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.

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

Mmmm…Raw Cookie D’oh!

For several years now, the government has told Americans to put down the tube of raw cookie dough and step away. New warnings about the harrowing dangers of cookie dough were announced by the FDA last week, right before our 4^th of July holiday. Seriously? You’ve been eating the stuff ever since your BFF started dating your ex in high school. What’s the big deal?

Where did things start to go wrong for Barney? Could it have been the raw cookie dough?

In this crazy, hustle and bustle world, who has the time to wait for the cookies to be cooked? Raw cookie dough allows you to savor all of the yummy cookie goodness without the grueling task of popping them into the oven and waiting 10 minutes, which feels like an eternity when you need your sugar fix. And then there’s the mess to clean up…who needs that?

So you defiantly crack open that tube and bury your face in the heavenly Play-Doh-like substance – nom nom. A few hours later, as you rest in content satisfaction on the couch, you begin to feel a great disturbance in The Force. An abrupt gurgle begins to percolate in your gut. Your stomach makes a demonic growl. Visions of volcanic eruptions suddenly waft through your woozy head. The horrific bout of bloody diarrhea that follows might be enough to convince you to listen to those pesky scientists at the FDA from now on. The intestinal apocalypse you experience may even have you wishing for death, but don’t do so lightly. Raw cookie dough has been known to kill.

Linda Rivera died in 2013, a victim of eating a few spoonfuls of raw cookie dough. Over 70 other people were sickened during this outbreak, which started in 2009 and affected mostly teenage girls and children.

How could something that tastes so good be so bad for you? Your first instinct might be the raw eggs in the dough, which could be contaminated with a common food poisoning bacterium, Salmonella. While this is indeed possible, the latest round of scares stem from flour contaminated with a particularly nasty strain of the bacterium Escherichia coli (E. coli). Shiga toxin-producing E. coli O121 has been identified as the culprit behind a massive recall of contaminated flour made by General Mills. Most E. coli strains are harmless, but this one is so not harmless.

Now you might be wondering:  how does E. coli, a bacterial species that inhabits the gut, get into flour? Flour comes from grain grown in fields where animals may do their business - not the kind of "chocolate chips" you want in your cookie dough! But the grain is not normally sterilized because manufacturers assume that people would actually cook the items made from that flour, which kills the E. coli. However, some people just want the “goods” and not the “baked” part.

The Shiga toxin produced by this type of E. coli is the cause for the alarm – these are proteins made by the bacteria that can bind to receptors on our cells, particularly in the intestine and the kidney, which is why people experience bloody diarrhea and renal failure when infected. Once inside our cells, the Shiga toxin can bind to our ribosomes, which make our cellular proteins. When our cells can’t make proteins, they eventually die.

E. coli bacteria are kind of scruffy-looking, but those “hairs” are actually flagella the bacterium uses to get around. About 10,000 of these can fit on the head of a pin. It only takes 10 of the more virulent strains to make you seriously ill.

Over 40 people have been sickened from the recent outbreak, almost a baker's dozen requiring hospitalization. There have been no deaths to date, and deaths from cookie dough remain extremely rare…but it has happened and is a most unpleasant way to leave the world. So cook your cookies or risk tossing them later.

The FDA also warned that pizza dough, “play clay” made from dough, or “flour crafts” that kids sometimes play with, can also lead to food poisoning. Even if they don’t eat it, the E. coli can get onto their hands, which usually end up in their mouth before they get washed.

In light of these cookie dough poisonings, manufacturers have started to use only pasteurized eggs and, more recently, heat-treated flour to destroy the bacterial culprits. However, they still caution that consumers cook the product properly to be on the safe side.

What about those of us who enjoy our desserts within a dessert, namely cookie dough ice cream? You can breathe easy - cookie dough ice cream is okay to eat because it is typically made with heat-treated flour and pasteurized eggs.

To put things in perspective, E. coli contaminated spinach sickened nearly 200 people and killed 3 of them in 2006. The point is not to eat more cookie dough instead of spinach (sorry)…but to handle and prepare ALL food properly no matter what it is.

Putting it all together, if you are making cookie dough or cake batter from scratch, odds are the flour you're using has not been heat-treated to kill bacteria, so there is a chance it could be contaminated. Even if it is not under the recall, the flour should be treated as you would any other raw food. If you must play cookie dough roulette, some companies are stepping up to the (kitchen) plate and making some that lacks eggs and uses heat-treated flour.

Contributed by:  Bill Sullivan

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Thorpe, C. (2004). Shiga Toxin--Producing Escherichia coli Infection Clinical Infectious Diseases, 38 (9), 1298-1303 DOI: 10.1086/383473

Obrig, T. (2010). Escherichia coli Shiga Toxin Mechanisms of Action in Renal Disease Toxins, 2 (12), 2769-2794 DOI: 10.3390/toxins2122769

Star Wars Midi-chlorians On Earth?

Star Wars Episode VII: The Force Awakens was a HUGE success and is being released on Blu-ray and DVD today. Fans seems to be in agreement that J.J. Abrams did a better job reviving the franchise than George Lucas did with the Star Wars prequels, which caused a great disturbance in the Force.


While Jar Jar Binks soured the prequels for most people, one of the other sticking points was the Midi-chlorians. The what? Let's review. In the original series, the Force was described by Obi-Wan Kenobi as "an energy field created by all living things. It surrounds us, penetrates us, and binds the galaxy together." In episode I, Qui-Gon Jinn delivered the buzzkill message that the mysterious Force actually had a biological explanation. Instead of saying, “The Force is strong with this one”, one may as well say, “The Midi-chlorians are numerous in this one.”


Watching the interview below, Abrams appeared to show disdain for the whole "Midi-chlorian" idea, not even mentioning them in the new film.

According to Wookieepedia, “Midi-chlorians were intelligent microscopic life forms that lived symbiotically inside the cells of all living things. When present in sufficient numbers, they could allow their host to detect the pervasive energy field known as the Force.” A collective groan could be felt through movie theatres worldwide, as if millions of voices suddenly cried out in terror…

To a cell biologist, it sounds like Lucas drew his inspiration from the mitochondria, which are bacteria-like symbionts that work with our cells to provide energy. They even look like they might be cousins (see below). But that is where the similarities end. Unlike Midi-chlorians, mitochondria do not allow us to tap into energy fields…no matter how much we try to quiet our minds to hear our mitochondria speak to us.

Midi-chlorian (left) and mitochondria (right). Brothers from another mother?

 

But a strange and provocative paper by Alexander Panchin and colleagues proposes an unorthodox new idea called the “biomeme hypothesis”, which posits that the impulse behind some religious rituals could be driven by mind-altering parasites.

Let that sink in for a moment. Might your religion, or any number of other activities, be driven in part by parasites or symbionts in your brain? Before you dismiss the idea too quickly, think about the rabies virus. This super tiny virus is notorious for altering the behavior of dogs (and other animals, including people). Rabies can make even the most docile of dogs become uncharacteristically aggressive so that they bite and spread the virus. Rabies virus is just the tip of the iceberg; there is no shortage of parasites that are known to eerily alter their host’s behavior.

Rabies makes dogs aggressive to enhance viral transmission. The virus can get into a new host by causing its current host to bite others.

Central to Panchin’s hypothesis is the idea that certain religious rituals may facilitate the transmission and spread of parasites. The authors site that holy springs and holy water are replete with numerous microbes, including human pathogens. Sacred in Hinduism, the Ganges River probably contains the most, as an estimated 200 million liters of untreated human sewage is dumped into it every day. Bathing in this “purifying” water has led to the development of multiple diseases, such as cholera.  The Hindu “side-roll” ritual is associated with Cutaneous Larva Migrans, also known as “creeping eruption of the skin”, which is caused when the skin becomes infected with parasitic hookworm larvae. Performed in Muslim communities, ritual ablution, which involves irrigation of the sinuses, has been proposed to be a potential risk factor in contracting Naegleria fowleri (the infamous “brain-eating amoeba”) in Muslim communities. Outbreaks of respiratory infectious diseases and meningococcal disease are common amongst Hajj congregation in Mecca. The transmission of herpes has been reported in the Jewish circumcision method known as metzitzah, which involves the sucking of blood from the wound. Finally, many sacred relics are kissed or handled by many worshipers, offering additional routes for the potential transmission of multiple infectious agents.

While it is clearly demonstrable that certain religious rituals have inherent health risks, there currently is no direct evidence that any of the possible infections transmitted can influence the victim’s behavior (other than causing them to see a doctor). Until new data arrives, we are left with the conclusion that the rituals people engage in stem from cultural memes rather than biological. But one thing is clear:  you should use some hand sanitizer next time you dip your fingers in the holy water.

Contributed by:  Bill Sullivan
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Panchin AY, Tuzhikov AI, & Panchin YV (2014). Midichlorians--the biomeme hypothesis: is there a microbial component to religious rituals? Biology direct, 9 (1) PMID: 24990702

A 5,300 Year Old Stomach Ache

In 1991, one of the best preserved mummies was found frozen in the Ötztal Alps, a mountain range near the border of Austria and Italy. This 5,300 year old man was named Ötzi and has been fascinating nosey scientists ever since. So far, scientists have learned about Neolithic fashions and dietary habits, and even identified his cause of death...solving one of the oldest “cold cases” in CSI history. (For the curious, poor Ötzi appears to have been attacked. He took a blow to the head and an arrow to his shoulder).


The well-preserved remains of the “iceman” named Ötzi.

Remarkably, genetic studies of folks living in Austria today reveal that Ötzi has some living relatives. Researchers found that at least 19 people may share a common ancestor with Ötzi, but the odds of one being a direct descendent of Ötzi himself are very remote. Some of these living relatives can be seen in a series of commercials for the auto insurance company Geico:

 

Ötzi provides a window into our past - a glimpse of what life might have been like 5,300 years ago. It turns out that Ötzi suffered from many of the same problems that we still have to contend with today. His body shows signs of heart disease, tooth decay, and joint pain, possibly caused by Borrelia borgdorferi, the bacteria that causes Lyme disease. The latest secret that scientists Frank Maixner and Albert Zink have coaxed out of Ötzi is that he was infected with another bacterial species that still causes grief in millions of people here and now:  Helicobacter pylori.

This is an artist’s rendition of Ötzi. But scientists didn’t just find a 5,300 year old human ancestor that day. They also found 5,300 year old bacteria.

Thanks to a landmark study in the 1980s, we now know that Helicobacter pylori is a causative agent of gastritis or stomach ulcers. Previously, doctors believed that stomach ulcers were simply caused by environmental factors - too much stress, spicy food, or smoking. But Drs. Barry Marshall and Robin Warren had a “gut feeling” that this model was wrong after they repeatedly found bacteria in the peptic ulcer biopsies from patients.

For decades, doctors believed that gastric ulcers were caused by stress. The idea that they were caused by a bacterial infection was a profound discovery and revolutionized treatment of this common ailment.

A lot of medical professionals had a hard time swallowing the idea that gastric ulcers were really an infection. Marshall and Warren faced great difficulty getting their results published in scientific journals. Many other doctors at the time mentioned how controlling the acid in the stomach usually helped patients feel better, and they balked at the idea that bacteria could survive in the acidic milieu of the stomach. Today, we now know that some bacteria can thrive in even the most inhospitable of places, including areas of high acidity. Helicobacter pylori is one such “acidophile” – it grows best under acidic conditions. This also explains why some ulcer patients recover after taking medication that reduces stomach acid; acid reducers cause a gastric climate change that is less favorable to the growth of Helicobacter pylori.

On June 12, 1984, Barry Marshall drank a culture of live Helicobacter pylori. He developed an ulcer, which he successfully treated with antibiotics. A tabloid newspaper first covered “the guinea-pig doctor” story, alongside stories of alien abductions and celebrity gossip. Ultimately, the stunt finally convinced the skeptics and won Marshall and Warren the Nobel Prize in Physiology or Medicine for 2005.

How do we get infected with Helicobacter pylori? The bacteria can be contracted through saliva or accidental ingestion of material coming out of the other end of a person. Somewhere along the way, a little poo from an infected person got into your food/water (or on your hands) and found its way into your gut. As gross as that sounds, it must happen a lot because Helicobacter pylori is present in the gut of billions of people. However, it causes ulcers in only 10% of them. 

Scientists don’t currently know why the bacteria attack the stomach lining of some people but not others. But if you are one of those unlucky few, the damage caused by the bacteria allows stomach acid to pass through the protective lining, which can cause bleeding and digestive problems, and obviously a lot of pain and discomfort.

But thanks to the renegade efforts of Barry Marshall, doctors now know how to treat gastric ulcers more effectively with a simple course of antibiotics. It is perhaps no surprise to you now that our old friend Ötzi had Helicobacter pylori in his tummy. The bug is very common and easily contracted, especially in his day when hand sanitizers were not easily accessible. Whether Ötzi’s Helicobacter pylori actually caused a gastric ulcer is hard to say, as his stomach lining was not preserved well enough to draw firm conclusions. One day we may find a specific type of genetic mutation in people prone to stomach ulcers, which would allow us to revisit the question.

If you want to learn more about the cracking of the stomach ulcer mystery, check out the following video.

 

Contributed by:  Bill Sullivan, Ph.D.

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Williams AC, Edwards HG, & Barry BW (1995). The 'Iceman': molecular structure of 5200-year-old skin characterised by Raman spectroscopy and electron microscopy. Biochimica et biophysica acta, 1246 (1), 98-105 PMID: 7811737


Tito RY, Knights D, Metcalf J, Obregon-Tito AJ, Cleeland L, Najar F, Roe B, Reinhard K, Sobolik K, Belknap S, Foster M, Spicer P, Knight R, & Lewis CM Jr (2012). Insights from characterizing extinct human gut microbiomes. PloS one, 7 (12) PMID: 23251439


Maixner, F., Krause-Kyora, B., Turaev, D., Herbig, A., Hoopmann, M., Hallows, J., Kusebauch, U., Vigl, E., Malfertheiner, P., Megraud, F., OSullivan, N., Cipollini, G., Coia, V., Samadelli, M., Engstrand, L., Linz, B., Moritz, R., Grimm, R., Krause, J., Nebel, A., Moodley, Y., Rattei, T., & Zink, A. (2016). The 5300-year-old Helicobacter pylori genome of the Iceman Science, 351 (6269), 162-165 DOI: 10.1126/science.aad2545

Living Off Nothing But Coffee

Can you imagine living off nothing but coffee? Some of us probably feel like we do at times, if not for the taste then for the buzz the caffeine brings. Caffeine makes us feel more alert because it structurally resembles a molecule called adenosine.

Caffeine and adenosine are like brothers from another mother.

 Adenosine accumulates in our brain the longer we stay awake, binding to its receptors to induce that sleepy feeling we all get after a long day. It is the body’s way of signaling to the brain that it has had enough and needs to shut down for a while. If you disagree with your body, the ingestion of caffeine can help. Due to their structural similarity, caffeine competes with adenosine for binding to adenosine receptors; however, adenosine receptors do not execute the signal to shut down when bound to caffeine. In other words, the body is trying to throw a pass to sleep but caffeine blocks the receiver.

Some people can’t get to their happy place without a cup of joe in the morning. By the way, the term “cup of joe” is likely to have originated from “cup of jamoke” - “jamoke” being a combination of locales noted for their coffee goodness, “Java” and “Mocha”.

But that’s not all. Caffeine also ramps up adrenaline production, which increases your heart and breathing rates, and primes your brain and muscles for action. You feel a boost from coffee because the caffeine blocks the signal to sleep and fools your body into thinking it is under attack.

 

Like other drugs, people can build up a tolerance to caffeine, requiring more and more of the drug just to achieve the sensation of that original buzz. And the road to addiction is a short one, indeed. People love their coffee so much that the threat of a shortage can send them into a panic, which is perfectly captured in this scene from Airplane II.

 

How much coffee can people safely consume? According to the FDA, 400 mg (4 cups of brewed coffee) per day appears to be safe for most healthy adults. While it is estimated to take about 140 cups (8 oz size) of coffee to kill, you can get there a lot quicker with pure caffeine powder. A single tablespoon can be lethal, prompting the FDA to issue this warning to consumers.

But there is a creature on Earth that can tolerate much, much more. In fact, it eats coffee beans for breakfast. And lunch. And dinner. And everything in-between. Amazingly, the coffee berry borer eats nothing but coffee beans!

The coffee berry borer is a small but devastating beetle that lays waste to coffee crops. It subsists solely on coffee, capable of drinking any Starbucks junkie under the table.

Scientists have recently discovered how the coffee berry pest can tolerate toxic levels of caffeine. Do they possess a special gene that can detoxify caffeine? Do they have receptors that don’t bind caffeine? No…evidently, the answer does not lie in the genome of the beetle, but in its gut.

 

Like most other living creatures, the coffee berry borer houses a microbiome in its intestinal system. Several species of bacteria, such as Pseudomonas fulva, that reside in the gut of coffee berry borers are wizards at breaking down caffeine. The gut bacteria from coffee berry borers found around the world were put into culture medium containing caffeine as the primary nutrient so researchers could identify which species grew the best in this condition. P. fulva was the most common; subsequently, this bacterial species was found to carry a gene known to degrade caffeine.

To further test this hypothesis, researchers gave the beetles antibiotics to deplete their intestinal microbiome. Beetles without their gut bacteria lost the ability to break down caffeine. When fed some P. fulva before their coffee bean diet, the beetles excreted no caffeine, indicating that they were able to detoxify it once again.

Assuming no adverse effects, ingestion of P. fulva might help humans break down caffeine. A better alternative to decaf?

The scientists speculate that altering the beetle’s microbiome might provide a new approach in the battle against this pest. However, antibiotics are a precious commodity in treating human disease, so this could be a reckless idea as the introduction of antibiotics into the field has the potential of generating resistant bacteria.

From an evolutionary perspective, the study serves as an example of how organisms can adapt to a new niche without genetic modification. By acquiring specific types of bacterial symbionts, the coffee berry borer is uniquely able to live off nothing but coffee.

In the video below, you can learn more about this research and similar studies being performed at Lawrence Berkeley National Laboratory:
 

 

Contributed by:  Bill Sullivan

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See the news release at ScienceDaily.
 

Ceja-Navarro, J., Vega, F., Karaoz, U., Hao, Z., Jenkins, S., Lim, H., Kosina, P., Infante, F., Northen, T., & Brodie, E. (2015). Gut microbiota mediate caffeine detoxification in the primary insect pest of coffee Nature Communications, 6 DOI: 10.1038/ncomms8618