The Smartest Guys in the Room

The Mayo Clinic just published Ten Things You Should Know About Antibiotic Resistance. The interesting thing about the article is that all ten things actually refer to just one thing: the mcr-1 gene.

Mcr-1 has become the gene of interest in antibiotic circles because (1) it has already conferred resistance on colistin, an antibiotic of last resort and (2) it’s promiscuous: it easily goes from one bacterium to the next leaving “superbugs” in its wake. The upshot, warns the CDC, is that this gypsy gene could turn all species of bacteria into superbugs thereby rendering our antibiotics useless.

Bacteria GT3

 

To really appreciate what’s happening here we turn to Columbia School of Medicine oncologist, and Pulitzer prize-winning author, Siddhartha Mukherjee MD, and his new and important book, The Gene: An Intimate History. He explains how genes “travel”:

Throughout the biological world genes generally travel vertically — i.e., from parents to children … the gene never leaves the living organism or cell [the body].

Rarely, though, genetic material can cross from one organism to another — not between parent and child, but between two unrelated strangers. This horizontal exchange of genes is called transformation. Even the word signals our astonishment: humans are accustomed to transmitting genetic information only through reproduction — but during transformation, one organism seems to metamorphose into another.

Transformation almost never occurs in mammals. But bacteria, which live on the rough edges of the biological world, can exchange genes horizontally. To fathom the strangeness of the event, imagine two friends, one blue eyed and one brown eyed, who go out for an evening stroll — and return with altered eye colors having exchanged genes.

 

In fact, it’s even stranger than that. Since bacteria exchange genes between different species, it would be as if, to continue Mukherjee’s analogy, we took our dog out for an evening stroll, and returned with altered eye colors having exchanged genes. Bacteria, writes Mukherjee, are “capable of trading genetic material like gossip, with scarcely an afterthought; free trade in genes [is] a hallmark of the biological world.”

So why are bacteria able to trade genes like gossip while we humans can only do it so cumbersomely through reproduction? For reasons of self-defense and species survival, says MIT-Harvard professor of medical biology, Eric Lander, PhD.

Bacteria have been around for some 3 billion years Lander reminds us. And for that whole time they have been at war with each other as well as with viruses. And what is a bacteria’s weapon of choice? Antibiotics: It is bacteria and other microorganisms that invented them (penicillin from mold, for example); we humans merely discovered their existence. And to defend against these antibiotics — to stay alive — bacteria have had to evolve various mechanisms to defeat them: what we call antibiotic resistance.

And not only have bacteria been perfecting and evolving these resistance mechanisms for 3 billion years, they turn over new generations — new genetic variants — every 20 – 25 minutes.

That’s why, Lander says, when it comes to genetic engineering we sit at the feet of bacteria — they are the experts. You see it in the contrast with us mortals: Our current version, H. sapien, has been around a mere 100,000 or so years. It takes a relative eternity, 20 – 25 years or so, to produce a new generation (of genetic variants), and we have zero ability to trade genes horizontally, i.e., between one person and another.

So back to mcr-1, an antibiotic weapon that has evolved in bacteria. What if it “escapes”? So far it has been found in E. coli in the gut of hospital patients and has defeated colistin, a “last resort” antibiotic.

But what if E. coli engages in genetic “free trade” and hands over its mcr-1 gene to one of our biggest threats, the common hospital and nursing home bug, MRSA, conferring even further antibiotic resistance on this superbug?

What then?

(Dr. Lander’s comments are available online at: https://www.edx.org/course/introduction-biology-secret-life-mitx-7-00x-3, Lecture 15: Cloning: Purifying a Gene.)

 

The Backstory: When we use antibiotics, why do the bacteria fight back?

The brief video below is a plea to reduce our use of antibiotics. As the more we use them, the more the bacteria find ways to resist them, thereby rendering our drugs ineffective. So much so that a UK government-commissioned report predicts that Superbugs will kill more people than cancer by 2050.

But why do bacteria fight back against our drugs? Why don’t they just lay down and die like we wished they would?

The answer lies in the long — long — history of bugs. Theirs too has been a struggle for survival. But they have one distinct advantage over us: they’ve been doing it since almost the beginning of time.

Here’s how infectious disease specialist Brad Spellberg, MD, explains it in his book Rising Plague: The Global Threat From Deadly Bacteria And Our Dwindling Arsenal To Fight Them:

Human beings did not invent antibiotics, we merely discovered them. Virtually all of the antibiotics we now use are either harvested directly from microbes or are made synthetically based on the design of naturally occurring antibiotics. … Microbes first invented both antibiotics and resistance mechanisms to defeat those antibiotics more than two billion years ago. In contrast, antibiotics were not discovered by humans until the first half of the twentieth century. Hence, microbes have had collective experience creating and defeating antibiotics for twenty million times longer than Homo sapiens have known antibiotics existed. Indeed, so experienced and successful are bacteria at developing resistance to antibiotics that some have actually evolved to be able to survive by ingesting and using antibiotics as their only food source!

And oncologist, researcher, and Pulitzer prize-winning author, Sid Mukherjee, MD, reminds us in his new book The Gene: An Intimate History, that bacteria’s two billion plus year history has been a struggle for survival against another vaunted enemy too — the virus:

“Bacteria have been at war with viruses for so long and with such ferocity that like ancient conjoined enemies each has been defined by the other: their mutual animosity has been imprinted in their genes. Viruses have evolved genetic mechanisms to invade and kill bacteria. And bacteria have counter-evolved genes to fight back. ‘A viral infection is a ticking time bomb … A bacterium has only a few minutes to diffuse the bomb — before it gets destroyed itself.’”

As you watch the video and see the six ways bugs fight off our drugs — thus becoming Superbugs — remember, they’ve refined this protection over some two billion years. In other words, they’re here to stay. Then we show up with “our” antibiotic weapons a mere 75 years ago. So as between their weaponry and ours, and in the ensuing arms race between us, whose side is history on?

Cost of Surgical Site Infections to the Healthcare System

Surgical site infections (SSI) affect 2-3% of patients who undergo surgery. SSIs usually occur due to bacteria and/or other microbes infecting the site of surgery due to improper preparation for the surgery and/or poor care of wounds post-surgery. Healthcare workers take extra precautions to prevent SSIs and subsequent complications.

The rate of surgical site infections is showing an increase in recent decades because of an increase in reporting, longer average life spans, and the presence of antibiotic-resistant bacteria1.  Due to this increasing rate and varying degrees of severity of SSI, an important question to ask is: What is the cost of surgical site infections to the healthcare system?

The healthcare system incurs large costs due to SSI. According to an investigative study written by scholar and orthopedic surgeon Joshua A. Urban: “Surgical site infections may account for as much as $10 billion annually in direct and indirect medical costs”. Another study conducted by economist R. Douglas Scott II stated that healthcare-associated infections (HAI), of which SSIs are a subset of, accounted for $4.5 billion in 1992—this number has since grown2. Direct costs include hospital visits, readmission, additional surgery etc. Indirect costs include post-care costs like lost wages, loss of functional capacity, and loss of mental health. An experimental study conducted in the United States resulted in a $3382 average cost per SSI1. This study also took into account costs and conditions outside of the hospital and cited “[…] shortened postoperative stays, as well as outpatient and same-day surgery […]” as factors increasing the risk of SSI1.  A similar study conducted in Canada yielded an average cost of $3383. It is important to highlight the varying degrees of severity for a surgical site infection. Some are superficial and can be treated with wound draining and cleaning therefore exhibiting less of an economic cost. However, some SSIs are severe and require additional surgery and can even affect internal organs—these SSIs exhibit a high economic cost.

Joshua A. Urban also investigated several studies relating to more serious surgical site infection cases.  Cost analysis of patients who underwent “coronary artery bypass grafting or cardiac valve surgery” resulted in costs between $14,000 and $20,000.1 Another cost analysis for patients at the Hospital for Special Surgery in New York who developed infections in joint arthroplasties yielded results that “exceeded the Medicare reimbursement by $27,000 and the private insurance reimbursement by $18,000”.  This caused this hospital to lose somewhere between $1.2 million and $1.4 million. If these costs are similar in hospitals around the world, it is evident that severe SSIs cost the healthcare system millions or even billions of dollars.

Surgical site infections are often easily preventable either with proper preparation before surgery or proper care after surgery. Additionally quick diagnosis and treatment of an SSI can prevent it from developing into a more serious condition. However, with the rise of antibiotic-resistant bacteria, new and innovative methods and technologies must be explored and implemented to treat the abundance of SSIs in hospitals.  This in combination with proper protocol and precautions with healthcare-workers may reduce the frequency and severity of SSIs significantly.

References:
1Urban, Joshua A. “Cost Analysis of Surgical Site Infections.” Surgical Infections 7, no. 1 (2006). 2006. Accessed June 16, 2016. doi:10.1089/sur.2006.7.s1-19.
2Scott, R. Douglous, II. “The Direct Medical Costs of Healthcare-Associated Infections in U.S. Hospitals and the Benefits of Prevention.” The Direct Medical Costs of Healthcare-Associated Infections in U.S. Hospitals and the Benefits of Prevention, March 2009. March 2009. https://www.cdc.gov/HAI/pdfs/hai/Scott_CostPaper.pdf.

Methicillin Resistant Staphylococcus aureus (MRSA) and Surgical Site Infections (SSI)

Surgical site infections (SSI) can affect anyone who has undergone or plans to undergo surgery. Certain precautions must be taken by healthcare workers and patients to prevent infections of healing wounds from surgery. SSIs occur in 2-3% of surgeries in health care facilities. Methicillin Resistant Staphylococcus aureus (MRSA) is a common species of bacteria found to be the cause of many SSIs.1 This species is one of many antibiotic resistant bacteria contributing to the growing problem of antibiotic resistance (ABR).

MRSA infections are prevalent in many SSI cases. An experimental study conducted by the St. John’s Mercy Medical Center found that 28.5% of all Surgical Site Infections were caused by MRSA. Additionally, an increase in MRSA infections is associated with the administering of post-operative antibiotics.1 This makes sense because the antibiotics administered either have no effect on already present MRSA or create conditions that allow resistant traits in bacteria to form.

MRSA infections are also associated with many factors in healthcare facilities. Same-day admission accounts for 41% of patients infected with MRSA.1 This could be attributed to the lack of wound monitoring and care. Furthermore, post-operative hospitalization lasting more than 3 days is responsible for around 58% of MRSA infections1.  This proportion of cases may be due to the extended exposure to pathogens in hospitals and/or from other patients. Perhaps hospitals need to be cleaner than they already are.

From the study studies shown, MRSA is evidently an important problem with respect to surgical site infections. The treatment of MRSA is also prolonged and more complicated as the bacteria responsible for the infection is resistant to certain antibiotics. While these infections may be treatable by other antibiotics, it is possible that a patient may be infected by a species of bacteria that is resistant to multiple drug types.

In order to mitigate these risks, new alternatives to antibiotics should be employed that is effective against antibiotic resistant bacteria. Furthermore, those alternatives should not further escalate the problem of antibiotic resistance.

References

Manian,, Farrin A., P. Lynn Meyer, Janice Setzer, and Diane Diane. “Surgical Site Infections Associated with Methicillin-Resistant Staphylococcus Aureus: Do Postoperative Factors Play a Role?” Oxford Journals. 2003. Accessed June 16, 2016. https://cid.oxfordjournals.org/content/36/7/863.full.pdf.

Common Multi-Drug Resistant Pathogens

Through several evolutionary mechanisms, bacteria are able to acquire antibiotic resistant traits. For example, one of these mechanisms is the enzymatic inactivation of drugs where the bacteria produce certain chemical compounds to neutralize the effect of an antibiotic. Because of the abundant use of antibiotics in recent decades, bacteria have not only developed resistance to certain types of antibiotics but have become resistant to multiple drugs simultaneously. These bacteria are included in what is termed multi-drug resistant organisms (MDRO). There are several common multi-drug resistant bacteria’s found around the world.

An especially notorious and robust multi-drug resistant species of bacteria is Methicillin-Resistant Staphylococcus aureus (MRSA). Methicillin was an antibiotic developed to fight penicillinase-producing Staphylococcus aureus, a classification of S. aureus resistant to the antibiotic penicillin.1 This trend of resistance shown by S. aureus demonstrates its ability to adapt and curve the efforts of antibiotic development. MRSA is also known to be resistant multiple drugs including aminoglycosides and chloramphenicol.1 Furthermore, MRSA is also known to be resistant to disinfectants and is a common source of infection in the hospital setting.

According to the CDC, MRSA is responsible for over 70,000 infections per year2.

Another common multi-drug resistant bacteria is Vancomycin-resistant Enterococci. Enterococci are found in the environment but also live in the human intestinal tract and in the urinary system. In general, Enterococci are known to be harmless, but in some cases cause infection in people with weak immune systems.3 Similar to Methicillin discussed earlier, Vancomycin was developed in order to battle Enterococci resistant to penicillin and other drugs. This again illustrates the ability for bacteria to quickly adapt to the effect of antibiotics and render them useless.

The Public Health Agency of Canada cites several ways to prevent the spread of Vancomycin-resistant bacteria. The important aspect is attention to proper sanitary precautions especially in hospitals and clinics. Enterococci are known to survive on surfaces like door handles for several days so regular disinfection of prone areas is also important.

Perhaps the most harmful species to be discussed in this article is multi-drug resistant Tuberculosis. Tuberculosis is a bacteria that generally causes infection in the lungs causing the patient to develop high fever, chest pain and coughing up blood. Multi-drug resistant Tuberculosis is defined as Tuberculosis resistant to at isoniazid and rifampin, the two most effective drugs at fighting this bacteria.4

Preventing the spread of Multi-drug resistant Tuberculosis is of the utmost importance as the symptoms a patient can develop from infection is severe and potentially life threatening and its resistance to drugs make it hard to treat.

These common Multi-drug resistant bacteria make it difficult for healthcare professionals to treat associated infections. These robust organisms find ways to side-step the efforts put forward by antibiotic development and adapt to changing environments. Fortunately, new technology and therapies like antimicrobial Photodisinfection (aPDT) are effective against multi-drug resistant bacteria and does not create the selective pressure that gives rise to more resistance in bacteria.

Sources:
1http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2839888/
2http://www.cdc.gov/mrsa/tracking/
3http://www.phac-aspc.gc.ca/nois-sinp/vre-erv-eng.php#q1
4http://www.cdc.gov/tb/publications/factsheets/drtb/mdrtb.htm

Dude, I want my money back

Imagine showing up at the pharmacy, prescription in hand for your bacterial-driven chest infection, only to be told, Sorry, we’re out of that—as if you were ordering soup of the day at Olive Garden and arrived shortly before closing.

That’s what’s meant by a post antibiotic era where the basic equation is (1) Bugs have become increasingly resistant to the antibiotics we have thus rendering them ineffective, therefore (2) We should have been developing new antibiotics all along but, oops, we never did get around to it.

The reason is money. It costs more than $2.5 billion and takes more than ten years to develop a new medicine. Which is all well and good if thw problem is, say, cancer, heart disease, diabetes, or arthritis, in which case you’ll be on a costly drug for the rest of your life.

Antibiotics, on the other hand, have a major flaw: they actually cure your illness—in a week. And they don’t cost much either. So if you’re in charge of The Very Big Drug Company of America, guess where you’re going to put your R & D money (you have shareholders to satisfy too, remember).

We’re sharing the interview below because it’s a smart discussion on where we’re at with the resistance issue in general. The return on investment discussion begins at 8:45. And we meet the interesting Hazel Barton, PhD, who isn’t waiting around for drug companies to discover new antibiotics. As these drugs are purified from organisms found in nature, her scientific life of adventure seeks them out through deep cave exploration.

Nasal Decolonization Prevents Surgical Site Infections

Surgical site infections (SSI) occur when tissue after surgery becomes infected with pathogens like bacteria.  According to a study conducted by the CDC, SSIs are responsible for 21% of Healthcare-Associated Infections present in hospitals (An infection received during medical treatment in a healthcare facility is termed a Healthcare-Associated Infection)1.  SSIs can vary in severity causing skin irritation and inflammation, but can also develop into more serious conditions affecting internal organs1. If you have ever had surgery, it is likely healthcare workers took precautions against SSIs—perhaps you or a loved one have been affected by SSIs.  Fortunately, there are methods to prevent surgical site infections; a procedure known to reduce the presence of SSIs is nasal decolonization.

Nasal decolonization involves eradicating bacteria present in the nasal cavity. A species of bacteria especially present and pathogenic in the nasal cavity is Staphylococcus aureus that can be killed using antibiotics like Mupirocin and Methicillin2. However, like most species of bacteria, Staphylococcus aureus is known to exhibit antibiotic resistance (especially with Methicillin), which can inhibit proper nasal decolonization. New methods of nasal decolonization like antimicrobial photodynamic therapy (aPDT), with technology like MRSAid, have proven to be effective in eradicating antibiotic resistant Staphylococcus aureus. Furthermore, aPDT is a procedure that does not create selective pressure in populations of bacteria that give rise to resistant traits. aPDT could lessen the chances of you receiving an SSI after surgery.

In several experimental studies, nasal decolonization was found to decrease occurrence of SSIs. A study conducted by Lonneke G.M. Bode et al of The New England Journal of Medicine employed the antibiotic mupirocin for nasal decolonization. The rate of infection in patients that underwent nasal decolonization was 3.4% compared to patients that did not undergo the procedure that had an infection rate of 7.7%3. If your doctors performed this procedure before you had surgery, then you would be less likely to contract a potentially serious surgical site infection. However, as mentioned earlier, some populations of bacteria can exhibit antibiotic resistance and nasal decolonization using antibiotics can prove to be ineffective. In a study conducted by E.Bryce et al of The Journal of Hospital Infection, aPDT was used for nasal decolonization with the objective of reducing surgical site infections. Results showed a decrease in the presence of SSIs in patients who received aPDT treatment (1.6% vs 2.7%)4. It is evident that aPDT is also an effective method for nasal decolonization.

While both studies discussed were able to reduce the likelihood of Surgical Site Infections, aPDT is a robust technology that is also effective against antibiotic-resistant populations of bacteria. This is especially important, as antibiotic resistance is a growing problem in modern medicine. SSIs can prove to be serious conditions in the most severe circumstances, but can ultimately be prevented by procedures like nasal decolonization. How do we ensure these procedures are more regular and present in healthcare facilities?

References:
1“Healthcare-associated Infections.” Centers for Disease Control and Prevention. 2016. Accessed June 14, 2016. http://www.cdc.gov/hai/surveillance/.

2“Nasal Decolonization of Staphylococcus Aureus with Mupirocin: Strengths, Weaknesses and Future Prospects.” Journal of Antimicrobial Chemotherapy. May 18, 2009. Accessed June 14, 2016. http://jac.oxfordjournals.org/content/64/1/9.full.

3Bode, Lonneke G.M. “Preventing Surgical-Site Infections in Nasal Carriers of Staphylococcus Aureus.” The New England Journal of Medicine, January 7, 2010. Accessed June 14, 2016. http://www.nejm.org/doi/full/10.1056/NEJMoa0808939#t=abstract.

4Bryce, E., T. Wong, L. Forrester, B. Masri, D. Jeske, K. Barr, S. Errico, and D. Roscoe. “Nasal Photodisinfection and Chlorhexidine Wipes Decrease Surgical Site Infections: A Historical Control Study and Propensity Analysis.” The Journal of Hospital Infection 88, no. 2 (October 2014). Accessed June 14, 2016.

http://www.journalofhospitalinfection.com/article/S0195-6701(14)00224-2/abstract
http://www.cdc.gov/hai/surveillance/
http://jac.oxfordjournals.org/content/64/1/9.full
http://www.nejm.org/doi/full/10.1056/NEJMoa0808939#t=abstract

http://www.journalofhospitalinfection.com/article/S0195-6701(14)00224-2/abstract

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.

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