Anti-bacterial soaps: why they do far more harm than good


There is an entire aisle in the supermarket devoted to cleaning products, many of which contain antibacterial chemicals. The most common, Triclosan, is found in about 75% of antibacterial soaps. Triclosan (2,4,4’ –trichloro-2’-hydroxydiphenyl ether) is a synthetic antibacterial chemical that was developed in the 1970s for use in hospital scrub rooms, but it has since made its way into hundreds of the products we use every day, all without formal FDA approval or safety studies.  Not only is Triclosan a common ingredient in hand soap, it’s also in children’s toys, toothpaste, deodorant, cosmetics, bedding, clothing, cutting boards, and much more, often marketed under trade names such as Microban®.

It doesn’t stay in those products…

A Center for Disease Control study in 2008 found that 75% of people have Triclosan in their urine. The chemical has also been found in breast milk, amniotic fluid, nasal secretions, and blood plasma, so it is obviously absorbed quite easily into our bodies.

Why is this bad?

Studies in animals and in cultured human cells have shown that Triclosan reduces heart and muscle function by as much as 25%. And this is after just 20 minutes, at doses equal to normal daily exposure. While a healthy person might not notice any difference, this could be a real problem for someone with already impaired cardiac function.

Triclosan has also been shown to alter levels of hormones, including estrogen and testosterone, and can have negative effects on thyroid function. In children, exposure to the chemical increases incidence of allergies. It isn’t yet known if this is a direct effect, or if Triclosan simply kills off too many of a child’s normal, protective bacteria, altering their developing immune function.

Killing off your ‘friendly’ bacteria is never a good idea, because it leaves that formerly occupied space wide open for infection, or to be covered by a bacterium that is resistant to antibacterials. Remember how Triclosan is absorbed into your bloodstream and later turns up in nasal secretions? It turns out that this enables Staph. aureus to bind to certain proteins in the nasal cavity and colonize it. Three in ten people carry Staph naturally in small, harmless amounts, but when it’s given an opportunity to take over, it will, and 85% of Staph infections are caused by our own bacteria

What about all of that Triclosan going down the drain?

Triclosan is one of the most frequently found chemicals in our rivers and streams, and it doesn’t break down easily, so it tends to build up in the environment (and, by the way, in our own bodies). When it reacts with chlorinated water, commonly found in homes in cities and towns with a central water supply, it can form chloroform, a potentially carcinogenic compound.

It does kill bacteria, as promised by those ads…

But it doesn’t work any better than plain soap and water would, even the FDA says so.  And this completely unnecessary chemical is adding to the growing problem of antibiotic resistance.  Triclosan works by blocking an enzyme that bacteria need to make a certain fatty acid that is part of their cell membrane.  The mechanisms bacteria develop to get around this problem and become resistant to Triclosan are often the same mechanisms they use to develop resistance to antibiotics.  Studies have shown that bacteria which have developed resistance to Triclosan are also now resistant to important antibiotics, including erythromycin, ciprofloxacin, ampicillin and gentamicin. All without ever coming in contact with these drugs.

Ironically, Triclosan has no effect at all on viruses, which cause the majority of the illness people are trying to avoid in the first place, such as colds, flu, and the norovirus.


What about alcohol-based hand sanitizers?

They are safe and relatively effective, as long as the alcohol content is at least 60%. Less than that, and they are too dilute to kill bacteria, with 70% being the most effective concentration. Alcohol kills bacteria and viruses physically, not chemically like antibacterials and antibiotics, so they can’t develop resistance to it. Alcohol disrupts lipids (fats) in the bacterial membrane (its ‘skin’), causing it to begin to fall apart. The alcohol can then enter the cell and denature the proteins there, killing the bacterium. If the percentage of alcohol to water is too high (greater than 75% or so) it evaporates before it can get inside the bacterial cell, and doesn’t do any good. Keeping this in mind, you need to use enough alcohol-based hand sanitizer so that it doesn’t evaporate too quickly from your skin.  Your hands should feel wet for at least 15 seconds, or longer.

And what works best of all for germ-free hands?

That’s right, plain old soap and water. Soap works in two ways. First, it loosens dirt and germs from our skin and washes them away. Second, it has the same kind of physical killing power as alcohol. Remember those fats that hold bacterial cell membranes together? Just think about how well soap breaks up the grease on your dishes. It breaks apart bacteria in much the same way. To eliminate the majority of germs from your hands, you should wash them for at least 24 seconds

Why doesn’t soap and alcohol hurt our own cells?

Our cells have the same kind of lipid-based membrane as bacterial cells do, but we are much better protected. The outer layers of our skin have high amounts of a protein called keratin that forms a tough barrier to protect them from physical assault. As the keratin builds up and gets too thick, the outer cells die, which is why our skin is constantly shed and replaced. When soap gets into a cut, our nasal passages or our eyes, which are not protected by keratin, it stings. This is because the soap is damaging our cells just like it damages bacteria. Your body protects itself from this damage by increasing fluids to wash the irritant away, which is why your eyes and nose water when you get soap in them.



Allmyr, M. 2006. Triclosan in plasma and milk from Swedish nursing mothers and their exposure via personal care products. Science of the Total Environment 372(1): 87-93

Calafat, A.M.  2008.  Urinary concentrations of Triclosan in the U.S. population: 2003-2004. Environ. Health Perspect. 116(3): 303-307

Cherednichenko, G., 2012. Triclosan impairs excitation-contraction coupling and Ca2+ dynamics in striated muscle. PNAS 109(35)

Rule, K.L, Ebbett, V.R., and Vikesland, P.J. 2005. Formation of chloroform and chlorinated organics by free-chlorine-mediated oxidation of Triclosan. Environ. Sci. Technol. 39(9): 3176-3185

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Chickens Eggs and Salmonella


‘Bernice’, our farm’s favorite chicken


Salmonella is a type of bacteria that was discovered in 1887 by an American veterinarian named Daniel Elmer Salmon (hence the name), and there are over 2,000 strains that we know of. Salmonella is actually quite common in the environment and even in our own gut, but luckily only some of those thousands of strains are harmful to humans. Many of those harmful strains happen to be carried by birds and other animals, including chickens, as a small part of their normal gut flora. All chickens can have varying amounts of Salmonella in their bodies, no matter how clean their surroundings are kept.

So how does Salmonella get into eggs?

It usually doesn’t. Nature has worked very hard to ensure that the inside of an egg is protected from Salmonella and other bacteria in the environment. When a hen lays an egg, she also deposits a natural antibacterial coating over the surface, often called the “bloom” or the “cuticle”. After all, eggs are meant to be incubated by the hen for three weeks, and if bacteria get inside during that time, the developing embryo would most likely die. There are lots of tiny pores in the eggshell that allow oxygen to get in, and the antibacterial bloom helps to keep bacteria from entering as well.

Since chickens carry Salmonella within their bodies, occasionally a hen might lay an egg with a small amount of Salmonella inside. This happens very rarely. On average 1 in every 20,000 eggs laid contains Salmonella bacteria, and even then it’s a tiny amount, most often five or less bacteria. It usually takes at least 100 Salmonella bacteria to make someone sick.  Bacteria can sometimes get in through the shell, especially if it’s damaged or cracked.

     Factory farm eggs increase risk

In factory farms, thousands upon thousands of chickens are crowded together, making it very easy for diseases to spread. Baby chicks are raised in isolation from adults and also fed antibiotics, which means they never acquire the natural gut microbes that normally protect adult birds from being colonized by large numbers of potential human pathogens like Salmonella.

In this environment, the bacteria that do colonize poultry tend to be the ones that have become resistant to the antibiotics the hens are fed. Chickens under high stress are also more likely to have large amounts of Salmonella, since stress hormones have been shown to increase the bacteria’s growth rate.

To wash or not to wash…

Washing removes most of the protective bloom from the surface of the shell, but In the U.S., producers are required to wash their eggs, at a temperature at least twenty degrees warmer than the inside of the egg. The logic behind the higher temperature is that cold water could cause the contents of the egg to contract, drawing contaminants inside through the pores. After washing, commercially produced eggs are then rinsed with a chemical sanitizer (which can also enter the egg) and dried, because bacteria cannot go through the pores of an egg without moisture as a vehicle to carry them across.

In Europe, there are very different thoughts on egg safety. European laws prevent producers from washing eggs at all, so that the natural antibacterial “bloom” remains intact. In European supermarkets, eggs are not refrigerated, because if they begin to warm up as you bring them home, condensation can form on the surface, and since bacteria needs a moist surface in order to enter an egg, this increases that chance of bacteria getting inside.


freshly laid eggs from our own flock…

And buying eggs from your local farmer?

In contrast to large factory farms, happy, free-roaming hens are less likely to be stressed and more likely to have a normal, diverse gut flora that are in competition with each other and preventing a prevalence of pathogens like Salmonella. In uncrowded conditions, there is less likely to be a large build-up of bacteria in the environment, and in the absence of antibiotics, diverse communities of bacteria vie with each other for resources, not allowing any one type to become dominant.

So are eggs from small farms safer? I know which ones I’d rather eat…








H. pylori: old friend, new enemy?



Up until the 1980s, doctors and scientists believed that gastritis and stomach ulcers were caused by peptic acid eroding the lining of the stomach. Then, two scientists from Australia, Dr. Barry J. Marshall and Dr. J. Robin Warren, made a discovery that changed everything: most people who suffered from ulcers also had a bacterial infection that was causing inflammation of the stomach lining. The newly discovered bacterium was named Helicobacter pylori, and doctors soon found that treatment with antibiotics could effectively cure most ulcers.  Good news for ulcer patients.

In 2005, Marshall and Warren were awarded the Nobel Prize for Physiology or Medicine for discovering H. pylori and its role in gastric disease, which led to wide-spread news and media coverage. People everywhere were hearing about this ‘bad stomach bacteria that you didn’t want to have’, but a few years have passed, and we are beginning to understand that it’s just not that simple.  You might want to have it, or you might not… it depends…

We now know that humans (along with many species of animals and birds) have been colonized by H. pylori for at least 60,000 years, and probably longer. We know this because geneticists can calculate average mutation rates of the bacterium’s DNA as it travelled along in the first Homo sapien exodus from Africa.

We seem to have lived together quite peacefully with H. pylori until very recently in human history. Not long ago, just about every human on the planet was colonized with H. pylori. It was (and still is) part of our normal microbial flora, but today only about half of all people are still carrying it.

Ironically, infection with H. pylori has been linked to gastritis and peptic ulcers, both of which have been on the rise in the last hundred years or so, just when the incidence of H. pylori infection is rapidly declining.  And, peptic ulcers were very uncommon before the 20th century, when just about everyone was infected with H. pylori.

Also practically unheard of before modern times was gastroesophageal reflux disease (GERD), a disease that has been increasing steadily, and is most common in people who aren’t colonized by H. pylori at all. GERD is not common in people who have H. pylori. So, here we have a bacteria that we apparently lived peacefully with for much, if not all, of our time as Homo sapiens, not even knowing it was there, and now suddenly we can’t live with it, can’t live without it…

What went wrong?

As it turns out, being colonized with H. pylori causes your stomach to produce less acid, and since humans have been colonized with the bacterium for so long, the ‘less acid’ state has become normal for us. Now, remove the H. pylori from the equation, and what happens? That’s right, a lot more acid is produced, and the incidence of GERD goes up as well.

But then why the ulcers?

Most people who are colonized with H. Pylori never get ulcers, but those that do have an abnormally low Treg response in their gastric system. ‘Treg’ is short for ‘regulatory T cells’, and their job is to keep the immune system in check, for example turning off the inflammatory response after fighting off a disease, or preventing the immune system from attacking things that aren’t really dangerous to us (and causing allergic reactions).

We have learned that much of our Treg response depends on our immune system learning early on in childhood what is friend and what is foe, and exposure to a large variety of bacteria early in life is important for all that to be sorted out. Yet with the advent of antibiotics, disinfectants, and improved sanitation, we are exposed to far less bacteria, both ‘good’ and ‘bad’, now than ever before in our history. Studies have already shown that children raised on farms where they are exposed to a wide variety of bacteria have far less incidence of asthma and other autoimmune diseases.

When we are not exposed to H. pylori as a child, our immune system does not recognize it as part of our normal gut flora when we acquire the bacteria as an adult. This means the Treg response doesn’t effectively control inflammation in the lining of the stomach, and ulcers can result. The excessive use of antibiotics may also have selected more virulent strains, which outcompete the more harmless ones..

And cancer?

Yes, prolonged infection with H. pylori is linked to stomach cancer, or at least it has been in the recent past, and here’s where things get even more complex. It seems that you need pretty close contact in order to pass H. pylori from person to person, and therefore in the history of our co-evolution, families, tribes, and other close-knit groups tend to share the same strain of the bacteria. Over time, people and their local strain of H. pylori adapt to one another’s small differences.

But now people have started moving around faster and farther than ever before, and are constantly encountering new strains of H. pylori. If you’re already colonized by your own familiar strain, that’s not really a problem. But if you acquire H. pylori for the first time from a ‘stranger’, it’s more likely not to agree with you and cause inflammation and other changes that might eventually lead to cancer.

A fascinating study of two populations in Colombia illustrates how closely H. pylori has evolved with its human hosts. One of these populations lives in the mountains, and is of Amerindian descent. The other population, living near the coast, is of largely African descent. Both populations have the same rate of colonization with H. pylori, yet gastric cancer rates are much higher among the Amerindian population.


When scientists sequenced the genomes of the H. pylori, they found that the bacterial strains colonizing the coastal population were largely of African descent, as were the people. But the bacteria colonizing the Amerindian population were largely Southern European. This mismatch seems to have led to a greater incidence of cancer.

Unfortunately, the absence of H. pylori also leads to an increase in cancer, because of the association of GERD with esophageal changes that can eventually become malignant.

We still have lots to learn about our physiological relationship with microbes, but now that the microbiome has moved into the spotlight, we are on the verge of a new age of understanding, and perhaps a more targeted and refined approach to medical care.



Atherton, J.C. and Blaser, M.J. 2009. Coadaptation of Helicobacter pylori and humans: ancient history, modern implications. J Clin Invest. 119(9): 2475-2487

De Sablet, T. 2011. Phylogenetic origin of Helicobacter pylori is a determinant of gastric cancer risk. Gut 60(9): 1189-1195

Why is it that I can call someone in Siberia on my cell phone, yet most species of bacteria living right in my garden haven’t even been identified yet?


Good question.

In just a gram of healthy garden soil, there are millions of bacteria, representatives of an estimated several thousand species. Several thousand species… just in a pinch of the soil we gardeners have our hands in most every day. That, in itself, is mind boggling.

But even stranger, in this age of cutting edge science, is that most of these bacteria haven’t even been identified yet.  Why? Well, as it turns out, less than 10% of soil bacteria can be cultured (grown) in the laboratory, and even those that can be cultured might look and ‘act’ so similarly it can be difficult to tell them apart, even by looking at them under a powerful microscope.

Why can’t they be cultured? Microbiologists rely on growth media, or ‘food’ that allows one or two tiny bacteria in a sample of soil to multiply into thousands so that they can see and study them, but most soil dwellers are very picky eaters. They have trillions of neighbors to compete with, and they’ve learned to eat some very strange things to get by. Many are involved in complex food chains, needing the products of plants, fungi, or other bacteria to survive.

Then the world of DNA sequencing came along…

…And with it a new way to find new types of bacteria that have been hiding all of these years right under our feet. When searching for new bacteria, or just looking to see who’s who in a sample of soil, scientists can now look directly at their genes, often a particular gene called 16S rRNA. This gene encodes a structural component of the bacterial ribosome, but that’s not really important. What’s important about 16S rRNA, is that all bacteria have this gene, it’s always exactly the same at the beginning and the end of the gene sequence, and in the middle there are slight differences from one species to the next (called variable regions) that we can use to tell them apart.

Here, we come to a process known as PCR, or the ‘polymerase chain reaction’. This is a way to make lots of copies of one specific gene within a sample of thousands, and relatively quickly (usually within a few hours). When you watch a crime show on TV, and they put the little tube with a DNA sample into a machine and shut the lid, this is what they’re doing, only they’re trying to ID a criminal, not an obscure Bacillus that might be found clinging to a radish.



PCR works by taking advantage of DNA’s natural replication (copy making) process that happens every time a cell divides. Polymerase is an enzyme that moves along a strand of DNA, adding the correct nucleotides (building blocks) as it goes. As the PCR machine cycles through a series of temperatures, the DNA is unwound from its double helix, the polymerase attaches to newly single strand of DNA, makes a copy, falls off, and then the cycle starts again. This continues until there are thousands of copies of the gene of interest.

But wait, if our sample of soil has thousands of bacteria, each with a few thousand genes, how do we make copies of just 16S rRNA? The answer is in short pieces of DNA that are added to the reaction, called ‘primers’. These ‘primers’ match the sequence at the very beginning and very end of the gene we want to copy, and when they come across their perfect match (in this case 16S rRNA), they grab on. These short sections of now double stranded DNA are just what the polymerase needs to start making copies. So if we put primers that match the beginning and the end of 16S rRNA into the mix, we copy this specific gene so many times that it can be separated from the original sample. It can then be ‘sequenced’ by another machine, which can read the individual nucleotides as they pass by. Now the gene sequence can be compared to a database to see if it matches 16S rRNA genes from any known bacterium. If it doesn’t, a new species has most likely just been discovered!



So, now that we have PCR machines and DNA sequencers, we can go to town on discovering new species of bacteria, right?  Discover them, yes, that’s the easy part.  But unfortunately, it takes much longer to learn what they’re like and what they do, let alone what they eat or how they interact with other organisms.

We have some work to do…


Your compost pile… what’s really going on in there?


When you throw organic matter onto your compost pile, it immediately begins to decompose, thanks to the trillions of bacteria that we share our environment with, along with fungi and molds, protists, and higher organisms such as worms and insects.  They all play a role.

There are two different types of decomposition, aerobic (in the presence of oxygen) and anaerobic (without oxygen), and each has its own set of associated organisms. In your compost pile, you want aerobic decomposition to be favored, because anaerobic decomposition produces bad smells and amines, some of which are toxic to plants. If your compost pile starts to smell like rotten eggs or ammonia, you need to turn it to let in more air.

Bacteria make up 80-90% of the organisms in your compost heap, and because different types of bacteria take turns doing different jobs, the process from kitchen scraps to soil happens in three distinct phases. There are billions of bacteria in a single teaspoon of healthy compost, and they use many different enzymes to break organic material down into nutrients and humates (the complex of organic matter left over after decomposition).

The first phase of decomposition is carried out by the mesophilic and psychrophilic bacteria, which consume all of the readily available, easy-to-eat organic matter. As they do this, the resulting energy production causes the temperature of the compost pile to increase. Psychrophilic bacteria are most active at around55°F, although they can even be at work (very slowly) during the cold winter months, while the mesophilic bacteria favor temperatures of 70º to 100º F.

As soon as the temperature rises above 100º F, the thermophilic (heat-loving) bacteria take over, with members of the genus Bacillus dominating the crowd. The inside of the compost pile can be raised to 130º to 160º F at this point. Bacillus bacteria have the ability to form protective endospores, which can lie in wait in the soil until conditions are favorable for them to thrive. When the compost pile reaches 160ºF, it’s too hot for the Bacilli, and they return to their spore form to wait until things cool off.

At the highest compost temperatures, 140º F and above, almost all bacterial species that might be harmful to plants or humans have died off, and above 160º F, only members of the genus Thermus might be active, if they’re present. These are the same bacteria that evolved to live in hot springs and near thermal vents.

Once the compost cools down again, micro-organisms from the surrounding environment move in, including the actinomycetes (although some species of actinomycetes are also present during the thermophilic phase as well). Actinomycetes are a bacterium that forms long, thin filaments through the compost or soil, and they may look like a spider web if you see them in your compost pile. These bacteria are very important in breaking down the “tough” stuff like the cellulose of wood or bark, the things none of the other bacteria want to eat. They are also responsible for making enzymes that give soil that wonderful ‘earthy’ smell.

This final phase of decomposition goes on indefinitely, as bacteria continue to breakdown smaller and smaller components of organic matter into all of the nutrients that make our gardens thrive.


Endosymbiosis: your mitochondria once had a life of their own…

Symbiotic relationships, where two or more organisms benefit from each other, are everywhere in nature. Once in a while, this relationship is taken a step further, and one organism actually engulfs the other. If all goes well, they live happily ever after, each benefiting from the other.

For example, the protist (single-celled animal) Hatena arenicola, has the ability to engulf a green algae cell, and then use it to gain photosynthetic nutrition. In the beginning of a relationship like this, both participants remain separate organisms, still capable of surviving on their own. Sometimes, though, they begin to take over vital functions for each other, and become stuck with one another for life.

Something just like this must have happened over a billion years ago, at the time when the very first Eukaryotic (animal, plant and fungi, i.e. ‘higher organism’) cells were evolving.  Within every one of our cells, we personally have the evidence of this long-ago endosymbiotic event.

     Our mitochondria.



The mitochondria, present in almost all higher organisms, are responsible for producing most of the chemical energy that cells need to function, through aerobic respiration. They are essential, and without them, we couldn’t survive… or use oxygen. The ability to conduct aerobic respiration was a significant evolutionary advantage to that first eukaryotic cell.  Anaerobic bacteria still use fermentation for their energy, which is far less efficient, but still handy if you want to make wine.

     But it wasn’t always this way for the mitochondria…

Mitochondria were once independent bacteria, living side by side with what would become the first plant and animal (eukaryotic) cells, until they began forming an eventually irreversible partnership after one engulfed the other. Once the bacterium was within the eukaryotic cell, changes took place over millions of years as two separate organisms learned to live together.

The mitochondrion still bears the mark of its origin as a bacterial cell. It has its own cell membrane and its own DNA, completely separate from the cell it resides in, and when the cell divides, the mitochondria divides too, separately.  It makes a copy of its DNA and then pinches in half, exactly like a bacterial cell does.

The DNA of our mitochondria is very similar to the Rickettsial bacterium, making this genus its closest living relative today. The Rickettsia which survives today still needs to enter a eukaryotic cell in order to live and reproduce, even if it doesn’t stay there permanently.  It causes diseases such as typhus and Rocky Mountain Spotted Fever.

In plants, a second endosymbiosis occurred, this time of a bacterium capable of using sunlight to produce energy. Thus, the chloroplast was born.

Because the mitochondrium has its own genome, separate from that of its host cell, it’s inherited differently in both plants and animals. When an egg and sperm meet, each has one-half of the full genome, and at fertilization, these genes recombine to form a completely new and unique genetic combination. But the mitochondria inherited by the offspring come only from the egg cell, and are transferred intact. Thus, you have exactly the same mitochondrial DNA as your mother, and her mother before her, etc., with only occasional small and random changes. This is why mitochondrial DNA is a favorite tool for scientists trying to trace the movement of populations over long periods of time.

So thank you, long ago Rickettsia species, for allowing us to breathe air, because quite frankly, the anaerobes haven’t gotten very far at all.