Blogs / The Loom

I’ve been thinking a lot about bedbugs recently, because…well, because that’s part of my job description. I was asked to be on a radio show a couple weeks ago to talk about the rising tide of bedbugs in the United States (note to self: don’t pick up old mattresses left out on trash day). But I also think they’re pretty interesting. (Traumatic insemination, for starters…) And, thanks to Alex Wild, Annie Liebowitz to the arthropods, I now also think they’re rather lovely. If you haven’t checked out his blog, do.

[Note: To all the professional exterminators who are trying to post crypto-ads for their companies in the comments, please don't bother. I'll delete it. Why not buy a real ad from Discover and support the site?]

Glad to see an old tongue-eating friend is back in the news.

Radiolab and parasites. A match made in parasitic heaven. If you haven’t discovered this excellent radio program, check out the first episode of their sixth season. During the first 20 minutes of the show, I persuade the hosts of the show, Jad Abumrad and Robert Krulwich, that parasites are not degenerate or evil, but rather sophisticated creatures that have a huge influence on humanity and the entire natural world (the basic message in my book, Parasite Rex). The rest of the show delves into some particularly cool parasite tales. Check it out.

When I first learned about the fungus Cordyceps, I refused to believe.

I was working on a book about the glories of parasites, so I was already in the parasitic tank, you could say. But when I read about how Cordyceps infects its insect hosts, I thought, this simply cannot be. The spores penetrate an insect’s exoskeleton and then work their way into its body, where fungus then starts to grow. Meanwhile, the insect wanders up a plant and clamps down, whereupon Cordyceps grows a long stalk that sprouts of the dead host’s body. It can then shower down spores on unfortunate insects below.

I mean, really.

Yet this video from David Attenborough faithfully depicts the actual biology of this flesh-and-blood fungus. I also discovered that Cordyceps is not the only species that drives insect hosts upward. You don’t even have to visit a remote jungle to see one. Here in the United States, houseflies sometimes end up stuck to screen doors thanks to a fungus called Entomophthora muscae. And the lancet fluke Dicrocoelium dendriticum uses the same strategy to get into cows.

Call me naive, but I assumed that creatures as freakish and wonderful as Cordyceps and company would attract enormous amounts of scientific attention. Yet I was frustrated to discover that hardly any research has been carried out on their powers of manipulation. That’s a shame, because you cannot assume that these parasites are indeed manipulating their hosts. It’s possible, but it’s just a hypothesis that requires testing. One alternative explanation might be that when insects get infected with these parasites, they just lose their bearings. What looks like an adaptation to us–getting your host to a good place for spreading your offspring–may just be a coincidence.

So it is with great delight that I see that David Hughes of the University of Exeter and his colleagues are bringing some real science to bear on these X-Files creatures. Based on their research, these creatures have indeed evolved finely tuned adaptations for using their hosts. In fact, they’re even more sophisticated that I had given them credit for.

The scientists are studying a fungus in Thailand called Ophiocordyceps unilaterius. It doesn’t infect just any insects, but only ants. And it doesn’t infect just any ant, but almost always infects a single species, called Camponotus leonardi, a species that makes its nests high in trees and wanders around the forest floor for food. If Ophiocordyceps really has evolved to manipulate its host, then the scientists predicted that the manipulation would boost their reproductive success in a number of ways. The alternative explanation would be that,  as has been shown with other parasites, they don’t actually benefit from the change in their hosts.

The scientists dissected infected ants to see how the parasites used up their bodies to grow. They also looked around the jungle to see where the ants ended up. It turns out that the ants don’t end up randomly scattered across the jungle. Instead, Ophiocordyceps-infected hosts are concentrated in “ant graveyards.” The scientists took careful measurements of the conditions in these graveyards, looking for any common factors they might share. They also plucked some infected ants from their leaves and moved them to different spots to see how their position affected their success in infecting other ants.

The death grip of the ant is very precise. All ants bite the underside of a leaf (another species of Ophiocordyceps is known to make its hosts bite bark, and another bites twigs). The scientists found that 98% of the ants bit a leaf vein. Most of the ants ended up on leaves on the north-northwest side of the plant. The ants ended up on leaves low to the ground–at a height of about 25 centimeters. It just so happens that there are consistent differences in the air conditions at different heights in the jungle. The higher you go, the drier and warmer the air becomes. This is telling, because the rate at which fungi grow is very sensitive to humidity and temperature. Studies on fungi similar to Ophiocordyceps show that they need very humid conditions to grow well, and temperatures between 20 and 30 degrees C.

When the ants ended up in this particular kind of spot, the fungus grew in the same consistent pattern. It developed an orange tube that ran the length of the animal, rich in carbohydrates. A big black ball of fungal tissue grew in the ant’s abdomen, and white threads, known as hyphae, spread through the rest of the body. Within 24 hours after death, the hyphae began to emerge out of their host, making the ants fluffy. Some of the hyphae grew out to contact the leaf, lashing the host in place. By the second day, a pinkish stalk began pushing out of the ant’s head. As the entire ant became covered in a mat of hyphae, the stalk grew to be twice as long as the ant itself. At first the fungus produces asexual spores, but after a week or so, the stalk produces sexual spores. Each night, both kinds of spores rain down on an area of about a square meter on the forest floor.

When the scientists moved infected ants higher up into the canopy, the fungi grew abnormally and never fully developed. On the other hand, when the scientists moved the ants to the ground, the ants simply disappeared–devoured most likely by other animals or washed away by rain.

The scientists published their findings recently in the journal American Naturalist. There they conclude that the ant becomes what Richard Dawkins would call an extended phenotype–an extension of the parasite itself, which helps it pass on its genes to the next generation. In a jungle, animals and plants evolve to exploit distinct niches. Ophiocordyceps exploits a niche of its own by directing its host to a place in the canopy where it can find the best conditions for growing quickly. (It should be pointed out that only infected ants end up on the underside of north-northwest leaves 25 centimeters up from the ground–it’s not the sort of place a healthy Camponotus leonardi is found.)

The resting place of the ants benefits the fungus not just because the humidity and temperature are good. It also helps the fungus extend the usefulness of the ant corpse. On the underside of a leaf, the ant’s body is protected from sunlight and heavy rain. The fungus also protects its cadaverous house by making antibiotics to keep other microbes from invading and stealing the valuable food inside. Far from destroying the ant’s body, the fungus uses its hyphae to strengthen the insect’s exoskeleton into what the scientists call “a protective case.” Inside the ant, the scientists propose, the fungus builds its orange tube in order to store up nutrients from the ant’s fluids, so that it can fuel its own growth more reliably over the long term. These adaptations together may allow the fungus to produce a steady shower of spores for days on end in order to infect as many unlucky ants below as possible.

Like their hosts, parasites face many threats to their survival these days. Just as overfishing may wipe out my dear namesake tapeworm, I worry about the rampant deforestation of tropical forests, which may wipe out not just trees, but the insects that depend on them, and the fungi that depend on them in turn. We should not wish extinction on Ophiocordyceps, as gruesome as it may be. It has much to teach us. We might even borrow some of its tricks–Ophiocordyceps antibiotics show promising signs of fighting against malaria and cancer. And it would be a true shame for this particular bit of science fiction to disappear from the world of science fact.

[Image: PLOS One, via Creative Commons Licence]

Chimpanzees get AIDS.

This is an important discovery, but what intrigues me most about it is how the discovery was made. It is a story of two kinds of science, both of which are essential to getting a deeper understanding of life, but which today are staggeringly out of balance.

In the 1960s, Jane Goodall carried out some of the first long-term studies on chimpanzees in the wild. Goodall made important observations, noting that chimpanzees can be surprisingly cooperative but also quite violent, with troops engaging in war-like conflicts.

Goodall’s research was part of a long tradition of going to where the animals are, and tracking them for years on end. Goodall didn’t take giant crates of lab equipment with her to Tanzania; instead, she brought patience and careful observation.

Of course, doing this sort of science poses some serious challenges. Field biologists often end up studying relatively few individual animals, because they’re so hard to find. Small sample sizes always make sweeping generalizations risky. Animals in the wild are also embedded in a marvelously complex environment. They are influenced by a vast number of variables–the weather, the food supply, the latest disease outbreak, the latest kerfuffle between the top male and his younger rivals. The state of an animal at any moment may be influenced by many of these variables, making it even harder to uncover important underlying rules of its natural history. And since this kind of science takes so long, it can seem meager if you only learn about it through the papers that the scientists publish.

The contrast between Goodall’s kind of science and, what goes on in, say, a virology lab is enormous. Instead of just watching viruses, scientists can run experiments to test hypotheses–experiments that are controlled with exquisite precision. Scientists can genetically alter viruses to discover how each bit of its genetic material helps (or doesn’t help) it infect its host. They can carefully select the hosts to infect, comparing two sets of hosts for instance that might differ only in one particular cell receptor. They can trace the virus’s journey through the cell and out again; they can sequence viral genes as easily as you might crack open a fortune cookie. And they can churn out many papers a year on what they discover.

The divide between these different kinds of biology has existed for decades, as I wrote in this essay for PLOS Computational Biology. That divide has led to some unfortunate biases. Natural history is sometimes treated like glorified butterfly-collecting. Meanwhile, lab-based molecular biology is sometimes seen as sterile and pointlessly reductionist. But it would be a mistake for one side to think it could live without the other. Understanding the origin of AIDS is a case in point.

In 2007, an estimated 33 million people worldwide had HIV infections, and an estimated 3.1 million people were dying of AIDS-related causes every year. Yet, as diseases go, HIV is a latecomer. Scientists only became aware of it in the early 1980s, when it was still relatively rare, after which it swiftly became a global epidemic. Scientists have tried to search through medical records and blood samples for earlier cases of HIV infection that might have been overlooked. The earliest sample of HIV comes from a blood sample taken from a patient in Kinshasa, the capital of the Democratic Republic of Congo, in 1959.

The mysterious appearance of HIV led to many speculations about where it came from–including accusations that vaccination campaigns introduced it into people with vaccines contaminated with a monkey virus. But when scientists reconstruct the evolutionary tree of the virus and its relatives, they can reject those claims.

As soon as scientists discovered HIV, it was clear that it belonged to a group known as the lentiviruses. Lentiviruses are small particles with spiky knobs on their surface, and they encode their genes in RNA. They infect mammals, such as cats, horses, and primates, typically invading certain types of white blood cells. Genetic studies revealed that HIV is most closely related to strains of lentivirus that infect monkeys and apes–known as simian immunodeficiency virus, or SIV for short. HIV is not actually a single lineage. It is several different strains with different origins.

There are two main forms of HIV, HIV-1 and HIV-2. HIV-2, which is relatively mild, evolved from SIV that live in a monkey called the sooty mangabey. The story of HIV-1, which  causes the vast majority of AIDS cases, is more complicated, as this diagram shows. (It comes from my upcoming book, The Tangled Bank: An Introduction to Evolution.) This tree reveals that it is actually several strains, all of which jumped from chimpanzees.

Scientists first discovered SIV in chimpanzees by looking at captive animals. But in order to get a sense of the true diversity of the virus, they had to leave the relative comforts of laboratories and head out to the places where chimpanzees live. Wild chimpanzees don’t take very well to a blood draw, so scientists developed methods for extracting virus DNA from the feces chimpanzees leave behind. But in order to find those chimp feces, you have to find the chimps (and the trees in which they spend the night).

These studies showed that two subspecies of chimpanzees carry SIV, but HIV-1 has only evolved from one, P. troglodytes trogloydytes, found in west Africa around Kinshasa (marked Ptt on this tree). Goodall’s central African chimpanzees, Pan troglodytes schweinfurthii, have SIV of their own (Pts).

These studies indicate that SIV evolved into HIV as hunters killed apes and monkeys to sell in a growing “bush-meat” industry. Viruses in the blood of the primates could have entered cuts in the skin of the hunters, where a few of them mutated and evolved adaptations to their new host.

Knowing the structure of the HIV tree allows scientists to pinpoint those adaptations. It turns out, for example, that as all three strains of HIV-1 evolved from chimp virus ancestors, they all acquired the same new amino acid in the same position in the same protein. No strain of SIV in chimpanzees produces that amino acid. This mutation altered a gene encoding the shell of the virus, and experiments suggest that it was crucial to the success of the new HIV strains in humans. It’s possible that the mutation allowed the virus to do a better job of manipulating its new hosts into building new copies of itself.

Of course, AIDS is more than just a virus. Once a person is infected with HIV, it may take years for the virus to wipe out his or her immune system, allowing a menagerie of parasites to move in. When scientists studied captive chimpanzees infected with SIV, they didn’t see anything that looked like AIDS. This was intriguing to say the least. Perhaps the chimpanzees and the viruses had coevolved to a peaceful coexistence. When HIV-1 jumped to humans, its evolution took a nasty turn.

But what about chimpanzees out in the real world? Do they get AIDS? That’s a very short question that has taken a very long time to answer. A team of scientists set up shop at Jane Goodall’s study site in Gombe National Park, and took advantage of her decades of field work to track 94 individual chimpanzees for nine years. They searched chimpanzee feces for SIV, and then kept track of the chimpanzees themselves, observing their health, their offspring, and their lifespan. When the chimpanzees died, the scientists autopsied them to see what effect, if any, SIV had on them.

The results, published today in Nature, are stark. Out of the 94 chimpanzees, 17 had SIV. The SIV-infected chimpanzees had a mortality rate 10 to 16 times higher than the uninfected chimpanzees. Fewer infected female chimpanzees gave birth than uninfected ones, and none of their babies survived to a year. Pathologists found that dead infected chimpanzees looked like they had AIDS, with a lower level of immune cells called CD4+ T cells and damaged lymph tissue.

This discovery raises all sorts of questions. The Gombe chimps get sick, but not as sick as humans do from HIV-1. Why? There’s no evidence that SIV jumped into humans from P. t. schweinfurthii. Instead, it jumped three or more times from P. t. troglodytes. As far as anyone knows, those chimpanzees don’t get AIDS. But, then again, nobody has yet published a study like the one that has just come out on the Gombe chimps. What will that study reveal, if anyone ever carries it out? Is P. t. trogolodytes the source of a recent infection of both humans and the Gombe chimps?

And what’s particularly interesting, to me at least, is the fact that scientists had not noticed chimp AIDS before. Robin Weiss, an HIV researcher at University College London, and Jonathan Heeney of the University of Cambridge, published a commentary in Nature in which they suggest that the artificial conditions in which captive chimpanzees live protect them from AIDS. Out in the real world, where chimpanzees face an onslaught of pathogens, infections may activate the immune system in a way that brings on the virus’s attack and, ultimately, AIDS.

In other words, only the slow-cooked science pioneered by Jane Goodall allowed scientists to discover one of the most fundamental facts about a virus that has become one of the most devastating scourges humanity has faced in modern history. Slow-cooked science may provide more clues in the future–but only if its value is recognized, and only if chimpanzees can survive SIV and all the other threats to their survival these days.

[Goodall image: Jane Goodall's Chimpanzees]

Long after I’m dead, there will be stingrays swimming the Arafura Sea infested with tapeworms that bear my name.

There are about 1.8 million species with names, out of an estimated 8 to 9 million species in total.  In 2007 alone, scientists named 18516 new species. Naming a species is actually the final step in a long, slow journey. It starts with the discovery of an organism that looks like it just might not belong to any known species. Scientists then search the scientific literature to see if it is indeed new to science. If it is, they inspect it in painstaking detail, observing all the information one might be able to use to identify another organism as belonging to the same species. This is not the sort of work a gene-sequencing robot can do for you on your lunch break. This is natural history, old school.

This tapeworm was discovered in 1999. Janine Caira of the University of Connecticut and Kirsten Jensen of the University of Kansas were traveling aboard the Ocean Harvest, a commercial trawling ship sailing the Arafura Sea off the north coast of Australia. The fisherman pulled up a massive whip-ray belonging to a species never seen before (shown below). Caira and Jensen were particularly interested in what lurked inside the fish: its tapeworms.

There are some 6000 species of tapeworms named so far. Some species live inside people. Others live inside beetles. Others live inside frogs. Not only do tapeworms live in a huge range of animal hosts, but the life cycle of a single species may take it through several different species–a shrimp, a fish, a sea bird, and back to the shrimp, for example. Scientists know a lot about a few species of tapeworms, but most of them live in familiar hosts like ourselves. But unfamiliar hosts have tapeworms too. Caira and her colleagues have traveled the world over to cut open sting rays, sharks, and other cartilaginous fishes to search for new species of tapeworms. And more often than not, they find them.

The tapeworms they found that day in 1999, belonged to a genus called Ancanthobothirum. They were small, measuring less than an inch long. Caira and Jensen dropped some of them into alcohol so that they could extract DNA later, and dropped the rest into formalin, which preserved the parasites so that they could be studied under a microscope without decaying. That task fell to Carrie Fyler, who was writing her dissertation on Acanthobothrium, which contains 165 known species. After studying the tapeworms Caira and Jensen brought back, Fyler determined that there were at least five new species among them, all gathered from a single fish.

Last year Fyler asked me to come to the annual meeting of the American Society of Parasitologists, where she had organized an entertaining session on parasites in popular culture. There were talks on parasites in the movies, in art, and in poetry. Fyler asked me to give a talk based on my own experience writing blogs, articles, and an entire book, Parasite Rex, on these marvelous beasts. At the meeting, Fyler told the audience how the book had helped propel her into parasitology. What she didn’t tell them was that she was working on a paper describing the five whip-ray tapeworms, and that she was doing me the honor of naming one of them for me. Now, at last, the paper has come out in the journal Folia Parasitologica. Meet Acanthobothrium zimmeri.

I’m happy to report that A. zimmeri is an excellent parasite. It has the bizarre anatomy that you’d expect from a tapeworm–an animal that has abandoned brains, eyes, and mouth, and has turned its skin into inside-out intestines. Its head is festooned with a distinctive set of suckers, hooks, and muscular pads, which it presumably uses to clamp onto the gut of its host. Like other tapeworms, the rest of its tiny body (1.5 to 3.1 millimeters long) is made up mostly of segments, each of which carries both testes and ovaries. (I note, without comment, that each segment’s vagina is described as “thick-walled, sinuous.”)

When I first discovered I was going to have a species named for me, I was overwhelmed by delusions of grandeur. But at the parasitology meeting, I was quickly brought back down to Earth. Fyler mentioned to another tapeworm expert that she was naming a species for me, and he said, “Yeah, I guess that makes sense. Acanthrobothrium is kind of tall and thin like you.”  Apparently naming species was not the hallowed ritual I imagined. It is actually rather routine, because biologists have so many species to name. In fact, species can be named for all sorts of odd reasons. Carl Linneaus, who first invented the whole two-part Latin name system we still use today, liked to name weeds for his scientific enemies. Fyler named the other four tapeworms found in the whip-ray for (1) the ship that Caira and Jensen were on (A. oceanharvestae), (2) her grandfather “Pop” (A. popi), (3) James Rodman at the National Science Foundation (A. rodmani), and (4) Jim Romanow, who took care of the microscopes Fyler used (A. romanowi).

I’m still grateful for Fyler’s gesture, and I still can’t help feeling some vaguely paternal pleasure at seeing how A. zimmeri helps scientists learn a little bit more about the diversity of life and how that diversity evolved. Fyler and her colleagues compared its DNA to other Acanthobothrium species and discovered something interesting: the five species that live in the one fish are not closely related to each other. Instead, their closest relatives live in other whip-rays. Somehow their ancestors must have made the leap from one host to another, and somehow they must have made a place for themselves in the crowded ecosystem that is the inside of a whip-ray’s gut.

For now, that leap remains almost entirely a mystery. Scientists have no idea what sort of life cycle A. zimmeri and its relatives have–what happens to the eggs that are released from the whip-rays, or what other hosts they may have to invade first before finally ending up in another whip-ray. Like its whip-ray host, A. zimmeri’s intermediate hosts probably have yet to get a name of their own.

I hope some day scientists do figure out my namesake’s lifecycle, but I also worry that their time may be running out. Whip-rays, like many other rays and sharks, are in serious trouble these days thanks to reckless overfishing. And whenever one species becomes extinct, it can take other species with it. Switching host species is an exquisitely rare event, and so it’s likely that A. zimmeri can only live in one species of whip-ray. When its host goes, it may disappear as well. Extinction is inevitable in the grand scheme of history: all species disappear after several million years, give or take. I just hope that A. zimmeri, along with the rest of the world’s diversity, doesn’t go sooner rather than later.

Yet more totally weird examples of parasites manipulating their hosts. Viruses make aphids sprout wings. Bacteria keep spiders from making silken balloons to float away from home. All the details are at Mystery Rays From Outer Space.

I’ve just discovered an online game called Killer Flu, presented by the UK Clinical Virology Network. I’ve been fairly leery of video games that try to present science in the past, because they either skimp on the science or skimp on the game. Killer Flu seems, on first inspection, to get fairly close to the happy medium.

You have to get a flu outbreak going in three months by infecting as many people as you can. There are lots of challenges, such as tough immune systems, and special tricks, such as infecting people who are likely to infect lots of other people. The game is bogged down by a few big blocks of text that pop up to explain how the flu virus spreads–something that a few paragraph breaks or separate windows could take care of easily. But those drawbacks are more than compensated by the elegant, SimCity like interface.

I’m curious what living, breathing virologists and epidemiologists think of it. All I know is that I am going to try to avoid this web site, because I have a lot of work to do today. And for me, that’s as high a compliment as I can pay to a game.

Mental Floss has a nice two-post line-up of the weirdest mind-controlling parasites that we know of (1, 2). Some will no doubt be familiar to readers of the Loom, but others may be disturbingly new.

Update: Also check out Discover’s own gallery of parasitic horrors.

You have to hand it to those little flu viruses–with just a few genes apiece, they can infect us humans by the millions, and we can barely keep up with their evolution. In tomorrow’s New York Times, I’ve written a natural history of the flu, looking at how influenza viruses mutate, swap genes, undergo natural selection, cross species barriers, and  adapt to new hosts. The new strain of swine flu (or perhaps more precisely, the new strain of human-and-bird-flu-viruses-swirled-up-inside-pigs-and-then-mixed-with-other-pig-viruses-that-descend-from-human-and-bird-flus-as-well) is just the latest chapter in this baroque evolutionary tale.

Marcel Salathe, a biologist I know at Stanford, is running a very cool study on swine flu psychology that you can be a part of. Here’s the dope from Marcel:

 As you have heard in the news, there has been an outbreak of swine flu in Mexico and the United States. There is a possibility that this situation might develop into a pandemic if the virus continues to spread around the globe. The news media report excessively about this threat, and while health officials urge people to stay calm, there is an increased level of anxiety in the population.

Models have predicted that when a disease breaks out, changes in behavior in response to an outbreak, and in particular in response to information about an outbreak, can alter the progression of an epidemic. While this makes intuitive sense, there is no good data to test such a hypothesis. One of the major problems is that emotional reactions and behavioral response to an epidemic is generally assessed quite some time after the epidemic has fizzled out.

We would like to address this problem by starting a survey about risk assessment and personal responses to a potential epidemic as it unfolds – that is, right now.

Please help us achieve this goal by filling out a simple questionnaire (link below) – it shouldn’t take more than five minutes.

This is the link:
https://opinio.stanford.edu:443/opinio/s?s=1403

I’ve just taken the survey, and I can vouch it’s quick and painless. When Marcel has results to share, I’ll make sure we get his analysis. So please help him out–take the test and spread the word.

Excellent lecture on parasites from Jim McKerrow, courtesy of FORA.TV. McKerrow helped me out long ago with information and pictures of blood flukes when I was writing Parasite Rex. But he can deliver great tales about all sorts of critters inside you.