How we Think: The United Nations Addresses Silent Violence

At the United Nations in New York this week, as the heads of state of 140 nations gather to address the pressing issues of the day — growing armed conflict, terrorism, and the massive refugee crisis — they will also spend a full day confronting the harm caused by the emerging global crisis of antibiotic-resistant infections.




One reason for the UN action is the sheer size of the number of people affected. The worldwide carnage of death caused by resistant infections is conservatively estimated at 700,000 people. In the US alone, the annual number is put at 23,000. But a compelling new investigation called “The Uncounted,” says that number grossly underestimates actual deaths — “a tiny fraction of the actual toll” — mainly because states simply do not record deaths by resistant infections, do so for only a few types of drug-resistant infections, or do not record consistently. Instead, the death will be listed as organ failure or simply as an infection that couldn’t be treated.

The near future is even more worrying. According to a widely-accepted study by the UK government, drug-resistant infections will kill an extra 10 million people a year worldwide – more than currently die from cancer – by 2050.

The second reason for the UN concern is less obvious but more insidious: Antibiotics have to be used in the treatment of most immunocompromised patients who, by definition, face a higher risk of infection. For example, burn victims, cancer patients undergoing chemotherapy, women undergoing c-sections, organ transplant patients, and even people undergoing routine surgery. And in all cases, the elderly, especially, are at risk. And so without effective antibiotics these procedures become even more dangerous.

Addressing this second issue three years ago the chief medical officer of Britain, Sally Davies MD, described it as “a ticking time bomb,” and that “the growing resistance to antibiotics should be ranked along with terrorism on a list of threats to the nation.”

The UN sees it that way too and thus their action today in putting harm caused by bacteria on equal footing with harm caused by bullets and bombs.

Notice that in all three cases the harm is broader than just death. Antibiotic-resistant infections don’t just kill you, they also do you violence: they scar, cause amputations, necessitate multiple surgeries, stays in the ICU, repeated hospitalizations, and cause infections that once “treated” can lay dormant and strike again at any time even years later. That translates into a lot of pain and suffering, for both the affected individual and for their families. In the US alone, for example, the Centers for Disease Control says at least 2,000,000 people contract resistant-infections every year.

So when Dr. Davies, head of the conservative British medical establishment, publicly states that resistant infections should be ranked with terrorism as a national threat is she exaggerating or does she have it about right?

If your loved-one has died, or is missing a limb, or has been traumatized, should it matter whether it was caused by a bullet, a bomb, or bacteria?

In marshaling our resources to combat harm should it matter any less that with bacteria the violence is silent and unseen?

Seeing Evolution in Action

It’s one thing to hear or read about evolution, and quite another thing to actually watch it in action. In fact, it’s pretty much impossible to do since by definition evolution occurs over generations, not a single lifetime. But a powerful new video from the Harvard Medical School lets us do just that: Watch bacteria as they evolve and move across a 4 foot long petri dish — it looks like a mini-football field — through increasing concentrations of an antibiotic that would ordinarily kill them. (Here is the full report from the Harvard Gazette.)

So why aren’t the bacteria killed by the drug? Because each time the bugs reach a higher concentration of antibiotic they stop, change their DNA (they mutate), thereby developing resistance to the drug. The mutants with the higher drug resistance reproduce and then continue their trek across the antibiotic field.

By the time they reach the middle of the field they have become resistant to 1,000 times as much antibiotic as would have killed them before their first mutation. In similar research at Harvard, bacteria developed resistance to 100,000 times as much antibiotic as would have killed them initially.

The real-world experiment took place over 11 days. The time-lapse video captures the whole process in 2 minutes.

There’s a few things to notice. When bacteria evolve they don’t remain stationary, they spread: here they moved a distance of 2 feet as they developed their drug resistance. Second, the bacteria continue to press forward in the direction of the drug that should kill them, rather than sitting still or heading to safer territory. It’s almost as if they want a fight! And third, the experiment shows us how easily bacteria evolve mutations that are resistant to extremely high concentrations of an antibiotic in just a short period of time.

It is because bacteria spread and mutate so easily — that is who they are — that the UN General Assembly has convened a one-day high-level meeting on Antimicrobial Resistance this-coming September 21 at the UN Headquarters in New York. Since seeing is believing, if the UN hasn’t seen the film we hope that someone brings this remarkable work to their attention.

Annals of Antibiotics: What has the human race gone and done this time?

You’d be forgiven for overlooking it: In the middle of a 6-page report (unfortunately, a subscription is required) about the large number of people using antibiotics without a prescription, is the rundown of where people are getting them:

“The major source of antibiotics used without a prescription was a store or pharmacy in the United States (40%), followed by antibiotics obtained from another country (24%), antibiotics obtained from a relative or friend (12%), antibiotics left over from previous prescriptions (12%), and veterinary antibiotics (4%).”

Dog confusedVeterinary meds? It wasn’t until I came across a CNN interview with one of the lead authors of the study, Dr. Barbara Trautner, that I understood the significance: We’re stealing antibiotics from our pets!

The researchers at the Baylor School of Medicine in Houston, Texas, didn’t anticipate this finding either. That’s why they didn’t even bother to ask about it in their survey. The only reason they discovered the “thefts” is that people who took the survey actually wrote it into their answers, saying it is one way they get off-prescription antibiotics.

Four percent of people using pet meds may not sound like much, but consider the math. The researchers randomly surveyed 400 people from 3 outpatient public health clinics in Harris County, Texas, and found that 5% of them were using nonprescription antibiotics. Harris County has an adult population of 3,285,000, and therefore, the researchers say, the 5% figure suggests that 131,400 primary care patients are using nonprescription antibiotics. And 4% of that figure — the percentage of people taking pet meds — is 5,256. Now multiply that number by the adult primary care patient population across the country — and you get a whopping number of people doing this.

And even that large number is likely to be an underestimate because, as mentioned, the survey didn’t provide for that answer, and because, quoting from the study, “Respondents might deny practicing self-medication, especially if they are aware that this is inappropriate behavior and if they are interviewed in a health care setting.”

Dr. Trautner warns us that we don’t want to be taking pet meds: “We metabolize things differently than animals do, and these drugs are formulated for animals.”

If a patient were ever to ask her about taking their pet’s medication, she said, she would compare it with how chocolate can be poisonous for dogs but fine for humans. Similarly, it may be dangerous for humans to take drugs that are created for an animals’ system.

And that’s on top of the fact that we don’t want to be taking (human) antibiotics in the first place without having seen a doctor because, as the study points out, we may not even need them. So without even any upside, the study points out that a number of things could go wrong, such as: an adverse drug reaction, a superinfection, the masking of an underlying infectious process, and harm to the bacteria in our body that we need for good health.

And should we actually require an antibiotic, we will need the right kind, taken at the right dosage level, at the right frequency, and for the right duration — none of which can be figured out through self-help.

Meanwhile, if our pets could talk we can imagine what they might say about our misusing antibiotics — especially if they caught us taking theirs … “Bad Human,” comes to mind.






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:, 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.

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.

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.


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.

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.


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?

1“Healthcare-associated Infections.” Centers for Disease Control and Prevention. 2016. Accessed June 14, 2016.

2“Nasal Decolonization of Staphylococcus Aureus with Mupirocin: Strengths, Weaknesses and Future Prospects.” Journal of Antimicrobial Chemotherapy. May 18, 2009. Accessed June 14, 2016.

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.

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.

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