90 Years Ago, A Contaminated Petri Dish Changed The World

Scientists throw away contaminated petri dishes every day. There is probably a frustrated researcher chucking her petri dishes into the bin right now as you read these words, cursing at the contaminant that ruined her experiment. 

In those petri dishes are soft beds of agar that bacteria feast upon. Hundreds of bacterial colonies grow on the agar, each one containing millions of bacterial cells. But fungal spores lurk in the air, and if one of them happens to land on the agar, it may grow better than the bacteria. When a mold appears in a researcher’s bacterial dish, it is not a good thing.

Alexander Fleming stares menacingly at a plate of bacteria.

Unless you were keeping your eyes peeled for a substance that can kill bacteria. In the 1920’s, a scientist named Alexander Fleming at St. Mary’s Hospital in London was doing just that. Fleming was growing colonies of Staphylococcus aureus bacteria on his petri dish plates. Staphylococcus aureus is commonly found on the skin, where it normally lives in peace. But it can turn into a deadly troublemaker if it finds its way into the bloodstream. One of Fleming’s first discoveries was that snot could kill the bacteria. He soon isolated the murderous enzyme (lysozyme), but it proved to be a rather weak assassin with no viable therapeutic potential. Besides, it would have been a marketing nightmare...what would you call it? Snoticide? Boogie bombs?

One fateful autumn day in 1928, Fleming arrived at his laboratory to a pile of petri dishes that needed cleaning. While sorting through them, he noticed a mold growing on one of his culture dishes of Staphylococcus aureus. Fleming had undoubtedly seen a contaminated dish of bacteria before, but something more caught his eye that day. It turned out to be the discovery of a lifetime – one that has saved an incalculable number of lives.

As Louis Pasteur said, “Chance favors only the prepared mind.” Fleming’s mind was prepared, and he was always on the lookout for things that could kill bacteria. On that contaminated plate of Staphylococcus aureus, he astutely noted that bacterial colonies grew better if they were farther away from the mold. In fact, no colonies could grow next to the mold. He figured that the mold was producing a substance that was actively killing bacteria that dared to come near it. The miserly mold would want to do this so it could have all the nutrients to itself. Fleming named this mystery bacteria-slaying substance penicillin, since the species of contaminating mold was called Penicillium.

The famous plate showing bacterial colonies being
killed by the mold, Penicillium.

Fleming published this extraordinary finding in the British Journal of Experimental Pathology in 1929 and the world…paid absolutely no attention to it at all. Pathogenic bacteria continued to lead tens of millions of people to early graves through the 1930’s. Fleming was no chemist, so he was not in position to isolate the active ingredient in the mold that was killing the bacteria. He needed help. But try as he might, Fleming couldn’t get other scientists interested in the promise of mold as a remedy for bacterial infections.

In hindsight, that seems crazy. But there were practical issues that dampened enthusiasm for his idea. At the time, fungi were very difficult to grow in bulk, and the strain of Penicillium Fleming promoted produced very little penicillin. Fleming’s follow-up studies also suggested that penicillin would not work well in the clinic. Because it was so rare, he was forced to use low doses in his attempts to treat ill patients. He also applied the “mold juice” topically on the skin instead of injecting it into the bloodstream, which would have been far more effective. These poorly designed experiments led many to the false conclusion that penicillin was an impotent bacterial assassin. You can imagine the skeptics dismissing his work: “First snot, now mold juice? C’mon, Fleming.” Consequently, Fleming’s discovery laid dormant for over a decade.

In 1939, while leafing through back issues of the British Journal of Experimental Pathology, a chemist at Oxford named Howard Florey decided to revisit Fleming’s ignored penicillin paper. Together with Ernst Boris Chain, this dynamic duo produced a highly purified mold extract and injected it into mice with sepsis. They soon published the striking result that their Penicillium extracts cured the mice of this deadly bacterial infection.

Imagine Fleming’s response when he woke up one day to read this report! Fleming was thrilled that someone was making use of his old work and immediately called Florey to arrange a visit to their laboratory. Chain was surprised to hear that he would get to meet Fleming, as he was under the impression that Fleming had passed away. The trio won the 1945 Nobel Prize in Physiology or Medicine and inspired many microbiologists to search for more bacteria-killing microbes out in the wild. Before long, our medicine cabinet was filled with additional antibiotics like erythromycin, tetracycline, streptomycin, and many more. These wonder drugs were being produced naturally by microbes found in the dirt, on rotting foods, and even in the throat of a chicken. Scientists left no stone unturned in their hunt for weapons of microbial destruction.

It took ten years before a pair of scientists took Fleming's paper on penicillin seriously. It makes one wonder: How many other medical treasures are buried in obscure scientific journals?

The story would have a happy ending were it not for two things. In an interview after his Nobel acceptance speech, Fleming gave a very prescient warning about the reckless overuse of antibiotics: "The thoughtless person playing with penicillin treatment is morally responsible for the death of the man who succumbs to infection with the penicillin-resistant organism." Unfortunately, we failed to heed Fleming’s premonition and now face an imminent threat of “superbugs,” bacterial strains that have evolved resistance to these precious medicines. Poor Fleming...ignored twice, but later proven correct on both accounts. Second, virtually no one is in the business of antibiotic discovery anymore because it does not generate high profits like medicines for chronic conditions, which patients must take every day for the rest of their lives. Considered together, Fleming’s near-century old discovery may soon be ineffective and we will return to the “pre-antibiotic” era when a simple scratch from a rosebush could mean death. We need more “prepared minds” in research and in business to keep the antibiotic pipeline strong.

Contributed by: Bill Sullivan

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Bill is writing a book! PLEASED TO MEET ME: The Hidden Forces Shaping Who We Are arrives in August 2019 from National Geographic Books.

Unsung Heroes In Our Battle Against Infectious Disease

Humanity has always been at war with infectious agents, but it wasn’t until 1860 when Louis Pasteur famously theorized that microbes (first observed by Antony van Leeuwenhoek in the 1600s) cause disease. It took another 70 years before Alexander Fleming noticed that Penicillium mold produced a substance that killed bacteria. While most people are familiar with these luminaries in the field, have you heard of Francesco Redi, Ignaz Semmelweis, Theobald Smith, Mary Hunt, and a cow named Blossom? In this presentation, we celebrate some of the “unsung heroes” whose victories are often neglected from the infectious disease saga.

In the talk below, Dr. Bill Sullivan, a professor at the Indiana University School of Medicine, takes us on a fascinating tour through medical history, answering these questions and more:

How did we figure out that microscopic creatures can make us sick?

Why were milkmaids considered to be so beautiful and what does that have to do with vaccination?

How were starfish important to the discovery of the immune system?

What do you mean penicillin wasn't the first antibiotic?

Watch the talk "Unsung Heroes In Our Battle Against Infectious Disease" by Bill Sullivan here.

The Rise Of Superbugs: How Bacteria Defeat Antibiotics

News stations are constantly warning us about the threats of climate change, hackers, and another season of Fuller House, but what doesn't get enough press is the rise of superbugs. We're not referring to a new species of insect aliens from Starship Troopers, but rather old enemies right here on Earth. Enemies so small that a microscope is required to see them, yet so mighty that just a few of them can spell the end of your existence.

No, that's not what we mean by superbug. We're talking about pathogenic bacteria.

Throughout human history, we've been locked in an ongoing struggle with infectious disease. For much of our existence, pathogenic bacteria have wiped out huge swaths of people and kept our average life expectancy under 50 years. But thanks to the discovery of antibiotics in the early 20th century, most people are no longer dying from skin infections, pneumonia, and tuberculosis.

Alexander Fleming's discovery that a mold (Penicillium notatum) produces a substance (penicillin) capable of killing bacteria revolutionized medicine, giving us the upper hand in the war on infectious disease. However, we are now losing our advantage in this war.

Since the advent of penicillin in the 1940s, antibiotic discovery and research exploded, filling our medicine cabinets with lots of other wicked bacteria-killing drugs with crazy names like the macrolides, tetracyclines, fluoroquinolones, aminoglycosides, and more. By the 1960s, we became so complacent with our pharmacological arsenal that the majority of antibiotic research ground to a halt. Consequently, very few new antibiotics have been developed in the last half-century, leaving us caught with our pants down in the wake of bacteria that have evolved resistance to our current supply of antibiotic drugs.

Speaking of being caught with our pants down, a recent case in point is Neisseria gonorrhoeae, the bacteria that causes gonorrhea. Once easily treated with a shot of penicillin, gonorrhea has quietly evolved resistance to multiple types of antibiotics over the years. Since there is now a danger of gonorrhea being untreatable once again (!), Neisseria gonorrhoeae is considered a superbug by the CDC. Pat Benatar warned us that "Love is a Battlefield"...and now the Huey Lewis request, "I Want a New Drug", takes on an urgent new meaning.

Gonorrhea used to be a very serious infection before the discovery of antibiotics. Today, scientists are sounding the alarm that the bacteria responsible for the infection may no longer be treatable if it continues to evolve resistance and we fail to develop new antibiotics.

There are 26 antibiotic drugs approved for use in the US. Just this week, the news broke that an elderly woman died in Nevada after losing a battle with a stubborn superbug. She succumbed to an infection caused by CRE - carbapenem-resistant enterobacteriaceae (carbapenem is one of our "last resort" antibiotics that is only used when others have failed). In other words, the bacteria that killed her was immune to every single antibiotic we have in our arsenal.

So how do bacteria develop resistance to our medicines? There are at least four different ways. One, bacteria can mutate, or change, the protein that is targeted by the antibiotic. For example, penicillin inhibits a bacterial enzyme called transpeptidase, which is required by the bacteria to build its cell wall properly. Bacteria that acquire a DNA mutation that makes a slightly different version of transpeptidase can become resistant to penicillin (the new version can still build the cell wall, but no longer interacts with penicillin). A related strategy bacteria can use involves increasing the amount of the drug target; in other words, the bacteria could make more transpeptidase - too much for the drug to inhibit effectively.

Two, the bacteria can acquire a gene that makes a protein called penicillinase, which can directly attack the penicillin compound and cut it up. Some bacteria already have this gene and can pass it along to other bacteria that do not have it. Penicillinase is like a bomb diffuser - the bacterial equivalent of Sergeant First Class William James in The Hurt Locker.

Three, bacteria can mutate proteins that are needed for the antibiotic to get into the bacteria cells. Finally, bacteria can also use "efflux" proteins to pump out the antibiotic. These two related strategies effectively keep the antibiotic out of the bacteria and away from its target. A cartoon summary of these mechanisms of antibiotic resistance is shown below.

In summary, bacteria have many ways to combat the drugs we use to kill them. We need to step up our game and fast if we want to stay ahead of the devastating infections bacteria inflict upon us. We need more kryptonite to defeat the superbugs!
 
For more on why bacteria develop resistance to antibiotics, check out this informative video from Everyday Elements.

Contributed by:  Bill Sullivan

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Blair, J., Webber, M., Baylay, A., Ogbolu, D., & Piddock, L. (2014). Molecular mechanisms of antibiotic resistance Nature Reviews Microbiology, 13 (1), 42-51 DOI: 10.1038/nrmicro3380

Pull Up A Stool And Let's Talk About Your Microbiome

A medical case report recently made headlines supporting the notion that the bacteria inside our gut have something to do with the size of our gut.

Clostridium is a nasty strain of bacteria that is resistant to many antibiotics. Normally, the many other species of bacteria in the gut keep Clostridium in check, but when those friendly bacteria are wiped out during antibiotic therapy, Clostridium can thrive and produce severe inflammation (colitis) and diarrhea. This can develop into a serious illness that claims the lives of 14,000 Americans every year.

A novel way to treat this condition is through use of fecal microbiota transplant (FMT). In other words, the patient ingests the intestinal bacteria from a healthy person to replenish their own stock and get Clostridium back under control. We will leave it to your imagination as to how doctors collect the good bacteria, but let's just say you can make some decent money if you're willing and able to donate. Thankfully for patients, FMT is available in pill form.

As unappealing as it sounds, fecal transplants - which repopulate intestinal bacteria in the recipient - are proving to be very effective in treating some serious ailments. 

As reported recently, a young woman with a stable weight of ~130 pounds had to undergo FMT to fight a Clostridium infection. The good news is that she beat the infection, but the bad news is that she gained 34 pounds in 16 months, classifying her as obese with a BMI of 33. Even more alarming is that she could not lose weight despite being on a supervised liquid diet and exercise program. The donor for the FMT (her teen daughter) was overweight, but otherwise in good health, so doctors are now recommending that FMT donors be of normal weight.

In light of this news, here's a beginner's guide to the tiny creatures calling you "home"...

You are not just a person – you are an ecosystem. Your body is home to trillions of microscopic critters, including viruses, bacteria, and fungi, living on or inside you. Collectively, these communities of microbes constitute what is called your “microbiome”.

And there are more of “them” than “you” – the number of microbes inhabiting your body is larger than the number of cells making up your body! To put this in perspective, it has been estimated that your microbiome weighs about 3 pounds. Good news if you’re on a diet – when you step on the scale tonight, feel free to subtract 3 pounds of stuff that isn’t “you” per se.

A new study concerning our microbiome seems to be coming out each week, so it is time we get to know our microbial roommates.

1. Where does your microbiome come from?

We are born virtually sterile, but quickly receive an infusion of bacteria from our mom, first through the birth canal and then through the milk. Over 900 species of bacteria have been found in breast milk, and these are the pioneers that settle into your gut, which appears to stabilize by the age of 3. Of potential interest are babies born by caesarean section or those who are fed formula instead of breast milk. Babies delivered via C-section do in fact have a different microbiome and may be at higher risk for certain types of allergies and obesity (more on this below). Our microbiome continues to receive fresh new imports as we move through, inhale, and ingest our environment.

How much of you is really you? There are more microbes in your body than the number of cells making up your body. We are just now beginning to appreciate the many things they do for us.

2. Your microbiome is like your own personal “germ cloud”.

You’ve probably noticed that everyone’s home smells a little different. Sometimes this is due to cooking, pets, or the amount of trash they let accumulate, but it is also due in part to the microbiome of the inhabitants. Researchers have found that you are surrounded by a “germ cloud”, and you leave pieces of your microbiome wherever you go like a trail of breadcrumbs. It might even be possible for police to use microbiomes to track people one day like they currently use fingerprints or DNA. In other words, you have a “microbiome fingerprint” that is left behind like a germ echo wherever you go.

This “germ cloud” may also explain how dogs can track people so easily. The byproducts generated by the millions of bacteria living on your skin are aromatic (odorous), producing a scent that is released into the air as you move. Animals with a keen sense of smell can get a whiff of these aromatic compounds and follow them to the source.

Speaking of “germ clouds”, if you ever wondered if it is possible to fart out germs, some brave scientists have sniffed out the answer to this question. You can read about the results here.

3. Antibiotics substantially alter your microbiome.

We take antibiotics to get rid of pathogenic bacteria that make us sick. The problem is they are not selective, so they destroy a lot of our friendly bacteria in addition to the bad guy. We need these friendly bacteria to do all sorts of things – to name just a few:  they help us digest food, make vitamins, and build anti-inflammatory compounds.

Another important thing our microbial friends do is keep infections in check. For example, yeast infections from pathogenic fungi can arise if good bacteria are not around competing for resources. And some bacteria, like the nasty Clostridium difficile, are naturally resistant to many antibiotics. When good bacteria are killed as collateral damage in an antibiotic treatment, the growth of Clostridium can run amok. These bacteria secrete a toxin that causes diarrhea and they can lead to a life-threatening superinfection in some patients.

4. Your microbiome may protect you from allergies or obesity.

Several recent studies have correlated unusual microbiome composition with the presence of certain allergies. Dr. Hans Bisgaard has shown that infants harboring fewer species of gut bacteria have an increased risk of developing certain allergies as they grow up. More recently, Dr. Catherine Nagler has shown that certain bacterial species offer protection from peanut allergies.

Dr. Martin Blaser has found that administration of penicillin to mice soon after birth altered their gut microbiome in such a way that it made them more prone to obesity as adults. Remarkably, the tendency to grow obese is transferrable to germ-free mice – in other words, by transplanting the microbes from the penicillin treated mice to normal mice made the normal mice more susceptible to weight gain.

Studies such as these make it tantalizing to speculate that we may be able to treat certain ailments in humans by altering our microbiome with specific probiotic regimens. Maybe they could even slip these bacteria into our peanut butter instead of deadly Salmonella.

5. How do scientists study the microbiome?

Advances in DNA sequencing have allowed scientists to rapidly map the genomes for many microbial species, which provides us with a “genomic fingerprint”. We can process samples swabbed from the skin or body cavities, or process stool samples, for DNA sequencing. Usually just sequencing the 16S ribosomal RNA gene is enough to distinguish one bacteria species from another.  

It should be mentioned that some scientists are issuing cautions about over-interpreting microbiome studies. Many of the studies altering the microbiome have been performed in mice, so it remains to be determined to what extent the findings can be extrapolated to humans. Furthermore, many of the methods used to alter the microbiome in lab animals do not faithfully mimic what humans do with antibiotics. For example, in some studies the investigators give large doses of antibiotics over unusually long periods of time to see an effect in lab animals, which does not equate to the typical dosing of antibiotics in humans. Finally, many of these studies are correlative and have not yet definitively demonstrated causation. There is a big difference between correlation and causation.

6. So should I take my microbiome into my own hands?

Much more research needs to be done to assess the true impact of the microbiome versus other factors that come into play, such as host genetics, diet, and the environment. It is argued that some microbiome studies are hyped up and way overblown. Long story short:  if you or your child becomes sick with an infectious agent, it is not wise to withhold antibiotic treatment out of fear that it will cause allergies or obesity. If you are overweight, a healthier diet and plenty of exercise is going to do much more than any probiotic pill. In fact, there is little evidence that the popular probiotics on the market do anything to remedy the wide-ranging health problems some claim to treat, although there is data showing potential benefit in treating some gastrointestinal maladies, especially acute diarrhea caused by rotavirus.

Go here to learn more about the NIH human microbiome project.

Contributed by:  Bill Sullivan, Ph.D.

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Lax S, Smith DP, Hampton-Marcell J, Owens SM, Handley KM, Scott NM, Gibbons SM, Larsen P, Shogan BD, Weiss S, Metcalf JL, Ursell LK, Vázquez-Baeza Y, Van Treuren W, Hasan NA, Gibson MK, Colwell R, Dantas G, Knight R, & Gilbert JA (2014). Longitudinal analysis of microbial interaction between humans and the indoor environment. Science (New York, N.Y.), 345 (6200), 1048-52 PMID: 25170151

Bisgaard, H., Li, N., Bonnelykke, K., Chawes, B., Skov, T., Paludan-Müller, G., Stokholm, J., Smith, B., & Krogfelt, K. (2011). Reduced diversity of the intestinal microbiota during infancy is associated with increased risk of allergic disease at school age Journal of Allergy and Clinical Immunology, 128 (3), 646-65200000 DOI: 10.1016/j.jaci.2011.04.060

Cox, L., Yamanishi, S., Sohn, J., Alekseyenko, A., Leung, J., Cho, I., Kim, S., Li, H., Gao, Z., Mahana, D., Zárate Rodriguez, J., Rogers, A., Robine, N., Loke, P., & Blaser, M. (2014). Altering the Intestinal Microbiota during a Critical Developmental Window Has Lasting Metabolic Consequences Cell, 158 (4), 705-721 DOI: 10.1016/j.cell.2014.05.052

Stefka, A., Feehley, T., Tripathi, P., Qiu, J., McCoy, K., Mazmanian, S., Tjota, M., Seo, G., Cao, S., Theriault, B., Antonopoulos, D., Zhou, L., Chang, E., Fu, Y., & Nagler, C. (2014). Commensal bacteria protect against food allergen sensitization Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.1412008111

Williams NT (2010). Probiotics. American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists, 67 (6), 449-58 PMID: 20208051

Alang, N., & Kelly, C. (2015). Weight Gain After Fecal Microbiota Transplantation Open Forum Infectious Diseases, 2 (1) DOI: 10.1093/ofid/ofv004

Attack Of The Germs!

No one likes being sick, especially with the flu. The body aches, the fevers, and the congestion all leave us desperate for ways to end the misery. Indeed, it’s growing increasingly hard to ignore the commercials telling us to stock up on flu-fighting products, like disinfectants and hand sanitizers. But how much do these items really help you avoid becoming the flu’s next victim, and do they have other consequences that we should be aware of?

Let’s first take a look at how many of the popular disinfectants work. Cleaners like Lysol have different types of salts in them that kill germs by disrupting important protein interactions, which causes the pathogen to stop functioning normally. These salts can also work by breaking up the membrane that surrounds bacteria and some viruses, essentially breaking open the pathogen and causing everything inside it to leak out. In both of these cases, the germs stop growing or are killed altogether.

Alcohol-based hand sanitizers work in a similar manner. At concentrations of at least 60%, ethyl alcohol (or ethanol) is effective at killing some viruses, including influenza viruses. Ethanol works by changing the shape of proteins, and therefore interferes with their ability to properly interact with other proteins. Ethanol can also disrupt membranes.

 

Image of Influenza virus from the CDC highlighting proteins on the outer surface that help the virus infect cells, and the viral genome located inside.

While killing off the germs that can make us sick sounds like a good way to stay healthy, the problem with using disinfectants and sanitizers to do this is that these products kill nearly all of the microbes in our environment. While there are many microbes that make us sick, there are also many that we need to help keep us healthy. If we kill those microbes off too, then we may put ourselves at risk for developing other health problems. 

On and within our bodies live millions and millions of good microbes that do things from helping us digest food, to helping keep bad microbes out of our bodies. These good microbes encompass the population known as the microbiome. The microbiome populations shift depending on the location of the body. For example, we have good bacteria that live on our skin, the population of which differs from the population of good bacteria that live in our digestive tracts. There is increasing interest in exploring the functions of the different microbiome populations, and many studies are showing that the microbiome has important roles in keeping us healthy. For example, it is thought that irregularities in the gut microbiome population may have a role in some inflammatory bowel diseases like Crohn’s disease and ulcerative colitis. It is possible that killing off the beneficial microbes in and on our bodies counteracts any good effect from killing off germs.

 

Keeping our good microbes around is only part of the story. According to the CDC, we are currently on the brink of a public health crisis due to the increasing numbers of microbes that are becoming resistant to common antibiotics. Due to our overuse and misuse of antibiotics, we have created strains of bacteria that are no longer susceptible, or able to be killed, by standard treatments. As bacteria populations are constantly exposed to antibiotics, many of those bacteria will be killed because they are sensitive to the antibiotic, but there will be some that are naturally able to withstand the actions of the antibiotic. Eventually, the population of bacteria that was initially a mix of sensitive and resistant will transition to a population of bacteria that is completely resistant, as all of the susceptible bacteria are killed off. What is the impact on us? In 2013, the CDC reported that at least 2 million people in the United States become infected with antibiotic-resistant bacteria, and that at least 23,000 of these people die from their infections.

Perhaps the most well-known case is MRSA, or methicillin-resistant Staphylococcus aureus. Staph bacteria are common and normally cause minor skin infections; however, MRSA has been highlighted in the media several times over recent years due to the outbreaks of invasive infections it has caused due to its resistance to standard antibiotics. MRSA is but one example of the bacterial strains that develop resistance to antibiotics due to constant exposure to them.

As we continue the cycle of overuse and misuse of antibiotics, we eventually will find ourselves at a point where no antibiotics will be effective against bacterial pathogens. Many public health experts suspect that point is near. There is reason to believe that constant use of disinfectants will eventually lead to the development of germs that are resistant to those disinfectants, just as we see happening with bacteria and antibiotics.

So how do we keep ourselves healthy without potentially setting ourselves up for other health problems later? We can start by limiting our use of disinfectants, and go back to simpler, tried-and-true methods of preventing the spread of communicable diseases. Despite the popularity of disinfectants and hand sanitizers, the CDC still maintains that hand-washing is one of the best ways to avoid spreading and catching viral and bacterial infections from others. Wash your hands before you eat, and avoid touching your hands to your eyes and nose.  If you are sick, do your best to sneeze or cough into the crook of your elbow (i.e., do the “Dracula sneeze”) rather than into your hands, and wash your hands frequently to avoid spreading your germs to others.

 

Of course, use soap that does not contain antimicrobial additives, like triclosan, to avoid encouraging the development of strains resistant to this compound. Soap is a potent killer of germs all by itself - it does not need supplemental antibiotics. While some companies are moving away from including triclosan, it is still present in many products, so be sure to check your labels.

Disinfectants have their place; they’re good for cleaning up food preparation areas that have come into contact with raw meat, for example. And, in times when you’re without clean water and soap, hand sanitizer can be a great tool for keeping your hands clean. But as with most things in life, these items should be used with care and arguably in balance with other washing methods in order to avoid creating greater problems down the line.

Contributed by:  Kelly Hallstrom
Visit Kelly’s blog, You Don’t Have To Be A Rocket Scientist
Follow Kelly on Twitter.

 

CDC Threat Report on Drug-Resistant Bacteria:

http://www.cdc.gov/drugresistance/threat-report-2013/

CDC and hand washing:

http://www.cdc.gov/handwashing/

 

Greenblum, S., Turnbaugh, P., & Borenstein, E. (2011). Metagenomic systems biology of the human gut microbiome reveals topological shifts associated with obesity and inflammatory bowel disease Proceedings of the National Academy of Sciences, 109 (2), 594-599 DOI: 10.1073/pnas.1116053109