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.

 

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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.

 

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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:

mrsamap

 

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.

Life is Counterintuitive

Quick – which has more bugs, a man’s shaggy beard or a man’s clean-shaven face?

A man’s beard typically has more than 100 different kinds of bacteria rummaging through it. But beards are actually less likely to harbor infection-causing and antibiotic-resistant bacteria than a clean-shaven face. In fact, not having a beard actually increases your chances threefold of having methicillin-resistant Staphylococcus aureus (MRSA) on your face, according to a recent study.

Guess which face is more likely to attract MRSA?

Guess which face is more likely to attract MRSA?

There seems to be two reasons for this. Micro-abrasions caused by shaving – tiny cuts in the skin – are thought to better support bacterial colonization and proliferation. Second, when you get a competitive environment like a beard where there are many different bacteria, they have to fight for food resources and space, so they produce their own antibiotics in order to kill off the competition – i.e., other bugs.

So how do we get these critters off of our freshly-shaved faces? We know that good hygiene is the best way to shed bugs and prevent the spread of bacterial infections, so we will want to wash our face with the new-age antibacterial soaps. After all, our grandparents used just regular soap and water and surely we’ve come a long way since then.

Well, not so fast, because studies are saying that our grandparents had it right: so ditch the antibacterial soaps and disinfectants and get back to good old-fashioned soap and water. The reason is that soap and water clean by loosening and lifting dirt, oil, and microbes from surfaces so they can be easily rinsed away with water.

Antibacterial products, on the other hand, leave surface residues – bugs. But not the usual ones. The ones left over – the survivors — constitute a small subpopulation of the original group. And they survived because they were armed with special defense mechanisms. These guys then reproduce as their weaker relatives perish, until they fill all the space previously occupied by the now dead bugs. And that’s how you end up with a face full, or a countertop full, of antibiotic-resistant bacteria like MRSA.

Scientists have identified two antibacterial agents in particular that they think select for antibiotic-resistant bacteria – triclosan and triclocaraban: so you want to stay away from any product that contains either one.

Stuart Levy, MD, of the Tufts University School of Medicine and author of The Antibiotic Paradox, sums it up this way: That antibacterial soaps and disinfectants select for bacteria that survive their onslaught illustrates yet another counterintuitive proposition: “What doesn’t kill you makes you stronger.”

 

MRSA in Motion

Ever wonder what MRSA bacteria do all day?

The traditional answer is they sit around, eat, and, especially, multiply (exponentially).

And until last month it was also thought that they remained in one spot because, well, no one had ever seen them move and, besides, they have no “legs,” the tail-like flagella that are typically used to propel bugs. Then the University of Nottingham published a study that says MRSA not only move, they move over distances that are incredibly vast compared to the size of the individual cells.
Humor - BT

Apparently they get around in large groups and leave behind a trail of MRSA bacteria as they go. Visually, it looks like a comet moving across the night sky. Interestingly, they also seem to have some ability to navigate because they are capable of avoiding other bacterial colonies. But it remains a mystery as to how they’re able to move: they don’t have flagella (tails) and no other means of propulsion were discovered.

The study has important treatment implications because pathogen movement determines how it colonizes its host – that would be us — and this in turn determines how much harm it can do. For instance, if you know your enemy is then you know where to target, but if it moves about that complicates things.

And finally, it raises this question: If MRSA can move, does that mean other bugs can as well? Because if that’s the case, it tells us we have a ways to go before we arrive at optimal treatment for infectious disease – which is both good news and bad.

Here’s a video provided by the researchers showing MRSA in motion. Warning: it’s not quite as exciting as watching a comet zip across the night sky:

Overcoming Antibiotic Resistance: We’re All In It Together

The Americans and the Brits are leading the worldwide fight against antibiotic resistance. And just today, Britain’s Chief Medical Officer, Professor Sally Davies, and her colleagues, published a 4-minute video (below) asking us to play our part in overcoming this problem. And that’s the point: WE created the problem, and WE – you and me – and not just the medical community, have to do the right thing to overcome it.

What makes this medical issue different than most is that when we misuse antibiotics we don’t just jeopardize our own health, we also jeopardize the health of others, particularly those we live with. Professor Davis explains: “When we use antibiotics when we don’t need them, or when we don’t finish the full course when we are given them, this gives bacteria in our bodies the opportunity to develop resistance to antibiotics. These bacteria that are resistant then multiply and spread so that the next time someone [else] needs an antibiotic to treat a bacterial infection, they don’t work.”

That’s why Davis’s message is aimed at parents. Because if parents get it wrong with one of their children they are also jeopardizing the health of their other children, and themselves.

The number one rule in all of this is: Please Stop Asking for Antibiotics! For instance, they don’t work for the common cold or the flu. Trust your doctor to know when you and your family will need antibiotics. You don’t need to ask for them. But if you are prescribed antibiotics make sure you finish the course – don’t save them – to make sure you kill off the infection.

A New Twist on Germ Warfare: The U.S. Government’s Pathogen Predators Program

The context is new but we’re familiar with the theory: The enemy of your enemy is your friend.

Using germs to fight germs is the idea behind the Pathogen Predators program of the US Defense Advanced Research Projects Agency (DARPA), which began last May. It’s based on the way bacteria behave in nature. As they compete for resources such as food and living space, bacteria fight a war against each other and have been doing so since their inception – 4 billion years ago. Those that survived have evolved ways of attacking other bacteria. In response, the defenders with stronger protections were favored, and the assailants, in turn, evolved even better weapons, and so on.

This digitally colorized electron micrograph shows your immune system in action: A white blood cell (blue) attacking MRSA (yellow). But when the immune system fails – the usual case with resistant germs - and antibiotics continue to loose their effectiveness - then what?

This digitally colorized electron micrograph shows your immune system in action. A white blood cell (blue) is attacking MRSA (yellow). But when the immune system fails – the usual case with resistant germs  like MRSA – and antibiotics continue to loose their effectiveness , then what?

Studying that arms race and picking and choosing what may work for us is the focus of the research. For example, Bdellovibrio bacteriovorus, is found in the soil. It attacks prey bacteria by embedding itself between the host’s inner and outer cell membranes, and begins to grow filaments and replicate. The host bacterium eventually explodes and releases more B. bacteriovorus into the environment. In another case, a team has engineered the gut bacterium Escherichia coli to produce peptides that kill Pseudomonas aeruginosa, a microbe that causes pneumonia.

But researchers warn that the enemy of your enemy isn’t always your friend. Some of these predators will attack you too, just as MRSA does. So they have to tease out which ones are toxic to us, and which pathogens (prey) the predators are effective against.

One more thing. From the perspective of bacteria, antibiotics, most of which come from the soil, are simply another front in their battle against one another. We tend to think of ourselves as Lords of the Universe, but when it comes to germ warfare we are relative newcomers dating back mere decades to the advent of the era of antibiotics in the 1940s. In other words, in this war, our ‘enemy’ has had a 4 billion year head start. So by using our know-how to harness theirs, DARPA wants to treat not just battlefield infections, but especially those that are stubbornly resistant to antibiotics – a problem that concerns all of us.

 

 

 

 

 

 

 

 

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