The Public Can Learn Medicine in the Digital Age

How do you get the public on board with the rising global plague of drug-resistant infections that kill 700,000 people a year and are estimated to eventually surpass deaths by cancer?

You go digital: The people at FutureLearn, a division of the Open University, are offering a free online 6 week course called “Antimicrobial Stewardship: Managing Antibiotic Resistance,” to a worldwide audience. And it’s an eye-opener.

Their teaching philosophy is that “learning should be an enjoyable, social experience, so our courses offer the opportunity to discuss what you’re learning with others as you go, helping you make fresh discoveries and form new ideas.” So for example after each presentation there’s a (well-used) discussion forum where you address the issues presented and answer the questions posed.

But it was something else that really got my attention: The course confronts head-on the human realities — the human frailties — that are an inevitable part of healthcare delivery. For example, in the very first video (below) that sets the stage for the entire course, we’re presented with an infectious disease outbreak at a hospital where the following issues, among others, are presented:

1) An ill-informed CEO – a physician – who seems more concerned with the reputation of the hospital and reassuring the public that everything’s under control than with coming to grips with the outbreak itself.

2) The power differential between doctors and patients and how that undermines healthcare. The wife of a patient remarks, “I just thought he’d be okay and protected … I suppose I should have said something, really. But you don’t like to, do you? Consultants know best, and I don’t want to upset anyone, especially when Bill’s relying on them to perform his operation.”

3) Nurses and other staff who are too busy to do their job. And so, for example, they allow a patient recovering from a drug-resistant infection to “help” other patients by keeping them company and assisting with their feeding.

4) Conflicts that arise even about which antibiotic to use: The national guidelines say one thing, hospital guidelines might say another, and within the hospital itself the attending physician will often push a “blockbuster” drug instead of following the microbiologist’s recommendation.

5) And of course the ever-ubiquitous issue of hospital staff following their hygiene rules about as much as the rest of us follow speed limits.

Most courses in science and health shy away from looking at the mistakes practitioners themselves make. But not here; and note that the course is offered by hospital insiders. For instance, it’s run by Professor Dilip Nathawani, an infectious diseases physician who leads a national antibiotics stewardship program in the UK and is chair of the British Society for Antimicrobial Chemotherapy. With respect to the 5 issues presented above, he admits, “Sadly, what you have seen is not an unusual scenario in many hospitals and departments across the world.”

Putting the healthcare workers and the public in the same classroom at the same time is empowering. We learn their language, and we can understand healthcare delivery from their perspective. On the issue of drug-resistant infections, this is the next best thing to going to medical school or to nursing school yourself.

Here’s the video that introduces the fact pattern that the course is based on:

“We are … not innocent victims of the antibiotic resistance phenomenon”

Think of antibiotic use this way: If there were only one car in our community we would be acutely aware of our responsibility not to misuse it. For if we did, the day would surely come when the car would be needed to get to work or take our child to the hospital — but it would not start, or perhaps it would breakdown along the way.

Antibiotics, much like the car in this example, are also a community resource says Stuart Levy, MD,  Director of the Center for Adaptation Genetics and Drug Resistance at the Tufts University School of Medicine in Boston.

Dr. Levy is also an author, and the very name of his powerful book tells the tale: The Antibiotic Paradox: How The Misuse of Antibiotics Destroys Their Curative Powers. He describes how our collective misuse renders antibiotics ineffective:

“The bacteria lining of our skin and intestinal tract form a protective ‘armor’ against invasion by pathogens. If, during antibiotic therapy, this protective coat is killed or diminished, resistant disease-causing bacteria can find a niche and multiply. Once they reach critical numbers, they can cause illness and, if resistant, will be harder to treat …. The problem is that in most cases no harm is evident and so the practice continues. Multiply this one instance by all those individuals worldwide … and the magnitude of this indiscriminate use should become obvious.”

Making diseases “harder to treat” means needless suffering. For example, multiple admissions to the hospital, unplanned surgeries (10 for this MRSA-infected NFL player), and admissions to the ICU. This is especially so for the vulnerable, such as cancer patients who, as Levy points out, 25 – 30% die from infection, about half of which are infections resistant to antibiotics.

Here’s how we contribute to this needless suffering: We get antibiotics without prescription, from friends and family, say. When we do get them by prescription we’ll prematurely stop use and store them for another day. Or we’ll go to a physician and demand them. For example, Levy tells the story of an aggressive patient: “Doctor I know what I have and I know what I need. I want so ampicillin. And don’t give me the 250mg tablets; they don’t work. I want the 500 mg pills.” But the biggest mistake of all is asking for antibiotics for things they don’t fight such as infections caused by viruses like colds, flu, most sore throats, bronchitis, and many sinus and ear infections.

When we do these things — when we misuse antibiotics — we set the stage for illness. In other words, as Levy puts it in his book, “We are … not innocent victims of the antibiotic resistance phenomenon.”

The following seminar on antibiotic resistance remains one of the best out there on the subject. Put on by the Harvard School of Public Health, Dr. Levy is one of the three panelists:

The New Recruit: Bad Bugs Have Acquired a New Weapon. And It Has Has Us Stymied

The ‘Klingons’ are gaining the upper hand.

Imagine: We’re locked in a struggle for survival against our age-old enemy, the Klingons. Increasingly resistant to our weapons, we now hear they have a new recruit—‘Gene,’ code name ‘MCR-1’—who has been travelling the planet dropping off a blueprint for a new weapon. The plan shows affiliated resistance groups how to build a device that disables anything we can throw at them thus rendering them virtually invincible. And just last week we learned that Gene has entered the United States. Captured at a military hospital in Pennsylvania, though not before he shared his weapons plan with at least one local resistance group, Gene is being interrogated at the Walter Reed Army Institute of Research. The key question: Who else has Gene given his blueprint to for making this new weapon?

Bacteria GT3

The analogy refers to a study published last week about a bad bug, E coli, that was resistant to the last-resort antibiotic colistin and, the researchers fear, to all antibiotics: “The recent discovery of a … colistin-resistance gene, mcr-1, heralds the emergence of truly pan-drug resistant bacteria,” write the authors. Tom Frieden, MD, who runs the US Centers for Disease Control, calls this an alarming development that could mean “the end of the road” for antibiotics.

The study concerned a 49 year old woman at a military hospital in Pennsylvania being treated for an E coli-driven urinary tract infection. Her antibiotic therapy wasn’t working so the doctors sequenced the E coli genome to see if they could figure out why. It turns out that the E coli had recruited a brand new gene, mcr-1, that acts as a blueprint for making an enzyme that attacks and defeats any antibiotic thrown at it.

It’s the first known case of the gene appearing in the United States. Researchers at Walter Reed are studying the gene to see how to defeat it. Meanwhile, the discovery raises two urgent issues: How prevalent is the gene in the US and elsewhere; and, crucially, even if it’s not prevalent, will it become so because it spreads easily, like the common cold, say.

The gene has been found primarily in E coli, but has also been found in other members of the E coli family of bugs, such as Salmonella and Klebsiella pneumonia. These mcr-1 gene-containing pathogens have so far gotten into humans, animals, food, and environmental samples, on every continent, and have even been found in a hospital patient in Canada.

But the real problem is this: The gene has the ability to spread beyond the E coli family to all bacteria. That’s why people like Dr. Frieden are so concerned: the E coli became resistant to the antibiotics not through mutation, but by acquiring a roving snippet of DNA called a plasmid—a ‘taxi cab’ for genes— that carries the resistance-conferring mcr-1 gene. And just like taxis, these plasmids can quickly and easily deliver their gene passengers to their destination, in this case, to other bacteria.

Here’s the concerning scenario. Right now antibiotic-resistant bacteria kill at least 23,000 people in the US each year and seriously hurt two million more. What if this new mcr-1 gene infiltrates MRSA, say, that is already so ubiquitous in hospitals and, increasingly, in the community? What will the numbers be then?

One more thing. Our understanding of the world around us is increasingly being driven by the biological sciences, especially genetics (for example, the project announced yesterday to synthesize the Human Genome). In order to properly assess the disease risks we face, and to have intelligent, informed discussions about these risks, we have to find a way to keep up with this ever- expanding body of knowledge.

The following video is offered for that reason. It’s from the Open Access course at the University of British Columbia. They say it’s “all you really need to know about DNA, in 3 minutes.” Notice, for example, the difference between a chromosome, DNA, and a gene. Enjoy:

BBC Knowledge Explainer DNA from Territory on Vimeo.

Unintended Consequences: Antibacterial soaps, disinfectants, and antiseptics don’t kill bad bacteria. Instead, their use results in more of them

Triclosan and triclocarbon are the ingredients to avoid. Soap and water, or an alcohol-based cleanser is the way to go.

Triclosan and triclocarbon are the ingredients to avoid. Soap and water, or an alcohol-based cleanser is the way to go.

It seems that we humans have this ability to get things not just wrong, but dangerously backwards.

In one of the more popular stories in the New York Times this week, we learn that we cannot sustain weight loss by dieting and, more troubling, that dieting will actually cause you to gain weight and even to become obese. The reason is our internal biology: in response to fewer calories coming in, our brain declares a “state of emergency” and issues orders to our body to: burn less calories, increase the release of hunger-inducing hormones and, make eating more rewarding. Ouch!

And in our homes, yet another counterintuitive and unintended event is taking place too: we are turning our homes into antibiotic-resistant bug-filled tombs, leaving us more vulnerable than ever to harder-to-treat illness. We even work hard at this, daily, through our increased use of antibacterial containing household products: soaps and shampoos, antiseptics, and disinfectants. This practice will not only not kill the bad bugs, it will create the very conditions that allow them to proliferate and spread.

It goes like this. In every population of bugs in our homes and on us, most are susceptible to our killing agents — an antibiotic drug or an antibacterial chemical in a cleaning product. But there are some bugs that aren’t susceptible. These ones we call resistant, i.eresistant to the killing agent. So after we use our chemical “weapon” and kill off the susceptible population, the surviving resistant ones have all that extra real estate to reproduce and spread. Which they do at a rapid clip: they can produce a new generation in an hour (we take around 20 years), thus producing dozens of new generations overnight, each one resistant to that antibacterial weapon. This diagram nicely illustrates how it works


But not only is this new generation bacteria resistant to the particular drug or cleaning agent used against it, it also develops something called “cross-resistance”: the ability to resist many different kinds of drugs or antibacterial agents. It becomes what in common parlance is referred to as a “superbug.” That’s generally accepted science these days, a conclusion long-ago reached by Dr. Stuart Levy, MD, Director, Center for Adaptation Genetics and Drug Resistance, Tufts University, and explained in his book The Antibiotic Paradox: How the Misuse of Antibiotics Destroys their Curative Powers.

In other words, the more we clean our homes with these products the more we surround ourselves with bugs that our antibiotic drugs having less and less effect on. So if we succumb to infection by them, we guarantee ourselves a longer and more difficult to treat illness, or one that can’t be treated at all. For example, Dr. Levy reports that exposing low-level resistant methicillin-resistant staph aureus (MRSA) bacteria to an antibacterial agent (similar to chemicals used in disinfectants), increased that MRSA’s resistance by 10-fold to antibiotics. So with an aging demographic and an increasing emphasis on home care versus hospital care, it matters how we clean our homes.

The devil is in the detail, warns Dr. Levy. Be on the lookout for the 2 suspects in the household cleaners that drive the proliferation of these resistant bugs: triclosan and triclocarbon. Read the labels, Dr. Levy says, and steer clear of these 2 guys unless your doctor says otherwise and explains how to use them. For instance, you would wash your hands for 2 or 3 minutes, not 3 or 5 seconds, as we typically do. Dr. Levy advises normal soap and water for hand washing; and peroxides, and chlorinated bleaches, for use as antiseptics and disinfectants, respectively. In the case of hand washing, the addition of a cleaning alcohol “produces a significant additive effect,” he says.









Early Childhood Exposure to Antibiotics Increases Your Chances of Becoming Overweight in Middle Age, Especially so for Women

It’s well understood that industrial farms purposefully enhance the growth of their livestock by giving antibiotics to young animals. If that’s the case with food animals, could our widespread use of antibiotics to treat infections in children be having the same effect?

The question was posed by Martin Blaser, MD, director of the Human Microbiome Program at NYU and president of the Infectious Diseases Society of America. In a series of mice experiments that he and his colleagues began in 2007 that he describes as “the most exciting work of my career,” Dr. Blaser answers the question with a decisive yes: Early life exposure to antibiotics, he says, can permanently change development leading to larger size and more fat, especially in women.












Dr. Blaser’s findings, laid out in his 2014 book Missing Microbes: How the Overuse of Antibiotics is Fueling Our Modern Plagues, can be summarized as follows:

(1) The early childhood years are a critical period in a child’s development and so the earlier they are exposed to antibiotics the more pronounced the effect of larger size and more body fat.

(2) The effect was present across all antibiotics tested.

(3) Short term exposure to antibiotics — mimicking a child’s periodic exposure to antibiotics — showed identical effects: getting antibiotics for 4 weeks or 8 weeks was the same as getting antibiotics for 28 weeks.

(4) The effect was noticed earlier in males; with females it arrived in middle age, and in both cases it persisted for their entire life span.

(5) Mixing a high-fat diet with an antibiotic exaggerated the effect dramatically: males put on 25% more body fat, but female body fat increased 100% — it doubled their body fat.

(6) Blaser reports that his findings are consistent with a human study linking obesity with antibiotic use in young children. He cites the well-known British research that tracked over 14,000 children from birth for the next 15 years. Blaser’s team reviewed the data and found that “children who received antibiotics in the first six months of life became fatter” than those who took antibiotics later on.

Thus, concludes Blazer: “So on the farm, in our mouse experiments, and in an epidemiological study of human children, there was consistent evidence that early-life exposure to antibiotics could change development leading to larger size and more fat.” (my emphasis)

We can to varying degrees combat body fat with diet and exercise, but Blaser’s use of the phrase “larger size” bears further scrutiny. In his experiment with mice that most resembled how children take antibiotics — “Instead of low doses, mice got the antibiotics just like children, full therapeutic doses for just a few days in several pulses” — he found a sobering effect that cannot be countered with diet or exercise:

[M]ice that received amoxicillin showed increased bone area and mineral content for the duration of the experiment. Perhaps the effect was permanent because they received the drugs so early in life. And since amoxicillin is the most frequently prescribed drug in childhood, I can only wonder if that’s the drug that most promotes the recent increases in human height.









The Antibiotic-Food Animal-Human Health Connection: When we Feed our Food Animals Antibiotics to Make Them Grow Faster, There Will be Consequences

carlos don 2When 12-year-old Carlos Don went off to summer camp his mom and dad didn’t expect him to come back looking deathly pale with a 104 degree fever. Carlos had to be admitted to the ICU of Children’s Hospital near his home in Poway, in southern California, where he was diagnosed with a MRSA-driven pneumonia in both lungs. Doctors induced a coma and put Carlos on a ventilator to give his lungs a rest. He was eventually “hooked up to so many machines and had so many people surrounding him, we could barely see him,” his mother, Amber Don, wrote.

We don’t know how the MRSA got into Carlos. But he didn’t catch it at a hospital, where it typically lurks. Instead, Carlos confronted it somewhere ‘out there,’ in the environment, where bad bugs like MRSA are increasingly being found. One big reason: the non-therapeutic use of antibiotics as growth-promoters in industrial-scale food-animal farming—in essence, steroids for animals to make them grow bigger, faster—a practice that is banned in Europe.


Industrial farming 1


Over 8 tons of antibiotics are fed every year to the more than 8 billion food animals in the US alone, resulting in a “massive selection” for resistant bacteria, writes Stuart Levy, MD, in The Antibiotic Paradox: How the misuse of antibiotics destroys their curative powers. With the upshot that resistant bacteria will develop in an animal within 2 – 3 days; from there it will spread to the other animals, then to the farm workers and their families, continuing outward to nearby communities, states, and even globally.

Crucially, Levy’s research team found that it doesn’t seem to matter what antibiotic is used on the food animals. Resistance will develop not just to that drug, penicillin or tetracycline, say, but to multiple drugs, as many as ten. And so when we eventually need one of those drugs to treat an infection, the drug-resistant bacteria have already been built into us through the chain of events shown in the following chart, put together by Dr. Levy’s group:

Food Animals Tufts 2

Levy’s chart illustrates something else too: Our usual rendition of nature as a “quiet environmental scene belies the extensive activity going on at the microscopic level,” writes Dr. Levy (my emphasis). “In fact, bacteria … are multiplying, metabolizing, and exchanging genes … among all participants … throughout the world, including people, animals, fish, birds, insects, and plants.”

That “extensive activity” affects all of us, as it did young Carlos Don that summer at camp. His mother, Amber, tells us the rest:

I remember him lying there on the hospital bed … He was petrified, but was trying to be so brave. I lied to my son for the first time in his life at that moment. He asked me if he was going to die, and I told him no. I told him he was going to be just fine, squeezed his hand, and gave him a kiss and told him I would see him shortly and that I loved him. He told me he loved me too. Those were the last words I ever heard my son say to me.

Pictures and memories are all I have left of him, and you can’t give those hugs or tuck those in bed at night. The day I picked up his urn from the mortuary I also picked up my daughters from school. While waiting in my car for the girls, I sat and watched my son’s friends laughing and playing around outside the school. While they were doing what normal 12-year-olds do, my son’s remains sat in a box in the back seat of my car. He should have been out there laughing and playing with them.








Big Bird

If you’ve ever eaten chicken that tastes like rubber, it may not have been the chef’s fault. It could be something called ‘woody breast,’ chicken laced with veins of fibrous meat that tastes gummy or as if there’s a knot in the meat, the Wall Street Journal reported this Tuesday.

To meet the growing global demand for white meat we have bred chickens and livestock to grow bigger more quickly. To do that we use antibiotics as growth promoters to help animals add extra flesh. And so over the past 50 years, average chicken weights in the U.S. have roughly doubled, while the time it takes for birds to pack on the pounds has been cut in half:

Basic CMYK


But there are side effects to this practice. The so-called woody breast is one; forcing baby chicks to keep up with adult-size bodies results in heart failure, and legs that break because they’re unable to bear the weight, are others. But it’s not just the chicken that suffers from too-rapid growth; you and I do as well, in the form of infectious disease that’s resistant to treatment, the consequence of a chain of events that began with feeding our chickens those growth promoting antibiotics.

Stuart Levy, MD, is the Director of the Center for Adaptation Genetics and Drug Resistance at Tufts University in Boston, and the author of The Antibiotic Paradox: How the Misuse of Antibiotics Destroys Their Curative Powers. In his book, Dr. Levy tells us what happens when we use antibiotics for growth promotion in food animals.

In essence, we manufacture bacteria (bugs) that are resistant to multiple antibiotics. In fact, his team found that a single bug can be resistant to as many as 10 different drugs: “It’s almost as if bacteria strategically anticipate the confrontation of other drugs when they resist one,” says Dr. Levy.

The resistant bugs are mobile: they move between the penned-in animals then to humans; first locally, then spread nationally and even internationally.

The food supply becomes contaminated. Proper cooking will usually kill the bug but problems will arise before cooking as the bugs contaminate kitchen surfaces, for example, when you place the meat there prior to cooking.

And once a bug becomes resistant to a drug, its effect on human health can be felt even decades later when that bug infects someone and their ensuing disease is antibiotic-resistant.

In other words, while antibiotics help sustain intensive food production, their uncontrolled use on farms is turning animals into reservoirs of hard-to-kill bacteria that can spread rapidly and globally.

Levy’s principles of the spread of resistant organisms generalize across bacteria and animals raised for food. We see this, for example, with the Pennsylvania research that nicely shows how antibiotic use in industrial pig farms is making us sick. They tracked the movement of MRSA from those “farms” to the local people and put together a map of their findings. Each red dot is the home address of a person that had a MRSA infection. The blue bits are the pig farms:



So what is the future of using antibiotics for growth promotion? Food demand will continue grow if for no other reason than our world population of over 7 billion will increase by more than 2 billion by 2050, says the UN.

Speaking to Bloomberg News this week, Vincent Doumeizel, a vice president of Lloyd’s Register Quality Assurance in London, where he focuses on food safety and sustainability, said the solution isn’t to ban bactericidal drugs on farms: “It’s absolutely impossible at the moment. Banning them would just collapse the current production system overnight.”

“That leads us to the next question: are animals a good way to get protein?” Doumeizel said. “That’s a big concern because we won’t be able to feed 9 billion people with animal protein.”

Is Doumeizel right? Is our future, judging by the top graphic, an even Bigger Bird?

What do you think?









It’s In Our hands

What’s the best way to prevent the spread of drug-resistant organisms — and thus infection — in a hospital? “The critical thing that all of us as healthcare providers can do is clean our hands between patient contact: and that is the number one, two, and three action to keep our patient safe,” says Dr. John Embil, Director of Infection Prevention and Control at Winnipeg’s Health Sciences Centre.

elderly 1The problem, though, is in the execution: our health- care workers are notoriously non-compliant when it comes to following hand hygiene rules. So Lona Mody, MD, professor of medicine at the University of Michigan Medical School, had a different idea: Instead of focusing on the healthcare worker, why not focus on patient hand hygiene, especially patients who are vulnerable to infection, such as the elderly?

The first question for Mody, then, was to see whether these patient’s hands were indeed “dirty” with bad bugs; because if they were, her approach would be a good one. (The hands were targeted for analysis because that’s what we use most to pick up and drop off the little beasties.)

Mody’s group examined the hands of patients, whose average age was 76, discharged from Detroit-area hospitals on their way to after-care facilities. Once in the facility the hands were examined again, weeks or months later. Dr. Mody’s team found that (1) 25% of all patients were colonized with at least one bad bug on their hands upon admission (2) this number shot up to 34% in the same patients in less than 6 months in the facility, and (3) these bad bugs persist in the facility thereby increasing the risk of transmission to other frail patients.

As high as these numbers are they underrepresent the overall burden of colonization. Patients already in the facility weren’t examined, only new arrivals. The researchers only looked for MRSA, VRE, and gram-negative bacteria which, taken together, represents less than half of the 18 drug-resistant pathogens that the Centers for Disease Control and Prevention list as real “threats” to our health. And only the hands were checked for bugs: we know that staph aureus, for example, tends to congregate in the nose.

The high level of colonization matters because studies show that between 1 and 4 and 1 in 7 people who are colonized go on to become infected. That means re-admission to hospital and an increased risk for surgery, admission to an ICU, and even death.

Accordingly, Dr. Mody concludes: “We believe that it is critical to … implement novel programs that reinforce patient hand hygiene.”

Dr. Mody is right for one other reason as well: from a healthcare perspective, the gathering storm of an aging population. In the US, 2011 ushered in the first of approximately 77 million Baby Boomers, born from 1946 through 1964. By 2030, there will be about 72.1 million people over 65, more than twice their number in 2000.

Yet the fastest-growing segment of the total population is the “oldest-old”— those 80 and over. Their growth rate is almost 4-times that for the total population, and will more than triple from 5.7 million in 2010 to over 19 million by 2050.

These people will need healthcare. And surely it’s a truism that the measure of a society is found in how it treats, not so much its well off, but its most vulnerable citizens, such as the sick and the elderly. Dr. Mody’s modest patient hand hygiene proposal would go a long way towards living up to such a standard. She argues, “We also believe that patient advocates should have an active voice in developing and implementing such programs. We think that patient engagement in this area may in fact energize healthcare worker hand hygiene.”

In other words, this too, is in our hands.

Copper Pajamas: An 18-year old school girl beats scientists to a MRSA remedy

A flurry of news stories surfaced last week about the newly published research of University of South Hampton’s Bill Keevil, PhD, that says MRSA is destroyed by copper within minutes of coming into contact with it. Not just MRSA, but other bacteria as well, plus viruses and fungus. For example, if you put 10 million MRSA bacteria on a copper surface their number will shrink to 0 in an hour. But when you put the same amount of MRSA on a stainless steel surface they’ll survive for months.

Amber McCleary: At age 16 she began research that saved a MRSA-infected friend’s life after a team of doctors were unable to.

Amber McCleary: At age 16 she began research that ultimately saved a MRSA-infected friend’s life after a team of doctors were unable to.

This matters because 1 in 20 people contract a hospital-acquired infection, and of those, 1 in 20 die. Change hospital surfaces, bed railings, door handles, and so on to a copper alloy and those numbers are vastly reduced. And if someone does contract a MRSA infection, a copper-based gauze, gown, or bandage, may do the trick.

No one understands this better than Amber McCleary and Gemma Wilby. Back in 2012, when Amber was 18, she heard that family friend Gemma had contracted a severe MRSA infection after giving birth to her first child, by cesarean section. Gemma remembers, “My c-section scar spread 10 inches from hip to hip and I was in excruciating pain.”  Despite emergency surgery, maggot therapy and a daily ­cocktail of drugs, her MRSA couldn’t be brought under control – and she was warned she could die.

Two years earlier, when Amber was just 16, she happened across a video by none other than Dr. Bill Keevil, talking about the antimicrobial properties of copper. Fancying herself an inventor, Amber spent 18 months researching the issue and she carried out various lab tests which proved bacteria couldn’t survive on a copper gown versus the standard hospital gown.

So by the time Gemma was in the hospital fighting for her life, Amber was ready. She brought in copper pajamas, bedding, socks, and a hospital gown for Gemma. (Since copper is a metal the fabrics were a blend of 60% copper, 20% cotton, and 20% bamboo.) Gemma was skeptical at first but within a couple days she felt much better and noticed the open wound was decreasing in size. “It was incredible,” said Gemma, “the nurses took swabs from my stomach daily and they always came back infected with MRSA, but a few days after wearing the copper-infused clothing, they came back negative. You wouldn’t think something so simple could make such a huge difference but I could feel the difference in my skin almost overnight. Instead of feeling lethargic I felt brighter, more alert and healthier. More importantly, I was healing. It was a miracle.”

The “miracle” is actually sound science according to Dr. Keevil. Copper overcomes pathogens in 3 ways: it destroys their cell walls and the contents spill out like air from a balloon; it kills the DNA; and it stops cellular respiration – all within seconds of contact with pure cooper.

That a 16-year old schoolgirl inventor would soon go on to save someone’s life based on her work sounds like a too-good-to-be-true Disney film. Except in this case art would imitate life. Here’s a talk given by Dr. Keevil to the Royal Society of Medicine in London, discussing his research on copper and pathogens, where he concludes with these words: “And of course Amber’s company are coming out with copper fabrics, clothing, and dressings, and this offers the future for prophylaxis and therapy.”

More than Just a Skin Infection: A Science Journalist Describes her Family’s Encounter with MRSA

The term “skin infection” doesn’t set off alarm bells for most people. They’re pesky, perhaps embarrassing, but with the right ointment or medication it shouldn’t be much of a problem. But that’s not the story Sonia Shah tells, a career science journalist and mother of two. In her recent book “Pandemic: Tracking Contagions from Cholera to Ebola and Beyond,” and in an interview with NPR, she describes something else entirely; something that few of us would imagine.

Sonia Shah

Sonia Shah

Ever-so-innocently it began: her son’s complaints about that frayed knee bandage, well-earned by his Huckleberry Finn-style outdoor adventures. The red stain in the middle of it probably meant the scab re-opened—the boy just needed to slow down. But when Sonia saw him limping a few days later she peeled off the bandage and: “We found a mountain range of pus-filled boils. One peak summited at over an inch – an inch! – and had wept a sickly stream of liquid into the gummed-up bandage.”

Down at the pediatrician’s office came the diagnosis of a methicillin-resistant Staphylococcus aureus (MRSA) infection, a barrage of heavy duty antibiotics, and instructions to carry out “a brutal regime in which we’d have to force the pus out of the boils using hot compresses and vice-like squeezing. This would be … excruciatingly painful, since the layer of pus extended deep into the tissue … Each drop would have to be meticulously captured and disposed of, lest it find its way into a microscopic fissure in our skin or worse, embed itself in our rugs, sheets, couches, or counters where it could lie in wait for up to a year.”

Which meant the family was at risk: her other son, the father of her two children, and Sonia herself. They probably hadn’t seen the last of this as they were told of whole families who came down with MRSA continually re-infecting each other for years. Another physician warned that her son could have lost his leg.

They acted fast: “We washed. We laundered. We maintained a sterile box with hand sanitizers, disposable gauzes, and antiseptic sprays. A set of cast-off pots lived on the stove for boiling bandages and compresses, which we did religiously. One doctor recommended twice-weekly 20 minute baths in a bleach solution – ½ cup per bath – for months or even years. You know, we first started fighting them with lots of antibiotics and getting them lanced and doing all this stuff with – you know, going to the doctor for them all the time, and then it turned out that if you just sort of stopped everything, they kind of went away on their own.”

But none of the various physicians, Sonia believed, quite knew how to prevent the infection from re-occurring, or from spreading to the rest of the family.

Sure enough, her son’s second bout hit a few months after the first, requiring another round of semi-toxic antibiotics.

A third MRSA infection appeared on the inside of his elbow after another few months. By this time, Sonia says, “There was no doubt: MRSA lived inside his body. Because there was no fissure in this protected bit of skin that would have allowed an external invader to creep in. My husband squeezed five tablespoons of pus from the swollen lesions.”

Then MRSA jumped to Sonia herself. Six months after her son’s boils healed a burning spot appeared on the back of her thigh. “I could see a small spider bite, one that felt as if a torch were being held to my skin. At the doctor’s office she took her scalpel to it and started to dig. Half an hour later I staggered home in tears with a giant wad of gauze to soak up the MRSA-infested pus that poured out for days.”

A pattern emerged: An eruption of boils in random places, popping up unexpectedly, they’d last for weeks, slowly get more and more painful, and it would debilitate movement: “Like, I would get a lot on my legs so it would be hard to drive, it would be hard to bend down; sometimes it was hard to walk.”

Sonia said something else was happening too: “The lack of a clear consensus [how to stop it], the open-minded time frame, and the repellant nature of the treatment began to shake our resolve. We started to wonder: Are they making it up [as they go along]?” (My emphasis.)

In other words, MRSA, even at the level of a “skin infection,” undermines the body and the mind—even the mind of Sonia Shah, who, you would think, is as fortified as they come. Both her parents are doctors. Sonia has a BA in neuroscience. She just published, “Pandemic,” (above), her third book in 10 years about disease-causing bugs. She has given two TED Talks on the subject, and has lectured at universities across the country, including Harvard and MIT. The father of her children and the man with whom she lives is a PhD in molecular biology whose research focuses on pathogens, how they spread disease, and the implications for antibiotic resistance and treatment.

Yet their resolve and faith in medicine has been shaken. So if it would do that to them, what would it do to us? What does it do to the more than 80,000 people who are felled by a “severe” MRSA infection every year, as the Centers for Disease Control calls them?

As for the future, Sonia says, “I think we might always have MRSA. It’s not really known, and this is sort of the problem.  Whether it’s going to come back and be a problem again. If we had surgery, if we had, you know, an accident, would it spread to other parts of our body? It’s like, we really don’t know the answers to those questions. For now we’re fine, and, you know, this is the world we live in. So it’s just a risk you have to live with.”

For life.

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