As you may be aware, I have a thing for parasites. So it was with great pleasure that I read through the latest issue of the Journal of Experimental Biology, which is entirely dedicated to the ways in which parasites turn hosts into zombies. What’s particularly newsworthy is that scientists are finally getting down to the biochemistry that allows them to pull the marionette strings. I’ve written a piece for the New York Times on the state of “neuroparasitology,” which will appear in print in next Tuesday’s Science Times. But you can read it now online.
The world, it bears reminding, is far more complicated than what we can see. We take a walk in the woods and stop by a rotting log. It is decorated with mushrooms, and we faintly recall that fungus breaks down trees after they die. That’s true as far as it goes. But the truth goes much further. These days scientists do not have to rely on their eyes alone to observe the fungus on a log. They can drill into the wood, put the sawdust in a plastic bag, go to a lab, and fish the DNA out of the wood. A group of scientists did just this in Sweden recently, sequencing DNA from 38 logs in total. They published their results this week in the journal Molecular Ecology. In a single log, they found up to 398 species of fungi. Only a few species of fungi were living in all 38 logs; many species were limited to just one.
Consider that on your next walk in the woods. The one or two types of mushrooms you see on a log are an extroverted minority. The log is also filled with hundreds of other species that don’t make themselves known to you. Their invisible exuberance is a paradox. The fungi that live on rotting logs all make a living by releasing enzymes that break down wood. It’s puzzling that so many species can coexist in a log this way, instead of a single superior fungus.
The forces that drive up the diversity of fungi in a log are similar to the ones that fosterer the thousands of species of microbes in our bodies. For one thing, a log or a human body is not a uniform block of tissue. They both have geography. A microbe adapted to the acid bath of our stomach won’t fare well on the harsh desert of the skin. Likewise, what it takes to succeed as a fungus in a branch is different from what it takes in the heartwood of the trunk.
The human body changes over time, and a rotting log does, too. Babies are colonized by pioneer microbes, which alter the chemistry of their host and make it more welcoming to late-arriving species. The pioneers on a fallen log may include the spores of some species of fungi lurking in trees while they’re still alive. They burst into activity as soon as the tree crashes to the forest floor. Other species, delivered by the wind or snaking up through the soil, find it easier to infiltrate a log that’s already starting to rot. The early fungi may go after the easy sugar in the log, while later species unlock the energy in tougher tissues, like lignin and cellulose. Which particular pioneer starts to feed on a log first can make it inviting to certain species but not others.
Warfare also fosters diversity in a log. The fungi inside a log battle each other for food, spraying out chemicals that kill off their rivals. Each species has to balance the energy it puts into making enzymes to feed and weapons for war. Sometimes the war ends in victory for one species, but very often the result is a deadlock that leaves several species in an uneasy coexistence. There are more peaceful forces at work in a log, too. Many species of fungi in a log depend on each other. One species may feed on the waste produced by another, and supply another species with food in turn.
The world in a log influences the world as a whole. If it wasn’t for wood-rotting fungi, forests would be strewn with the durable remains of dead trees. When the first massive forests spread over the land 350 million years ago, fungi hadn’t yet adapted to decomposing logs. Instead of turning to soil, many trees ended up as coal. The great age of coal ended about 300 million years ago–right around the time that tree-rotting fungi emerged. Their emergence may have brought the age of coal to an end.
Three hundred million years later, that coal is coming back up to the surface of Earth to be burned. Some scientists are investigating fuels that could replace climate-warming ones like coal. One possibility is to pull out the energy-rich sugar locked up in the lignin and cellulose of crop wastes or switchgrass. On our own, we would not be able to perform the necessary alchemy. But fungi know how, and so scientists are sequencing the genomes of wood-rotting fungi to borrow their tricks. This is big-scale science: the genomes of over a dozen species have been sequenced or are in the sequencing pipeline. Yet a single log may contain twenty times more fungus genomes. At the moment, we can say for sure that the few mushrooms we see on a rotting log are far from its full reality. But it will be a long time before we know how all the parts of that reality fit together.
In the past few weeks, there’s been a string of horrific tales of cannibalism and other zombie-esque behavior in the news. How to explain a handful of reports of people doing the unspeakable? One answer circulating around these days is that it must be parasites. And for some journalists, the question demands a call to the Centers for Disease Control to find out what they’re hiding from us!
1. Andy Campbell of the Huffington Post asked the CDC if some kind of zombie virus was to blame for the recent attacks. On June 1, he reported on HuffPo’s Politics page the following scoop:
“CDC does not know of a virus or condition that would reanimate the dead (or one that would present zombie-like symptoms),” wrote agency spokesman David Daigle in an email to The Huffington Post.
The Huffington Post entitled Campbell’s hard-hitting investigation, “Zombie Apocalypse: CDC Denies Existence Of Zombies Despite Cannibal Incidents.” That’s perhaps the finest deployment of the word despite in the history of journalism.
The story, by the way, received 65,797 likes on Facebook.
2. The Daily Caller picked up Campbell’s expose later that day, essentially reposting his whole piece. But Daily Caller reporter Michael Bastasch also salted his cut-and-paste with a few pieces of his own research. For example, Bastasch reports, some people “have claimed it was caused by the LBQ-79 virus.”
The Daily Caller headline: “CDC: No zombies, despite cannibal attacks.”
Can’t those pointy-headed government pencil-pushers see what’s in front of their own dismembered noses???
3. Andy Campbell must have bitten Michael Bastasch’s ear, because the idea of parasite-induced zombification has infected the editorial offices of the Daily Caller. On June 4, a minute before midnight, Josh Peterson, Tech Editor at the Daily Caller, posted a new story:
Clearly, this story could not wait for the morning, presumably because zombies prowl the night.
Here’s how last night’s story starts:
The Centers for Disease Control and Prevention (CDC) recently denied knowing of “a virus or condition that would reanimate the dead (or one that would present zombie-like symptoms),” after a series of instances of cannibalism across the country were reported, but remains silent about the effect of zombie-inducing parasites that live in human brains.
The parasite is Toxoplasma gondii. Lifting material reported here at Discover, Peterson describes how Toxoplasma alters rat behavior, reducing their fear of cats, the final host for the parasite. About one in five humans carries Toxoplasma too, as do many mammals, including pigs.
Now–watch as Peterson makes an Olympic-quality pivot off of the pig and back into the horde of zombies:
While pigs are known to engage in cannibalism, no known correlation between the parasite and cannibalism has been found.
France also has a high prevalence of Toxoplasma-infected people.
The Daily Caller’s inquiry to the CDC about why it omitted parasites from its denial, and about the possibility of the cannibals having been infected by the Toxoplasma, however, was met with silence.
Silence! Perhaps the CDC spokespeople simply couldn’t pick up their phones, because they were busy holding their heads in their hands, wondering how their clever zombie attack survival guide had gotten them into this mess, and how they’re going to get out of it.
As someone who has written a lot about the sinister powers of parasites, I’d be right in the thick of it to report on any genuine information on a zombie-parasite outbreak–if there was one. But there isn’t. While some people may laugh off these “reports” from the Daily Caller or the Huffington Post, others may take them–or subsequent rumors–seriously. So let me just lay out the reality of what parasites can do to the brain:
1. Some parasites do control the brains of their hosts. There are viruses and fungi that drive their insect hosts to the tops of plants, so that the parasites can shower down on new hosts, for example. Some flatworms that infect fish cause them to thrash around at the surface of the water, to make them easier pickings for birds, inside of which the flatworms can reproduce. Parasitic wasps rob cockroaches of their will, so that the wasps can lay eggs on them, which then invade their docile host. Other parasitic wasps turn their hosts into bodyguards. After they emerge from caterpillars, their dying hosts fight off other insects that would try to eat the pupating wasps. It’s important to note that the most extreme examples of host manipulation come from tiny-brained animals such as insects or fish–not people.
2. A cannibalistic zombie is no benefit to a parasite. Host manipulation generally shows all the signs of natural selection at work. Mutations to genes in the parasites gradually give them the ability to alter the behavior of their host more and more, in ways that boost the odds that the parasite will be able to reproduce. But what possible good could come from a parasite that caused its host to kill other people? That just robs you (the parasite) of a potential host. Not smart. And so it should come as no surprise that scientists have never found a parasite that causes cannibalism. (Tasmanian devils spread cancer to each other by biting each other’s faces, but they don’t need cancer’s help to get into fights. The cancer cells just go along for the aggressive ride.)
3. Fine, but what about rabies? The rabies virus is pretty creepy, both in its manipulation of its host and in its deadliness. You get rabies from the saliva of an infected animal that bites you, and the virus then slips into the nervous system. Rabies infection makes animals aggressive–and thus more likely to bite new victims. The horror of rabies infection has haunted us for thousands of years (for more, check out the wonderful book, Rabies: A Cultural History of the World’s Most Diabolical Virus by Bill Wasik and Monica Murphy, coming out next month. Wasik, an editor at Wired, sent me the book a few months back, and I loved it.)
But the reality is that rabies does not produce armies of human zombies trying to bite other people. It is possible to get infected by someone’s saliva, but it’s an extremely rare occurrence. We humans are a dead end for the virus. It depends on other animals to continue circulating from host to host.
And, again, let’s think this through. Rabies is 100% deadly unless you get treated. But it stays in circulation because its hosts remain alive long enough to bite other animals before they die. Dismembering a victim and eating him for dinner, or chewing off his face under a Florida overpass are not going to do a virus much good.
4. But what about the LBQ-79 virus? I read about it on the Daily Caller! Couldn’t that be a rabies-like virus that makes people cannibalistic zombies? There is no such thing.
5. But there is such a thing as Toxoplasma, right? Absolutely. Toxoplasma is one of my favorite parasites. And there’s a lot of evidence now that it can influence human behavior–albeit in subtle ways. Kathleen McAuliffe lays out the current science nicely in this story in the March issue of the Atlantic.
But again, let’s work through this. Toxoplasma only alters its animal hosts to make them easier prey for the parasite’s final host. All effects on humans seem to be pale shadows of that strategy. (And, just like rabies, we are a dead end for Toxoplasma.) So how do we get from making your host easy prey to becoming a zombie cannibal?
Also, bear in mind that the parasite dwells in the brains of over a billion people. It’s been there for centuries, if not thousands of years. Only now is it suddenly turning people into cannibals? No self-respecting science-fiction scriptwriter would try pitching that idea to Hollywood. Unfortunately, the editors at the Daily Caller have lower standards than that.
[Update: I originally wrote that Bastasch was the author of the second Daily Caller story. Fixed. Also, I accidentally block quoted some of my own text, giving the impression it was in the Daily Caller. Fixed.]
[Second update, 5:10 pm: On Twitter, Peterson responded to this post by writing, “Nice piece, but why’d you leave out the parts about it being related to mental disorders?” and, later asking, “So you’re content in not explaining the effect of the parasite on the brain in your piece, then?”
In case I wasn’t clear enough by linking to McAuliffe’s story, let me be clear now: a number of studies suggest that an exposure to Toxoplasma may influence people’s personality. It has also been identified as a risk factor for schizophrenia. Here’s one recent review in Developmental Neurobiology that presents evidence of a raised risk in people who were exposed before birth. (Other studies have found that other infections can also raise the risk.)
But I find Peterson baffling. Is he suggesting that we can explain an outbreak of cannibalism by pre-birth exposure to Toxoplasma, leading decades later to schizophrenia, leading to cannibalism? If so, it’s not only ridiculous, but it’s insulting to the 2 million people who suffer from schizophrenia in the United States, as well as their families.]
At some of my recent talks, I’ve been running into people who’ve been annoyed that they forgot to bring a book of mine to get signed. You really couldn’t think of a better way to cheer up a writer, and so I feel the need to reciprocate.
So if you’ve gotten a book of mine and want to get it signed, I’ve printed up some bookplates that I can autograph and send to you.
Just to ensure I’m not signing bookplates for alien robots who will take these bookplates to their home planet to…do whatever evil thing alien robots do with bookplates from science writers…please follow these steps:
1. Take your picture with the book.
Optional step 3. For those on Twitter: instead of emailing me your photo, you can upload it to Twitter (mentioning my Twitter name @carlzimmer). Be sure to email me your address, too, so that I know where to send the bookplate.
So far, I’ve got three bookplates–one for Parasite Rex, one for Science Ink (in matching Goth type), and one for Planet of Viruses. (See below). It’s weirdly easy to produce these things, so I’m happy to take requests for my other books.
Whenever I give a talk about my book Parasite Rex, I try to gather together the creepiest images of parasites that I can. Every time, there’s one kind of parasite that summons an instant reaction: a mix of laughter, sucked-in breaths, and gasps of recognition. I speak, of course, of the parasites that eat your tongue.
I only mean you if you’re a fish. Some species of isopods (crustaceans related to the less creepy crabs and lobsters) will swim into the gill of a fish, make their way to its mouth, and devour its tongue. It will jam its legs into the gills to hold itself in place, facing forward, its eyes gazing out of the fish’s mouth, taking the very place of the tongue it just ate.
I was first introduced to these disturbing creatures by Matthew Gilligan, an invertebrate zoologist at Savannah State University. I had come across a disturbing picture of one of these parasitic isopods in a paper he published in 1983 and sent him an email, asking questions about it. I wondered what the isopods did once they were done devouring the tongue. As far as Gilligan could tell, they stopped eating the fish once they had made a place for themselves in its mouth. Perhaps afterwards, they fed on the animals that the fish itself caught. After all, the fish that Gilligan and others had caught with these isopods were still alive and seemed healthy. Gilligan’s response made me wonder if perhaps the fish simply used the hard-shelled back of the parasite as its own tongue.
Since then, a new generation of scientists have studied these mysterious parasites, and it looks as if their dealings with their hosts are not as peaceful as once thought. In 2003, for example, scientists studying isopods in a fish farm off the coast of Turkey found that sea bass with the parasites in their mouths had lower blood counts than ones that still had their tongues intact. It seems that the isopods act like blood-drinking mouth leeches.
In a new paper in the Biological Journal of the Linnean Society, British researchers have followed up on these studies with a big survey of the Mediterranean, inspecting striped sea bream for tongue parasites. They compared two populations of the fish that were closely related to each other but lived in very different environment. One population, off the coast of France, lived in a marine protected area. The other, off the coast of Italy, is heavily fished. In the protected waters, the scientists found, 30 percent of fish had the parasites in their mouth. In the fished waters, 47 percent did.
Take a moment to let that sink in. Almost a third to almost half of these fish open their mouth and look as if they came out of a science fiction movie. Having recently just eaten bream for the first time, I’m relieved to find out that the parasite does not cause human disease. Still, next time I eat fish I may have some disturbing images in my head.
The scientists found not only that there are more parasites in the heavily fished waters. They also found that parasites took a heavier toll there. Fish with tongue parasites ended up smaller and lighter in the heavily fished waters than infested fish in the refuge.
These differences all seem to come down to fishing. A lot of studies on many species of fish have shown that heavy fishing can drive the evolution of small fish. Fish that get to be sexually mature faster may be more likely to have offspring than fish that take their time to reach bigger sizes. In that rush, harvested fish may end up unable to defend themselves against enemies, including tongue-eating parasites.
It would be interesting to see what the rates of tongue parasites are in other heavily fished and protected parts of the world. If this pattern holds up, it may turn out that overfishing has made the world a more alien place.
There are times when I want to retitled this blog The Continuing Adventures of Parasitic Wasps and Their Unfortunate Hosts. Because there are just so many stories of these sinister insects and how they lay their eggs inside other animals. That’s no surprise, really, because there are hundreds of thousands of species of parasitic wasps on Earth, all evolving in different directions as they adapt to their host’s defenses.
Last week, for example, I reported in the New York Times about a newly discovered defense that flies use against certain wasps: when the wasps inject their eggs into the flies, the flies drink alcohol to literally turn the parasites inside out.
Since then, I’ve become obsessed with another species of wasp that attacks aphids. The battle between these two species–and their many allies–makes the story of the boozy flies seem positively pedestrian.
The wasp is known as Aphidius ervi, and its hosts are aphids. Because aphids are major pests on farms and in gardens, researchers have turned A. ervi into a biological weapon against them. If you so desire, you can order 250 mummified aphids with wasps ready to emerge through the mail for $69.95.
To find an aphid host, A. ervi wasps take advantage of the struggle between the aphids and the plants they eat. When a plant gets nibbled by an aphid, it releases a cocktail of molecules into the air. The wasp detects those chemicals, sniffing its way to the plant–and to the aphid.
The wasp may lay only a single egg inside an aphid, or it may choose to lay additional ones. Along with her eggs, the wasp will also inject a venom that stunts the growth of the aphid’s own ovaries–thereby stopping the host from wasting energy on its own reproduction so that there’s more food for the wasps. The wasp eggs have no yolk, so they depend entirely on their host from the start. When the wasp egg hatches, the larva develops a thick, tentacled blanket of cells that extends out into the aphid’s body and draw in nutrients–in other words, a placenta. The placenta also buds off a special class of cells that swim through the aphid’s body, releasing enzymes that degrade the aphid’s cells and bind fatty acids, making it easier for the wasp to feed on its host.
But there’s a big puzzle about A. ervi’s strategy. No matter how many eggs it lays in an aphid, only a single adult wasp at most emerges from a host. Why the extra eggs?
In many cases, no wasp emerges at all. That’s because the aphids have defenses of their own. Their immune cells go after the wasp larvae. And in addition to their own defenses, many aphids are home to allies–namely a species of bacteria called Hamiltonella defensa. Some aphids are infected with the bacteria and pass it down from parents to offspring (or spread it by sex). The bacteria produce a toxin that sickens the wasps and keeps them from developing. Weirdly, Hamiltonella defensa only protects the aphids if they are, in turn, infected by a virus of their own, which carries the wasp-attacking toxin gene. (See Ed Yong’s post for details.)
That would be remarkable enough. But now scientists have discovered another dimension in this multi-species battle. A team of researchers led by Kerry Oliver at the University of Georgia has found that the wasps can tell the difference between aphids that are protected by bacteria, and the ones that are defenseless. Into the defenseless aphids, they lay only a single egg. And into the protected aphids, they are more likely to lay two or more. Oliver found that the wasps seem to boost their odds of surviving against the bacteria by boosting their numbers. It’s possible that the extra venom and enzymes let the wasps grow despite the poison supplied by the bacteria and their viruses. No matter how exactly the extra eggs help, Oliver’s finding hints at an answer to the puzzle of the wasp’s egg laying patterns.
How the wasps can figure out that the aphids have friends inside, the scientists cannot say. It’s possible that when the wasps lay the first egg, they can probe the chemistry of the aphid and figure out if it’s infected with H. defensa. Oliver and co. raise an even more intriguing possibility. The aphids infected with H. defensa seem to release fewer alarm pheromones in times of trouble. Perhaps they are blase about parasites because of their protection. It’s possible that the wasps have evolved to use that clue to tell whether they need to lay extra eggs.
Regardless of which trick they actually use, Aphidius ervi is my favorite parasitic wasp. But it will probably not keep the trophy for long.
Reference: Parasitic wasp responses to symbiont-based defense in aphids. Kerry M Oliver, Koji Noge, Emma M Huang, Jamie M Campos, Judith X Becerra and Martha S Hunter. BMC Biology (in press)
(For much more on the wasps, see my book Parasite Rex)
One of the most interesting features of Google’s new social media service, Google+, is Google+ Hangout On Air. A group of people get onto G+ all at once, fire up their computers’ cameras, and have a conversation. Google puts whoever is speaking at the moment on the main screen. You can join a hangout if it’s public or if you have an invitation, and–coolest of all–it automatically records the conversation and throws it onto Youtube.
Right now only a few people have access to this service. I jealously watched fellow Discover blogger Phil Plait talk about exoplanets last month. (You can too.) And then I got invited to join the folks at the Singularity Hub for a hangout, too. It’s up on Youtube, and you can also see it embedded here below. We talked about all sorts of things–from mind-controlling parasites to bird flu to using viruses to cure antibiotic-resistant bacteria to the future of ebooks and much more.
I deeply crave this technology. I used to participate in a primitive forerunner of this, known as Bloggingheads. I bowed out due to editorial differences, but I still think the basic system is an exciting medium. I hope Google opens up their Hangout On Air service to more people, because it could be a whole lot of fun.
One mission of the Loom is to champion unjustly neglected forms of life. And so I spend a lot of time blogging about the sinister powers of parasites. But I don’t want to leave you with the impression that hosts are simply helpless bags of grub. Hosts have evolved defenses to ward off parasites, and those defenses can be just as baroque and marvelous as the adaptations of their parasites.
And so let me point you to a story I’ve just written for the New York Times. If you think you’ve got it bad with parasites, with your cold viruses and stomach bugs, just think what it’s like to be a fly like Drosophila melanogaster. Wasps land on you, inject eggs in your body, and turn you into an extra on the set of Aliens. It now turns out that these flies have a secret weapon. It’s booze. And it turns out to destroy the parasitic wasps in perhaps the most horrific way imaginable.
This was the very first article I’ve ever written where I was able to quote a scientist who said–without prompting or reading off a cue card: “The flies self-medicate by getting schnockered.”
[Image: Photo by raysto – http://flic.kr/p/aoe5xF ]
In 1494, King Charles VIII of France invaded Italy. Within months, his army collapsed and fled. It was routed not by the Italian army but by a microbe. A mysterious new disease spread through sex killed many of Charles’s soldiers and left survivors weak and disfigured. French soldiers spread the disease across much of Europe, and then it moved into Africa and Asia. Many called it the French disease. The French called it the Italian disease. Arabs called it the Christian disease. Today, it is called syphilis.
I’ve been intrigued by the murky history of syphilis for a few years now. The text above is from the start of an article I wrote for Science in 2008. At the time, scientists were split between two explanations for sudden appearance of syphilis at the end of the fifteenth century. According to one, it was caused by bacteria that had evolved in the New World and were brought back to Europe by Columbus’s crew. But other researchers found many skeletons with signs of syphilis in Europe, Africa, and Asia that appeared to have been from long before Columbus’s voyage. They argued that it must have started in the Old World, perhaps before people even left for the New World some 15,000 years ago.
As I explained in the article, one way to test these hypotheses is to survey the evolution of the bacteria. A group of researchers based at Emory University came across bacteria infecting Indians in Guyana that was genetically close, but not identical, to syphilis. They suggested syphilis had evolved in the New World from a common ancestor of both pathogens. Columbus’s crew may have picked it up when they visited the New World and then brought it home to Europe. Unfortunately, by the time doctors had gotten the bacteria from the jungles of Guyana to a laboratory where it could be analyzed, the DNA was in bad shape, so they couldn’t come to a firm conclusion.
Recently, I caught up with one of the scientists on the team, Kristin Harper, who is now at Columbia University. She didn’t have any new genetic results to talk about, unfortunately, although she may before long. In the meantime, she pointed me to a new review she has published in the Yearbook of Physical Anthropology. She and her colleagues took a look at the bones that scientists have pointed to as evidence for the antiquity of syphilis in both the New and Old World, and passed judgment about just how good the evidence was that they did, indeed, have syphilis, and not some other disease that can deform bone. The scientists also took a close look at the dating of the bones, since the timing of syphilis’s origin is so crucial to the entire debate.
The trouble with a lot of past research, Harper says, is that scientists have come up with new ways to diagnose syphilis in ancient bones without offering good evidence that their criteria are good. “Paleopathology is kind of the wild west of science, in that the ‘rules’ are still in their infancy,” Harper said. “We set ourselves the challenge of using only evidence-based diagnostic criteria in this paper and tried to be similarly stringent about dating.”
The scientists looked at 54 reports from both hemispheres. Most of the Old World bones failed to meet at least one of the standard requirements for a diagnosis of syphilis, such as distinctive pits on the skull or swelling in the long bones of the arms and legs. But when they looked at the Old World bones that had been dated to before 1492 that did make the grade, they ended up throwing all of those bones out, too. The evidence that these Old World bones were from before 1492 turned out to be weak. They tended to come from coastal regions, where people eat lots of fish. Fish are full of carbon from deep in the ocean, which has a different balance of isotopes than that found on the land. The ocean carbon gets into the bones of coastal people, where it can throw off estimates of their age by centuries. A close examination of these coastal Old World bones led the Emory scientists to conclude that they belonged to Europeans who died shortly after Columbus’s voyage.
“In contrast,” Harper told me, “we found definite cases of treponemal disease [syphilis] hailing from the New World that stretched back thousands and thousands of years.”
Harper and her colleagues conclude that there’s no good evidence for syphilis in the Old World, and plenty in the New World. They continue to argue that syphilis traveled east across the Atlantic.
It’s intriguing if Harper turns out to be right. Europeans brought smallpox and other pathogens to the New World which decimated its residents. Syphilis, it seems, is one pathogen that went the other way.
[Update, 12/19 7 pm: Some of the comments prompted me to edit this piece for clarity.]
If you’re a regular reader of the Loom, you’re no doubt familiar with the parasite Toxoplasma gondii. If you’re not, now is the perfect time to meet this sinister creature which may very well be residing in your brain. It seems like every year or two, it gets more remarkable, and today it’s taken another step into awesomeness.
Here’s a quick Toxoplasma primer. It’s a single-celled protozoan that reproduces inside the digestive tract of cats. The cats poop out egg-like Toxoplasma cells into kitty litter and dirt. Other animals take up the parasite, which makes its way into their tissues, especially the brain. There it forms cysts that can linger for years or decades. Only if that animal gets eaten by a cat can Toxoplasma complete its life cycle.
This life cycle opens up opportunities for Toxoplasma to evolve. For example, natural selection should favor mildness in the parasite in its hosts, because cats do not like to eat corpses. And, indeed, Toxoplasma is fairly harmless, only causing trouble to people with suppressed immune systems. (Hence the rule that pregnant women should not handle kitty litter. If they get infected by Toxoplasma for the first time, the parasite runs amok in the fetus.) On the other hand, if there’s any way for the parasite to increase the odds that it can get from prey to cat, natural selection may favor genes for that strategy too.
And it turns out that Toxoplasma does have that very ability. In studies on rats, scientists have found that infected rodents lose their fear of the scent of cats. In fact–and please remember, I am a science writer, not a Hollywood script doctor–the rats may even become sexually aroused by the smell of cats. They embrace their doom, and the parasite benefits.
These findings have lots of interesting implications for humans, because perhaps a quarter of all people on Earth carry these parasites in their heads, where they no doubt secrete their mind-altering compounds. There’s some preliminary work that suggests some changes to the personality of infected people, but nothing definitive.
That would be enough for Toxoplasma to earn its place in the Parasite Hall of Fame. But, no, it needed to go one better.
It turns out that rats and other non-cat hosts can spread Toxoplasma to each other through sex. The first reports have only just emerged from studies on dogs and sheep. Recently Ajai Vyas, a neuroscientst at Nanyang Technological University in Singapore, decided to see whether rats can spread Toxoplasma the same way. In the journal PLoS One, he and his colleagues describe how they mated infected males with uninfected females. They found Toxoplasma in the male rats’ semen, and, after mating, in the female rats’ vaginas. And later, they found signs of Toxoplasma in the female rat brains.
These are Toxoplasma cysts moving from rat to rat, so this exchange is kind of like a side track on the parasite’s life cycle. But it still benefits Toxoplasma, because it means it can infect even more potential prey that may get eaten by cats. And so the logic applies once more: if Toxoplasma can raise the odds of getting from infected males to uninfected females, it may have more reproductive success.
You know where this is going–it’s turning into a David Cronenberg horror movie with an all-rodent cast. Vyas wondered if there’s any difference in how female rats mate with infected and uninfected males. So he and his colleagues put a male rat with Toxoplasma at one end of a two-armed maze, and an uninfected male in the other arm. Females then got to choose which rat to approach. Vyans found that they preferred the infected males, spending more time with them and mating more often.
In other words, Toxoplasma makes its host sexy, in order to get into other hosts through sex.
As I wrote in Parasite Rex, many parasites have evolved the ability to manipulate hosts. But I was disappointed to find no good examples of parasites that manipulate the sexual behavior of their hosts. In fact, female rats have actually evolved to steer clear of male rats infected with some other parasites. They can detect these infections even when the male rats look healthy, and they avoid these males to avoid getting sick. Now Vyas’s research suggests that there is at least one parasite that manipulates sex. Toxoplasma may be exquisitely unusual among parasites. But it’s also possible that there are other sex-hijacking creatures lurking out there. As for what this means for humans, I should point out there’s zero evidence of it moving from person to person, nor is there any evidence of it affecting the sexual behavior of humans. Then again, nobody has looked. For now, you can just let your inner Cronenberg take matters from here….