Thanks to Mandarb for posting this clip from Weeds I was wondering about yesterday. I should point out that it’s a very abridged version of my original piece on the radio. For example, it sounds as if I’m giving God my own personal forgiveness for parasitic wasps. I was actually talking about a letter written by Darwin in which the wasps figured in his musings about God.

And I have to say that I’m not much closer to figuring out what parasitic wasps have to do with the show’s plot. I guess I’ll have to watch the whole episode. But–for the record–here it is:

I have a strange job. A few weeks back I was wandering through the aisles of the local Walmart, searching for bug spray, when my phone rang. A very excited Robert Krulwich was calling. As I drifted past the potato chips and plasma-screen TVs, he declared to me with great excitement that I was going to be on the cable series Weeds.

Now, I’m pretty sure that if I had actually auditioned for the show, I would remember it. Or at least I could find some trace of the experience over on IMDB, searching for my name in the role of Pothead #8. So there I was at the store, getting totally lost trying to figure out what Krulwich was saying.

Gradually, the story emerged: a few months ago, I joined Krulwich and his partner in radio crime, Jad Abumrad to tape a couple segments for their fine show, RadioLab. In one of those segments, I describe the glories of parasites, focusing on one surgically fiendish wasp. Apparently the people at Weeds are RadioLab fans and sometimes work bits of it into their own show. And apparently, they are using my ramblings–at great length, I’m reliably informed–in the season premiere. What deeper meaning that Jad, Robert, and I could bring to their show, I can’t say–in part because I don’t have cable TV, so I’m not a regular viewer.

Suffice to say, it was a very long bug spray run. The new season airs tonight. If anyone sees it, fill me in! And if I can get my mitts on the clip, I’ll post it.

[Update: We've got it]

When I’ve traveled abroad, I’ve gotten my share of jabs for hepatitis and other diseases. But for malaria, the best I could hope for was to take malaria-blocking drugs like Lariam, which gave me weird dreams at night and made me feel as if someone was tugging my hair all day.

For people who live in countries with malaria, these prophylactic drugs just aren’t practical. Given that 800,000 people a year die of malaria, why don’t we have a good vaccine for it? It’s not for lack of trying–in fact, this year marks the 100th anniversary of the first attempts to make a malaria vaccine.

To understand this epic fail, I talked on my latest podcast with Irwin Sherman, a malaria expert and author of The Elusive Malaria Vaccine: Miracle or Mirage?.

Check it out.

Everything is connected. And when I say everything, I include you, dear reader, and the tapeworms of Madagascar. They carry a hidden history of our entire species.

I’m sure we’d all prefer that there was no such connection. Tapeworm are not just gross, but they are pretty much the polar opposite of the human existence. They have no brain. They have no eyes. They lack mouths and guts, having turned their body inside out, absorbing food through its surface. Most of their hideously long body is made up of segments, each of which contains its own supply of both eggs and sperm. To reproduce, the tapeworm fertilizes its eggs, either with its own sperm or another tapeworm’s, and then sheds its segments. Once out of the body, those segments can crawl around on the ground on their own.

But, like it or not, tapeworms–or at least the pork tapeworm Taenia solium–has an intimate relationship with us. After all, it can only live in our guts as an adult, where it will dwell for years and grow over 20 feet long. Without us, these tapeworms would simply not exist. From the safety of our guts, they can shed six egg-loaded segments a day, each of which contains 50,000 eggs. If a pig swallows one of these eggs, it hatches in the animal’s instestines, drills its way into the abdominal cavity, and finds a muscle to infect. There it dwells in a barely visible cyst, for years if need be. In order to complete its life cycle, it must get into another human, which it does if a human eats a piece of infected, undercooked pork.

Carrying an adult tapeworm around in your gut may be disturbing, but it’s not the worst thing a tapeworm can do to you. Sometimes people get infected with the eggs of pork tapeworms, rather than the cysts. Instead of developing into an adult, the tapeworm treats you like a pig. It invades your muscles, where it makes a cyst. Sometimes the tapeworms can get into people’s brains. These cysts can trigger dangerous reactions from our immune systems, and can sometimes be fatal. This disease, known as cysticercosis, is relatively rare in the United States. Only 221 people died of it between 1990 and 2002. But in other parts of the world, it’s a lot worse, with ten percent or so of the population of many countries showing signs of having had the disease.

Madagascar is one of those countries. In the highlands, over 20% of people have antibodies to cysticercosis. To get a better handle on the epidemiology of the disease, medical researchers at the Pasteur Institute of Madagascar have traveled around the country, gathering tapeworm from different regions. They isolated DNA from 13 of the samples and then compared their genetic sequences to see how they were related to one another, and to tapeworms from other parts of the world.

The family tree of tapeworms they got was strangely ancient and alien. In many cases, the closest relatives of tapeworms on Madagascar are not other tapeworms on Madagascar. The tapeworms that live in the southwest part of the island are closely related to tapeworms hundreds of miles away, in Africa. The tapeworms in other parts of the island are more closely related to tapeworms thousands of miles away, in south Asia.

The scientists then tallied up the mutations in each lineage of tapeworm to figure out how long ago they had split off from a common ancestor. All the T. solium tapeworms the scientists studied descend from a common ancestor that lived about 680,000 years ago. The southwest Madagascar tapeworms and the tapeworms of Africa share a common ancestor that lived 235,000 years ago. All of the Madagascar and Asian tapeworms share a common ancestor that lived about 260,000 years ago. The Madagascar tapeworms and their very closest Asian relatives share an ancestor that lived 85,000 years ago.

So how on Earth did one remote island end up with two such deeply split lineages of tapeworms in their pigs? The answer is like a guided tour thorugh the evolution of our species, rolling right on through the history of civilization.

Along with pork tapeworms, there are two other species of Taenia that live in humans. One, T. asiatica, also cycles between people and pigs, but only in Asia as the name suggests. The other, T. saginata, moves between people and cows. Both of these human tapeworms use domesticated hoofed mammals (known as ungulates) as their intermediate hosts. Pigs and cows were only domesticated within the past 11,000 years or so. The best way to find clues to how these tapeworms colonized us is to compare them to the 39 species of Taenia tapeworms that infect wild animals. Eric Hoberg, a parasitologist at the U.S. Department of Agriculture, and his colleagues have found that most Taenia tapeworms form cysts in wild ungulates, such as antelopes, and then become adults in the carnivores that eat their intermediate hosts. The closest relatives of all three human tapeworms live in Africa. Hyenas are the hosts of the closest relatives of pork tapeworms, while lions are the hosts of the closest relative to the other two species, T. saginata and T. asiatica. Hoberg and his colleagues compared the mutations in the DNA of T. saginata and T. asiatica and found that their common ancestor lived somewhere between 780,000 and 1.71 million years ago.

The new results from Madagascar fit in nicely with Hoberg’s results. Hundreds of thousands of years ago, our ancestors lived in Africa, where they scavenged meat from ungulates. In so doing, it appears, they stepped into the life cycle of Taenia tapeworms. Tapeworms that might have ended up in the gut of a hyena or a lion ended up in the gut of our ancestors instead. Over thousands of years, some populations of these tapeworms adapted to our scavenger ancestors. These were the common ancestors of today’s human tapeworms, whose great antiquity is now recorded in the DNA of living tapeworms.

As hominins expanded their ranges both within Africa and beyond it, they carried their tapeworms along for the ride. As hominins scavenged new game, the tapeworms adapted to new intermediate hosts. Hominins gradually developed the skills and weapons to hunt game, offering still more opportunities for their tapeworms. Neanderthals and other hominins hunted wild boar as well, and it’s likely that we infected them with the ancestors of today’s pork tapeworms.

Starting about 11,000 years ago, humans domesticated pigs many times over, both in East Asia and in the Near East. Now the trip from host to host became riduclously easy for the tapeworms. Instead of waiting for its wild boar host getting speared by a hunter, it could make the journey on the dinner plate. Judging from the deep split in the evolution of pork tapeworms, the parasites must have made two separate shifts from wild boar to domesticated pigs, in both East Asia and the Near East.

The genealogy of the tapeworms also matches up nicely with the human history of Madagascar. People only arrived on the island 2000 years ago. They came from two directions. Bantu farmers sailed from the west from Africa across the Mozambique channel. Asians came from the east, traveling thousands of miles across the Indian Ocean from Indonesia. Malagasy culture emerged from the mingling of these two origins. That culture also includes the livestock that the Bantu and Indonesians brought to the island. And those animals brought parasites with them that had been separated for almost 700,000 years, reaching back to a time when our ancestors had yet to invent fire or spoken language.

[Image: Chiang Mai University]

If blogs could have mascots, the Loom’s would be the Emerald Cockroach Wasp (Ampulex compressa). Back in 2006, I first wrote about the grisly sophistication of this insect, which turns cockroaches into zombie hosts to be devoured by their offspring. Since then I’ve blogged from time to time about new research on this parasite’s parasite. Last year I sang the praises of the Emerald Cockroach Wasp on the NPR show Radiolab, and, to my surprise, brought some peace of mind to a very scared kid.

Scientists still don’t understand the wasp very well, though, and so I decided last night to see if anyone had discovered something new about it recently. It turns out Ram Gal and Frederic Libersat, two scientists at Ben Gurion University in Israel, just published a paper in which they reveal one of the secrets to zombification. In effect, they identified the seat of the cockroach soul.

Before I describe the new results, let me just refresh your memory about what the Emerald Cockroach Wasp actually does.

Like many parasites, the Emerald Cockroach Wasp manipulates its host’s behavior for its own benefit. As I explain in Parasite Rex, parasites make their hosts do lots of different things (get them into the body of their next host, act as a bodyguard, or build them a shelter to name a few examples). The Emerald Cockroach Wasp needs a live, tame cockroach to feed its babies.

When the female wasp is ready to lay her eggs, she seeks out a cockroach. Landing on the prospective host, she delivers two precise stings.

The first she delivers to the roach’s mid-section, causing its front legs buckle. The brief paralysis caused by the first sting gives the wasp the luxury of time to deliver a more precise sting to the head. The wasp slips her stinger through the roach’s exoskeleton and directly into its brain.

She injects another venom that robs the cockroach of the ability to start walking on its own. The wasp takes hold of one of the roach’s antennae and leads it, like a dog on a leash, to its doom: the wasp’s burrow. The roach creeps obediently inside and sits there quietly as the wasp lays her egg on its underside. The wasp leaves the burrow, sealing the opening behind her.

The egg hatches, and the larva chews a hole in the side of the roach. In it goes. The larva grows inside the roach, devouring the organs of its host, for about eight days. It is then ready to form a pupa inside the roach. After four more weeks, the wasp grows to an adult. It breaks out of its pupa, and out of the roach as well. Only then does the zombie cockroach die.

The zombifying sting has long fascinated scientists. It does not paralyze the roach. It does not put it to sleep. If the zombie roach is frightened, it jumps in the air like a normal roach, but then it fails to run away. What does the wasp understand about the nervous system that we do not?

The cockroach brain is not a brain like ours–a single solid lump of neurons like the one in our head. It’s actually a group of linked clusters of neurons, called the cerebral ganglia. Some studies have suggested that one of those clusters, called the sub-esophageal ganglia (SEG), boosts the signals required for an insect to start walking. So Gal and Libersat decided to see how wasps would behave if the roaches they stung were missing the SEG.

Normally, the wasps only spends about 15 seconds inserting its stinger into the cockroach’s head. But when Gal and Liberset destroyed the SEG in roaches, the wasps were flummoxed. They spent over three minutes poking and prodding inside the cockroach’s head. By contrast, when the scientists cut the nerve running from the SEG to the roach’s body (marked here as NC), the wasps didn’t spend any extra time delivering the sting. It thus appears that the wasps zero in on the SEG to zombify their host.

Gal and Libersat took a closer look at the SEG of zombified cockroaches. Using an electrode, they measured the activity of the SEG. They discovered that the neurons in the SEG became quiet. They spontaneoulsy fired half as often as the neurons in the SEG of normal cockroaches. And a puff of air on the antennae of the zombified roaches–which usually triggers a roar of activity in the SEG so that the insect can escape–produced only half the normal activity in the neurons.

To cap off the experiment, Gal and Libersat then pretended to be wasps. They injected wasp venom directly into the SEG of healthy cockroaches. The injection zombified the roaches. The insects barely moved on their own, and they hardly budged in response to a terrifying puff of air. Gal and Libersat could only zombify the cockroaches with a shot to the SEG, however. If they injected the venom into a neighboring cluster of neurons (marked here as SupEG), the roaches flitted about as if nothing had happened.

While this study does a good job of pinpointing the place where the wasps perform their neurosurgery, it does not close the book. The SEG is actually a complicated maze of neurons. Gal and Libersat are now investigated exactly where in the SEG the wasp sends its stinger, and what precisely its venom does to those particular neurons. The Emerald Cockroach Wasp will no doubt make yet another visit to the Loom in years to come, because it has more to teach us.

Here’s a wonderfully disturbing new species of leech that you don’t want to find up your nose. For background, check out my profile of its discoverer, Mark Siddall, in the New York Times.

Did pregnancy tests help drive frogs extinct around the world? In my latest podcast, I talk to wildlife disease expert Peter Daszak about his research on how germs can drive animal species to extinctions, and jump from animals to us. Check it out.

Measles looks to be 1000 years old. It jumped from cattle. And you can read more about it here.

Can the bacteria in our bodies control our behavior in the same way a puppetmaster pulls the strings of a marionette? I tremble to report that this wonderfully creepy possibility may be true.

The human body is, to some extent, just a luxury cruise liner for microbes. They board the SS Homo sapiens when we’re born and settle into their assigned quarters–the skin, the tongue, the nostrils, the throat, the stomach, the genitals, the gut–and then we carry them wherever we go. Some of microbes deboard when we shed our skin or use the restroom; others board at new ports when we shake someone’s hand or down a spoonful of yogurt. Just as on a luxury cruise liner, our passengers eat well. They feed on the food we eat, or on the compounds we produce. While the biggest luxury lines may be able to carry a few thousand people, we can handle many more passengers. Although the total mass of our microbes is just a few pounds, the tiny size of their cells means that we each carry about 100 trillion microbes–outnumbering our own cells by more than ten to one.

It’s important to bear in mind that you can carry this galaxy of microbes around and enjoy perfect health. These microbes, for reasons that are not entirely clear, behave like well-mannered passengers. They do not barge into the kitchen, take a cleaver to the cooks, and then eat all the food. Aboard the SS Homo sapiens, the crew includes a huge staff of security guards armed with lethal chemical sprays and other deadly weapons, ready to kill any dangerous stowaway (also known as the immune system). For some reason, the immune system does not unleash its deadly fury on the microbes–even when the microbes are fairly close relatives to truly dangerous pathogens.

In fact, our microbial passengers may actually help out the cruise liner’s crew. They can close up the ecological space in our bodies, so that invading pathogens can’t get a solid foothold. Some species in our guts can break down our food in ways that we can’t, and synthesize certain vitamins and other compounds beyond our biochemistry. The genes that the microbes carry–millions of them–expand our biochemical powers enormously.

To understand the human microbiome better, scientists have been cataloging the microbes in and on people’s bodies, and they’ve been sequencing their DNA. (Listen to my recent podcast with biologist Rob Knight for more.) Yesterday, Nature published a head-spinningly huge study on the microbiome from a team of European and Chinese researchers. Lurking in the stool of 124 volunteers, the scientists found, were 3.3 million microbial genes. The scientists identified a core of bacteria species carried in most people’s guts, as well as other species that varied from person to person.

As Ed Yong rightly points out, this study is most impressive as a titanic database. It is not the Theory of Everything for the human microbiome. That will take a lot longer to build, because the microbial ecosystem inside of us is so complex. Individual species don’t just sit in isolation, surviving in their own special way. Microbes cooperate with one another to get the food they need and produce the conditions in which they can thrive. In Microcosm, for example, I write about research suggesting that E. coli–a minor member of the gut ecosystem–may keep oxygen levels low enough for other species to invade and dominate. And it’s not as if there is some Platonic ideal of a microbiome that we all carry around with us from birth to death. The diversity of microbes I carry is different from the one you carry, and they both change over our lifetimes. Every time we take a dose of antibiotics, for example, the balance can change dramatically. And as the diversity of microbes changes, so do its ecological functions.

Which brings me, at last, to the possibility that the human microbiome can become our puppetmaster.

First some background. A lot of parasites have evolved the ability to manipulate their hosts for their own benefit. (I get into more detail about this in my book Parasite Rex and in this segment of the show Radio Lab.)

Very often, the parasites cause hosts to do things that help the parasites, instead of themselves. For example, a protozoan called Toxoplasma needs to get from rats to cats, and to help the process along, it makes rats lose their fear of cats. Parasites can also change the diet of their host as well as the way in which their hosts digest their food. Parasitic wasps living inside caterpillars, for example, cause catepillars to convert the plants they eat into compounds that supply quick energy (good for wasp larvae growing quickly) instead of storing them as fat for their own metamorphosis.

I was reminded of this sinister manipulation by a paper that was published in Science today by Rob Knight and his colleagues. They built on previous research that revealed that mice genetically engineered to be obese have different kinds of microbial diversity in their guts than normal mice. Scientists have found that if they transfer microbes from an obese mouse to a regular mouse that has had all its own germs stripped out, the recipient mouse will develop extra fat. In the case of these obese mice, it appears that the microbes become less efficient at helping the animals digest food, triggering a series of changes that leads the mice to be fat.

Knight and his colleagues discovered a different–and more disturbing–way that microbes can make mice fat. They started out by engineering mice so that they didn’t produce a protein normally found on the surface of gut cells, called TLR5. TLR5 can recognize bacteria, and some studies suggest that the cells can then pass along signals to the immune system, possibly sending a stand-down command so that the immune system doesn’t start trying to kill the microbes (and end up killing gut cells too).

Born without TLR5, mice got 20% fatter than normal. Not only that, but the mice had lots of other familiar symptoms that go along with being overweight, such as high levels of triglyceride, cholesterol, and blood pressure. Without TLR5 exerting its soothing influence, the mice suffered from chronic inflammation, probably thanks to the low-level war they were waging on their microbes. And things got worse for the mutant mice when they had to eat a high-fat diet. They gained more weight on a high-fat diet than regular mice, suffered even more inflammation, and even ended up diabetic.

The obesity of these TLR5-deficient mice was not the result of inefficiency, as in previous studies. Instead, the mice wanted to eat more–about 10 percent more than regular mice. Knight and his colleagues restricted the diet of the mutant to what the regular mice ate. A lot of their symptoms went away. So the change in their behavior was critical to their weight change.

The scientists also discovered that the make-up of the microbial diversity changed significantly in the mutant mice. Were the microbes giving the mice their symptoms? To find out, Knight and his colleagues knocked out the microbes with antibiotics. The mice ate less, put on less fat, and showed less diabetes-like symptoms.

To isolate the effects of the microbes even more, the scientists transferred them from mutant mice into the bodies of ordinary mice that had first had all their own germs stripped out. Remember–these mice have a normal set of TLR5 receptors. The scientists found that the microbes made the recipient mice hungry–and also made them obese, insulin resistant, and so on.

So here we are. Mice with a genetic make-up that alters the diversity of their gut microbes get hungry, and that hunger makes them eat more. They get obese and suffer lots of other symptoms. Get rid of that particular set of microbes, and the mice lose their hunger and start to recover. And that distinctive diversity of microbes can, on its own, make genetically normal mice hungry–and thus obese, diabetic, and so on.

When I first learned of this work, I asked Knight–with a mix of dread and delight–whether the microbes were manipulating their hosts, driving them to change their diet for the benefit of the microbes. He said he thinks the answer is yes.

This discovery doesn’t just have the potential to change the way we think about why we eat what we eat. (Am I really hungry? Or are my microbes making me hungry?) It also provides a new target in the fight against obesity, diabetes, and related disorders. What may be called for is some ecological engineering.

[Update: Links to papers fixed.]

In my newest podcast, I talk to a kind of viral Indiana Jones. Michael Worobey of the University of Arizona chases down the evolutionary origins of viruses such as HIV and the flu no matter what it takes–including getting dangerously ill in the middle of a civil war. Check it out.

Plush Alien Facehugger out of stock and not back until mid-2010?? This is an outrage–let’s get to work, people!

Last March a new kind of flu came on the scene–the 2009 H1N1 flu, a k a swine flu. Hatched from an eldritch mingling of viruses infecting humans, birds, and pigs, it swept across the world. Here in the United States, the CDC estimates that between 41 and 84 million people came down with swine flu between April and January. Of those infected, between 8,330 and 17,160 are estimated to have died. For more details on the evolution of this new flu strain, here’s a video of a lecture I gave in November.

This flu strain has been nothing if not surprising. It was lurking around in humans for several months, undetected, before becoming a planetary infection. And before that, the ancestor of the virus was circulating among pigs for a decade, again unknown. And while the new swine flu has killed some 10,000 people in the United States alone and many more abroad, it has proven to be relatively low key–as flu goes. Some 30,000 people die in the United States every year from seasonal flu, the cocktail of flu strains that show up year in and year out.

Now the swine flu is surprising us once more. It has dwindled away to very low levels and stayed there. Meanwhile, the seasonal flu, which was expected to kick in at some point as well this flu season, is a virtual no-show. The San Francisco Chronicle has the story. In this CDC chart of total reports of flu-like symptoms, you can see that we’re in a deep trough. At this point in previous years, we were fast approaching the peak of the flu. This season, the peak came months ago, at the height of the fall swine flu outbreak.

When swine flu started to crash, some observers expected it to bounce back soon, as other flu strains have in the past. Ian York, at his blog Mystery Rays from Outer Space, offers some interesting ideas about why this hasn’t happened. He suggests that the virus has been stymied by pre-existing immunity in a lot of old people, new immunity from vaccinated children, and the protection that infected survivors now have. In other words, the virus just doesn’t have enough hosts now to sustain a new outbreak.

It’s possible that the swine flu’s raging success in the fall may have also led to the weird situation we’re in right now, with no seasonal flu at exactly the time you’d expect it. One possibility is that getting sick with swine flu provides some cross-immunity to seasonal flu. Another is ecological: the swine flu outcompeted seasonal flu so effectively at the start of flu season that the seasonal flu hasn’t been able to get a toehold since.

That, of course, could change. Seasonal flu has been known to peak as late as March. And while flu may be in a lull in the United States, it’s doing just fine in other parts of the world. For example, a nasty kind of flu called influenza B is raging around China right now according to the Chronicle. In normal years B makes up a pretty small fraction of US flu. But this is no normal year.

Scientists did a better job tracking the 2009 H1N1 outbreak than they have with previous emergent strains. They’ve got new machines to sequence virus genes, online databases to pool information from around the globe, and powerful computers to help figure out where the viruses came from. And yet, with just ten genes, the flu still continues to move enigmatically ahead of our understanding.