There are bacteria in the soil that can resist our antibiotics. That’s predictable – these drugs are our versions of natural compounds that bacteria have been assaulted with for millions of years. Of course, they would have evolved resistance.
There are also disease-causing bacteria in our hospitals and clinics that can resist our antibiotics. That’s predictable too – we expose ourselves, often unnecessarily, to high doses of such drugs. Of course, bacteria would have evolved resistance.
Here’s something fascinating though: some of the genes that confer resistance to the harmless soil bacteria are exactly the same as the ones that confer resistance to the devastating clinical ones. Exactly the same, DNA letter for DNA letter.
This new discovery, by Gautam Dantas, suggests that environmental bacteria may be supplying genetic weapons to the ones that kill us (or the other way around). I’ve written about this secret arms trade for The Scientist. Check it out.
New Scientist published a story yesterday stating that rosacea – a common skin disease characterised by red blotches on one’s face – may be “caused” (more on this later) by “tiny bugs closely related to spiders living in the pores of your face.” Tiny bugs that “crawl about your face in the dark”, lay eggs in your pores, and release a burst of faeces when they die.
This is the terrifying world of the Demodex mite. And by “terrifying world”, I mean your face. For anyone who wants to know more, and who isn’t currently clawing at their cheeks or bleaching their head (health tip: don’t), here’s everything you never wanted to know about your face-mites.
Say hello to my little friend
Mites are relatives of ticks, spiders, scorpions and other arachnids. Over 48,000 species have been described. Around 65 of them belong to the genus Demodex, and two of those live on your face. There’s D.folliculorum, the round-bottomed, bigger one (top image, above) and there’s D.brevis, the pointy-bottomed, smaller one (bottom image, above). These two species are evolution’s special gift to you. They live on humans and humans alone. Other Demodex mites have similarly specific preferences: D.canis, for example, is a dog-lover.
Both species are sausage-shaped, with eight stubby legs clustered in their front third. At a third of a millimetre long, D.folliculorum is the bigger of the two. It was discovered independently in 1841 by two scientists, but only properly described a year later by Gustav Simon, a German dermatologist. He was looking at acne spots under a microscope when he noticed a “worm-like object” with a head and legs. Possibly an animal? He extracted it, pressed it between two slides, and saw that it moved. Definitely an animal. A year later, Richard Owen gave the mite its name, from the Greek words ‘demo’, meaning lard, and ‘dex’, meaning boring worm. The worm that bores into fat. I can only assume that Simon and Owen spent the rest of their lives feeling a little itchy.
These mites are our most common ectoparasites (those that stay on the surface of our bodies, rather than burrowing inside). They’ve been found in every ethnic group where people have cared to look, from white Europeans to Australian aborigines to Devon Island Eskimos. In 1976, legendary mite specialist William Nutting wrote:
“One can conclude that wherever mankind is found, hair follicle mites will be found and that the transfer mechanism is 100% effective! (One of my students noted it was undoubtedly the first invertebrate metazoan to visit the moon!)”
But it’s hard to say exactly how common they are. The first estimate came from a 1903 study, which found the critters in 49 out of 100 French cadavers. The next count, from 1908, found them in 97 out of 100 German cadavers. The nationalities are probably a red herring. What’s clearer is that age matters. The mites aren’t inherited at birth, so each generation picks them up anew, probably from direct contact with our parents. Thanks, parents! If you’re under 20, good news! A French study from 1972 says that you’ve only got a 4 percent chance of carrying Demodex. If you’re old, bad news! You’ve almost certainly got Demodex somewhere.
The mites spend most of their time buried head-down in our hair follicles – the stocking-shaped organs that enclose and produce our hairs. They’re most commonly found in our eyelids, nose, cheeks, forehead and chin. That’s not to say they’re restricted to the face: Demodex has been found in the hairs of the ear canal, nipple, groin, chest, forearm, penis, and butt too. Generally, dry skin is a turn-off for them. They prize bodily real estate that’s flooded with oils (sebum). This explains why they love your face. It might also explain why their numbers are apparently higher in the summer, when hot temperatures ramp up sebum production.
A mite-y existence
How do Demodex mites spend their time? They eat! Some say they eat sebum, but Nutting thought that such a diet wouldn’t be nutritious enough. Instead, he said that they feast on the cells that line the follicle, sucking out their innards with a retractable needle in the middle of a round mouth. On either side of the mouth, D.folliculorum has a seven-clawed organ (a “palpus”) for securing itself to what it’s eating. “All of the structures formed a sharp, offensive weapon,” writes Xu Jing, who first looked at them under an electron microscope. (D.brevis, with its five-clawed palpus, was branded as “less offensive”.)
They crawl! They move about in darkness and freeze in bright lights. The fact that mites have been found on the surface of the skin suggests that they emerge from follicles at night for shadowy strolls across our faces. With their stumpy legs, they’re hardly fast. It would take almost half a day for Demodex to cover the distance from your ear to your nose.*
They don’t poo! The mite has no anus, and stores its waste in large cells within its gut. Nutting saw these as adaptations for a life spent head-down in a tightly closed space. When the mite dies, its body disintegrates and the waste is released. More on this later.
And they have sex! On your face! Their favourite hook-up spots are the rims of your hair follicles. Males outnumber females by three to five times, but this detail aside, Demodex sex lacks much of the horror found throughout the arachnid clan. No traumatic insemination. No cannibalism. The penis and vulva are hidden within the pairs of legs. (Jing wrote that D.folliculorum’s penis “looks like a small candle when it was elongated”. He failed to see D.brevis’s.)
After sex, the female buries into the follicle (if it’s D.folliculorum), or into a nearby sebaceous gland (if it’s D.brevis). Half a day later, she lays her eggs. Two and a half days later, they hatch. The young mites take six days to reach adulthood, and they live for around five more. Their entire lives play out over the course of two weeks.
People with rosacea should look away now
Are they parasites, or something more benign? For the most part, it seems that they eat, crawl and mate on your face without harmful effects. They could help us by eating bacteria or other microbes in the follicles, although there’s little evidence for this. Their eggs, clawed legs, spiny mouthparts, and salivary enzymes could all provoke an immune response, but this generally doesn’t seem to happen.
But like many of our body’s microscopic residents, Demodex appears to be an opportunist, whose populations bloom to detrimental numbers when our defences are down. Several studies, for example, have found that they’re more common in people with HIV, children with leukaemia, or patients on immunosuppressive drugs. Perhaps changes to the environment of the skin also allow the mites to proliferate beyond their usual levels.
In dogs, an overabundance of D.canis can trigger a potentially lethal condition called demodectic mange, or demodicosis. In humans, these blooms have been linked to skin diseases like acne, rosacea and blepharitis (eyelid inflammation). The New Scientist piece will undoubtedly bring this to many people’s attention, but scientists have been talking about such connections for decades. The rosacea link was first put forward in 1925!
Dermatologists have since repeatedly found that Demodex is more common in the cheeks of people with rosacea. In one study, those with the condition had an average of 12.8 mites per square centimetre of skin, compared to 0.7 in unaffected people. And according to an analysis of 48 separate studies, people with rosacea are eight times more likely to have a Demodex infestation. Obviously, correlation not causation, blah blah blah, you know the drill.
There’s plenty of anecdotal evidence about mite-killing treatments and clinical improvements (here’s the latest involving tea-tree oil), but very little in the way of hard clinical trial evidence. An example: metronidazole is sometimes used to treat Demodex infestations, and there’s evidence from three clinical trials that it’s effective at treating rosacea (a Cochrane review, and everything!). Then again, Demodex can survive high concentrations of metronidazole, so maybe the mites are irrelevant to the substance’s actions.
In the new review, covered by New Scientist, Kevin Kavanagh suggests that rosacea may be caused not by the mites themselves, but by the bacteria in their faeces. After all, antibiotics that kill the bacteria, but are harmless to the mites, can sometimes successfully treat rosacea. But again: more correlations. The bacterial angle is fascinating, though. We know so little about these creatures that colonise our bodies, and now we must contend with our even greater ignorance of the creatures that colonise their bodies. Down the rabbit-hole we go!
And finally, if all of this sounds unbearably revolting, spare a thought for people with acarophobia – the fear of mites and other “small bugs that cause itching.” What words of solace can we offer to them? Here’s Nutting:
“Those patients with acarophobia (approximately 12 have been seen in our laboratory) seem curable if they follow a prescription which includes a relaxing vacation at the beach. If they insist on a follow-up examination for hair follicle mites, the situation is a bit delicate because most will still be positive. Diplomacy will prevail—only two of our 12 have failed to respond!”
Images: top photos from Nutting, 1976, HAIR FOLLICLE MITES (ACARI: DEMODICIDAE) OF MAN.
* One review I read quoted their speed at 16 centimetres per hour. Another said 16 millimetres. Given the stubby legs, the centimetre value surely cannot be right, so I’m going with millimetres.
Icelandic horses can move in an odd way. All horses have three natural gaits: the standard walk; the two-beat trot, where diagonally opposite pairs of legs hit the ground together; and the four-beat gallop, where the four feet hit the ground in turn. To those, Icelandic horses add the tölt. It has four beats, like the gallop, but a tölting horse always has at least one foot on the ground, while a galloping one is essentially flying for part of its stride. This constant contact makes for a smoother ride. It also looks… weird, like watching a horse power-walk straight into the uncanny valley.
The tölt is just one of several special ambling gaits that some horses can pull off, but others cannot. These abilities can be heritable, to about the same extent that height is in humans. Indeed, some horses like the Tennessee Walking horse have been bred to specialise in certain gaits.
Now, a team of Swedish, Icelandic and American scientists has shown that these special moves require a single change in a gene called DMRT3. It creates a protein used in neurons of a horse’s spine, those which coordinate the movements of its limbs. It’s a gait-keeper.
Here’s an amazing fact: Adult robins have a magnetic compass in their right eye that allows them to sense the direction of the Earth’s magnetic field, and navigate when all other landmarks are obscured. Here’s an even more amazing fact: Baby robins have two such compasses, one in each eye. They lose the left one as they grow up.
Robins kick-started the study of magnetic senses in the first place. In the 1950s, a German biologist called Hans Fromme showed that robins would always try to escape from a cage in the same direction when it came time to migrate. Even though they had no visual bearings, they headed south-west, as if sunny Spain lay just beyond their cages. In 1966, the husband and wife team of Wolfgang and Roswitha Wiltschko showed that a powerful magnet could disrupt this constant vector, sending them skittering in all sorts of directions.
The Wiltschkos have been studying the magnetic sense of robins ever since. In the 1980s and 1990s, they showed that their compass depends on light. They need some of it, and blue-green wavelengths in particular, to find their way. And in 2002, they showed that the compass lies in just one eye – the right one. If they wore a one-sided goggle that blocked their left eye, they could navigate just fine within their featureless cages. If their right eye was blocked, they headed in random directions. It’s not just robins. They right-eye compasses that the Wiltschkos discovered also exist in Australian silvereyes, homing pigeons and domestic chickens.
Your body keeps its own time. It has an internal 24-hour “circadian clock” that drives the rise and fall of many molecules. Everything from brain activity to hormone levels waxes and wanes according to these molecular metronomes, which dictate how hungry, hot and sleepy we are.
They also affect how well we respond to medicine. Since the late 1980s, scientists have shown that drugs work better at certain times of the day. For example, the cancer drug cisplatin is more effective and less toxic if it’s given in the evening. Adriamycin is more of a morning drug. In another cancer trial, tailoring chemotherapy to these daily rhythms—a practice known as chronotherapy—made the same drugs more effective and reduced the frequency of toxic side effects.
Chronotherapy would seem to be a no-brainer but it hasn’t caught on widely. That may be partly due to scepticism, but there’s a more practical reason: it’s hard to read a person’s body clock. Some people are larks, others are owls. The ticks and tocks of the clock vary depending on age, sex, health, employment, and more. The clocks of two people can be half a day apart. How do you administer a drug at the right time if you can’t tell that time?
The conventional way would be to take blood samples every hour or so for 24 hours, and measure the concentrations of melatonin—a hormone that rises in darkness and falls in light. Melatonin can be detected in saliva samples but because the hormone is found in such low concentrations, the process can’t be automated. As such, it’s labour-intensive work that takes days and tightly controlled environmental conditions. If you have patients to treat, you rarely have such luxuries.
Takeya Kasukawa and Masahiro Sugimoto from the RIKEN Center for Developmental Biology have a better way. Their team have developed a “metabolite timetable” that plots how dozens of molecules rise and fall in relation to one another. With this timetable, they could accurately read a person’s internal clock with just two blood samples, taken 12 hours apart.
When Delta Airlines refused to let Arijit Guha board a plane because his T-shirt made passengers uncomfortable, others made Delta aware of their outrage. When Samsung infringed Apple’s copyright, a jury of independent peers awarded Apple more than $1 billion in damages. When Republican Todd Akin claimed that women could stop themselves from becoming pregnant if raped, people called for his head.
These recent events all illustrate a broad human trait: we seek to punish people who do wrong and violate our social rules, even when their actions don’t harm us directly. We call for retribution, even if we have nothing specific to gain from it and even if it costs us time, effort, status or money to do so. This “third-party punishment” is thought to cement human societies together, and prevents cheats and free-riders from running riot. If you wrong someone, and they’re the only ones who want to sanction you, the price of vice is low. If an entire society condemns you, the cost skyrockets.
Do other animals do the same thing? It’s not clear, but one group of scientists believes that our closest relative – the chimpanzee – does not. Katrin Riedl from the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany found that chimpanzees will punish individuals who steal food from them, but not those who steal food from others. Even if the victim was a close relative, the third party never sought to punish the thief. These were the first direct tests of third-party punishment in a non-human animal, and the chimps got an F.
That being said, there’s an interesting new study showing that people can learn new information when they sleep. Earlier work tells us that we can certainly strengthen existing memories when we slumber, but actually adding new information is different. And retaining that information when we wake up, even if we have no actual awareness of what we learned, is just plain cool.
I wrote about the new study for The Scientist. Head on over.
Image by Alessandro Zangrilli
We aren’t single individuals, but colonies of trillions. Our bodies, and our guts in particular, are home to vast swarms of bacteria and other microbes. This “microbiota” helps us to harvest energy from our food by breaking down the complex molecules that our own cells cannot cope with. They build vitamins that we cannot manufacture. They ‘talk to’ our immune system to ensure that it develops correctly, and they prevent invasions from other more harmful microbes. They’re our partners in life.
What happens when we kill them?
Farmers have been doing that experiment in animals for more than 50 years. By feeding low doses of antibiotics to healthy farm animals, they’ve found that they could fatten up their livestock by as much as 15 percent. You can put the antibiotics in their feed or in their water. You can give the drugs to cows, sheep, pigs or chickens. You can try penicillins, or tetracyclines, or many other classes of antibiotics. The effect is the same: more weight.
Consistent though this effect is, no one really understands why it works. The safe bet is that the drugs are exerting their influence by killing off some of the microbiota. Now, Ilseung Cho from the New York University School of Medicine has confirmed that hypothesis. By feeding antibiotics to young mice, he has shown that the drugs drastically change the microscopic communities within their guts, and increase the amount of calories they harvest from food. The result: they became fatter.