determined by exclusion of HCA, so all suspected CA cases after chart review subsequently underwent interview. Overall, 13% of such suspected CA cases were reclassified to HCA after the interview revealed information missing from the record. All CA and some HCA isolates were subjected to pulsed-field gel electrophoresis (PFGE), as well as standard microbiological investigation to determine speciation and resistance patterns, and PCR was used to confirm persistence of the mecA gene. Finally, samples of 26 CA and 26 HCA isolates were sent to the French reference laboratory, where blinded assays were performed for a compendium of toxin-associated genes in the 2 sets of organisms.
During 2000, there were 4612 patients with S aureus isolates from the reference facilities. Of these, 1100 were MRSA, with 937 (85%) classified as HCA, 131 (12%) as CA, and 32 (3%) not classified because of insufficient information. The proportion of CA cases was higher in areas of the state outside of the greater Minneapolis-St. Paul area (OR, 1.66; CI, 1.24-2.15). CA patients were younger (median age, 23 vs 68 years), even after exclusion of data from 2 pediatric hospitals (median age, 30 vs 70 years). Also, CA-MRSA patients were more likely to be nonwhite (OR, 3.13) and have lower median household income compared with HCA-MRSA and especially the general population.
Underlying conditions were uncommon among children < 18 years of age with CA-MRSA, with only 9% having previous dermatologic illness. Most adults, on the other hand, had some health risk, with tobacco use (19%), diabetes (17%), dermatologic illness (13%), chronic obstructive pulmonary disease (6%), and hypertension (6%) most notable.
CA-MRSA was more likely than HCA-MRSA to be manifested as cutaneous or soft-tissue disease (OR, 4.25). Respiratory (OR, 0.22) and urinary (OR, 0.04) disease were much less common in the community. There was no significant difference in the incidence of bacteremia (4% among CA, 9% among HCA). Remarkably, 61% of CA patients were initially treated with ineffective antibiotics. Unfortunately, detailed outcome analysis was not possible.
Resistance patterns differed between CA and HCA strains, with the former generally susceptible to a wider range of non beta-lactam antibiotics, particularly ciprofloxacin (OR, 1.90) and clindamycin (OR, 1.46) or all 4 of the following: ciprofloxacin, clindamycin, gentamicin, and trimethoprim-sulfamethoxazole (OR, 5.88). A single PFGE clonal group accounted for 62% of CA-MRSA, with similar rates for all demographic subgroups. A second clone was also associated with a lesser number of CA cases. The following virulence factors were significantly more common in CA-MRSA: Panton Valentine leukocidin (PVL); enterotoxins A, C, and K; accessory gene regulator 3; and SSCmecIV).
PVL was present in 77% of CA, but only 4% of HCA isolates tested (OR, 5.01), and was almost always (90%) associated with skin infection in community patients. This cytotoxin has been found in different CA strains on 3 continents and seems to enhance tissue necrosis and leukocyte dysfunction by membrane injury.
The investigators, since they are from public health agencies, offered important clinical suggestions based on their data. It is important to know the prevalence of CA-MRSA in your community, and be particularly alert to children with aggressive skin infection. All such children should be cultured for MRSA. If there is a history of contact with a patient with CA-MRSA or sufficient risk factors to suggest epidemic spread, empiric therapy with clindamycin or ciprofloxacin should be considered, rather than vancomycin. Surgical drainage should be performed when appropriate. Public quarantine and nasal or skin decolonization procedures are not necessary. Rather, physicians should educate patients and their families, as well as the general public, that CA-MRSA is an emerging threat and that suspected infections need prompt management.
JAMA December 10, 2003 (Volume 290, Number 22)
Vandenesch F, Naimi T, Enright MC, et al. Community-acquired methicillin resistant Staphylococcus aureus carrying Panton-Valentine leukocidin genes; worldwide emergence. Emerg Infect Dis. 2003;9:978-984.
Oral hygiene has been proven to help reduce healthcare-acquired pneumonias (HAPs), including ventilator-associated pneumonia (VAP) and aspiration pneumonia.
In fact, the CDC now requires acute care hospitals to “develop and implement a comprehensive oral hygiene program" for patients at risk for healthcare-associated pneumonia.
For more exhaustive information regarding HAP AND VAP, go to:
Do germs communicate? Many scientists think so and are betting the chatter may hold the key to developing the next generation of drugs to fight killer superbugs.
The conventional wisdom has long been that the carpet-bombing approach is the best way to fight infection. But as evidence of bacterial bonding has mounted in the past decade, researchers are now focusing on antibiotics that will break down the lines of communication.
In the last 20 years, the number of scientists working in this field has jumped from a few solitary researchers to thousands. In Britain, the strategy is one of the top research priorities of a newly formed center dedicated to stopping superbugs.
“Bacteria are a bit like an army going into battle,'' said Dr. Paul Williams, professor of molecular biology at the center at Nottingham University. “Only when they've got strength in numbers do they tell their troops to start firing.''
The thinking is that if bacterial communication can be interrupted, the microbes might be incapacitated before doing any damage. And by not killing off the bacteria, they won't have the Darwinian opportunity to evolve into resistant strains.
Scientists are still years away from producing a commercially available drug. But if the strategy proves successful, it could open the way for new weapons against superbugs such as the deadly MRSA superbug — whose infection rate has jumped dramatically in the last two decades.
Researchers refer to the bacterial communication system as “quorum sensing.'' Just like in a company boardroom, a quorum is needed before any major action can be taken.
Bacteria communicate with each other by sending out a chemical signal that is in turn picked up by special receptors. Williams and his colleagues are developing enzymes to destroy the signal molecules.
Experts are also trying to break into other bacterial social activities. For instance, bacteria congregating to form a “biofilm'' achieve a type of super-resistance.
“If we can break them up, we can kill them,'' said Dr. Pete Greenberg, a microbiology professor at the University of Washington. Greenberg is working on methods to disable a bacteria that frequently attacks people with cystic fibrosis.
New strategies to fight bugs that don't end up boosting their immunity would be a big boost. Pharmaceuticals companies have been reluctant to invest in traditional antibiotics because many germs can develop resistance within months. The last new classes of antibiotics appeared in the 1990s.
“With only one or two antibiotics that are effective against a major pathogen, we are potentially living on borrowed time,'' warned Dr. Richard James, director of Britain's newly established Centre for Healthcare Associated Infections at Nottingham University.
“Unless we do something to change the situation, we are facing a post-antibiotic apocalypse.''
James, who is not involved in quorum sensing research, believes that it is one of the most promising avenues to developing new antibiotics. “Perhaps the answer to the problem of increasing bacterial resistance is for us to be even more clever than the bacteria,'' he said. “We could do this if we have antibiotics that disable the bacteria, which may then allow the host's immune system to kick in.''
Still, there are no guarantees that antibiotics based on quorum sensing will work. For instance, it's uncertain if knocking out communication lines in later stages of an infection would have any impact.
“There are no experiments to show that in a raging infection, a quorum sensing inhibitor could calm it down,'' said Greenberg. “It might already be too late by the time patients turn up with an infection.''
But with no new antibiotics on the horizon, scientists say new strategies must be attempted.
“Drugs that inhibit quorum sensing are in the unproven category, but there is still a possibility they could work,'' said Dr. Anthony Coates, a professor of medical microbiology at St. George's Hospital Medical School in London. “Quorum sensing might produce very effective antibiotics, but they might only work on specific species of bacteria,'' he said, adding that further tests on existing compounds is needed.
“The cupboard is running bare, and without any new antibiotics, we have to keep trying.''
By Maria Cheng
Associated Press, London
01 February 2007