by Wendy Orent DISCOVER MAGAZINE
From the July-August special issue, published online July 17, 2009
For 300 years, scientists thought of bacteria as individual killers, like a bunch of piranhas. Recently, we've found that's almost entirely wrong.
Perhaps you notice it after a visit to the dentist.You pass your tongue across the front of your teeth and they feel slick and squeaky-clean. Four hours later, although you might not yet be able to tell the difference, the beginning of a rough fuzz is growing. These are streptococci, the first bacterial settlers in the film that saliva deposits on your teeth. Another four hours and the bridge germs, the fusobacteria, have climbed on board. They are the ones that make it possible for the really bad actors, like Porphyromonas gingivalis, to grab on and start building colonies.
By the next morning, if you still have not brushed your teeth, a definite fuzzy scum is starting to form. If you could look at that fuzz under a microscope without disturbing its structure, you would see towers or entire communities of bacteria, each building upon others. Some of those microbes are dangerous indeed. P. gingivalis not only grows in the pockets of your gums, helping to loosen your teeth from your jaws, but also causes the release of inflammatory chemicals that get into your circulation, complicating diabetes treatment and possibly increasing the risk of heart disease. Traces of the germ have also been found in arterial plaque.
If you have ever been admitted to a hospital, it is very likely you have experienced another, related kind of scary bacterial growth—and in this case you almost certainly did not notice it. Hospitalized patients are routinely hooked up to urinary catheters that enable doctors and nurses to measure urine flow (not incidentally, the catheters also liberate health-care workers from having to take patients to the bathroom). Swiftly coated by a conditioning film made of proteins in the urine, the catheters are then inexorably covered by layers of interacting bacteria, which alter the chemistry of their surface and can cause crystals to form. Within a week, an infection is growing on the catheters of 10 percent to 50 percent of catheterized patients. Within a month the infection has reached virtually everyone.
These slimy bacterial colonies, known as biofilms, add a remarkable new dimension to our understanding of the microbial world. Ever since Louis Pasteur first grew bacteria in flasks, biologists have pictured bacteria as individual invaders floating or swimming in a liquid sea, moving through our blood and lymph like a school of piranhas down the Amazon.
But in recent years, scientists have come to understand that much, and perhaps most, of bacterial life is collective: 99 percent of bacteria live in biofilms. They vary widely in behavior. Sometimes these collectives are fixed, like a cluster of barnacles on a ship’s hull; other times they move, or swarm, like miniature slime molds. Bacteria may segregate into single-species biofilms, or they may, as in the case of dental bacteria, join together in groups that function like miniature ecological communities, competing and cooperating with each other.
The unifying factor in all these biofilms—the thing that makes them so strange and wonderful and dangerous—is that their cooperation is, in a sense, verbal. Using streams of chemicals that they pump outside their cell walls and membranes, they “talk” incessantly, among their own clones and species and even to unrelated bacteria dwelling nearby. Understanding that chatter could be vital for gaining the upper hand in the endless battle against infectious disease.
Biofilms were first discovered in 1978 in the clear waters of a frigid mountain stream in British Columbia. Microbiologist William Costerton, now of Allegheny General Hospital in Pittsburgh, and his team of scientists wondered why there were so few bacteria in the water, while billions upon billions of the germs nestled in the crevices of the streambed’s rocks. “We were finding 9 bacteria per milliliter in the water, but there must have been 100 million in a square centimeter when we took a rock out of a stream and brought it down to the lab,” Costerton says.
The bacteria were not just sitting idly on the rocks, he found. They were forming complicated structures, cities of germs encased in a slippery substance the bacteria exude called an exopolysaccharide matrix. This slime protects them from grazing amoebas and provides them with food that is excreted by bacteria within the biofilm or even bits of DNA released when other germs die.
When Costerton published his results, he coined the term biofilm and introduced a whole new understanding of how bacteria behave. “We reasoned one stubborn fact,” he recalls. “Bacteria have no idea of where they are. They are just programmed to do their thing.” In other words, they are always going to form biofilms —whether they are living on a rock or in the human body.
Two years later Tom Marrie, a young doctor working in Halifax, Nova Scotia, examined a feverish homeless man who had wandered off the street and into his emergency room.
The man had a raging staph infection and, on his chest, a lump the size and shape of a cigarette pack. It was an infected pacemaker, Marrie reasoned. For three weeks the man was given huge doses of antibiotics but did not get better, so Marrie and his team decided to operate. They invited Costerton to sit in. “If there were ever going to be a biofilm infection in a human being, it was going to be on the end of that pacemaker,” Costerton says. “We took out the pacemaker and there was our first medical biofilm. It was a great big thick layer of bacteria and slime, just caked on.”
Biofilms on implants are now recognized as a serious and growing health problem. Bacterial infections hit 2 percent to 4 percent of all implants. Of the 2 million hip and knee replacements performed worldwide each year, 40,000 become infected. More than a third of these infections lead to amputation, and not with very successful results: Most of those people die. “Implant operations have a 98 percent success rate, so people don’t want to talk about the infections,” Costerton says. “They’re a bit of a disgrace, really.”
Biofilm infections are not limited to implants. They can be found in the bodies of the young and the healthy. Many children suffer from undiagnosed biofilm infections in their ears, which require months of oral antibiotic therapy while the underlying infection smolders untouched. Millions of others live with chronic biofilms: urinary tract infections in women that last for years; prostatitis that no antibiotics permanently cure; bone infections (osteomyelitis) that cripple and immobilize people for the rest of their lives. Each year roughly 500,000 people in the United States die of biofilm-associated infections, nearly as many as those who die of cancer.
As Marrie’s experience shows, biofilms repel antibiotics, although scientists do not fully understand how. Some drugs cannot fully penetrate the biofilm’s protective matrix. In other cases, even though most of the germs die, enough remain alive to regroup and develop another biofilm. The matrix also keeps its resident germs under cover, hiding the chemical receptors on the bacteria so that drugs cannot latch onto them and kill the germs.
The study of this newly discovered behavior is rooted in the basic and ancient biology of bacteria. Geneticist Bonnie Bassler of Princeton University thinks group-living bacteria may give us a window onto the origins of multicellular life. “Bacteria grow best when each one does its own thing…together,” she says. “Bacteriologists had it wrong for the past 300 years—bacteria don’t live alone.”
As these social bacteria talk to each other, we can now listen in. Bassler and other scientists are learning how to eavesdrop on the chemical language of bacteria, seeking ways to scramble or block those messages. Disrupting the formation of films could be a powerful way to neutralize harmful infections.
Originally trained as a biochemist at Johns Hopkins University, the blue-eyed, athletic Bassler walked into a lecture hall on a whim in the late 1980s to listen to a talk by geneticist Michael Silverman of the Agouron Institute in La Jolla, California. It was one of only a handful of talks that the notoriously reserved Silverman had given in 10 years. Bassler was riveted by what she heard. Silverman talked about how bacteria make light inside the inch-long luminescent squid that live in the shallow waters off the Hawaiian coast.
Infant squid cannot glow until they excrete a mucuslike net to entrap the ubiquitous luminescent bacteria floating in the water. The squid draw captured bacteria into their “light pouches,” where the bacteria are bathed in nutrients —a diet richer than what they can find outside in the sea. In return, the bacteria (Vibrio fischeri, a close relative of the cholera germ) produce a dim blue-green light that is directed downward through small reflective organs in the squid to shine into the water below. When the squid swim at the ocean surface at night, hunting for shrimp, they are invisible to predators below because they look like moonlight on the water. Both squid and bacteria benefit. “The host wants the light, the bacteria get fed,” Bassler says.
The glow of V. fischeri provides an instructive glimpse into the communal behavior of bacteria. Autoinducers (chemical signaling molecules that produce more of themselves inside the cell) control the switch that turns the light genes off and on. Each bacterium secretes a bit of this light-evoking substance into the environment. When a crowd of bacteria and their autoinducers become dense enough, the lights in all the bacteria switch on at once. “This counting of heads is called quorum sensing,” Bassler explains. More broadly, this is how bacteria coordinate their actions in large groups: When the local concentration of autoinducers gets high enough, the bacteria know a crowd is present, and they flip over from solitary mode to group behavior.
The autoinducer molecule that triggers bacterial glow is made by a protein called LuxI, which has a very focused effect. “The molecule that the LuxI protein makes is acylated homoserine lactone, or AHL,” Bassler says. “Each LuxI protein and the molecule it produces is species-specific. There are two kinds of bacteria, and each talks in a different language. Gram-negative bacteria [which have a thin cell wall surrounded by an outer membrane] use the AHLs as autoinducers, while gram-positives [which have a thick cell wall] use peptides. This is a very ancient split.” When the V. fischeri make enough AHL autoinducer—called AI-1 for short—the cells wink on. But that is far from the only autoinducer.
Working with a related bacterium, Vibrio harveyi, in the early 1990s, Bassler discovered another kind of chemical signal that a wide range of bacteria emit. In many species this chemical, called autoinducer 2 (AI-2) has properties of a waste product, says molecular biologist Stephen Winans of Cornell University. AI-2 is the by-product of a complex process of metabolism in these species. Not all bacteria create AI-2, however. According to Winans, eons ago one line of early bacteria began to break down waste products along a pathway leading to the excretion of AI-2; another line did not. The latter are the bacteria that eventually gave rise to eukaryotic organisms, including humans. “That’s why you don’t excrete ?AI-2,” Winans says.
But Bassler found that AI-2 is much more than a waste product. “This little leftover molecule,” she says, got pressed into service as another bacterial language, one that can carry messages between different kinds of germs. Most forms of quorum sensing, including V. fischeri’s luminescence circuit, act as a private language—that is, each germ speaks only to others of its own kind. But AI-2 is a kind of bacterial Esperanto, Bassler determined. After she and her team purified the small AI-2 molecule and its protein receptor, they were able to show that the two form a lock-and-key structure, the telltale sign of a chemical signaling mechanism.
The big question was, what are different germs saying when they talk to each other? Bassler says that in some instances—such as in dental biofilms, in which some 600 species may be growing at a time—AI-2 is necessary for collective or cooperative behavior. First, though, the bacteria must be right next to each other to receive the signal, especially in a dynamic system like the mouth, where saliva is constantly washing across the teeth. The earliest colonists on freshly cleaned teeth, the streptococci, produce only low levels of AI-2; the fusobacteria produce moderate levels. The appallingly destructive germs love a very high level of AI-2, which sends them into overdrive. “They grow like gangbusters,” says Paul Kolenbrander of the National Institute of Dental and Craniofacial Research of the National Institutes of Health.
Quorum-sensing molecules also play an important part in bacterial virulence, or deadliness. If a lethal germ released toxic chemicals immediately after entering the host’s body, the immune system would quickly sense the toxin and go after the invader. So it pays for bacteria to wait, stealthily multiplying until the unwitting host is full of them. Then they can release their toxins all at once, overwhelming immunity and sickening or killing the host.
In their more recent work, Bassler and her colleagues are searching for ways to scramble the quorum-sensing signals of cholera germs. The researchers have demonstrated that in test tubes a particular chemical, called CAI-1, can induce deadly cholera cells to turn off their virulence genes.
Building on our understanding of how germs communicate, Naomi Balaban, a molecular biologist at Tufts University, has spent 17 years studying Staphylococcus aureus, a strain of bacterium that is the main cause of hospital-acquired infections.
Antibiotic-resistant forms of S. aureus, known collectively as methicillin-resistant Staphylococcus aureus, or MRSA, have spread widely in hospitals throughout the world, forming long chains of infection. There are 19,000 MRSA-associated deaths in the United States alone each year.
Other forms of MRSA have begun to spread outside of hospitals; one strain, known as USA300, is especially deadly. It has infected and killed children and athletes, and no one knows where it came from or exactly how it spreads, though athletic locker rooms have been implicated in some cases. Like other forms of staph, USA300 can form invisible biofilms outside the body, making it almost impossible to eradicate. It is difficult to judge the actual prevalence of MRSA, since many staph infections do not get much more serious than a small pimple.
Some cases do progress, though, and they may cause debilitating and almost untreatable soft-tissue infections like cellulitis and folliculitis, pneumonia, and often-fatal heart infections, or endocarditis. Another form of staph, Staphylococcus epidermidis, grows commonly in sheets of invisible biofilm on our skin, where it is normally benign. But if it is introduced into the body during a medical procedure—especially if a joint implant, catheter, or pacemaker is contaminated during insertion—both S. epidermidis and S. aureus can form dangerous biofilms that often cannot be treated without removal of the infected implant.
Balaban has discovered that all forms of staph, whether in a free-floating state or in a biofilm, have a complex form of chemical communication that can activate the agr (accessory gene regulator) system, producing a number of toxins. Somewhat controversially, Balaban also claims to have discovered another system that controls the agr system. The second system involves two proteins known as RNAIII activating protein (RAP) and TRAP, which Balaban calls “the most beautiful protein in the world.” TRAP is RAP’s target protein, Balaban says. It is found both on and within the staph cell. S. aureus secretes RAP into the environment, where the chemical collects and binds to the TRAP molecules on the cells.
When enough RAP molecules adhere to enough target molecules, staph bacteria switch on their cell-to-cell communication and stress-response systems and begin producing the toxin that makes them so lethal. S. aureus bacteria, depending on their strain, can produce 40 or more different toxins. The toxins break down the cells in the host—which could very well be you—in order to release nutrients to the germs. That is why staph infections can be so destructive. When there are enough staph germs present, the host’s immune system is overwhelmed, and tissues are destroyed at a frightening rate, leading sometimes to shock and death.
Balaban reasoned that if she could find a way to block RAP from reaching its target molecule, she could break down the signaling system that allows the release of staph’s devastating toxins. She discovered a chemical she calls RIP (RNAIII inhibiting peptide), which blocks RAP from linking to its target. It is as if an outfielder were standing ready to catch a fly ball heading his way, but he already has a grapefruit in his mitt, preventing the ball from going in. If RAP does not reach its target molecule, the whole communication process breaks down, toxins do not get made, and human immune cells converge on the now-helpless staph germs, ready to mop them up. Balaban claims that RIP can have this effect on free-floating and biofilm-embedded staph alike.
Bacteriologists had it wrong for the past 300 years—bacteria don’t live ?alone. They grow best when each one does its own thing...together.
Some researchers remain unpersuaded by Balaban’s work, however. Richard Novick of the NYU Langone Medical Center, a well-respected staph expert who was also Balaban’s postdoctoral adviser, insists that the TRAP protein does not have any known role in staph biology. In a series of letters to the journal The Scientist, he argues that only one quorum-sensing system has been discovered in Staphylococcus: the agr system. Neither Novick nor any other scientist has been able to reproduce Balaban’s RAP/TRAP experiments in the laboratory. Novick does acknowledge, though, that RIP works. “I don’t question that it has activity.
But whatever it’s doing, it’s not inhibiting agr,” he says. “I would guess it could work by interfering with assembly of a biofilm. It should not have any effect on planktonic Staphylococcus. If it did, I would have to revise my view.”
Despite these questions, RIP—which Balaban discovered in Novick’s laboratory—is in the first stages of preclinical testing as a new kind of antibiotic. It costs millions of dollars to develop drugs and get them tested in animals before they can ever be used in clinical trials for safety and efficacy in humans. Fortunately, Balaban has found a naturally occurring chemical equivalent to RIP: hamamelitannin, an extract of witch hazel bark. She has shown that this old-fashioned household remedy, long used by Native Americans, also serves to knock the ball from the outfielder’s mitt. In her tests, hamamelitannin has the same chemical effect as synthetically produced RIP.
by Wendy Orent DISCOVER MAGAZINE
by Peggy Macdonald
Walt Disney World Recreation Examiner
July 16, 2009
Swine flu has not prevented guests from visiting Walt Disney World.
Walt Disney World had another brush with swine flu (H1N1) last week after a group of Mississippi tourists who had stayed at Disney's Pop Century Hotel were treated at Florida Hospital in Celebration, FL. The Mississippi group's chartered bus was en route to Mississippi when 12 to 14 members of the group began to experience flulike symptoms, according to the Orlando Sentinel.
Although one member of the tour group informed the Orlando Sentinel that at least one case of swine flu was confirmed, the test for the H1N1 virus takes several days, and it is unlikely that the hospital could have received results of the test so quickly.
Guests who visit the Walt Disney World resort come into frequent contact with other guests and surfaces that tens of thousands of guests touch each day. The moment a guest enters a Disney theme park, the guest is asked to place his or her index finger on a touch pad to verify that the park ticket belongs to him or her. The touch pads are not cleaned after each use, and Disney does not provide hand sanitizer. There are no sinks in the immediate vicinity of the touch pads.
The Disney parks would decrease the potential spread of swine flu and other diseases by installing hand sanitizer stations at the entrance to the parks. Hand sanitizer should also be made available near the attractions, so guests can clean their hands after touching safety bars and other ride surfaces. Swine flu at Disney World first made headlines last spring, when a girl traveling from Mexico was diagnosed with the disease. Although the girl's family did not stay on Disney property, they attended the Disney parks.
The swine flu/H1N1 virus is spreading across Central Florida. At the University of Central Florida, ten cases of the virus have been confirmed to date. The infected exhibited mild symptoms and either recovered fully or are currently being treated for the disease.
Swine flu treatment:
Swine flu has not led to decreased attendance at Walt Disney World's theme parks. Relatively few people have died from the disease in the United States. According to physician Robert Walton, M.D., when otherwise healthy patients receive immediate treatment with antiviral medication upon the first sign of infection, their chances of recovery are strong.
Swine flu prevention tips:
Wash your hands frequently with soap and water. Ideally you should wash your hands for at least 20 seconds.
Carry hand sanitizer for use inside the parks. You will undoubtedly come into contact with door handles, counters, and other surfaces that could be contaminated with germs. Tens of thousands of park guests and employees touch these surfaces daily.
Be prepared and keep your hands clean.
Refrain from touching your mouth, eyes, or nose in order to prevent the spread of germs. Make sure you wash your hands before eating or placing any objects in your mouth.
Cover your mouth and nose with a tissue when you sneeze or cough. Dispose of the tissue in the trash and wash your hands after sneezing or coughing.
Do not travel if you are sick. Instead call a doctor to discuss your symptoms and potential treatment.
Study shows pathogens may transfer between patients and dogs in healthcare facilities.
By Wendy Bedwell-Wilson ( dogchannel.com)
Posted: June 23, 2009
A new study of therapy dogs shows these canine workers do more than share smiles; they can also share bacteria commonly found in hospitals.
In a paper titled, “Contamination of pet therapy dogs with MRSA and Clostridium difficile,” published online on March 28, 2009, in the Journal of Hospital Infection, researchers from the University of Guelph in Ontario, Canada, reported that methicillin-resistant staphylococcus (MRSA) and C. difficile may have been transferred to the fur and paws of these canine visitors when patients handled or kissed the dogs, or through exposure to a contaminated healthcare environment.
Investigators examined 26 therapy dog-and-handler teams between June and August 2007. Twelve teams visited acute-care facilities and 14 visited long-term care facilities. Prior to each visit, the dog’s forepaws and their handlers’ hands were tested for MRSA, vancomycin-resistant enterocci and C. difficile. In addition, the investigator sanitized her hands, handled each dog, then tested her hands for the same pathogens.
Testing was repeated on departure from the facility. The dog-and-handler teams were observed at all times during the visits, and all interactions with patients and staff were closely monitored.
Prior to the visits, none of the tested pathogens were found on the hands of the investigator or the handlers, or the paws of the therapy dogs. But after visiting an acute-care facility, one dog was found to have C. difficile on its paws. It was observed giving its paw to many of the patients.
When the investigator’s hands were tested after handling another dog that had just visited a long-term care facility, MRSA was detected, suggesting the dog had acquired MRSA on its fur. It had been allowed onto patients’ beds and was seen to be repeatedly kissed by two patients.
Finding MRSA on the hands of the investigator who petted a dog after its visit to the facility suggests that dogs that have picked up these pathogens can transfer them back to people. Even transient contamination presents a new avenue for transmission, not only for the pathogens evaluated in the study, but potentially for others, such as influenza and norovirus.
The authors conclude that to contain the transmission of pathogens through contact with therapy animals, all patients and handlers should follow recommended hand-sanitation procedures.
“It’s unrealistic to think that we can sanitize an animal visitor’s body between patients,” says investigator Sandra Lefebvre of the University of Guelph’s Ontario Veterinary College. “But we can and do ask human visitors to sanitize their hands so they don’t spread germs.”
More People Dead From U.S. HAIs in One Decade Than Total Toll of Americans Who Died in Battle in All Wars
Victoria Nahum, Safe Care Campaign
According to the U.S. Veterans Administration's latest numbers (Nov. 2008), the total fatalities of all soldiers who ever died during battle is 651,030. This number includes all wars the U.S. has been involved in, beginning with the American Revolution.
As awful as it is, having lost our good men to the ravages of war, unbelievably, this terrible number is far less than the number of patient fatalities caused by health care and community acquired infections just in the last decade.
Genetic “pieces” of the 1918 flu virus, which killed between 50 and 100 million people worldwide, were likely circulating between pigs and people two to 15 years before the pandemic struck, according to a new study published in Proceedings of the National Academy of Sciences.
Catch two different flu viruses at once and a new one can emerge, something scientists call reassortment. Birds are the ultimate origin of influenza viruses, but because pigs can catch both bird and human flu strains, they’ve long been recognized as a species mixing vessel [AP].
The research shows that lethal flu strains may be the result of such reassortment of pre-existing strains, not a sudden genetic “jump.” It’s a cautionary tale for those studying the current swine flu outbreak, say researchers, as the findings suggest that the swine flu virus could evolve slowly over many years into a more dangerous form.
The analysis found that the 1918 epidemic was most likely created by interactions between human seasonal influenza and a flu strain circulating in pigs, which may have originated in birds. It had [previously] been thought that the 1918 virus emerged quickly, directly from a bird form [USA Today].
To come to the new conclusion, scientists used a computer program to construct flu strains’ evolutionary trees and find their common ancestors. They entered the genetic information of all known strains, including those that infect people, pigs, and birds. The program worked backward from genetic relationships and estimated dates to find where and when bits and pieces of deadly strains arose.
According to the new analysis, some genes of the  virus may have been circulating as early as 1911. “Our results show that, in terms of how the virus emerged, it looks like much the same mechanism of the 1957 and 1968 pandemics, where the virus gets introduced into the human population over a period of time and reassorts with the previous human strain”
[Technology Review], says lead author Gavin Smith. The study showed that genetic variants of the 1968 flu, which killed nearly 34,000 people in the United States, began circulating one to three years earlier, while close relatives of the 1957 flu, which struck down about 70,000 Americans, circulated for two to six years before it struck.
The research offers clues as to how virulent strains develop and emphasizes the importance of monitoring existing ones. The authors’ biggest fear isn’t that the novel swine flu will mix with some regular winter flu as both types start circulating when cold weather hits — but that it might hang around long enough in places like China or Indonesia to [swap genes] with an extremely lethal bird flu that sometimes jumps from poultry to people [AP].
Information from the study could help scientists better predict which strains will arise, and whether these variants will be particularly deadly.
By Jeremy Laurance
THE INDEPENDENT - London
No parent can have read yesterday's headlines about the death of six-year-old Chloe Buckley from swine flu without a shudder. Teachers described the north London primary schoolgirl as "perfectly healthy" until she fell ill with a virus that her GP initially diagnosed as tonsillitis. Within 48 hours she was dead. Results of a post-mortem examination, which will confirm whether she had any underlying health problem, are awaited. A 64-year-old GP, Michael Day, from Bedfordshire, also died bringing the UK total of deaths to 17.
Does this mean the virus is becoming more severe?
No. The H1N1 swine flu virus is being intensively monitored around the world and there is no sign yet that it is mutating. That is to be expected. There is normally a period after a flu virus emerges when it continues to replicate and spread, before immunity to it grows (among those already infected) and it mutates into something else – which starts the cycle of infection all over again. Experts say that if deaths start occurring in clusters, that could be a warning sign that the virus is mutating into something more serious. For that reason all deaths should be scrutinised.
Why the disparity in people's reactions?
It is one of the many mysteries of flu. Some healthy individuals die each year from seasonal flu, while the majority of the population are only mildly affected, for reasons that are unexplained. Swine flu is so far causing only mild illness in the vast majority of people, but the most seriously affected have been predominantly young. Those with illnesses such as asthma, diabetes, and heart, liver or kidney disease and anyone with a suppressed immune system are more vulnerable. So are pregnant women – the growing foetus pressing on their diaphragm reduces their lung capacity and means if they get a respiratory infection it may be more serious. Obese people are also more vulnerable, possibly for the same reason. Of the UK's 17 deaths so far, at least 14 have been in people with underlying health problems.
Would these people have died anyway?
Probably not. Describing the victims as having underlying health problems conveys the impression that their deaths were unavoidable, even if they had not been infected. This is not the case. A person with asthma is vulnerable to flu because of their impaired lung function. But there is no reason why, if they can avoid the flu, they should not live a normal lifespan.
How many people have been affected in the UK?
The official tally is almost 10,000 cases confirmed by laboratory testing. But tens of thousands more, and probably hundreds of thousands, are estimated to have contracted the virus but not contacted their GP but dosed themselves with paracetamol and hot drinks at home. The Department of Health estimated that new cases were running at 8,000 a week and accelerating, with 100,000 cases a day predicted by the end of August. The age group most affected are children aged five to 14.
Is the death rate higher than for seasonal flu?
It is difficult to tell because there is a tendency in outbreaks of infectious disease to over-diagnose serious cases and deaths and underestimate the numbers infected (who may never contact their GP). Research published in Nature this week suggested that swine flu was nastier than ordinary seasonal flu, causing more lung damage in animals tested. Lung damage can lead to pneumonia, severe illness and death. A study published in Eurosurveillance last week concluded that the death rate was "relatively low... by historical standards". In an average year 4,000 to 12,000 mainly elderly people die from flu, and in an epidemic year that rises to 20,000 to 30,000. In the UK's last major epidemic in 1989-90, around 35,000 people died.
Will we all get swine flu?
No. Some people – the elderly – appear to have immunity against the virus, though it is not yet certain why. Having lived through previous seasonal epidemics and pandemics (in 1957 and 1968) they may have confronted a similar virus before and developed antibodies. Or it may be that the virus happens to have started spreading among younger groups and will reach the elderly later. The most serious illness has been in younger people. Current estimates are that 30 to 50 per cent of the population could be infected – compared with 10 per cent in an average seasonal flu year.
Is it unusual for flu to be spreading in the summer?
Yes. It hasn't happened for decades. Flu is a winter illness. The dampness and humidity in winter help the virus survive longer on surfaces like door handles so it can spread and people tend to mix more closely together in the colder, darker months. But swine flu has found the warm, dry days of summer no impediment, and has spread sooner than experts expected.
Why is the UK worse affected than other countries?
No one is sure. Heathrow is one of the world's major transport hubs, bringing travellers and their viruses from all over the world. The UK also has close links with North America, where swine flu began. The epidemic here may simply be more advanced than elsewhere, and other countries will catch up. Or it may be that we have more sophisticated surveillance systems and are better at tracking the spread of infection.
Is there a vaccine against swine flu?
Not yet, but it is on the way. The Government has ordered 130 million doses, enough to give a double dose – which will be necessary to induce immunity – to the whole population. First supplies are expected by the end of August, and enough vaccine to cover half the population is due by the end of the year. The remainder will be delivered in 2010. The Government will have to decide who is to receive the first doses. Children, the elderly, those with chronic illnesses, pregnant women and NHS frontline staff are likely to head the queue.
Is it a good idea to be vaccinated?
Probably, assuming it is safe and effective. Although swine flu is causing mild illness in most people now, most scientists think it will sooner or later mutate, possibly into a more virulent form. Experience in previous pandemics has shown that novel viruses may start by causing mild illness and end up causing more severe illness, two or even three years on. We could feel the effects of this pandemic for years to come and we don't yet know how severe it may turn out.
What else can we do?
Recognise the symptoms – sudden fever and sudden cough are typical of swine flu. Other symptoms may include headache, tiredness, aches and pains, diarrhoea, sore throat, sneezing, loss of appetite. Stay at home if you are infected and protect the vulnerable in your household by getting antiviral drugs – Tamiflu or Relenza – for them. Use a handkerchief to catch coughs and sneezes, wash your hands – a key transmitter of the virus – and clean surfaces such as door handles. Most people recover in a week, even without anti-viral medication.
Should we be afraid of swine flu? Yes and no. Why?
* Although it is causing mostly mild illness now, it could mutate and become more virulent
* It is spreading faster than expected and people with chronic conditions and pregnant women are at risk
* The most serious illness has been in younger people, unlike seasonal flu which is worse in the elderly
* Most people infected with swine flu have suffered nothing worse than a brief fever and a cough
* There is no sign yet that it is mutating, and even if it does it may not cause more serious disease
* With anti-viral drugs and a vaccine on the way we are better prepared than for previous pandemics
Associated Press July 17, 2009
LONDON — The World Health Organization says it will stop counting individual cases of swine flu.
Tracking individual swine flu cases is too overwhelming for countries where the virus is spreading widely, the agency says in a statement. WHO will no longer issue global totals of swine flu cases, although it will continue to track the global epidemic.
WHO says countries should look for signs the virus is mutating, such as changes in the way swine flu is spreading, surges in hospital visits or more severe cases.
The agency asks countries to report their first confirmed cases, then provide weekly case numbers with a description of their outbreaks.
WHO had reported nearly 95,000 cases including 429 deaths worldwide. But the numbers are outdated, with Britain estimating it had 55,000 new cases last week alone.
(AFP) – July 17, 2009
GENEVA — The World Health Organisation said Friday that the swine flu pandemic is moving around the globe at an "unprecedented" speed as it stopped giving figures on numbers affected.
The WHO said in a information note on its website Friday that it would focus on regular updates from newly affected countries, in order to keep track of the global progress of the new influenza A(H1N1) pandemic.
The influenza pandemic had "spread internationally with unprecedented speed," according to the global health watchdog.
"In past pandemics, influenza viruses have needed more than six months to spread as widely as the new H1N1 virus has spread in less than six weeks," the WHO said.
The agency said the counting of individual cases was no longer essential to assess the risk from swine flu but would focus on new countries to be hit by A(H1N1).
"WHO will continue to request that these countries report the first confirmed cases and, as far as feasible, provide weekly aggregated case numbers and descriptive epidemiology of the early cases," it added.
While it eased its overall reporting requirement, the WHO called on all countries to "closely monitor unusual events," such as possible clusters of severe or fatal infections, or unusual patterns that might be associated with worsening disease.
The policy shift was partly motivated by the "mildness of symptoms in the overwhelming majority of patients, who usually recover, even without medical treatment, within a week of the onset of symptoms."
"Moreover, the counting of individual cases is now no longer essential in such countries for monitoring either the level or nature of the risk posed by the pandemic virus" or to guide the best response, the UN health agency added.
In some countries, the investigation and laboratory testing of all cases had absorbed huge resources, leaving health systems with little capacity to monitor severe cases or exceptional events that might mark an increase in the virulence of swine flu.
"For all of these reasons, WHO will no longer issue the global tables showing the numbers.
July 10, 2009
By Althea Chang / Mainstreet.com
If the Obama administration devoted some of the $787 billion in economic stimulus funds to preventing deadly infections rampant in some hospital environments, billions of dollars would be saved in the long run, notes Consumer Reports… and not just by doctors.
How Infections Can Cost Us
Hospital acquired infections, by staph bacteria, for instance, slams patients with expensive bills and days of missed work. But they’re preventable, and health care reforms haven’t done enough to prevent them, according to Consumer Reports. Beyon that, hospital acquired infections costs the institutions $35 billion to $45 billion a year, according to Bill Vaughan, policy analyst for Consumers Union.
One especially difficult infection spreading in hospitals is MRSA, a type of staph skin infection caused by bacteria resistant to common antibiotics. Staph is present on the skin of about 25% to 30% of the population without causing an infection, according to the U.S. Department of Health & Human Services, but surgical wound infections, bloodstream infections, and pneumonia can also be caused by staph infections. People with weakened immune systems, like hospital patients, may be more likely to get an infection.
An Ounce of Prevention
Just like recommendations to prevent the spread of the H1N1 swine flu, everyday prevention methods are basic.
To prevent getting or spreading an infection, wash your hands thoroughly with soap and water or use an alcohol-based hand sanitizers, keep cuts and scrapes clean and covered with a bandage until healed, avoid contact with other people’s wounds or bandages and avoid sharing personal items such as towels or razors, the Centers for Disease Control and Prevention recommends.
In addition, to prevent the spread of staph bacteria, the CDC urges) those with infections to tell any healthcare providers of their condition to avoid spreading it to them and other patients.
From the CDC
July 10, 2009
On July 7, 2009 the World Health Organization announced the identification of a third person with oseltamivir resistant novel H1N1 virus infection.
All three people fully recovered after uncomplicated illnesses and did not have contact with each other. Two of the three people are reported to have developed illness while taking oseltamivir preventatively after an exposure to a close contact with novel influenza A (H1N1). The third person had no known exposure to oseltamivir.
Results from ongoing testing of novel influenza A (H1N1) viruses indicate that oseltamivir resistance remains rare.
The interim recommendations for the use of antiviral medications for chemoprophylaxis and treatment have not been changed http://www.cdc.gov/h1n1flu/recommendations.htm.
Judicious use of antiviral medications is recommended to reduce the possibilities of the development and spread of antiviral resistant influenza viruses.
Use of zanamivir or oseltamivir should be focused on treatment of persons with suspected novel H1N1 influenza who are 1) hospitalized or 2) at higher risk for complications due to influenza, even if hospitalization is not required.
Personal hygiene practices such as hand washing and practices to prevent the spread of an ill person’s respiratory secretions should continue during treatment because an infected person may continue to shed virus in respiratory secretions while on therapy.
Use of oseltamivir for chemoprophylaxis should be reserved for certain specific situations, such as when a person at high risk for influenza-related complications is exposed to a person with influenza.
Monitoring for antiviral resistance is ongoing and clinicians and state health departments should continue to follow state and national guidance for submission and testing of clinical specimens from persons with suspected novel influenza A (H1N1) virus infection.
More information will be provided as it becomes available.
Since the first cases of novel influenza A (H1N1) virus were detected in mid-April 2009, more than 94,500 people with confirmed infection have been reported worldwide.
Until recently, all novel H1N1 viruses tested have been susceptible to oseltamivir and zanamivir (neuraminidase inhibitors), and resistant to amantadine and rimantadine (M-2 channel blockers, or adamantanes).
The World Health Organization recently announced the identification of three persons with oseltamivir-resistant novel influenza A (H1N1) virus infection; all viruses had the same mutation that confers resistance, H274Y (H275Y in N1 numbering), in the neuraminidase protein.
On July 3, The Hong Kong Department of Health reported a resistant virus isolated from a 16 year-old girl who had a fever upon arrival at the Hong Kong International airport on June 11, 2009. Her symptoms began prior to boarding the plane in San Francisco, California. The patient had not taken antiviral agents and reported no illness among close contacts.
On July 2, 2009, a person infected with an oseltamivir-resistant novel influenza A (H1N1) virus was reported from Japan from an illness on May 15, 2009. This patient also became ill while receiving oseltamivir for chemoprophylaxis.
On June 29, 2009, the National Influenza Center in Denmark reported an oseltamivir-resistant novel influenza A (H1N1) virus from an unknown date. The virus was isolated from a patient who became ill while taking a chemoprophylaxis dose of oseltamivir to prevent influenza infection after exposure to an ill person.
Guidance for the use of antiviral agents for novel influenza A (H1N1) infection has not changed and is available at: http://www.cdc.gov/h1n1flu/recommendations.htm.
The use of antiviral agents for treatment should be prioritized; zanamivir or oseltamivir are recommended for the treatment of persons with suspected novel H1N1influenza who are 1) hospitalized, or 2) at higher risk for complications due to influenza, even if hospitalization is not required.
Initiation of antiviral therapy should be as early as possible, preferably within 48 hours since symptom onset; however antiviral therapy for hospitalized persons is recommended even if it is not possible to begin therapy until more than 48 hours after symptoms began.
Despite treatment with antiviral agents, including treatment with the neuraminidase inhibitors, patients may continue to shed influenza virus and some persons may shed up to four or more days after beginning therapy. Therefore, patients should continue good hand washing and respiratory hygiene practices during the entire period on therapy to prevent the transmission of virus to close contacts.
Antiviral agents to prevent infection with novel influenza A (H1N1) virus should be used judiciously.
Most people who are infected with novel influenza A (H1N1) virus have had a self limited illness and have recovered without the need for antiviral medications.
Inappropriate use of oseltamivir for chemoprophylaxis could contribute to the development of oseltamivir resistance among novel influenza A (H1N1) viruses and the circulation of resistant viruses in the community.
Use of antiviral agents for chemoprophylaxis can be considered for persons at higher risk from complications due to influenza, or for health care workers with an exposure to influenza due to inadequate personal protective equipment.
Appropriate administrative controls (e.g. having health care personnel stay home from work when ill, and triaging for identification of potentially infectious patients) and personal protective equipment should be used to reduce the need for post-exposure chemoprophylaxis among health care workers.
Antiviral agents are discouraged for prevention of illness in healthy children or adults based on potential exposures in the community, school, camp or other settings.
In addition, there is no safety data regarding long term or frequent use of antiviral agents in children, and limited data for healthy adults.
Efforts to monitor for antiviral resistance among novel influenza A (H1N1) viruses are ongoing in the United States and internationally, but detection of oseltamivir resistance among novel influenza A (H1N1) viruses has been rare to date.
Clinicians and clinical laboratories should continue to test patients for novel influenza A (H1N1) infection, especially hospitalized persons with suspect novel H1N1 influenza, and submit clinical specimens or viruses to the local public health laboratory as described by each state health department.
State laboratories should continue to test for novel influenza A (H1N1) and seasonal influenza viruses and follow guidance issued by CDC for surveillance.
Reports on antiviral resistance testing in the United States will be available at: http://www.cdc.gov/flu/weekly.
TABLE: Persons at Higher Risk for Complications of Novel Influenza A (H1N1) Virus
• Children younger than 5 years old. The risk for severe complications from seasonal
influenza is highest among children younger than 2 years old.
• Adults 65 years of age and older.
• Persons with the following conditions:
- Chronic pulmonary (including asthma), cardiovascular (except
hypertension), renal, hepatic, hematological (including sickle cell disease),
neurologic, neuromuscular, or metabolic disorders (including diabetes
- Immunosuppression, including that caused by medications or by HIV;
- Pregnant women;
- Persons younger than 19 years of age who are receiving long-term aspirin
- Residents of nursing homes and other chronic-care facilities.
For more information, please see the CDC website: http://www.cdc.gov/h1n1flu/recommendations.htm
Matthew B. Stannard, Chronicle Staff Writer
Wednesday, July 8, 2009
A San Francisco teenager has been diagnosed with a strain of swine flu that is resistant to the common antiviral drug Tamiflu - an important milestone in the pandemic's evolution.
The case suggests swine flu - a form of influenza Type A, subtype H1N1 - is capable of not only developing drug resistance but also spreading between humans in that resistant form, said Dr. Arthur Reingold, professor at UC Berkeley School of Public Health.
California Department of Public Health spokesman Ralph Montano said the teenager had developed some symptoms prior to a trip to Hong Kong but did not seek medical attention before boarding a plane.
"Hong Kong officials screened the teenager on June 11, upon arrival at the Hong Kong International Airport, and they detected a fever," he said. "The teenager was isolated in a Hong Kong hospital as a precaution and was discharged seven days later, which would be June 18."
The World Health Organization identified the teenager's virus as Tamiflu resistant Tuesday, one of three cases the organization has identified in the past two weeks.
It is not surprising that a Tamiflu-resistant form of the virus would develop, Reingold said: If a virus finds itself within a host that is taking an antiviral drug as a preventive measure, that virus may mutate to a form that can survive that drug.
The two other resistant cases - in patients in Japan and in Denmark - were taking Tamiflu prophylactically, said Dr Keiji Fukuda, assistant director-general of the WHO.
But the San Francisco teenager was not, which gives her case added significance, Reingold said, because it suggests she caught the resistant variant from somebody else.
The resistant strains remain treatable with another drug, generically known as Zanamivir, Fukuda said.
By Ginny Graves / CNN Health
When the swine flu burst onto the scene in April, the bug arrived with a few particularly ominous signs: The flu was resistant to a class of drugs often used to fight flu in the past, and experts were surprised that a nonhuman virus could have such rapid human-to-human transmission. Why was swine flu resistant to current medicines, and was this strain a new supergerm?
Doctors say keeping your hands clean is key to preventing supergerm infections.
Flu bugs develop drug resistance when a virus mutates in a way that makes medications ineffective. Overusing and misusing antiviral meds can cause the problem. But mutations can also crop up spontaneously, even when the drugs aren't overprescribed, said Dr. Anne Moscona, a flu expert and an infectious-diseases physician at Weill Medical College of Cornell University and New York Presbyterian Hospital.
"Swine flu seems to respond to Tamiflu, but we weren't sure at first. And we're seeing more strains of other types of flu, including some bird flu, that are resistant to it. That's been sobering for lots of people in public health because Tamiflu is the drug the country has been stockpiling for a possible pandemic," she said. "The issue we're facing now is 'What do we do if the drugs we're counting on don't work?'"
This question is being asked with increasing urgency these days, as more and more bugs, including some truly nasty bacteria, become impervious to the effects of our best drugs. Acne and some STDs aren't clearing up the way they once did.
More worrisome, methicillin-resistant Staphylococcus aureus (MRSA) -- bacteria that are resistant to methicillin, a common antibiotic -- now kills more people in U.S. hospitals than HIV, AIDS, and tuberculosis combined. And, scarier still, the bug is becoming increasingly common outside of hospitals, affecting everyone from infants with ear infections to young, healthy athletes. And MRSA, experts warn, is just the tip of the drug-resistance iceberg.
"Drug-resistant bacteria have developed in large part because of our overuse and misuse of antibiotics -- and it has led us to a crisis point," said Dr. Helen W. Boucher, a specialist in the division of infectious diseases at Tufts Medical Center in Boston, Massachusetts. "We're even seeing bugs today that are resistant to all antibiotics."
But while some germs may be outpacing our ability to kill them, we're not completely defenseless. In fact, there are plenty of things we can do to slow their spread. Here, five of the scariest threats right now, and what you can do to keep yourself and future generations safe.
Scary strains of flu
In 2005, two teenage girls in Vietnam died of avian (bird) flu. The news was alarming because both had been treated with Tamiflu, the drug governments stockpile to fight the avian virus. In fact, lab tests showed both girls had developed Tamiflu-resistant viruses. More bad news came in January of this year when researchers at the University of Colorado announced that more than 30 percent of the bird flu samples they analyzed were resistant to adamantanes, older antivirals doctors might use if Tamiflu doesn't work.
As of May this year, bird flu had killed 261 of the 424 people who have been diagnosed with it worldwide since 2003, according to the World Health Organization. "It's incredibly deadly," Boucher said. "It doesn't spread efficiently from person to person -- at least not yet -- but a pandemic flu still tops the list of scary health nightmares, even in the United States, because there's the potential for a highly contagious flu to sweep through the population before we can contain it."
Such a flu could kill thousands --if not hundreds of thousands-- of people, especially if the strain is resistant to Tamiflu. "It makes sense for countries to start adding Relenza, another newer antiviral, to their stockpiles, just in case we see a Tamiflu-resistant strain that's highly contagious," Moscona said.
Even if there are drugs that work against a virulent flu, they can't necessarily be relied on to contain an epidemic. "Antivirals only work if you take them within two days of the first symptoms, and they're much more effective if you take them in the first 6 to 12 hours," Moscona said.
Some good news: Researchers recently identified human antibodies that seem to neutralize some flu viruses, including the bird flu strain -- a finding that could lead to more-effective treatments. In the meantime, not getting the flu in the first place is a far better bet than trying to treat it. (In the United States, about 36,000 people die from the flu every year.) Health.com: 8 causes of chronic cough
To avoid it:
• Get an annual flu vaccination. The viruses in the vaccine (based on the type or strain of flu researchers think is most likely to hit) change every year, so get vaccinated each year -- and early. It takes about two weeks for flu-fighting antibodies to develop, so get vaccinated in September or early October to protect yourself from early-arriving bugs.
• Wash your hands. The flu virus can live for up to 72 hours on surfaces like doorknobs, light switches, and TV remote controls and if you get it on your hands and touch your eyes or nose, you could get sick. That makes hand-washing the most effective daily defense. Wash briskly with plain old soap and water for 30 seconds.
• Fight the flu with vitamin D. "One study found that people who took vitamin D supplements were less likely to have cold and flu symptoms," said Dr. Michael F. Holick, professor of medicine, physiology, and biophysics and director of the Vitamin D, Skin and Bone Research Laboratory at Boston University School of Medicine. Holick says 1,500 to 2,000 I.U. of vitamin D not only bolsters the immune system but also may help prevent infection.
Methicillin-resistant Staphylococcus aureus (MRSA)
In December 2005, when 14-month-old Bryce Smith came down with a cold -- his first ever -- the pediatrician told his mom he'd feel better in a few days. He didn't feel better, and by New Year's Day Bryce was in the emergency room. An X-ray showed that he had pneumonia, and a CT scan revealed something even scarier: His right lung was filled with a thick, gelatinous fluid.
The doctors rushed the baby into surgery, where they discovered he was infected with MRSA -- and the infection was so severe that it had eaten a hole through his lung. After 40 days on vancomycin, a superpotent antibiotic that can affect kids' hearing, Bryce pulled through. "But we're still worried about his hearing and how much damage the bacteria did to his lungs," his mom said.
Bryce's story is scary because it reflects a trend. "It's most worrisome that MRSA can infect completely healthy people with healthy lifestyles, something that was almost unheard of 15 years ago," Boucher said. About 12 percent of infections strike people who aren't hospitalized, a percentage that is likely to increase as MRSA becomes more widespread. Health.com: The truth about staph
Currently, about 40 percent of us have staph bacteria on our skin-- and it rarely causes a problem. But about 60 to 70 percent of staph in U.S. hospitals has developed resistance to methicillin. Worse, a small percentage of the bugs are now resistant to vancomycin, the drug that saved Bryce's life.
Although MRSA can cause pneumonia and blood infections and has recently been linked to children's ear and sinus infections, it most often causes skin and soft-tissue abscesses. A MRSA infection looks like a pimple, boil, or spider bite, but it may quickly worsen into an abscess or pus-filled blister or sore.
To protect yourself:
• Shun the staph. Wash your hands, especially after you've been in public places and touched handrails, grocery-cart handles, and other frequently handled objects. Experts estimate that staph is present on 2 to 3 percent of surfaces in public places-- more in hospitals. Regular soap and water will remove most germs. Alcohol gels or wipes and antibacterial soap work, too, but there's a chance that antibacterial soap contributes to antibiotic resistance, so it makes sense to avoid it.
• Cover up. Bandage all cuts, even paper cuts and blisters. Sterilize the stetho. Researchers recently found that one in three stethoscopes used by emergency-medical-service providers was contaminated with MRSA. Ask your doc to swab his scope with alcohol.
* De-germ the gym. Use a disinfectant wipe to swab the handlebars of equipment, and drape a clean towel over shared yoga mats and sauna and locker room benches. After each workout in a group environment, take a shower, soaping up thoroughly-- and be sure your kids who play sports do, too. Health.com: The germiest places in America
• Don't share. You're at increased risk of MRSA if you share razors, soap, towels, or other personal items. Schools, day-care centers, and gyms may harbor the germ -- one reason it's important to get children in the hand-washing habit.
Clostridium difficile (C. diff.)
Amy Warren, 41, thought she was dying when, several weeks after giving birth to her daughter, she began having severe abdominal cramps and dozens of daily bouts of diarrhea. After several medical tests, a doctor identified her infection as C. diff., a gut bug that, thanks to its virulence and prevalence in hospitals has earned it the distinction of being called "the new MRSA." (It sickens about a half-million people in the United States every year and contributes to between 15,000 and 30,000 deaths.)
Warren, who finally beat the infection after six months and three rounds of the potent vancomycin, said, "I had never even heard of C. diff. before. I've never been so sick in my life. I live in fear of getting this thing again."
C. diff. is one of the most aggressive killers of hospitalized patients. But it's increasingly affecting people in the community, and one of its most frightening qualities is that it can develop even after you've taken a single dose of antibiotics for a sinus infection, say, or a urinary-tract infection -- if the toxic bacteria is in your gut. "The drugs wipe out the healthy bacteria, which allows C. diff. to proliferate," Boucher said.
The bacteria can produce toxins that destroy the lining of the gut, causing everything from mild diarrhea to a deadly condition known as toxic megacolon, in which the colon walls become so thin they rupture. The type of C. diff. Warren had -- a mutated strain known as NAP 1, which has only appeared in the last decade -- is particularly dangerous, producing roughly 20 times the amount of toxin as older strains and responding less favorably to antibiotics.
To stay safe:
• Bust out the bleach. The bacteria's hardy spores can survive for months on most surfaces (even dry ones) and aren't killed with most cleaners. "You can only kill them with bleach," said Dr. Stuart Levy, president of the Alliance for the Prudent Use of Antibiotics and a professor of microbiology and medicine at Tufts University School of Medicine. On your hands, alcohol sanitizers do little to get rid of spores, but the friction of soap and water may remove it from your hands. "The best you can do is try to wash it down the drain," said Dr. Louis Rice, an expert on resistant bugs and chief of medical service at Louis Stokes Cleveland VA Medical Center. Also, be particularly vigilant about hand hygiene if you visit a hospital or extended-care facility; both are places where the toxin-producing bacteria thrive. Health.com: Five ways to prevent more antibiotic resistance
• Be proactive. If you have to take an antibiotic, take a probiotic at the same time to build up the healthy bacteria in your gut. "It might help protect against C. diff.," Boucher said.
Drug-resistant gram-negative bacteria
Last year, Mariana Bridi da Costa, a 20-year-old Brazilian model, was diagnosed with a urinary-tract infection, and within weeks a bacterial infection had spread throughout her body. In an attempt to stem the infection, her hands and feet were amputated. But complications from the infection killed her.
In 2007, Ruth Burns, 67, of Columbus, Ohio, had surgery to relieve a pinched nerve. "She was supposed to be in and out in 24 hours, but she developed pneumonia and meningitis," her daughter, Kacia Warren, said. Although she was treated aggressively with antibiotics, Burns died 17 days after her surgery. The cause of both deaths: drug-resistant gram-negative bacteria.
"These are some of the most antibiotic-resistant bacteria out there, and they can cause all sorts of infections," said Dr. Barbara Murray, director of the division of infectious diseases at the University of Texas Medical School. Although most infections occur in hospitalized patients, such as Burns, the numbers are quietly escalating in people who are not hospitalized, elderly, or immunocompromised.
"It's a problem that's poised to spin out of control," Boucher said.
The germ that killed Burns, Acinetobacter baumannii, is nicknamed "Iraqibacter" because it has caused deadly infections in soldiers wounded in Iraq. Until a few years ago, most strains of Acinetobacter could be killed with a variety of drugs; for those that couldn't, doctors relied on broad-spectrum antibiotics known as carbapenems.
Now, more and more strains of this bug are showing resistance to carbapenems, as are other gram-negative bacteria, including Pseudomonas aeruginosa, which killed Bridi da Costa; some strains of E. coli, the bug responsible for most urinary-tract infections; and Klebsiella pneumoniae, a strain of bacteria that causes a particularly severe type of pneumonia.
"The carbapenems are the best drugs we have against these bacteria," Boucher says. "Without them, we're looking at something pretty scary because there's almost nothing in the pipeline -- and gram-negative bacteria can be killers. They actually chew up the antibiotics used against them."
To fight back:
• Practice infection-protection. If you're having surgery, ask the surgeon about infection rates. "Surgeons know their rate of infection for various procedures, and you have a right to know, too," said Betsy McCaughey, founder of the Committee to Reduce Infection Deaths.
• Stay clean at the hospital. If you're visiting a hospital, wash yourself and your clothes right after. Don't use bar soap in any hospital bathroom or set your purse on the floor.
• Be pushy. Ask medical personnel to wash their hands. Don't be falsely assured by gloves, McCaughey warned. "If caregivers have pulled on gloves over dirty hands, the gloves are contaminated, too."
TB seems like the last thing you need to worry about in this day and age, but people in the United States still get the disease. (There are about 13,000 new cases a year.) In March and April alone there were reports of high school students in Florida, Pennsylvania, and New Hampshire being diagnosed with the illness.
"Two or three times a week there's news of an active TB outbreak somewhere in the United States," said Dr. Lee B. Reichman, executive director of the New Jersey Medical School Global Tuberculosis Institute. "For a disease that's supposed to have died out, that's a lot of sick people."
Although TB is treatable, new strains are cropping up that are resistant to antibiotics. Multidrug resistant TB (MDR TB) is impervious to at least two of the best first-line anti-TB drugs (isoniazid and rifampicin). Extensively drug-resistant TB (XDR TB), still relatively rare, is resistant to first- and second-line anti-TB medications, including injectable drugs. And both types are on the rise.
To keep it at bay:
• Get tested. If you've been around someone with active TB, ask your doctor to give you a blood or skin test.
• Take your meds. If you have TB that responds to drug treatment, taking the wrong dosage or stopping the drugs too soon (before the prescribed 6 to 9 months) may leave your body with lingering bacteria, and the germs that are still alive may mutate and develop resistance.