Author Archives: Zoe Gordon

Is This Clean? Common myths and real ways to clean up your act — and your hands

Well, I just checked my clock and, given the current viral season and the many robust little germs circulating, it seems like it is time. It’s time to let everyone know what they don’t know about the concept of ‘clean’.

Now you must be wondering what I’m talking about — you take showers, you wash your hands — but there’s more to it than that. The problem is that a lot of us have a mistaken impression of how ‘clean’ we, and objects around us are.

This is largely because we constantly underestimate microbes.

Now, before you start panicking, remember that the vast majority of bacteria are harmless to humans. This is more of a guide to correcting things we thought we knew so our habits can be a bit better for ourselves and everyone else.

Image credit: Burst via

Soap just isn’t a murderer

This is one I come across often. People believe that washing their hands with soap is sufficient to not just remove but kill all the germs on their hands.

This is not the case.

While antibacterial soaps may kill bacteria, the FDA determined it isn’t enough to differentiate it from normal soap in preventing illness. Antibacterial soap also contributes to the growing problem of bacterial resistance to antibiotics. So here’s what you need to know about soap to use it the most effective way — starting with how soap actually works.

As we all know, oil and water don’t mix. Washing your hands with water alone will get rid of a fair amount of the grime by physically pushing it away, but what it can’t move will be left behind. Here comes soap to the rescue.

Detergents (a group of chemicals including soap) are structured to bond to both oil and water. They will essentially grab the grime with one molecular arm and the water with the other, ensuring that everything washes away down the drain.

What does this mean for microbes? Well, soap doesn’t kill the bacteria, viruses, mold and other things — it just makes them easily slide off your hands. Even more important to understand is that this means that bacteria can live in and on soap. Simply putting the soap on your hands is not making your hands clean. The mechanical action of washing to remove dirt, grime, and the microbes within them is very important.

So the next time you go and wash your hands, scrub them for at least 20 seconds if you want to really get them clean, and rinse them off properly with running water. You could slowly count to twenty or try singing a song chorus, that way you know you’ve given it enough time to actually do its work. Try to get places like between the fingers and under the nails for the best effect.

Dry your hands when you’re through, wet hands are a nice place for more germs to land on. Note that the water temperature doesn’t actually matter.

A quick note on drying your hands: hot-air hand dryers have been shown to be sucking up bacteria from the air and dumping them on the newly washed hands. Use hand towels if they are available.

99% Invisible: Hand Sanitizer may not substitute

Hand sanitizer is another interesting one, with even typical pocket brands claiming to kill 99% of germs. I am not in the least disputing the truth of these numbers and under normal circumstances, this is an excellent percentage of anything. The thing is, we’re talking about microbes.

These organisms, when they settle down and multiply on a surface, easily exist in the millions. I am reluctant to show what a little dust will look like when left to grow on a microbiological plate for just two days.

With that in mind, let us do a little math — just a little, I promise.  Let’s say that there are only one million bacterial cells on your hand right now. They are mostly quite harmless, but you don’t like them living here and paying no rent so you rub on some hand sanitizer. This sanitizer kills 99% of them, leaving only 1% behind—but that’s 1% of a million. This means there are still ten thousand bacterial cells left alive on your hand. How about 99.9%? That is still a thousand. Well, this isn’t quite as clean as you thought it was, is it? Consider the germs’ multiplication power, and it’s clear to see why this isn’t such a good idea.

Now multiply that by dirt. Image via

According to the CDC and studies on the topic, you need to get hand sanitizer with 60% or higher ethyl alcohol concentration or it just isn’t doing enough. You want 99.99% kill and there are several good sanitizer brands that will offer this. It’s important to note, however, that hand sanitizer loses efficacy when your hands are visibly dirty or greasy. It also isn’t as effective at getting rid of certain viruses and stubborn bacteria as handwashing. And all this assumes you’ve used the sanitizer correctly—using the right amount and allowing it to dry on your hands (the directions are on the bottle).

So, given the choice between hand sanitizer and handwashing, wash your hands. In fact, hand sanitizer is most effective when used after washing the hands to get rid of stragglers. If it’s dirt you’re trying to get off and washing isn’t an option, consider using hand wipes then following up with your sanitizer. Otherwise, you just have dirt, sanitizer and the microbes it failed to kill cohabiting on your hands.

Doing well so far? I haven’t said anything you don’t know yet? Excellent. But, now it’s time to talk about (a personal pet peeve and) another cleanliness concern: sponges and washcloths.

Pictured: A low-tech dishwasher. Image via

It absorbs more than just water

If you’re like me, the unfortunate fact is that the only dishwasher in your home is you. Soap, water, and a sink are how you get your dishes done. And, of course, to get those plates cleaned good and proper you have your trusty sponge. But for how long do you keep Ol’ Reliable and how exactly are you using it?

To start with, we need to understand the nature of a sponge. A kitchen sponge is full of holes, is frequently coming into contact with food, and spends most of its time saturated with water or slowly drying. This means it has a lot of surface area for microbes to settle into, a good food supply to keep them well-fed and comfortable in there, and a nice water-rich environment conducive to growth. Such environments in other circumstances easily promote the growth of bacteria and mold, so why would the sponge be an exception?

Make no mistake — kitchen sponges are a hotspot for bacteria.

Your kitchen sponge habits make a very big difference to whether you are making your plates clean or, invisibly, much dirtier. There are many good habits that will help to reduce microbial transfer from your useful and squishy little incubator. So think to yourself if you’re using sponges the right way.

You should:

  • Rinse and squeeze out the sponge after every use. Leaving the food particles in a damp sponge creates excellent conditions for microbial growth.
  • Use different sponges for different things. If you are using the same sponge to wash your dishes, clean up your counters and wipe off your appliances, you are ensuring that all the varied bacteria in your kitchen are spread equally all over your kitchen. While cooked food coming off a plate is unlikely to contain things like Salmonella, that bit of raw egg that spilled on the counter earlier just might—and you don’t want to wipe that on your forks.
  • Change sponges at least monthly and discard a sponge the moment it becomes discolored or produces an off odor. The reason it smells like that is typically a combination of mold and bacteria having a party in your sponge.
  • You can also microwave sponges, which has proven effective in eliminating germs.

Now, with the more standard sponge care aside here is my personal suggestion for extending the lifespan of your sponges: rinse your dishes off with water before ever applying a sponge to them, this decreases the amount of food scraps in and on your sponge. 

If the lasagne has become one with the dish, leave the dish in the sink either with water in it or immersed in water for a short time. The particles will soften and be easily removed with running water and little hand rubbing. This way you don’t need to scrub the plate hard with the sponge and trap food particles inside it. Another pointer is that abrasives like steel wool do not and cannot substitute for a normal sponge. Instead, they leave scratches and depressions in the surfaces of dishes into which bacteria can settle. They are also far more difficult to clean.

Washcloths live a similar life. You know that weird smell it has? It’s not just your own personal eau de you, it is very probably the scent of fungus settling in for the long haul. The same thing happens when other fabrics are left in water for too long. That smell is mildew. Ensure that your washrags are properly rinsed out — ideally washed with soap in hot water—and hung up to dry properly after every use.

A few extra bits of information

Freezing food does not kill bacteria.

If it’s microbes you want to be rid of then heat is the way to go. Most fungi have a low tolerance for high heat, and if it feels hot to your touch most bacteria won’t like it too much either. Freezing, on the other hand, only causes them to slow down and stop reproducing for the time being. Once thawed, the bacteria start to multiply again. Keep this in mind when deciding which foods in your freezer to trust. Similarly, ice is not clean simply because it is frozen. An ice cube that falls on the floor is a dirty ice cube, don’t put that straight in your mouth.

For that matter, the Five-Second Rule is a lie.

Even as you inhale this very moment microbes are entering your lungs. That chip is picking up bacteria in the air on its way to the floor. You just need to accept that when you pick it up and eat it. It is what it is. Fortunately for you, most microbes are harmless—but please don’t eat a chip that fell in dirt.

On a more positive note, it turns out that sugar-free chewing gum is actually quite useful for teeth cleaning. Consider using it between meals when brushing your teeth isn’t immediately an option. It absolutely has to be sugar-free, however, or it will have a very opposite effect. It has been shown to be useful for removing bacterial buildup from the surfaces of and between teeth.

Now there are many more aspects we could explore, but for now, you should have the basics. So here’s a little tip to get you through the current flu season. Hands are by far one of the easiest ways to move germs around so remember not just your own cleanliness but the spaces around you. Keep track of public surfaces, like doorknobs and handrails, that your hands touch and try to be conscious of moving your hands to your face. Wash them often. Sanitize them for good measure if you want to. Stay safe, healthy and squeaky, shiny clean.

What’s the difference between birds and mammals

There is a huge variety of organisms on the planet and among them, members of the animal kingdom tend to captivate us humans the most. Birds and mammals are equally remarkable, but very different.

Numerically speaking, only a handful of living organisms have skeletons and an even smaller fraction of vertebrates can regulate their own body temperature. The classes Aves and Mammalia are the only groups that have this special warm-blooded trait and that often leads people to think that birds and mammals are very related—sometimes even that birds are a type of mammal.

The truth is, however, that these two classes are very different in a lot of ways. It’s quite a bit more than the fact that we can’t fly.

“I don’t think this will work out. You’re cute but we’re just too different.” Image credits: Pixabay.


Defining the Problem

To start with, mammals and birds are quite different through their very definitions. The definition of a bird requires feathers, a toothless beak, wings (usually allowing for flight), and the ability to lay hard-shelled eggs. Meanwhile, mammals have hair, give birth to live young, and the females produce milk from mammary glands — the structures for which the class is named.

That being said, there are a few species that blur the definitions a little bit.

On the issue of wings, care is taken to not focus too much on the flight itself as several bird species, like penguins, have modified wings specialized for movement through water. Of course, there are also many flightless birds. Meanwhile, there are mammals that have wings and can fly, bats. At the same time, monotremes (a group including the platypus and the echidna) make things even more complicated,

Monotremes defy mammalian definitions in favor of bird-like habits. Although they’re mammals, they lay eggs rather than giving birth to live young — although it has to be said that the platypus and echidna are extremely odd mammals and we shouldn’t generalize based on them (but that is a discussion for a different article).

With those facts noted, however, even the bat’s modified forelimb doesn’t possess feathers and even after laying eggs monotreme mamas are going to feed their growing young on a milk diet.

Judging books by covers

Being humans, it’s fair to assume we get the gist of what mammals are — at least the basics.

But, very few of us have taken the time to consider the specialized form of a bird. To start with, while there is quite a variety in mammalian silhouettes, the basic structure of the bird body is fairly consistent and generally quite different from a mammal’s. Even considering only the most standard mammal form, with four similarly-sized limbs and a tail, there is a notable difference in overall structure from birds.

Image credits: Karen Arnold.

Now, let us take a closer look. If you have a pet bird, feel free to smile at it and maybe it will return an excited stare.

Some mammalian smiles sport fangs, and the bird’s mouth can be just as sharp, but it will never quite be able to give you back that excited grin—because, unlike mammals, birds don’t have any teeth. The next thing to note is the most obvious, the nice somewhat rounded feathery bodies and, where a mammal would have forelimbs, birds sport wings. But that’s okay, while they don’t have hands to hold things, if you look a little lower they are sporting a lovely pair of wrinkly clawed feet.

Birds typically possess four toes, three facing forward and one facing backward — this is the part we typically think of as the bird’s feet. However, birds are typically digitigrade meaning that they are actually walking on their toes. What we think of as their knees are actually their ankles. Canines and felines are also digitigrade but, of course, the feet look quite different. And that is just an outside look. Let us get even closer.


An Even Closer Look

We really need to appreciate how specially a bird must be built to live its extraordinary life in the air.

The typical internal structure of a pneumatized bird femur.


Because they so well adapted for flight, their internal structures can be quite different from our own. Flying requires you to be both strong and lightweight and while we may be able to accomplish the first, no amount of arm flapping will ever get us off the ground.

Since they need to be so lightweight, airborne members of the class Aves have decided to drop the weight in the densest structures in the mammalian body, their bones. Birds possess many bones which are pneumatized (hollow), with crisscrossing struts, like columns on a building, to maintain their shape and structure. Those specialized for swimming like puffins and penguins have none, however. A bit of density helps when you need to go underwater and can’t simply fall from the sky.

But, this is just one of the major ways birds and mammals differ internally to aid in flight. Another fascinating structural difference between birds and mammals is the extraordinary avian respiratory system. Flight takes energy—a lot of it. Try flapping your arms all the way up and down just ten to fifteen times, exhausting isn’t it? Birds need to do this simply to get off the ground and many bird species are not adapted for gliding so they must ­always do this to stay above ground. Hummingbirds flap their wings up to twelve times each second. How can they even keep up with all this exertion?


Inhalation: the air sacs expand, pulling oxygenated air from outside into the posterior sacs and deoxygenated air out of the lungs into the anterior air sac. Exhalation: The air sacs contract, the posterior sacs pushing oxygenated air into the lungs and the anterior air sacs pushing oxygen-free air away from the lungs and back up the trachea. In this way, oxygenated air is always in the lungs. Image credits L. Shyamal via Wikimedia Commons.


Well, unlike in mammals, birds don’t have a simple system with two neat lungs in the chest. Their respiratory system takes up a large percentage of their bodies. What moves air though bird bodies aren’t their lungs, which don’t expand and contract as ours do. Instead, they have a complex system of air sacs which move air constantly in a cyclical system far more efficient than our own.

As a point of comparison, how the mammalian system works is that we inhale and our lungs fill with air.  Deep in the lungs, there are air sacs called alveoli, covered in capillaries, in which oxygen is exchanged for carbon dioxide in the blood. When this exchange takes place to a sufficient extent we exhale, then inhale again. This system means that air must reverse direction and there is a time when our lungs are devoid of usable oxygen. This, however, is not the case with birds. For them, air goes in one direction at all times, maximizing efficiency so that the lungs always have oxygen to process.

The last thing to mention is the cloaca. While most mammals—again, monotremes are weird—possess distinct regions for defecation, urination, and reproduction (the urethra and vagina actually have distinct exit points), birds work with a one-for-all approach. For these purposes, birds have a single structure called a cloaca. Avian waste is a combination of all solid waste products, leaving their waste two-toned. Instead of liquid urea, they release semi-solid uric acid which is the reason why bird feces left on a car erodes the paint.

So, though there are mammals that can fly and lay eggs, they can never quite be as birds are. Though we haven’t gone to great detail here, birds breathe, give birth, digest and even sing using structures different from those found in mammals. Interesting and complex though mammals are, they are mostly lacking the intricate anatomy needed for flight. Though mammals and birds are all warm-blooded creatures, with four-chambered hearts, that is roundabout where the similarity between mammals and birds ends. Altogether, birds and mammals are entirely different animals.

Evolution: What is it? How does it work?

This is an odd start, but before we get into complicated things I want to talk about something near and dear to my heart—corn. Once upon a time, the corn we know and love (at least I do), used to be something called teosinte, a small green plant that doesn’t look anywhere near as appetizing. It is hard to believe, I know, but something very interesting happened. In the area that is now Mexico, this plant was identified as having potential as a food crop, so farmers began intentionally growing it. Being good farmers, they thought that maybe if they kept the seeds of the biggest ones and kept planting those they would get more food out of it. As it turns out, they were right. After ten thousand years of only planting the ones that produced the biggest kernels, we ended up with maize as we know it today. It’s bizarre but entirely true and it happened through a process we call artificial selection.

In nature similar, very strange changes can happen to species over time given enough pressure by the environment around them. Evolutionary biology is essentially the study of how organisms have changed over time to develop into new species. The topic is a bit contentious, as we all know, but there are also many common misconceptions about exactly how this process works. Thinking about it as a whole is difficult, with many points where it is easy to get hung up and confused. So, instead of looking at the big strange picture, we should start with a closer look at the little parts that make up the concept. As we move into this article, remember that, ultimately, every species needs to survive and reproduce because that’s how species continue to exist. With that said, let us take a look!

Credit: Pixabay.

Getting Fit

Let us consider two individuals, Tom and Jack. Tom is long-limbed, athletic, lightweight, and doesn’t have much body hair. Jack is shorter, has a fair amount of hair, and a larger, higher-fat build. If you put both of these men in a forest, it is likely that Tom will have a bit of an advantage with traversing, climbing, et cetera. However, take the same pair and put them in a windy tundra and Jack will likely do a lot better in the harsh weather.

Every environment poses its own unique challenges. If you live in an area that has a lot of water, you will do a lot better if you can swim. If you live in an area that has a lot of plants and cover, predators are less likely to see you if you’re small and green. These factors contribute to something we call fitness which is a measure of how well you are built to survive and how likely you are to reproduce. In some ways, it’s a bit like physical fitness in humans. And, similarly, this fitness affects more than just your looks.

Genetics plays a huge role in this, and your genes (genotype) are expressed through your outward characteristics, called your phenotype. Small brown lizards living in a forest are displaying (‘expressing’) genes that give them the small and brown phenotype, and maybe even more than tell them to like staying on surfaces that match their color. Which brings us to the next main idea, a process called natural selection.

Selection Bias

Natural selection looks at the differences in the likelihood of survival and reproduction based on a species’ phenotype. Ultimately, in nature, creatures that have genes that result in fit phenotypes will survive and reproduce. This concept is where the term “survival of the fittest” comes from. The survivors live to have offspring and so genes in that population will, therefore, start leaning towards that fitter survivor genotype. Let us use an example.

Imagine that in a grassland there is a population of mostly large, green grasshoppers. They are doing well here because nature provides a lot of cover. This season, though, there isn’t much rain and the grassland starts turning brown and sparse. This means that the larger, brighter grasshoppers become much easier to see by predators and many of them get eaten. So, the next generation of grasshoppers ends up being mostly smaller and perhaps a bit less green, because the ones that best survived the change in the grasslands were the ones that were harder to see.

This is natural selection. Those built to survive in an environment will live long enough to have offspring, changing the gene variety in the next generation. The same process happens with plants, fungi, and microorganisms. An important thing to note here, though, is that this is only possible because a healthy population has a wide range of genes to choose from. Not all organisms of a species will be the same size or the same color or have the same features.

Darwin's Finches

Charles Darwin is considered the father of modern evolutionary biology. He developed his theory of natural selection by observing the variations among the species of the Galapagos Islands. He was best known for his study of birds, which all occupied different niches on these far islands but bore obvious resemblances to mainland species. Image credits: John Gould.

Over a long period of time and given a lot of pressure, a population of organisms can change in significant ways. The reason we are now having an antibiotic crisis is that, after many years of exposing bacteria to chemicals designed to kill them, the ones that had the gene quirks allowing them to survive are the ones that were able to multiply. So now we have a large number of antibiotic-resistant bacteria to contend with which have whole sections of DNA that exist only to counteract these drugs—but that, of course, raises a question. If they didn’t have these genes before, why do they have them now?

Mutant Power

Credit: Pixabay.

Credit: Pixabay.

Mutation is a major factor influencing the process of evolution. Every so often, when cells are dividing, the mechanisms that copy bits of genetic data make a mistake. While it can often result in problems, it sometimes creates just what an organism needs to survive. One reason why HIV has been so hard to cure is that its reproduction process is unstable and prone to genetic errors. What this means is that the medication will work on most viral particles, but not all of them. The virus is, therefore, constantly evolving and the ‘error’, mutant forms that help it survive to persist due to natural selection.

Some mutations are overtly harmful, like mutations in hemoglobin genes that cause sickle cell disease, where red blood cells curve into a “sickle” shape. The mutation makes the cells less efficient oxygen carriers and more fragile, and sometimes they cause painful blockages and organ damage. However, these mutations continue to persist because if a person is only a carrier, having received the variant gene from only one parent, it has a protective effect against malaria—a common disease in the parts of Africa where sickle cell is most prevalent. The fragility of the cell due to the hemoglobin structure means the cell will often rupture before the parasite can reproduce. But, since the remainder of their hemoglobin is normal, they don’t experience most of the severe effects seen in persons with the full form of the disease. The carrier phenotype is, therefore, fit. Natural selection is a strange process indeed.

So we have looked at mutation, natural selection, and fitness. We have looked at bacteria and viruses and how these factors have made them survive and evolve on a smaller faster scale. Now, how does that translate to bigger more complex things?

Making Sense of it All

Imagine that there is a ground-dwelling species of mammal that lives in a forest. Many of them are competing for the same food sources. A few of them, have started climbing in the hopes of finding another food source. A mutation comes which makes one offspring’s claws curve a bit more, causing that individual to be better at climbing. It survives to reproduce. A few generations down the line, all its descendants may have these curved claws. Somewhere along the line, a descendant is born with unusually long limbs which makes it better at both climbing and jumping, this individual’s offspring may well, do better than others—and so on. These minor changes can add up over time, just like the biggest teosinte kernels being intentionally planted. In nature, however, it takes far longer than a neat ten thousand years to produce something as different as maize.

Let this mammal group adapt for many thousands of years with natural selection favoring climbing habits and hunting in trees. At the end of that time if you were to take one of these climbing adapted creatures and put them alongside the ground dwellers they would look very different. They may have a different body form, make different sounds, have eyes that are adapted to seeing at a distance, and so on. And, because of the amount of mutation and genetic changes that brought them to this point, any offspring born of a mix of these two creatures would be sterile like a liger or mule. Just like that, you now have two different species. This also speaks to a common misconception, the idea that if one organism advanced from another, the first one should be gone. That simply isn’t how the process works.

In nature, creatures will exist side by side as one group remains the same and others experience changes due to environmental pressure. It is strange, and hard to fully appreciate, but we have a bit of evidence that can follow the trail. Think even of the liger I just mentioned, the mere fact that a lion and tiger—two distinct species from two different regions—can produce offspring means that their genotypes must be similar enough to make an embryo viable. We interpret this to mean that these big cats must have some ancestry in common.

What Do We Know?

Though it happens over a very long period of time in creatures that take longer to reproduce than bacteria or viruses, there are a few ways we can observe that evolution is an acting process. If an organism has advanced from one form to another, it stands to reason that there had to be some forms in between. Well, though we don’t always have all the bits of the puzzle, the fossils we find often help us fill these gaps. For example, between dinosaurs and birds we have found species of feathered, winged dinosaurs like Archaeopteryx.

There are also several odd cases in nature of organisms growing parts they have no need for. Some snake species and legless lizards retain a pelvic girdle with no real function, dolphin embryos in development still start to grow hind limb buds that retract after a time, and many cave-dwelling or burrowing species retain non-functioning eyes. The fact that the genetic machinery required to make these structures happen exists, presents as evidence that these genes had a purpose at some point in the organism’s history.

There are other factors to consider as well. Genetic evidence frequently shows fairly small differences between one species and another of a similar type that cannot reproduce with each other. In fact, genetic evidence shows that a large variety of organisms have a surprising number of genes in common—whales, humans, bats, and cats all have the same bones making up their forelimbs. But, this gets into very complex discussion and murky waters. This article really just serves to give a background of a concept. Take the information here, interpret and think about it as you will and, of course, there are many other great sources of information on the topic out there. Whether evolution on a larger scale makes sense to you or not, hopefully we can at least agree that these smaller processes of change are things we can observe. By now, I hope, the idea of what evolution is and how it works is at least a little bit clearer.

Prions — the Revenge of the Cows

Once upon a time, the idea that creatures too small to see made you sick was a concept that average people and doctors alike scoffed at. Think about it—if you didn’t already know about bacteria, wouldn’t the idea seem ridiculous? Without evidence, a person may as well have been telling you that tiny elves were attacking you. In relatively modern times, though, we have discovered that small organisms of all kinds are hard at work ruining our days. But as it turns out, whenever science thinks it has things figured out, something always steps up to the task of confusing us all. This time it was protein.

The Mystery

Now, we hear about bacteria and viruses all the time. More often than not, these are the causes of the illnesses we suffer. However, bizarre animal behavior, first officially noted in the 1730s, baffled scientists all the way through to the 1980s—and in the process of discovery turned our understanding of pathogens, and biology itself, on its head.

First, the Spanish observed strange behavior in their Merino sheep. The animals were walking strangely and pathologically scratching their bodies against fences. This led to the illness being called ‘scrapie’. Nearly two centuries later, in 1920, a disorder was noted in humans which caused degeneration of their brain tissue. This was named Creutzfeldt-Jakob’s disease, after the scientists who first noted this inexplicable phenomenon.

At the time, no one had noticed how similar the two diseases were. For one, they both had long incubation periods. In fact, in 1954 Sigurdsson proposed that scrapie was caused by a ‘slow virus’. No other form of pathogen known at the time fit this long incubation period. Scrapie took years to show symptoms, much like HIV. Meanwhile, in remote Papua New Guinea, an illness called kuru by the Fore people was officially noted—it looked a lot like Creutzfeldt-Jakob’s.

The Problem

By the 1960s, some scientists had begun to suspect that the agent of scrapie was not a virus at all but actually a protein. However, there was a very big problem­—this directly went against everything we understood about cells, the central dogma of molecular biology. In simple terms, it states that information moves from DNA to RNA to form proteins and doesn’t go in the opposite direction. Essentially, proteins can’t give instructions, so how could one be a pathogen?

However, after many failed experiments designed to inactivate the illness—conducted by such scientists as T. Alper, J. S. Griffith, and I. H. Patterson—a protein was one of the only options left. Then, in 1967, Griffith officially proposed that scrapie was caused by a protein and even suggested possible mechanisms. Finally, in 1982 Stanley Prusiner coined the term ‘prion’, stating that the illness was caused exclusively by proteins. The specific protein involved was referred to as the PrP (Prion Protein). Prusiner’s research went on to earn him a Nobel Prize in 1997.

The Bizarre Reality

At last, we knew what was causing scrapie and eventually realized that kuru and Creutzfeldt-Jakob’s (CJD) were the same sort of illnesses. It was all down to prions, proteins which are able to change their shape and structure such that they can fold into non-functional shapes. All that was left to do was figure out just how a protein could cause disease.

Such diseases are called transmissible spongiform encephalopathies (TSEs) and, in these diseases, the brain degenerates in such a way that gaps begin to form in the tissue. In other words, they cause your brain to essentially become Swiss cheese or, as the name suggests, like a sponge in appearance. The results of this degeneration are severe and, unfortunately, always fatal.


(A) Normal healthy brain tissue. (B) Brain tissue from the temporal lobe of a patient with Creutzfeldt-Jakob’s disease. Note the large spaces in the tissue where the prion proteins have caused damage. Image credits: Nephron via Wikimedia Commons and Sherif Zaki; MD, PhD; Wun-Ju Shieh; MD, PhD, MPH.

So how does a misfolded protein do all of that damage? The truth is that scientists still don’t really know the mechanism. However, a simplified way to look at it is that prions are highly charismatic proteins, able to ‘convince’ other proteins that their flawed structure is the right structure. The protein associated with most TSEs is called PrPC (for common), which is common in cell membranes in the normal configuration. It becomes a prion when it changes to PrPSC (for scrapie) which is the misfolded, infectious form of the protein.

Once consumed the PrPSC passes through the wall of the intestine by an unclear mechanism. Even more impressively, from there it manages to enter the central nervous system, apparently moving from nerve to nerve until it enters the brain itself. Upon encountering PrPC on a cell surface, it induces structural changes to occur, encouraging folding of the protein until it resembles the PrPSC form. Now satisfied that its work is done, the prion moves on to the next PrPC, showing itself off and spreading the good word about its bad conformation.

Photomicrograph of neurons in scrapie-infected mouse. The red stained areas show prion proteins in transit from one neuron to the next. Image credits: National Institute of Allergy and Infectious Diseases (NIAID)

Before long it has gained a crowd following that is also going forth to share this new shape with others. The newly converted PrPSC tend to like to group together, forming aggregate communities throughout the brain. These aggregates form amyloid fibrils, insoluble clusters of protein which accumulate to form plaques (a process also associated with Alzheimer’s). And thus the spongiform structure occurs, with gaps being left behind by this accumulation. Worse still, this form of the protein is resistant to proteases, enzymes which break down proteins.

Some known prion diseases include kuru, scrapie, and CJD, as well as bovine spongiform encephalopathy (mad cow disease), and fatal familial insomnia (FFI). In most cases, the disease develops spontaneously with no apparent explanation. Otherwise, a person could consume tainted meat, such as in human cases of mad cow disease and kuru. In some forms, such as FFI, genes coding for the faulty protein can be further passed to offspring.

Symptoms of these illnesses include poor coordination, confusion, memory loss, hallucinations. In some cases, patients will experience dementia, psychoses and persistent insomnia. There are few ways to actively avoid such incredibly rare diseases but the best you can do is ensure that your food comes from safe sources—also, try not to eat any suspicious brains.

If you want to learn more and in more detail, you can take a look at the links below:

Understanding Allergies: What they are and how they work

Allergies, you can’t live with them… and would gladly live without them. Unlike standard illnesses, rather than involving a shortcoming of the immune system, allergies actually happen when it becomes too reactive.

Yes, you have allergies because your immune system loves its job and is working overtime — it is called a hypersensitivity reaction. These reactions include autoimmune disorders as well as organ and graft rejections. But, here, I’ll give you the crash course on Type I hypersensitivity reactions, a.k.a allergies.

What causes allergies?

To answer this question we need to go down to the cellular level and take a look at our immune system. This system consists of many parts but what we’re mostly concerned with here are white blood cells — lymphocytes and granulocytes. Our cells are well trained to respond to threats and, like with a national military, we leave it up to their discretion and expertise to determine which foreign molecules (antigens) pose a threat. T lymphocytes, our generals, make these calls. Let’s meet these high-ranking members of the army.

Most of us have heard of antibodies, if only from watching cartoons. These defensive molecules are produced by our B lymphocytes — high ranking special forces who answer only to T cells. Polymorphonuclear cells (PMNs), named for their unusually shaped nuclei, are our soldiers and are the immune cells found in greatest numbers at sites of infection. They are also called granulocytes for the granules observed in their cytoplasm, which serve different functions for each cell type. Along with mast cells, these cells respond to lymphocyte orders to release granules.

“Sir, yes, sir!” 3D renderings of PMNs. From left: a basophil, eosinophil and neutrophil. Image credits: staff (2014). “Medical gallery of Blausen Medical 2014”. WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436.

Macrophages are our all-rounders – scouts, marksmen and information specialists. They are usually the first to identify strange foreign substances which they consume, break apart and then present segments (like snapshots) of them to the T cells. Now, the generals must decide if these strangers are worth waging war. T helper cells (TH, CD4+) give out orders and our cytotoxic T cells (CD8+) personally attack problem cells, like cancer cells.  Sometimes, unfortunately, they get it wrong. This is when you experience a hypersensitivity reaction.

Okay. So what is an allergy?

With the introductions out of the way, we can learn about the anaphylactic response. ‘Ana’ means ‘away from’ and ‘phylaxis’ means ‘protection’. Seasonal allergies, severe allergies, and rashes are typical type I (anaphylactic) reactions. Interestingly, this is the reaction you will have, not the first time, but the second time you are exposed to the same ‘threat’ – and every time after that. Our immune system is a learning system, this is the reasoning behind vaccination and why chickenpox won’t affect you the same way twice. Once threatened, your army remembers their enemy so they can mount a faster, stronger defense the next time.

“A new challenger appears!” False color electron micrograph of various pollen grains, a common allergy trigger. Image credits: Dartmouth College Electron Microscope Facility.

In our first response, our T cells send in our B cells to attack. Once activated they become bigger, scarier, plasma cells. Their weapon of choice is, of course, antibodies but particularly immunoglobulin E (IgE). The first time our body encounters a strange antigen, be it pollen, dust, animal dander etc., there is a chance we will produce IgE. Some of these attach themselves to mast cells, which behave the first time around. The second time, however, they hold nothing back. And so we get back to the anaphylactic response, characterized by vasodilation and bronchoconstriction – essentially, your blood vessels expand and your air passages close up.

The T cell signals, which tell your blood vessels to expand, are to allow cells like PMNs and mast cells to move more quickly to the site of the challenge. Unfortunately, in the case of allergies this is usually your respiratory tract and skin. Once the PMNs and mast cells see their enemy, all hell breaks loose. The IgE antibodies on the mast cells identify the evil pollen and trigger the cells to degranulate, along with the attacking basophils.

Diagram showing a mast cell with attached IgE (A) and its degranulation (B) once the deadly pollen grain antigen binds to it. Image credits: Zoe Gordon, ZME Science.

From these granules, among other pre-formed mediators, histamines come out. A bit like grenades, they do their job very well but create a mess while they’re at it. They are excellent vasodilators and help your army enter the area quickly, unfortunately, they also make those areas leak. Essentially, histamines help to cause your red, runny nose and watery eyes. In fact, histamines are also stimulating your nerves and making you sneeze and itch. This is the reason why the medication we take to unclog our poor sinuses and de-rash our skin are antihistamines.

  • Early phase reaction: Within 15 minutes

The reaction that occurs — swelling of the area, redness, inrush of cells — is a standard inflammation reaction. And we see this on our skin in the form of itchy rashes or hives. The redness is because the blood vessels have expanded. But what about bronchoconstriction? As it turns out, within ten minutes after exposure, other mediators (e.g. prostaglandins) in those granules trigger tightening of the smooth muscle in the respiratory tract. This is allergy induced asthma and can become life-threatening anaphylaxis.

  • Late phase reaction: 4-6 hrs later

The war is over, but those cells just don’t seem to want to go away. In fact, some reinforcements are still arriving. The acute symptoms are gone but the effects of their presence remains. Rashes and hives can last for weeks or even months. The bronchoconstriction is even more troublesome, usually peaking at 30 minutes and fading but sometimes recurring after a few hours.

  • Anaphylaxis

Anaphylaxis is a different situation than your standard type I reaction. It’s potentially life-threatening and often comes with some combination of these symptoms: visible inflammation, trouble breathing, a worrisome drop in blood pressure, gastrointestinal distress.  When the person’s face swells up and they can’t breathe, what they need is a shot of adrenaline!

The most well-known brand of portable epinephrine shots. Image credits: Intropin/ Wikimedia Commons.

Epinephrine shots are your go-to for anaphylaxis – the sooner the better. Why? Because adrenaline essentially causes the exact opposite effect of inflammation. It’s our fight or flight hormone. It makes us breathe better, pushes up our heart rate and constricts our veins to increase blood pressure and flow. Allergies only become more severe with repeated exposure, so if you have experienced anaphylaxis, ensure you walk with your shots and that there is a way for people to know.

Now you know

All in all, your pollen allergy is essentially equivalent to a stray beach ball rolling across the battlefield and immediately getting focus fired by every soldier on hand – because it looked funny. And it doesn’t seem to matter how many times they try to harmlessly roll by. In fact, over time, the soldiers get joined by an extra platoon, then tanks, and then the air force because those beach balls have got to go! And over a few bits of pollen, soldiers and bystanders have been lost.

Yes, it’s very strange to imagine, but a lot of the symptoms we associate with allergies and illness aren’t things that the invader is doing to your body, but things that your body is doing to you – fever, runny nose, itchy eyes, shortness of breath, rashes, and hives. Your body is making you miserable… in an attempt to protect you. But, remember, when it’s not an allergy, to appreciate that. It’s doing the best it can.



The Bacteria Files: Pseudomonas — What it is and why you should know about it

It may not be a household name on the level of E. coli or Salmonella, but this troublesome bacterium is very well known. In medicine and manufacturing, Pseudomonas is high on the list of things you don’t want to have nearby. It all comes down to one particular tendency it has: like a freeloader, a rash, or that one gray hair, once Pseudomonas shows up, it simply will not go away.

Pseudomonas is a genus of gram-negative, rod-shaped bacteria which use flagella for movement. They are typically found in soil and water as obligate aerobes (needing oxygen for survival), but also colonize plant and animal tissues. A colorful group, many of them produce blue-green pigments called pyocyanins. P. fluorescens, as the name suggests, produces a pigment that even glows in the dark. In a lab setting, seeing growth media turn green is a suspicious sign that the organism may be present.

Pseudomonas fluorescens under UV light. Image credits: Biotech Michael / Wikipedia.

A Hospital Hazard

When it comes to Pseudomonads as pathogens, P. aeruginosa is the star of the show. It likes to spend its time in hospitals, thriving on medical equipment, such as catheters and ventilators. It will settle on a surface, get comfortable, and form a large extended family — but it won’t be content to remain there. This microbial opportunist is simply waiting for the right moment to strike.

Supervillain that it is, it has quite a few accomplishments under its belt. Pseudomonas aeruginosa alone is associated with sepsis, pneumonia, dermatitis, urinary tract infections, and infections in cystic fibrosis patients and the otherwise immunocompromised. It’s also special within its genus because it is one of the only Pseudomonads that can maintain metabolism in the absence of oxygen. This is what enables it to stay functional in damaged lung tissue.

In cystic fibrosis, a genetic disorder causes cells to produce a much thicker, more viscous mucus than is typical. In the lungs, this blocks ducts and passageways, and generally makes it difficult for the natural defenses (such as cilia) to function. This is when your opportunist sees its chance. It enters with moist air from a contaminated ventilator, or simply from unwitting, unclean hands touching your face, and settles in the altered mucus of the lung. Now it can do the thing it’s most hated for: it forms a structure called a biofilm.

Scanning electron micrograph of P. aeruginosa. Image credits: Janice Haney Carr, USCDCP.

Once settled, the cells rapidly reproduce and then literally stick together, releasing cellular products to form a slimy matrix. In the end, you have layers and layers of bacteria forming on top of one another until all medication can truly do is cut away at the upper surface. And if the fact that it’s so anchored wasn’t enough, along with Staphylococcus aureus and Klebsiella species, P. aeruginosa is among the best known bacteria in the world for laughing in the face of antibiotics.

As it turns out, P. aeruginosa isn’t limited to only affecting humans from within. It can be the bane of any water bottling plant. Since they tend to live in springs, wells, and other natural sources, with one small error in the process, Pseudomonas could become attached to a factory line. And once the biofilm fully establishes on the equipment, no amount of scrubbing will make it go away. Heavy-duty chemical treatment is required. Their presence can be so pervasive, that manufacturers have been known to just toss out expensive equipment, rather than waste further resources trying to rid themselves of this plague.

Silver Linings

Still, it isn’t all bad news. Many Pseudomonads have made significant positive contributions to human activity as well — from antibiotics and research opportunities to even cleaning up our messes:

P. fluorescens, can be cultured to produce an antibiotic called Mupirocin, used in the treatment of highly resistant bacterial species. It is also found around plant roots and acts to protect them from fungal growths.

P. deceptionensis lives in the Antarctic and has provided multiple avenues of interest. Strain M1T has presented with a previously unknown internal structure called a stack, meanwhile strain DC5 produces silver particles during metabolic processes.

P. aeruginosa, P. putida and a few other species can decompose hydrocarbons and are used in bioremediation. In fact, a strain of P. putida is the first organism to be patented (with much difficulty) because of its potential for use in degrading toluene and naphthalene in soil, as well as converting styrene to a biodegradable plastic, without being a threat to human health.

Deception Island, Antarctica where P. deceptionensis was discovered. Image credits: W. Bulach / Wikipedia.

So, you see, even the worst of them can be used for positive things – it can break down hydrocarbons and is an excellent model for biofilm formation. As with most bacteria, the majority are harmless to humans. But it is always good to be informed and Pseudomonas is just one more thing you should know about.