MRSA is Methicillin-resistant Staphylococcus Aureus. Abbreviated MRSA.
MRSA are Staphylococci that are resistant to the antibiotic, methicillin, and other commonly used antibiotics such as penicillin and cephalosporins. These germs have a unique gene that causes them to be unaffected by all but the highest concentrations of these antibiotics. Therefore, alternate antibiotics must be used to treat persons infected with MRSA. Vancomycin has been the most effective and reliable drug in these cases, but is used intravenously and is not effective for treatment of MRSA when taken by mouth.
MRSA first cropped up among persons in hospitals and other health facilities, especially among the elderly, the very sick, and those with an open wound (such as a bedsore) or a tube going into their body (such as a urinary catheter or IV catheter).
MRSA has since been found to cause illness in the community outside of hospitals and other health facilities. MRSA in the community is associated with recent antibiotic use, sharing contaminated items, having active skin diseases, and living in crowded settings.
Skin infections caused by MRSA have clustered among injecting drug-users, Native Americans, prison inmates, and athletes in close-contact sports. Community-associated MRSA infections typically cause skin lesions (such as boils), but also can cause severe illness. Some children have died from community-associated MRSA.
The transmission of MRSA is largely from people with active MRSA skin infections. MRSA is almost always spread by direct physical contact, and not through the air. Spread may also occur through indirect contact by touching objects (such as towels, sheets, wound dressings, clothes, workout areas, sports equipment) contaminated by the infected skin of a person with MRSA.
MRSA infections are usually mild superficial infections of the skin that can be treated successfully with proper skin care and antibiotics. MRSA, however, can be difficult to treat and can progress to life-threatening blood or bone infections because there are fewer effective antibiotics available for treatment.
If someone has an MRSA infection, they can help from spreading it by keeping infections, particularly those that continue to produce pus or to drain material, covered with clean, dry bandages; by advising close contacts to wash their hands frequently with soap and warm water, especially if they change the bandages or touch the infected wound or potentially infectious materials; by not sharing personal items (such as towels, washcloth, razor, clothing) that may have had contact with the infected wound; by washing linens and clothes with hot water and laundry detergent and drying them in a hot dryer; and by telling healthcare providers that you have an antibiotic-resistant staph skin infection.
To help prevent the spread of MRSA in a health care setting, wash hands regularly with antimicrobial soap and warm water. When hands are not visibly soiled, alcohol-based hand sanitizer use is effective. Wear gloves when managing wounds. After removing gloves, wash hands with soap and warm water, or use alcohol-based hand sanitizer. Carefully dispose of dressings and other materials that come into contact with blood, nasal discharge, urine, or pus from patients infected with MRSA. Clean surfaces in patient rooms with commercial disinfectant or a 1:100 solution of diluted bleach (1 tablespoon bleach in 1 quart of water). Launder any linens that come into patient contact in hot water (>160°F) and bleach. The heat of commercial dryers improves bacterial killing.
Pennsylvania became the first state to publicly report the number of patients who contracted an infection while in one of its 168 hospitals last year. A recent report issued by the Pennsylvania Health Care Cost Containment Council (PHC4) indicates that deadly hospital infections are on the rise.
The topic of hospital infections has been controversial because the infections are usually transmitted by workers who do not wash their hands or by contaminated medical equipment. Quality control experts expect the report will be used by hospitals to improve infection control efforts, which range from requiring consistent hand washing to taking special steps to prevent patients on ventilators from getting pneumonia.
Listed below are some area hospitals’ infection rates
(per 1,000 patients):
· Butler Memorial 39.4
· Jefferson Regional 28.7
· Allegheny General - 19.9
· Mercy Hospital - 17.4
· St. Clair Memorial - 17.3
· UPMC Presby-Shadyside - 16.2
· Beaver Medical - 10.1
· West Penn Hospital - 9.4
· Westmoreland Regional - 9
· UPMC Passavant - 5.5
Ask for a hospital's infection rates before you decide where you want your next surgical procedure.
A report, released by the Pennsylvania Health Care Cost Containment Council, examined 1.6 million patients in 168 hospitals in the state in 2005. For the report, PHC4 grouped hospitals to account for differences in the severity and complexity of their cases and excluded certain patients with conditions that placed them at high risk for infection. State law requires hospitals to report four broad forms of infections: surgical site, urinary tract, pneumonia and blood stream.
According to the report, 19,154 patients acquired infections in 2005.
An average of 12.2 per 1,000 patients acquired infections, and those who acquired infections cost private heath insurers an average of $59,915 for hospital care, compared with $8,311 for those who did not acquire infections, according to the report (USA Today).
The report also found that: Patients who acquired infections spent almost 400,000 additional days in hospitals at an estimated cost of $1 billion or more (Philadelphia Inquirer).
The average cost of hospital care for patients who acquired infections was $185,260, compared with $31,389 for those who did not acquire infections.
The average length of hospital stays for patients who acquired infections was about 23 days, compared with about five days for those who did not acquire infections (Pittsburgh Post-Gazette).
2,478 patients who acquired infections died during their hospital stays, although PHC4 did not determine whether the infections caused their deaths; and the mortality rate for patients who acquired infections was 12.9%, compared with 2.3% for those who did not acquire infections (Philadelphia Inquirer).
Marc Volavka, Executive Director of PHC4, said, "This first hospital-specific report demonstrates Pennsylvania's robust commitment to reducing these serious, costly and largely preventable infections" (Pittsburgh Post-Gazette). He said that such infections result from "flawed processes" of care and hygiene, not from the treatment of sicker patients (Philadelphia Inquirer).
Roger Mecum, executive vice president of the Pennsylvania Medical Society, said, "There are too many infections, which are increasing mortality and hospital lengths of stay while adding billions of dollars in hospital charges." Lisa McGiffert, director of the "Stop Hospital Infections" campaign at Consumers Union, said, "This is really the first report of its kind in the U.S., where hospitals have actually identified infections and reported them to a state agency".
Healthcare quality experts said that the report might prompt additional efforts by hospitals to prevent infections.
The New England Journal of Medicine (N Engl J Med 2004;350:1422-9) states that as many as 1 hospital patient in 10 in the United States acquires a nosocomial infection; that's 2,000,000 patients a year. More than 80,000 people die each year from these virulent bacteria they acquire during medical procedures and/or while being cared for in trusted healthcare facilities. Estimates of the annual cost as high as $11,000,000,000.
Shockingly, TWICE as many people die from Hospital Acquired Infections as the number of people who die annually from Breast Cancer (41,000) or automobile accidents (39,189 in 2005.) Nationally, 5X as many people die from Hospital Acquired Infections annually as die of AIDS.
Nosocomial infections have nightmarish, far-reaching consequences even if you are fortunate enough to recover from yours. I am left with a lifelong incurable immune disease after recovering from mine. Before our son died the bacteria he was infected with pushed part of his brain into his spinal cord and killed the nerves he needed to breathe or move, causing him to become a ventilator dependent quadripilegic.
220 people per DAY in the United States are dying from Hospital Acquired Infections and yet no one seems to be batting an eye. Perhaps it's not as media-sexy as the scarier sounding Bird Flu or Anthrax but if you add up the number of national annual mortalities from AIDS, Bird Flu, West Nile Virus, Rabies, Anthrax and the war in Iraq all put together, there are still more people dying from infections they accidentally caught in our country's healthcare system.
Somebody needs to pay attention pretty quickly. So far, this silent epidemic, this unbelievable healthcare debacle is being addressed in a cavalier manner with “acceptable” casualties considered okay.
Trust me when I tell you this - When it's a treasured loved one's life at stake, there is no such thing as an acceptable casualty.
Enterobacter species are important nosocomial pathogens responsible for various infections, including bacteremia, lower respiratory tract infections, skin and soft tissue infections, urinary tract infections (UTIs), endocarditis, intra-abdominal infections, septic arthritis, osteomyelitis, and ophthalmic infections.
Risk factors for nosocomial (Hospital Acquired) Enterobacter species infections include hospitalization of greater than 2 weeks, invasive procedures in the past 72 hours, treatment with antibiotics in the past 30 days, and the presence of a central venous catheter. Specific risk factors for infection with nosocomial multidrug-resistant strains of Enterobacter species include the recent use of broad-spectrum cephalosporins or aminoglycosides and ICU care.
These ICU bugs cause significant morbidity and mortality, and infection management is complicated by multiple antibiotic resistance. Enterobacter species possess inducible beta-lactamases, which are undetectable in vitro but are also responsible for resistance during treatment. Physicians treating patients infected with these bacteria are advised to avoid certain antibiotics, particularly third-generation cephalosporins, because resistant mutants can quickly appear.
The crucial first step is appropriate identification of the bacteria. Antibiograms must be interpreted with respect to the different resistance mechanisms and their respective frequency, as is reported for bacteria belonging to this genus, even if the resistance mechanisms have not been detected by routine in vitro antibiotic susceptibility testing.
Enterobacter species rarely cause disease in a healthy individual. This opportunistic pathogen, similar to other members of the Enterobacteriaceae family, possesses an endotoxin known to play a major role in the pathophysiology of sepsis and its complications.
Although community-acquired infections are occasionally observed, nosocomial infections are, by far, the most frequent. Patients most susceptible to acquiring Enterobacter infections are those who stay in the hospital, especially the ICU, for prolonged periods. Other major risk factors include the prior use of antimicrobial agents, concomitant malignancy (especially hemopoietic and solid organ malignancies) hepatobiliary disease, ulcers of the upper gastrointestinal tract, use of foreign devices such as intravenous catheters, and serious underlying conditions such as burns, mechanical ventilation, and immunosuppression.
The source of infection may be endogenous via colonization of the skin, gastrointestinal tract, or urinary tract or exogenous resulting from the ubiquitous nature of these bacteria. Multiple reports have incriminated the hands of personnel, endoscopes, blood products, devices for monitoring intra-arterial pressure, and stethoscopes as sources of infection. Outbreaks have been traced to various common sources: total parenteral nutrition solutions, isotonic saline solutions, albumin, digital thermometers, and dialysis equipment.
Reprinted Excerpts from ABC News
Oct. 14, 2006: There's a deadly threat hiding inside America's hospitals. What's even scarier, your hospital is probably keeping it a secret.
Maureen Daly's mother was a healthy 63-year-old woman when she had surgery to fix a broken shoulder. However, after being admitted to the hospital, Daly's mother got an infection that left her immobilized on a respirator. Daly was told that life-threatening germs are an inevitable fact of hospital life. Daly was shocked. "I cannot accept that it would be a fact of life that you can walk into a hospital with a broken shoulder and leave practically dead," she said. Her mother died four months later.
Pennsylvania is one of only six states that has passed a law requiring the reporting of infections. Experts say public disclosure forces hospitals to reduce infection rates. Dr. Rick Shannon, Chief of Medicine at Allegheny General Hospital in Pittsburgh, looked at the data on patients in the hospital's intensive care units. He was stunned. "Fifty-one percent of everyone who got these infections died. Half the people who got one died," he said. Dr. Shannon wasted no time. He gave an order to the ICU staff. Reduce hospital infections to zero in just 90 days.
Staff nurses said they didn't think it could be done. But after just one week, the ICU staff identified the culprit. It wasn't a superbug - it was the staff. And the fact they each had their own way of washing hands, changing dressings, and putting in catheters. "No one actually knew what the right way to do it was. And not knowing what the right way to do it was that all these little errors could creep in that would lead to infection," Dr. Shannon said. A year later the results are impressive. Only one patient in the ICU has died from an infection.
Betsy McCaughey says it's important for the public to know about infection rates at hospitals. "The public has a right to this information. If you are going into the hospital, you should be able to find out which hospital in your area has a serious infection problem, so you can stay away from that hospital," she said. Her advocacy group is working to pass more state laws - like Pennsylvania's requiring hospitals to release this data.
And McCaughey says there's a simple thing you can do to keep yourself safe from dangerous germs in any hospital.
"Ask doctors and nurses to clean their hands before touching you. If you are worried about being too aggressive, just remember, your life is at stake" she said.
Ricki Lewis, Ph.D. (geneticist) wrote this piece for the FDA:
When penicillin became widely available during the second world war, it was a medical miracle, rapidly vanquishing the biggest wartime killer - infected wounds. Discovered initially by a French medical student, Ernest Duchesne, in 1896, and then rediscovered by Scottish physician Alexander Fleming in 1928, the product of the soil mold Penicillium crippled many types of disease-causing bacteria. But just four years after drug companies began mass-producing penicillin in 1943, microbes began appearing that could resist it.
The first bug to battle penicillin was Staphylococcus Aureus. This bacterium is often a harmless passenger in the human body, but it can cause illness, such as pneumonia or toxic shock syndrome, when it overgrows or produces a toxin.
In 1967, another type of penicillin-resistant pneumonia, caused by Streptococcus Pneumoniae and called Pneumococcus, surfaced in a remote village in Papua New Guinea. At about the same time, American military personnel in southeast Asia were acquiring penicillin-resistant gonorrhea from prostitutes. By 1976, when the soldiers had come home, they brought the new strain of gonorrhea with them, and physicians had to find new drugs to treat it. In 1983, a hospital-acquired intestinal infection caused by the bacterium Enterococcus faecium joined the list of bugs that outwit penicillin.
Antibiotic resistance spreads fast. Between 1979 and 1987, for example, only 0.02 percent of pneumococcus strains infecting a large number of patients surveyed by the national Centers for Disease Control and Prevention were penicillin-resistant. CDC's survey included 13 hospitals in 12 states. In 1994, 6.6 percent of pneumococcus strains are resistant, according to a report in the Journal of the American Medical Association by Robert F. Breiman, M.D., and colleagues at CDC. Today, as many as 100,000 people die per year in the United States due to antibiotic-resistant infection. Why has this happened?
"There was complacency in the 1980s. The perception was that we had licked the bacterial infection problem. Drug companies weren't working on new agents. They were concentrating on other areas, such as viral infections," says Michael Blum, M.D., medical officer in the Food and Drug Administration's division of anti-infective drug products. "In the meantime, resistance increased to a number of commonly used antibiotics, possibly related to overuse of antibiotics. Now we've come to a point for certain infections that we don't have agents available."
According to a report in the New England Journal of Medicine, researchers have identified bacteria in patient samples that resist all currently available antibiotic drugs.
The increased prevalence of antibiotic resistance is an outcome of evolution. Any population of organisms, bacteria included, naturally includes variants with unusual traits - in this case, the ability to withstand an antibiotic's attack on a microbe. When a person takes an antibiotic, the drug kills the defenseless bacteria, leaving behind - or "selecting," in biological terms - those that can resist it. These renegade bacteria then multiply, increasing their numbers a millionfold in a day, becoming the predominant microorganism.
The antibiotic does not technically cause the resistance, but allows it to happen by creating a situation where an already existing variant can flourish. "Whenever antibiotics are used, there is selective pressure for resistance to occur. It builds upon itself. More and more organisms develop resistance to more and more drugs," says Joe Cranston, Ph.D., director of the department of drug policy and standards at the American Medical Association in Chicago.
A patient can develop a drug-resistant infection either by contracting a resistant bug to begin with, or by having a resistant microbe emerge in the body once antibiotic treatment begins. Drug-resistant infections increase risk of death, and are often associated with prolonged hospital stays, and sometimes complications. These might necessitate removing part of a ravaged lung, or replacing a damaged heart valve.
Disease-causing microbes thwart antibiotics by interfering with their mechanism of action. For example, penicillin kills bacteria by attaching to their cell walls, then destroying a key part of the wall. The wall falls apart, and the bacterium dies. Resistant microbes, however, either alter their cell walls so penicillin can't bind or produce enzymes that dismantle the antibiotic.
In another scenario, erythromycin attacks ribosomes, structures within a cell that enable it to make proteins. Resistant bacteria have slightly altered ribosomes to which the drug cannot bind. The ribosomal route is also how bacteria become resistant to the antibiotics tetracycline, streptomycin and gentamicin.
Antibiotic resistance results from gene action. Bacteria acquire genes conferring resistance in any of three ways.
1.) In spontaneous DNA mutation, bacterial DNA (genetic material) may mutate (change) spontaneously (indicated by starburst). Drug-resistant tuberculosis arises this way.
2.) In a form of microbial sex called transformation, one bacterium may take up DNA from another bacterium. Pencillin-resistant gonorrhea results from transformation.
3.) Most frightening, however, is resistance acquired from a small circle of DNA called a plasmid, that can flit from one type of bacterium to another. A single plasmid can provide a slew of different resistances. In 1968, 12,500 people in Guatemala died in an epidemic of Shigella diarrhea. The microbe harbored a plasmid carrying resistances to four antibiotics!
Though bacterial antibiotic resistance is a natural phenomenon, societal factors also contribute to the problem. These factors include increased infection transmission, coupled with inappropriate antibiotic use.
More people are contracting infections. Sinusitis among adults is on the rise, as are ear infections in children. A report by CDC's Linda F. McCaig and James M. Hughes, M.D., in the Journal of the American Medical Association tracks antibiotic use in treating common illnesses. The report cites nearly 6 million antibiotic prescriptions for sinusitis in 1985, and nearly 13 million in 1992. Similarly, for middle ear infections, the numbers are 15 million prescriptions in 1985, and 23.6 million in 1992. And they've continued to rise ever since.
Causes for the increase in reported infections are diverse. Some studies correlate the doubling in doctor's office visits for ear infections for preschoolers between 1975 and 1990 to increased use of day-care facilities. Homelessness contributes to the spread of infection. Ironically, advances in modern medicine have made more people predisposed to infection. People on chemotherapy and transplant recipients taking drugs to suppress their immune function are at greater risk of infection.
"There are the number of immunocompromised patients, who wouldn't have survived in earlier times," says Cranston. "Radical procedures produce patients who are in difficult shape in the hospital, and are prone to nosocomial [hospital-acquired] infections. Also, the general aging of patients who live longer, get sicker, and die slower contributes to the problem," he adds.
Though some people clearly need to be treated with antibiotics, many experts are concerned about the inappropriate use of these powerful drugs. "Many consumers have an expectation that when they're ill, antibiotics are the answer. They put pressure on the physician to prescribe them. Most of the time the illness is viral, and antibiotics are not the answer. This large burden of antibiotics is certainly selecting resistant bacteria," says Blum.
Another much-publicized concern is use of antibiotics in livestock, where the drugs are used in well animals to prevent disease, and the animals are later slaughtered for food. "If an animal gets a bacterial infection, growth is slowed and it doesn't put on weight as fast," says Joe Madden, Ph.D., strategic manager of microbiology at FDA's Center for Food Safety and Applied Nutrition. In addition, antibiotics are sometimes administered at low levels in feed for long durations to increase the rate of weight gain and improve the efficiency of converting animal feed to units of animal production.
FDA is investigating whether bacteria resistant to quinolone antibiotics can emerge in food animals and cause disease in humans. Although thorough cooking sharply reduces the likelihood of antibiotic-resistant bacteria surviving in a meat meal to infect a human, it could happen. Pathogens resistant to drugs other than fluoroquinolones have sporadically been reported to survive in a meat meal to infect a human. In 1983, for example, 18 people in four midwestern states developed multi-drug-resistant Salmonella food poisoning after eating beef from cows fed antibiotics. Eleven of the people were hospitalized, and one died.
A study conducted by Alain Cometta, M.D., and his colleagues at the Centre Hospitalier Universitaire Vaudois in Lausanne, Switzerland, and reported in the April 28, 1994, New England Journal of Medicine, showed that increase in antibiotic resistance parallels increase in antibiotic use in humans. They examined a large group of cancer patients given antibiotics called fluoroquinolones to prevent infection. The patients' white blood cell counts were very low as a result of their cancer treatment, leaving them open to infection.
Between 1983 and 1993, the percentage of such patients receiving antibiotics rose from 1.4 to 45. During those years, the researchers isolated Escherichia coli bacteria annually from the patients, and tested the microbes for resistance to five types of fluoroquinolones. Between 1983 and 1990, all 92 E. coli strains tested were easily killed by the antibiotics. But from 1991 to 1993, 11 of 40 tested strains (28 percent) were resistant to all five drugs.
Antibiotic resistance is inevitable, say scientists, but there are measures we can take to slow it. Efforts are under way on several fronts - improving infection control, developing new antibiotics, and using drugs more appropriately.
Barbara E. Murray, M.D., of the University of Texas Medical School at Houston writes in the New England Journal of Medicine that simple improvements in public health measures can go a long way towards preventing infection. Such approaches include more frequent hand washing by health-care workers, quick identification and isolation of patients with drug-resistant infections, and improving sewage systems and water purity in developing nations.
Drug manufacturers are once again becoming interested in developing new antibiotics. These efforts have been spurred both by the appearance of relatively new bacterial illnesses, such as Lyme disease and Legionnaire's disease, and resurgences of old foes, such as tuberculosis, due to drug resistance.
FDA is doing all it can to speed development and availability of new antibiotic drugs. "We can't identify new agents - that's the job of the pharmaceutical industry. But once they have identified a promising new drug for resistant infections, what we can do is to meet with the company very early and help design the development plan and clinical trials," says Blum.
No one really has a good idea of the extent of antibiotic resistance, because it hasn't been monitored in a coordinated fashion. "Each hospital monitors its own resistance, but there is no good national system to test for antibiotic resistance," says Blum.
This may soon change. CDC is encouraging local health officials to track resistance data, and the World Health Organization has initiated a global computer database for physicians to report outbreaks of drug-resistant bacterial infections.
Experts agree that antibiotics should be restricted to patients who can truly benefit from them - that is, people with bacterial infections. Already this is being done in the hospital setting, where the routine use of antibiotics to prevent infection in certain surgical patients is being reexamined.
"We have known since way back in the antibiotic era that these drugs have been used inappropriately in surgical prophylaxis [preventing infections in surgical patients]. But there is more success [in limiting antibiotic use] in hospital settings, where guidelines are established, than in the more typical outpatient settings," says Cranston.
Another problem with antibiotic use is that patients often stop taking the drug too soon, because symptoms improve. However, this merely encourages resistant microbes to proliferate. The infection returns a few weeks later, and this time a different drug must be used to treat it.
Appropriate prescribing also means that physicians use "narrow spectrum" antibiotics - those that target only a few bacterial types - whenever possible, so that resistances can be restricted. There has been a shift to using costlier, broader spectrum agents. This prescribing trend heightens the resistance problem, write McCaig and Hughes, because more diverse bacteria are being exposed to antibiotics.
One way FDA can help physicians choose narrower spectrum antibiotics is to ensure that labeling keeps up with evolving bacterial resistances. Blum hopes that the surveillance information on emerging antibiotic resistances from CDC will enable FDA to require that product labels be updated with the most current surveillance information.
Many of us have come to take antibiotics for granted. A child develops strep throat or an ear infection, and soon a bottle of "pink medicine" makes everything better. An adult suffers a sinus headache, and antibiotic pills quickly control it. But infections can and do still kill. Because of a complex combination of factors, serious infections may be on the rise. While awaiting the next "wonder drug," we must appreciate, and use correctly, the ones that we already have.
Leon Bender is a 68 year old urologist in Los Angeles. Last year, during a South Seas cruise with his wife, Bender noticed something interesting: Passengers who went ashore weren’t allowed to reboard the ship until they had some antibacterial gel squirted on their hands. The crew even dispensed the gel to passengers lined up at the buffet tables. Was it possible, Bender wondered, that a cruise ship was more diligent about killing germs than his own hospital?
Cedars-Sinai Medical Center, where Bender has been practicing for 37 years, is in fact an excellent hospital. But even excellent hospitals often pass along bacterial infections, thereby sickening or even killing the very people they aim to heal. In its 2000 report “To Err Is Human,” the Institute of Medicine estimated that anywhere from 44,000 to 98,000 Americans die each year because of hospital errors - more deaths than from either motor-vehicle crashes or breast cancer - and that one of the leading errors was the spread of bacterial infections.
While it is now well established that germs cause illness, this wasn’t always known to be true. In 1847, the Hungarian physician Ignaz Semmelweis was working in a Viennese maternity hospital with two separate clinics. In one clinic, babies were delivered by physicians; in the other, by midwives. The mortality rate in the doctors’ clinic was nearly triple the rate in the midwives’ clinic. Why the huge discrepancy? The doctors, it turned out, often came to deliveries straight from the autopsy ward, promptly infecting mother and child with whatever germs their most recent cadaver happened to carry. Once Semmelweis had these doctors wash their hands with an antiseptic solution, the mortality rate plummeted.
But Semmelweis’s mandate, as crucial and obvious as it now seems, has proved devilishly hard to enforce. A multitude of medical studies have shown that hospital personnel wash or disinfect their hands in fewer than half the instances they should. And doctors are the worst offenders, more lax than either nurses or aides.
All of this was on Bender’s mind when he got home from his cruise. As a former chief of staff at Cedars-Sinai, he felt inspired to help improve his colleagues’ behavior. Just as important, the Joint Commission on Accreditation of Healthcare Organizations would soon be inspecting Cedars-Sinai, and it simply wouldn’t do for a world-class hospital to get failing marks because its doctors didn’t always wash their hands.
It may seem a mystery why doctors, of all people, practice poor hand hygiene. But as Bender huddled with the hospital’s leadership, they identified a number of reasons. For starters, doctors are very busy. And a sink isn’t always handy — often it is situated far out of a doctor’s work flow or is barricaded by equipment. Many hospitals, including Cedars-Sinai, had already introduced alcohol-based disinfectants like Purell as an alternative to regular hand-washing. But even with Purell dispensers mounted on a wall, the Cedars-Sinai doctors didn’t always use them.
There also seem to be psychological reasons for noncompliance. The first is what might be called a perception deficit. In one Australian medical study, doctors self-reported their hand-washing rate at 73 percent, whereas when these same doctors were observed, their actual rate was a paltry 9 percent. The second psychological reason, according to one Cedars-Sinai doctor, is arrogance. “The ego can kick in after you have been in practice a while,” explains Paul Silka, an emergency-department physician who is also the hospital’s chief of staff. “You say: ‘Hey, I couldn’t be carrying the bad bugs. It’s the other hospital personnel.”’ Furthermore, most of the doctors at Cedars-Sinai are free agents who work for themselves, not for the hospital, and many of them saw the looming Joint Commission review as a nuisance. Their incentives, in other words, were not quite aligned with the hospital’s.
So the hospital needed to devise some kind of incentive scheme that would increase compliance without alienating its doctors. In the beginning, the administrators gently cajoled the doctors with e-mail, faxes and posters. But none of that seemed to work. (The hospital had enlisted a crew of nurses to surreptitiously report on the staff’s hand-washing.) “Then we started a campaign that really took the word to the physicians where they live, which is on the wards,” Silka recalls. “And, most importantly, in the physicians’ parking lot, which in L.A. is a big deal.”
For the next six weeks, Silka and roughly a dozen other senior personnel manned the parking lot entrance, handing out bottles of antibacterial gel to the arriving doctors. They started a Hand Hygiene Safety Posse that roamed the wards and let it be known that this posse preferred using carrots to sticks: rather than searching for doctors who weren’t compliant, they’d try to “catch” a doctor who was washing up, giving him a $10 Starbucks card as reward. You might think that the highest earners in a hospital wouldn’t much care about a $10 incentive - “but none of them turned down the card,” Silka says.
When the nurse spies reported back the latest data, it was clear that the hospital’s efforts were working - but not nearly enough. Compliance had risen to about 80 percent from 65 percent, but the Joint Commission required 90 percent compliance.
These results were delivered to the hospital’s leadership by Rekha Murthy, the hospital’s epidemiologist, during a meeting of the Chief of Staff Advisory Committee. The committee’s roughly 20 members, mostly top doctors, were openly discouraged by Murthy’s report. Then, after they finished their lunch, Murthy handed each of them an agar plate — a sterile petri dish loaded with a spongy layer of agar. “I would love to culture your hand,” she told them.
They pressed their palms into the plates, and Murthy sent them to the lab to be cultured and photographed. The resulting images, Silka says, “were disgusting and striking, with gobs of colonies of bacteria.”
The administration then decided to harness the power of such a disgusting image. One photograph was made into a screen saver that haunted every computer in Cedars-Sinai. Whatever reasons the doctors may have had for not complying in the past, they vanished in the face of such vivid evidence. “With people who have been in practice 25 or 30 or 40 years, it’s hard to change their behavior,” Leon Bender says. “But when you present them with good data, they change their behavior very rapidly.” Some forms of data, of course, are more compelling than others, and in this case an image was worth 1,000 statistical tables. Hand-hygiene compliance shot up to nearly 100 percent and, according to the hospital, it has pretty much remained there ever since.
Cedars-Sinai’s clever application of incentives is certainly encouraging to anyone who opposes the wanton proliferation of bacterial infections. But it also highlights how much effort can be required to solve a simple problem - and, in this case, the problem is but one of many. Craig Feied, a physician and technologist in Washington who is designing a federally financed “hospital of the future,” says that hand hygiene, while important, will never be sufficient to stop the spread of bacteria. That’s why he is working with a technology company that infuses hospital equipment with silver ion particles, which serve as an antimicrobial shield. Microbes can thrive on just about any surface in a hospital room, Feied notes, citing an old National Institutes of Health campaign to promote hand-washing in pediatric wards. The campaign used a stuffed teddy bear, called T- Bear, as a promotional giveaway. Kids and doctors alike apparently loved T- Bear but they weren’t the only ones. When, after a week, a few dozen T- Bears were pulled from the wards to be cultured, every one of them was found to have acquired a host of new friends: Staphylococcus aureus, E. coli, Pseudomonas, Klebsiella, etc ...
Article by: Stephen J. Dubner and Steven D. Levitt authors of “Freakonomics: A Rogue Economist Explores the Hidden Side of Everything.” More information on the research behind this column is at www.freakonomics.com.
Reprint of article by Gloria Chang
British scientists have reported two cases of a "superbug" that thrives on the antibiotics used to kill it.
At St. George's Hospital Medical School in London, two patients, men aged 60 and 64, were treated with the antibiotic Vancomycin after they developed infections from a bacterium called Enteroccoccus faecium. But not only was the bug resistant to its antibiotic, an increasingly common phenomenon around the world, it evolved to become dependent on the Vancomycin, actually needing it to survive!
"What was unusual was that we found the organism had evolved into a Vancomycin-dependent strain," said Ian Eltringham, one of the doctors who reported the cases. "That meant the antibiotic intended to kill it was making it grow. The cure had become the killer."
Enterococcus faecium is normally a harmless bacterium found in the stomaches of most people. But for those with compromised immune systems, the bacterium can cause an infection. Many cases of Vancomycin-resistant enterococcus (VRE) have been reported in hospitals around the world, including Canada, as a result of widespread and overuse of antibiotics.
The first patient developed an infection after undergoing an operation for a ruptured esophagus and other antibiotics got him better. The second patient, admitted one month later, developed his infection after a routine operation and also eventually recovered.
The scientists reported their findings as early as 1996 in the journal Lancet.
They ask, "Have we at last witnessed the emergence of a true superbug?"
When microbes began resisting penicillin, medical researchers fought back with chemical cousins, such as methicillin and oxacillin. By 1953, the antibiotic armamentarium included chloramphenicol, neomycin, terramycin, tetracycline, and cephalosporins. But today, researchers fear that we may be nearing an end to the seemingly endless flow of antimicrobial drugs.
At the center of current concern is the antibiotic Vancomycin, which for many infections is literally the drug of "last resort," says Michael Blum, M.D., medical officer in FDA's division of anti-infective drug products. Some hospital-acquired Staph infections are resistant to all antibiotics except Vancomycin.
Now Vancomycin resistance has turned up in another common hospital bug, Enterococcus. And since bacteria swap resistance genes like teenagers swap T-shirts, it is only a matter of time, many microbiologists believe, until Vancomycin-resistant staph infections appear. "Staph Aureus may pick up Vancomycin resistance from enterococci, which are found in the normal human gut," says Madden. And the speed with which Vancomycin resistance has spread through enterococci has prompted researchers to use the word "crisis" when discussing the possibility of Vancomycin-resistant staph.
Vancomycin-resistant enterococci were first reported in England and France in 1987, and appeared in one New York City hospital in 1989. By 1991, 38 hospitals in the United States reported the bug. By 1993, 14 percent of patients with enterococcus in intensive-care units in some hospitals had Vancomycin-resistant strains, a 20-fold increase from 1987. A frightening report came in 1992, when a British researcher observed a transfer of a Vancomycin-resistant gene from enterococcus to Staph aureus in the laboratory. Alarmed, the researcher immediately destroyed the bacteria.
What type of bacterial evolution will be be fighting next?
Researchers have identified a promising new target in their fight against a dangerous bacterium that sickens people in hospitals, especially people who receive medical implants such as catheters, artificial joints and heart valves.
A substance found on the surface of Staphylococcus Epidermidis has, for the first time, been shown to protect the harmful pathogen from natural human defense mechanisms that would otherwise kill the bacteria, according to scientists at the Rocky Mountain Laboratories (RML), part of the National Institute of Allergy and Infectious Diseases (NIAID) of the National Institutes of Health.
Staph Epidermidis is one of several hard-to-treat infectious agents that can be transmitted to patients in hospitals via contaminated medical implants. The new report concludes that the substance known as Poly-gamma-DL-glutamic acid, or PGA must be present for S. Epidermidis to survive on medical implants. S. Epidermidis infections are rarely fatal but can lead to serious conditions such as sepsis (widespread toxic infection) and endocarditis (inflammation of the lining of the heart and its valves).
Because of the ability of PGA to promote resistance to innate immune defenses, learning more about the protein could lead to new treatments for S. Epidermidis and related Staphylococcal pathogens that also produce PGA, according to the RML scientists. In addition, they also are hoping that similar research under way elsewhere on Bacillus anthracis - the infectious agent of anthrax, which also produces PGA - will complement their work.
The report of the study, led by Michael Otto, Ph.D., appeared in the March edition of The Journal of Clinical Investigation. Collaborators, all scientists at RML in Hamilton, MT, include Stanislava Kocianova, Ph.D.; Cuong Vuong, Ph.D.; Yufeng Yao, Ph.D.; Jovanka Voyich, Ph.D.; Elizabeth Fischer, M.A.; and Frank DeLeo, Ph.D.
"Nosocomial, or hospital-acquired, infections are a worrisome public health problem made worse by the increase in antibiotic resistance," says NIAID Director Anthony S. Fauci, M.D. "This research has initiated a promising new approach that could result in the development of better ways to prevent the spread of many different Staph infections that can be acquired in healthcare settings."
The PGA discoveries came during Dr. Otto's research of how Staphylococcal bacteria biofilms contribute to evading human immune defenses. Biofilms are protective cell-surface structures. Biofilm formation does not depend on PGA, but other research in Dr. Otto's laboratory has indicated that PGA production is greater when a biofilm is present. Further, Dr. Otto says all 74 strains of S. Epidermidis that his group tested also produced PGA, as did six other genetically related Staphylococcus pathogens. "This could be very important to vaccine development because the PGA is present in every strain of the organism," Dr. Otto says. "If a vaccine can be developed to negate the effect of the PGA, it could be highly successful against all pathogens in which PGA is a basis for disease development, such as Staph and anthrax."
The group used genetic and biochemical analyses to show that PGA is produced in S. Epidermidis. They then used three S. Epidermidis strain - one natural, one altered to eliminate PGA production and one altered to produce excess PGA--to show that PGA protects S. Epidermidis from innate immune defense, human antibiotic compounds and salt concentrations similar to levels found on human skin. Dr. Otto's group also used mice fitted with catheters to demonstrate that the S. Epidermidis strain deficient of PGA was not able to cause infection while the other strains containing PGA did.
NIAID is a component of the National Institutes of Health, an agency of the U.S. Department of Health and Human Services. NIAID supports basic and applied research to prevent, diagnose and treat infectious diseases such as HIV/AIDS and other sexually transmitted infections, influenza, tuberculosis, malaria and illness from potential agents of bioterrorism. NIAID also supports research on transplantation and immune-related illnesses, including autoimmune disorders, asthma and allergies.
Staph Epidermidis is capable of clinging to tubing (as in that used for intravenous feeding, etc.), prosthetic devices, and other non-living surfaces, S. Epidermidis is the organism that most often contaminates devices that provide direct access to the bloodstream. The primary cause of bacteremia in hospital patients, this strain of Staph is most likely to infect those, whose immune systems have been compromised for any reason, and high-risk newborns receiving intravenous supplements.
S. Epidermidis also accounts for two of every five cases of prosthetic valve endocarditis. Prosthetic valve endocarditis is endocarditis as a complication of the implantation of an artificial valve in the heart. Although contamination usually occurs during surgery, symptoms of infection may not become evident until a year after the operation. More than half of the patients who develop prosthetic valve endocarditis die.
Staphylococcus Epidermidis, which is a common bacteria in the nipple ducts, is thought by some doctors to cause a subclinical infection and perhaps cause capsule contracture.
When the patient has few clinical signs except severe pain it suggests that the bacteria may be pseudomonas. This bacteria seems to irritate nerve endings more than other germs. Another rare infection is caused by mycobacterium fortuitum. This causes inflammation around the implant but no symptoms in other parts of the body. Patients do notusually have a raised temperature but about one in three have drainage from the surgical site.
Staph Epidermidis is a common member of the normal florae of skin and mucous membranes. Its large numbers and ubiquitous distribution make it one of the most commonly isolated organisms in the clinical laboratory. While at one time the appearance of S. Epidermidis in clinical material could be dismissed as contamination, it is now one of the most important agents of hospital acquired infections. Immunosuppressed or neutropenic patients are particularly at risk, as are individuals with indwelling catheters or prosthetic devices. It can also cause endocarditis in individuals with previous heart valve damage. The hydrophobic nature of the organism's cell surface facilitates its adherence to synthetic devices as well as damaged heart valves. Following initial colonization, a copious amount of extracellular polysaccharide or slime is synthesized, forming a protective biofilm around the colony. Because many isolates are multiply antibiotic resistant, these infections are very serious and can even be fatal.
Interestingly, Staph Epidermidis is normally resident in the skin flora, the gut and upper respiratory tract. It is a true opportunistic pathogen, requiring a major breach in the host's infection to establish infection, and invariably is hospital acquired. It is associated with skin penetration by implanted prostheses, for example Spitz Holter valves used to treat hydrocephalus, prosthetic heart valves, IV lines, intraperitoneal catheters and orthopaedic prostheses. It is a major cause of bacteraemia in neutropenics and in all infections there is a risk of endocarditis. It is also a serious neonatal infection, particularly in very low birth weight infants.
Staph Epidermidis produces some toxins but their significance is unknown. Adherence to a foreign surface is facilitated by the production of a viscous extracellular (proteoglycans) slime. Staph Epidermidis is coagulase negative.
This is a review of the biological properties of Staphylococcus Epidermidis describing its ability to colonise polymers and to form biofilms thus leading to chronicity of infection. It is known that capsular contraction after silicone breast implantation may be caused by chronic infection and the review supports the IRG's concern that low grade infection with an organism such as Staph Epidermidis could cause chronic ill health in some women who have had a breast implant.
Staphylococci are common causes of infections associated with indwelling medical devices. These are difficult to treat with antibiotics alone and often require removal of the device. Some strains that infect hospitalized patients are resistant to most of the antibiotics used to treat infections, Vancomycin being the only remaining drug to which resistance has not developed.
By Amanda Gardner, HealthDay Reporter
WEDNESDAY, Aug. 16, 2006
In Emergency Rooms across the United States, a tough-to-treat Staphylococcus bug is now the leading cause of skin and soft-tissue infections, a new study finds. Methicillin-Resistant Staphylococcus Aureus (MRSA) is resistant to many standard antibiotics that have been used for years, but it can still be effectively treated with one of several antibiotics, experts say.
"MRSA is now the most common cause of skin infections in most of the big U.S. cities," said researcher Dr. Gregory Moran, a Professor of Medicine at the University of California, Los Angeles, David Geffen School of Medicine. "When doctors are deciding if a patient needs antibiotics, they should be given them antibiotics that cover MRSA. That's a change from things we've been doing for a decade. This has changed. A different type of bacteria is now the most common cause of infections." The study is published in the Aug. 17 issue of the New England Journal of Medicine.
In the same issue of the journal, another study found that the antibiotic daptomycin is effective for treating bloodstream and heart infections caused by Staphylococcus Aureus bacteria. Based on this trial, the U.S. Food and Drug Administration has already approved the drug for use in these cases. Daptomycin has previously been approved for treating skin infections caused by S. Aureus.
MRSA was, for a long time, limited to hospitals, nursing homes and other health care facilities. "It began to change several years ago," said Dr. Pascal James Imperato, distinguished service Professor and Chairman of the Department of Preventive Medicine and Community Health, at SUNY (State University of New York) Downstate Medical Center in New York City. "We began to see it in people in the community who were not in hospitals."
The bacteria live uneventfully in the nose of many people but sometimes lead to serious infection. Symptoms can range from something as benign as an infected paper cut, to bloodstream infections, to infections of heart valves that can be fatal.
Community-associated MRSA most often appears on the skin as a boil or pimple that may be swollen, red and painful, and have a discharge.
Moran and his colleagues cultured skin or soft-tissue infections from 422 patients at emergency rooms in 11 cities across the United States. Of those 422 patients, 59 percent had MRSA. The prevalence of MRSA ranged from 15 percent to 74 percent, depending on the city. One genetic type (USA300) accounted for 97 percent of the samples, and 74 percent were a single strain (USA300-0114).
"We weren't surprised that it was the most common bug overall," Moran said. "But we didn't know how uniform it was going to be, and all across the U.S., it was remarkably similar. There's something about this particular strain [USA300] that gives it some survival advantage over other types." Almost all (98 percent) of the isolates had two toxins that make the germ more aggressive.
When tested, 95 percent of the MRSA samples could be treated with the antibiotic Clindamycin, 6 percent with Erythromycin, 60 percent with Fluoroquinolones, 100 percent with Rifampin and Trimethoprim-sulfamethoxazole, and 92 percent with Tetracycline. But in 57 percent of cases, doctors had prescribed an antibiotic to which the bacteria were already resistant.
In the second trial, Daptomycin was about as effective as standard therapy in treating patients. This trial was sponsored by Cubist Pharmaceuticals, which makes Daptomycin. "Daptomycin is an IV drug, so that's something that we would use for more serious infections that would need to be in the hospital," said Moran, who was not involved in this study. The infections studied were also not as uniform as the ones identified in the first study.
There are already several effective drugs for the type of skin and soft-tissue infections Moran studied. "Many of the drugs active against community strains of MRSA are older antibiotics that have been around for a long time," Moran said. "We don't really need to go with big, new, expensive antibiotics."
"Most infections occurring in the community are relatively mild and frequently resolve with very simple measures," Imperato added. People can prevent infections by not sharing towels, razors or other common items, and by washing hands with soap and water, experts say.
SOURCES: Gregory J. Moran M.D., Olive View-UCLA Medical Center, Sylmar, Calif., and professor, medicine, David Geffen School of Medicine, University of California, Los Angeles; Pascal James Imperato, M.D., distinguished service professor and chairman, department of preventive medicine and community health and director, master of public health program, State University of New York Downstate Medical Center, New York City; Aug. 17, 2006, New England Journal of Medicine
By Brandon Keim, Oct, 11, 2006
(Note: This is not an endorsement,)
When Jennifer Eddy first saw an ulcer on the left foot of her patient, an elderly diabetic man, it was pink and quarter-sized. Fourteen months later, drug-resistant bacteria had made it an unrecognizable black mess. Doctors tried everything they knew -- and failed. After five hospitalizations, four surgeries and regimens of antibiotics, the man had lost two toes. Doctors wanted to remove his entire foot. "He preferred death to amputation, and everybody agreed he was going to die if he didn't get an amputation," said Eddy, a professor at the University of Wisconsin School of Medicine and Public Health.
With standard techniques exhausted, Eddy turned to a treatment used by ancient Sumerian physicians, touted in the Talmud and praised by Hippocrates: honey. Eddy dressed the wounds in honey-soaked gauze. In just two weeks, her patient's ulcers started to heal. Pink flesh replaced black. A year later, he could walk again.
"I've used honey in a dozen cases since then," said Eddy. "I've yet to have one that didn't improve." Eddy is one of many doctors to recently rediscover honey as medicine. Abandoned with the advent of antibiotics in the 1940s and subsequently disregarded as folk quackery, a growing set of clinical literature and dozens of glowing anecdotes now recommend it.
Most tantalizingly, honey seems capable of combating the growing scourge of drug-resistant wound infections, including group A streptococcus - the infamous flesh-eating bug - and Methicillin-Resistant Staphylococcus Aureus, or MRSA, which in its most severe forms also destroys flesh. These have become alarmingly more common in recent years, with MRSA alone now responsible for half of all skin infections treated in U.S. emergency rooms. So-called superbugs cause thousands of deaths and disfigurements every year, and public health officials are alarmed.
Though the practice is uncommon in the United States, honey is successfully used elsewhere on wounds and burns that are unresponsive to other treatments. Some of the most promising results come from Germany's Bonn University Children's Hospital, where doctors have used honey to treat wounds in 50 children whose normal healing processes were weakened by chemotherapy.
The children, said pediatric oncologist Arne Simon, fared consistently better than those with the usual applications of iodine, antibiotics and silver-coated dressings. The only adverse effects were pain in 2 percent of the children and one incidence of eczema. These risks, he said, compare favorably to iodine's possible thyroid effects and the unknowns of silver - and honey is also cheaper.
"We're dealing with chronic wounds, and every intervention which heals a chronic wound is cost effective, because most of those patients have medical histories of months or years," he said.
While Eddy bought honey at a supermarket, Simon used Medihoney, one of several varieties made from species of Leptospermum flowers found in New Zealand and Australia.
Honey, formed when bees swallow, digest and regurgitate nectar, contains approximately 600 compounds, depending on the type of flower and bee. Leptospermum honeys are renowned for their efficacy and dominate the commercial market, though scientists aren't totally sure why they work.
"All honey is antibacterial, because the bees add an enzyme that makes hydrogen peroxide," said Peter Molan, director of the Honey Research Unit at the University of Waikato in New Zealand. "But we still haven't managed to identify the active components. All we know is (the honey) works on an extremely broad spectrum."
Attempts in the lab to induce a bacterial resistance to honey have failed, Molan and Simon said. Honey's complex attack, they said, might make adaptation impossible.
Two dozen German hospitals are experimenting with medical honeys, which are also used in the United Kingdom, Australia and New Zealand. In the United States, however, honey as an antibiotic is nearly unknown. American doctors remain skeptical because studies on honey come from abroad and some are imperfectly designed, Molan said.
In a review published this year, Molan collected positive results from more than 20 studies involving 2,000 people. Supported by extensive animal research, he said, the evidence should sway the medical community - especially when faced by drug-resistant bacteria. "In some, antibiotics won't work at all," he said. "People are dying from these infections."
Commercial medical honeys are available online in the United States, and one company has applied for Food and Drug Administration approval. In the meantime, more complete clinical research is imminent. The German hospitals are documenting their cases in a database built by Simon's team in Bonn, while Eddy is conducting the first double-blind study.
"The more we keep giving antibiotics, the more we breed these superbugs. Wounds end up being repositories for them," Eddy said. "By eradicating them, honey could do a great job for society and to improve public health."
Vancomycin is indicated for the treatment of serious, life-threatening infections by Gram-positive bacteria which are unresponsive to other less toxic antibiotics.
The increasing emergence of Vancomycin-resistant enterococci has resulted in the development of guidelines for use by the Centers for Disease Control (CDC) Hospital Infection Control Practices Advisory Committee.
Common adverse drug reactions (≥1% of patients) associated with IV vancomycin include: local pain, which may be severe and/or thrombophlebitis. Nephrotoxicity is an infrequent adverse effect (0.1–1% of patients). Rare adverse effects (<0.1% of patients) include: anaphylaxis, toxic epidermal necrolysis, erythema multiforme, red man syndrome (see below), superinfection, thrombocytopenia, neutropenia, leucopenia, tinnitus, dizziness and/or ototoxicity (see below).
Vancomycin needs to be given intravenously (IV) for systemic therapy since it does not cross through the intestinal lining. It is a large hydrophilic molecule which partitions poorly across the gastrointestinal mucosa. The only indication for oral vancomycin therapy is in the treatment of pseudomembranous colitis, where it must be given orally to reach the site of infection in the colon.
Vancomycin must be administered in a dilute solution slowly, over at least 60 minutes (maximum rate of 10 mg/minute for doses >500 mg). This is due to the high incidence of pain and thrombophlebitis and to avoid an infusion reaction known as the "Red man syndrome" or "Red neck syndrome". This syndrome, usually appearing within 4–10 minutes after the commencement or soon after the completion of an infusion, is characterised by flushing and/or and an erythematous rash that affects the face, neck and upper torso. Less frequently, hypotension and angioedema may also occur. Symptoms may be treated with antihistamines, including diphenhydramine.
Vancomycin activity is considered to be time-dependent – that is, antimicrobial activity depends on the duration that the drug level exceeds the minimum inhibitory concentration (MIC) of the target organism. Thus, peak levels have not been shown to correlate with efficacy or toxicity – indeed concentration monitoring is unnecessary in most cases. Circumstances where therapeutic drug monitoring (TDM) is warranted include: Patients receiving concomitant aminoglycoside therapy, patients with (potentially) altered pharmacokinetic parameters, patients on haemodialysis, during high dose or prolonged treatment, and patients with impaired renal function. In such cases, trough concentrations are measured.
Vancomycin has traditionally been considered a nephrotoxic and ototoxic drug, based on observations by early investigators of elevated serum levels in renally impaired patients who had experienced ototoxicity, and subsequently through case reports in the medical literature. However, as the use of vancomycin increased with the spread of MRSA beginning in the seventies, it was recognized that the previously reported rates of toxicity were not being observed. This was attributed to the removal of the impurities present in the earlier formulation of the drug, although those impurities were not specifically tested for toxicity.
Subsequent reviews of accumulated case reports of Vancomycin-related nephrotoxicity found that many of the patients had also received other known nephrotoxins, particularly aminoglycosides. Most of the rest had other confounding factors, or insufficient data regarding the possibility of such, that prohibited the clear association of vancomycin with the observed renal dysfunction.
In 1994, Cantu and colleagues found that the use of vancomycin monotherapy was clearly documented in only three of 82 available cases in the literature. Prospective and retrospective studies attempting to evaluate the incidence of Vancomycin-related nephrotoxicity have largely been methodologically flawed and have produced variable results. The most methodologically sound investigations indicate that the actual incidence of vancomycin-induced nephrotoxicity is around 5–7%. To put this into context, similar rates of renal dysfunction have been reported for cefamandole and benzylpenicillin, two reputedly non-nephrotoxic antibiotics.
Additionally, evidence to relate nephrotoxicity to Vancomycin serum levels is inconsistent. Nephrotoxicity has also been observed with concentrations within the "therapeutic" range as well. Essentially, the reputation of vancomycin as a nephrotoxin is over-stated, and it has not been demonstrated that maintaining vancomycin serum levels within certain ranges will prevent its nephrotoxic effects, when they do occur.
Attempts to establish rates of Vancomycin-induced ototoxicity are even more difficult due to the scarcity of quality evidence. The current consensus is that clearly related cases of vancomycin ototoxicity are rare. The association between Vancomycin serum levels and ototoxicity is also uncertain. While cases of ototoxicity have been reported in patients whose Vancomycin serum level exceeded 80 µg/mL, cases have been reported in patients with therapeutic levels as well. Thus, it also remains unproven that therapeutic drug monitoring of vancomycin for the purpose of maintaining "therapeutic" levels will prevent ototoxicity.
Another area of controversy and uncertainty concerns the question of whether, and if so, to what extent, Vancomycin increases the toxicity of other nephrotoxins. Clinical studies have yielded variable results, but animal models indicate that there probably is some increased nephrotoxic effect when Vancomycin is added to nephrotoxins such as aminoglycosides. However, a dose or serum level-effect relationship has not been established.
Microbial resistance to Vancomycin is a growing problem, particularly within health care facilities such as hospitals. With Vancomycin being the last-line antibiotic for serious Gram-positive infections there is the growing prospect that resistance will result in a return to the days when fatal bacterial infections were common. Vancomycin-resistant enterococci (VRE) emerged in 1987. Vancomycin-resistance emerged in more common pathogenic organisms during the 1990s and 2000s, including Vancomycin-intermediate Staphylococcus aureus (VISA), Vancomycin-resistant Staphylococcus aureus (VRSA), and Vancomycin-resistant Clostridium difficile. There is some suspicion that agricultural use of avoparcin, another similar glycopeptide antibiotic, has contributed to the emergence of Vancomycin-resistant organisms.
From the BBC, November 19, 2006:
A hand-held probe could cut the number of patients who develop infections following operations. The device can predict, as little as 12 hours after surgery, whether a wound is likely to become infected. The results could help doctors and nurses act quickly to prevent infections in the most vulnerable patients.
Details of the University Hospital of North Durham breakthrough feature in the British Journal of Surgery. To be able to identify those patients most at risk of infection at just 12 hours after surgery gives you the opportunity to actually do something about it. Surgical wound infections, including those caused by MRSA, are a significant cause of problems for patients trying to recover from major operations. Contamination of the wound with bacteria is one obvious cause for this, and there are strict hygiene procedures in place to try to minimise the risk of this in operating theatres and on wards.
However, some patients have a far higher risk of developing an infection. This is because not enough oxygen-rich blood is reaching their wound. This not only slows down healing, offering more time for an infection to take hold, but the lack of oxygen also hampers the body's immune system as it tackles harmful bacteria.
The new approach works on a simple principle - blood cells carrying oxygen are bright red, while blood cells which have no oxygen are purple in colour. The Durham team used a handheld device which bounces infra-red light into the skin around the wound. The signal that reflects back is different depending on the colour of blood cells in the wound.
The study looked at 59 patients recovering from abdominal surgery, who were scanned at 12, 24 and 48 hours after their operation, then examined a week later to check for signs of infection. In all, 17 patients developed an infection in their wound, and scans from these patients had suggested significantly lower levels of oxygen in the tissue surrounding the wound.
Lead researcher Dr David Harrison said it could make a real difference to patients. He said: "The beauty of this device is that there is no need to even remove the transparent film that is placed across the wound after surgery - it's completely non-invasive. Dr Andrew Berrington, a consultant microbiologist, said: "It sounds very promising, and is certainly a potentially useful development in infection control."
"The main questions are does it really predict infection with a high degree of accuracy, and if so does this translate into a genuine clinical benefit?" The technique is now to be the subject of a much larger clinical trial in the US after a major biotechnology firm found out about the Durham team's results.