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When Parasites Attack, Flies Diversify Their Babies’ Genes

Imagine an animal that reproduced by budding off genetically identical clones. This asexual creature doesn’t have to bother with finding or attracting mates: it is a self-contained factory for making more of itself. This sounds like a recipe for success, but asexual animals are far from successful. They exist, but they tend to be rare and precarious twigs on the tree of life—recently evolved, and likely to snap off at any time. By and large, the vast majority of animal life practices sex.

The asexual lifestyle falters because it presents a sitting target. If every new generation is genetically identical to the last, then predators, parasites, and rivals can easily evolve ways of outmanoeuvring them all.

Sex mixes things up—literally so. When the genes from a mother and father unite in their offspring, they are broken up, shuffled, and rejoined in new ways, through a process called recombination. This creates variety. In the recombinant youngsters, parasites face a diverse range of targets, and are unlikely to be able to hit all of them at once. The targets also move. Each bout of sex creates new combinations of genes that parasites must then adapt to. And when they do so, the combinations change again. As the Red Queen of Lewis Carroll’s Wonderland said, “It takes all the running you can do, to keep in the same place.”

These “Red Queen dynamics” have been a familiar part of evolutionary biology for many decades. But Nadia Singh from North Carolina State University has found a new and dramatic twist on the idea. She showed that fruit flies, after facing infectious bacteria or body-snatching wasps, produce more diverse offspring. It turns out that when parasites are around, the flies can somehow ensure that the next generation’s set of genes—their genotype—is even more thoroughly shuffled than usual.

“One way to look at it is that if parasites are specialising on any particular host genotype, then being different at all is good,” says Todd Schlenke from Reed College, Oregon, who was also involved in the study. “As long as you’re different from your parents, you’ll do well.”

There have been some hints of this before. Over the last century, scientists have found that all kinds of environmental factors, including temperature, stress, and age, can affect the frequency of recombination. In plants, those factors include infections. “I have always thought about whether the same is true for animals,” says Schlenke.

To find out, Singh worked with flies that had mutations in two genes that sit very close to one another: ebony, which darkens their skin; and rough, which changes their eyes from regularly dimpled domes into uneven and chaotic ones. Through clever breeding, Singh created strains of flies where the mutations were linked, so individuals either had both rough eyes and dark bodies, or neither. If she continued to breed them, and ended up with flies with just one mutation—say, rough eyes but light bodies—she knew they were the result of recombination. In these recombinant insects, the normal copy of one gene had been shuffled next to the mutant version of its neighbour.

Using these flies, Singh showed that when females are infected with an opportunistic bacterium before they could mate, they produced around 15 percent more recombinant larvae. Schlenke showed that an attack from a parasitic wasp could do the same. The wasp lays its egg inside the fly larva, which will be eaten from the inside-out unless its immune system can destroy the invader. If they survive, mature, and mate, they also produce more recombinant larvae than any flies which didn’t have to endure trial-by-wasp. By contrast, merely wounding the flies with needles had no effect; it was specifically infections, whether by bacterium or wasp, that led to more recombination.

And actually, they didn’t lead to more recombination. Schlenke and Singh found signs that the rate of shuffling doesn’t go up. What actually happens is even weirder. In a female’s reproductive system, several potential cells could turn into eggs, ready to be fertilised by males. It seems that, after infections, the females can somehow prioritise those cells in which recombination has already happened.

“It’s like the parents ‘know’ which of the cells are the recombinant ones and they’re preferentially making those into the embryos.  Or they know which are the non-recombinant cells and delete them,” says Schlenke. “It sounds crazy but it’s the least crazy of the crazy explanations.” It’s still unclear how the females actually pull this off.

“It’s almost like genetic engineering,” he adds. “People think: oh, what if you could engineer your child to be smarter, or have brown eyes, or whatever. That’s sort of what’s happening here. These parents are altering the genotypes of their offspring. They’re not specialising and going for a particular genotype, but they’re going for genotypes that are different from theirs.”

For now, the team only measured recombination within one small part of the fly genome—the section between the rough and ebony genes—and they don’t know if other sections are being shuffled to the same increased extent. They also haven’t shown that the extra shuffling leaves the new generation of flies in a better place when exposed to the same parasites. Do the larvae actually benefit? No one knows. “It does seem like a gap,” admits Schlenke.

It’s also unclear if the same effect exists in other animals, beyond fruit flies. What about us? Do human mothers give birth to children with more heavily shuffled genes after a bout of illness? “I wouldn’t be surprised either way,” says Schlenke. “It happens in plants and we’ve found it in fruit flies.”

Reference: Singh, Criscoe, Skolfield, Kohl, Keebaugh & Schlenke. 2015. Fruit flies diversify their offspring in response to parasite infection. Science http://dx.doi.org/10.1126/science.aab1768

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There’s More Than One Way to Decapitate An Ant

Tropical rainforests are home to lots of ants, which means that they’re home to lots of injured ants. Ant colonies frequently fight each other, leaving behind battlefields strewn with wounded workers.

That’s good news for phorid flies.

There are some 4,400 species of phorids. Although their lifestyles are diverse, a surprising number of them specialise in decapitating ants (or bees). The females lay their eggs inside their victims. When the maggots hatch, they move towards the ant’s head and eat its brain and other tissues. The brainless ant stumbles about in a fugue for weeks until its head eventually falls off. Sometimes, that’s because the fly has inflicted so much damage. In other cases, the maggot deliberately releases an enzyme that dissolves the connection between the ant’s head and body.

But in the rainforests of Brazil and Costa Rica, Brian Brown from the Natural History Museum of Los Angeles County has found a phorid that beheads ants in an entirely new way.

Brown is an authority on phorids and especially the ant-decapitating, bee-killing varieties. He has discovered around 500 species of them. In the field, he lures them in by crushing ants and other insects with forceps, and watching what arrives. Some phorids feed directly off the injured insects. Others lay their eggs inside. But one species, Dohrniphora longirostrata, did something different.

A female will land near a wounded ant and circle it. She darts in and out, touching the would-be victim and occasionally tugging on its legs and antennae. The goal, it seems, is to check just how incapacitated this incapacitated ant really is. If it’s too active, she retreats to find an easier mark.

Eventually, she climbs onto the ant and jams her mouthparts into its body. “The fly was nearly constantly in motion, probing from several angles,” writes Brown. “They made in-and-out, as well as rotational head movements.” In other words, she’s sawing.

A housefly’s mouthparts end in a spongy pad for soaking up fluids; in place of that, D.longirostrata has an extremely long proboscis, almost as long as its entire body. Under the microscope, the tip looks like a murderous Swiss army knife, with one fiendish spike and a couple of serrated steak knives. The fly jams this tip into an ant, cutting and severing. After some time, it yanks the head clean off.

Proboscis tip from Dohrniphora longirostrata. Credit: Brown et al, 2015.
Proboscis tip from Dohrniphora longirostrata. Credit: Brown et al, 2015.

The headhunting females typically dragged their bounty away, so Brown isn’t clear about what they actually do with the heads. They probably lay eggs inside. But the team sometimes saw the females slurping up the contents of the heads themselves, and upon dissection, these females never had mature eggs. Perhaps they need to gorge themselves on ant heads before their eggs can develop.

Brown has been crushing ants and watching flies for 30 years, in eight countries across South and Central America. In all that time, he has only ever seen this fly attacking wounded trap-jaw ants. It won’t target healthy workers that could easily overpower and kill them—the strike of a trap-jaw ant is among the fastest movements in the animal kingdom. It won’t attack injured crickets, grasshoppers, or termites either. It’s extremely picky, which means that even without the intervention of forceps-wielding biologists, there must be a lot of injured trap-jaws lying around the forest.

There are between 50 and 100 species of Dohrniphora flies and many co-exist in the same forests. Maybe they’re all picky specialists, each one decapitating its own preferred ant.

Reference: Brown, Kung & Porras. 2015. A new type of ant-decapitation in the Phoridae (Insecta: Diptera). Biodiversity Data Journal http://dx.doi.org/10.3897/BDJ.3.e4299

More: The world’s smallest fly is a phorid; at half a millimetre long, it could sit on a housefly’s eye, and probably decapitates really tiny ants.

Thanks to Alex Wild for the hat-tip.

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You Almost Certainly Have Mites On Your Face

Think of all the adults you know. Think of your parents and grandparents. Think of the teachers you had at school, your doctors and dentists, the people who collect your rubbish, and the actors you see on TV. All of these people probably have little mites crawling, eating, sleeping, and having sex on their faces.

There are more than 48,000 species of mites. As far as we know, exactly two of those live on human faces. While their relatives mostly look like lozenges on spindly legs, face-mites are more like wall plugs—long cones with stubby legs at one end. They don’t look like much, and most of us have never looked at one at all. But these weird creatures are almost certainly the animals we spend the most time with.

They live in our hair follicles, buried head-down, eating the oils we secrete, hooking up with each other near the surface, and occasionally crawling about the skin at night. They do this on my face. They probably do it on yours. A group of scientists led by Megan Thoemmes and Rob Dunn at North Carolina State University found that every adult in a small American sample had face-mites on their faces—something that was long suspected but never confirmed. If you want to find humanity’s best friend, ignore dogs; instead, swab a pore and grab a microscope.

As I wrote back in 2012, the mites were discovered in 1841, but only properly described a year later by German dermatologist Gustav Simon. He was looking at acne spots under a microscope when he noticed a “worm-like object” with a head and legs. Possibly an animal? He extracted it, pressed it between two slides, and saw that it moved. Definitely an animal. A year later, Richard Owen gave the mite its name, from the Greek words ‘demo’, meaning lard, and ‘dex’, meaning boring worm. Demodex: the worm that bores into fat. We host two species: Demodex folliculorum (bigger, round-bottomed) and Demodex brevis (smaller, short-bottomed).

Demodex brevis. Credit: Dan Fergus and Megan Thoemmes
Demodex brevis. Credit: Dan Fergus and Megan Thoemmes

Scientists have since found Demodex in every ethnic group where they’ve have cared to look, from white Europeans to Australian aborigines to Devon Island Eskimos. In 1976, legendary mite specialist William Nutting wrote “One can conclude that wherever mankind is found, hair follicle mites will be found and that the transfer mechanism is 100% effective! (One of my students noted it was undoubtedly the first invertebrate metazoan to visit the moon!)”

But it’s always been hard to say exactly how common they are. The first estimate came from a 1903 study, which found the critters in 49 out of 100 French cadavers. The next count, from 1908, found them in 97 out of 100 German cadavers. Most studies since then have fallen in the range of 10 to 20 percent.

But these censuses were all based on visual counts. Someone would apply cellophane tape to skin to pull the mites off, or scrape an oily patch of face with a small spatula, or pluck eyelashes and eyebrows. But the creatures live in our pores and aren’t easy to extract. They’re also unevenly distributed. You might have a population living in your cheek; I might have one on my forehead. Unless you’re scraping and taping and plucking all over someone’s face, you might miss their mites.

So Thoemmes did something different. She searched for their DNA. The mites have this helpful habit where they… er… have no anus and never poo. Instead, they release a lifetime’s worth of waste when they die. That contains their DNA, which gives away the presence of the mites even when the creatures themselves are inaccessibly hidden.

Thoemmes developed a test for Demodex DNA and recruited willing volunteers at “Meet Your Mites” face-sampling events. “We had really good responses,” she says. “People act grossed out at first, but they get excited when they see the mites under the microscope.” She recruited 253 volunteers and saw the actual mites on 14 percent of them, in line with previous estimates. She also checked for mite DNA in 19 adults… and found it on all of them. Those results are published today in PLOS ONE, but Thoemmes tells me that the team has continued their work and more than doubled their sample size. Same result.

Obviously, this is a small and unrepresentative sample, but it clearly shows that visual counts grossly underestimate the proportion of people with mites. That, combined with over a century of other studies, strongly suggests that the mites are to faces as smoke is to fire.

Or, at least, on adults. Thoemmes also sampled ten 18-year-olds and found Demodex DNA on just 70 percent of them. This fits with what earlier studies had shown—the mites seem to become more common with age. They’re rare on babies, more common on teenagers, and universal in adults. No one really knows where we get them from. Dogs get their face-mites during nursing, and humans might do the same—after all, one study found a lot of Demodex living in nipple tissue. But the fact that some teens aren’t colonised suggests that we pick up these creatures throughout our lives.

The team also compared their mite DNA to sequences from other parts of the world. They found that D.follicorum doesn’t have a lot of genetic diversity. The ones living on someone in China are probably very similar to those living on an American face. D.brevis, on the other hand, is much more diverse, and a single face can house many different lineages.

These differences probably reflect the lifestyles of the two species. D.brevis snuggles deeply in our pores and stays there. As we travelled the world, it hitched along and co-evolved with us, giving rise of many distinct lineages. D.folliculorum is a shallower resident, and may move between people more easily. Brevis epitomises insularity, folliculorum symbolises globalisation. “This is an arthropod that’s likely living on everyone’s body,” says Thoemmes. “That’s a huge deal. They could tell interesting stories about the spread of humans across the world.”

Considering how common these creatures are, there’s still so much we don’t know about them. We don’t know where our two face-mite species came from, or what their closest relatives are. We also don’t know how many other face-mites exist. Each Demodex species seems to stick to one mammal host, and humans, dogs, and cats all have more than one. There are over 5,000 species of mammals, which means that there could potentially be 10,000 species of Demodex left to discover.

For more on the habits of these wonderful creatures, and how they might affect our health: Everything you never wanted to know about the mites that eat, crawl, and have sex on your face

Reference: Thoemmes, Fergus, Urban, Trautwein & Dunn. 2014. Ubiquity and diversity of human-associated Demodex mites. PLOS ONE, citation tbc.

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The Barnacle That Eats Glowing Sharks

Most barnacles sit on hard surfaces, and filter small particles of food from the surrounding water. But Anelasma squalicola is an exception. It’s a parasitic barnacle that eats sharks, by fastening itself to their flanks and draining nutrients from their flesh.

Charles Darwin, history’s greatest barnacle fanboy, described Anelasma in his 1851 magnum opus, and suggested that it was most likely a parasite. He was right, but the creature is so rare that few scientists have been able to study it in detail. That changed when Henrik Glenner discovered a large group of velvet belly lantern sharks—small fish with glowing bellies—off the western coast of Norway. The sharks were infested with the parasitic barnacles.

Glenner’s team at the University of Bergen, fronted by David John Rees, have now shown that Anelasma is a newly-minted parasite. It has only just made the evolutionary leap from filter-feeding to parasitism, and still retains many of the traits of its former life.

“The chances of finding such an organism are incredibly slim,” says Glenner. “It would have a brief evolutionary existence compared to its suspension-feeding predecessor and its parasitic successor. For evolutionary biologists, a chance to study all aspects of the biology of such a creature is a rare gift.”

Barnacles, despite their outward appearance, are crustaceans like crabs and lobsters. You can see the resemblance if you cut their shells open. Inside, you’ll find a weird creature that looks like a distorted prawn, lying on its back, with its legs sticking upwards. These legs are called cirri—they’re long and feathery, and the barnacle beats them to draw water into its shell and to sieve food from that water. There are around 1,000 species of barnacle and they’re almost all like this.

Anelasma is not. It lacks a hard shell. Its cirri are still there, but they are small and useless for feeding. It has a mouth and gut, but there’s never anything in them.

Instead, it feeds with a unique organ called a peduncle, which looks like a yellow onion with tree roots sprouting out of it. It’s not connected to the animal’s gut. Instead, the peduncle may be a modified version of the stalk that allows other barnacles to anchor themselves onto rocks; Anelasma uses it to anchor itself in flesh. Once there, it absorbs nutrients through the root-like filaments.

Two barnacles in cross-section: Analesma (left) and Lepas (right).
Two barnacles in cross-section: Analesma (left) and Lepas (right). Ci = cirri; m = mouth; pd = peduncle; r = rootlets; ma = mantle. Credit: Rees et al, 2014, Current Biology.

There are other parasitic barnacles. The rhizocephalans (from the Greek for “head root”) target their own kin—crabs and other crustaceans. As adults, they consist of little more than an external sac, and a root-like digestive system that threads its way through the body of their victims. They also castrate their hosts and addle their minds, so that the crabs care for their parasitic bulge as if it were a clutch of their own eggs. Even the males do this.

Rhizocephalans are completely unrecognisable as barnacles. That’s typical of many parasites, which have so thoroughly adapted to their exploitative lifestyles that they look nothing like their closest relatives. Anelasma bucks the trend. It’s very clearly still a barnacle. It has evolved a completely new feeding system, but it still has traces of the old one (the cirri). “This is a highly unusual situation,” says Glenner. “The selection pressure for both getting rid of the old redundant feeding system, and for improving the novel one, would change the [shape] of such an organism very fast.” That it exists in its current form is an unexpected delight.

Anelasma’s DNA yielded even more surprises. It’s reasonable to think that it evolved from whale barnacles, which attach themselves to whales without parasitising them. After all, this family is already adapted to riding on free-swimming animals, and often bury deeply into their hosts’ skin. But Anelasma’s closest relative is actually Capitulum mitella, a traditional filter-feeding barnacle that lives on rocky Indo-Pacific shorelines. Not a whale barnacle. Also: really quite a long way from Norway!

This suggests that Anelasma might be the last survivor of a much broader group of barnacles. Indeed, C.mitella might be Anelasma’s closest relative, but the two diverged from each other during the Cretaceous period, 120 million years ago. Since that time, perhaps Anelasma’s dynasty spread throughout the world, only to mostly go extinct.

A velvet-belly lantern shark with two (?) Analesma barnacles attached to it. Credit:  Irvin Kilde
A velvet-belly lantern shark with two (?) Analesma barnacles attached to it. Credit: Irvin Kilde

Perhaps the weirdest thing about Anelasma is that it’s the only barnacle to parasitise a back-boned host. It’s not the others lack for opportunities. Many barnacles attach to whales, turtles, sea snakes and manatees. As Rees writes, there’s a “virtually endless food resource (tissue and blood) available just a few millimetres below the attachment site”. So why have so few of them evolved to tap into this nutritious seam?

No one knows. Glenner suspects that it’s just very hard for a barnacle to evolve the peduncle that Anelasma uses. It probably required a “rare combination of rare events” and his team are now trying to find out what those events were.

They also want to solve a few other mysteries about Anelasma. For example, how does it circumvent its host’s immune system? There’s never any inflammation around the buried peduncle, so the shark apparently treats the parasite as part of itself.

And why is it almost always found in pairs, sitting side by side on a lantern shark’s skin? It certainly doesn’t arrive in pairs. As larvae, Analesma is streamlined and can swim surprisingly fast in pursuit of sharks. But it settles independently, which is why some pairs contain a large individual (the longer resident) and a small one (the newer arrival). Perhaps, they eventually settle in pairs so they can always find a mate. Or perhaps these creatures have even more surprises left to discover.

Reference: Rees, Noever, Hoeg, Ommundsen & Glenner. 2014. On the Origin of a Novel Parasitic-Feeding Mode within Suspension-Feeding Barnacles. Current Biology. http://dx.doi.org/10.1016/j.cub.2014.05.030

More on barnacles: Poorly-endowed barnacles overthrow 150-year-old belief

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Parasite Forces Host To Dig Its Own Grave

If a bumblebee is attacked by a thick-headed fly, it’s doomed. The fly will lay an egg inside it and the larva will eat it alive. And if that wasn’t an ignoble enough fate, the larva also forces the bee to burrow into the ground. The soil is warm and safe, and makes for a better nursery for the developing fly. And the bee? The bee is as good as dead. For its last act, it might as well dig its own grave.

There are around 800 species of thick-headed flies or conopids, and they’re all parasites. They use the hard tips of their abdomens like can-openers to prise apart the body segments of bees and wasps, so they can lay an egg inside. They even do this while flying. A conopid can chase down a bee, grab it in mid-air, open it up, and implant it with an egg, without ever touching the ground.

The fly maggot takes just under two weeks to kill its host, first by draining nutrients from its bodily fluids and then by actually eating it. Shortly, after, it forms a pupa and transforms into an adult.

In 1994, Christine Muller discovered that the vast majority of infested bumblebees bury themselves. As soon as she put them on soil, they started to dig. This behaviour didn’t matter to the bees, but it was critical for the flies.

Conopids have yearly life cycles. The adults emerge in the spring after spending the winter as pupae, hibernating inside their dead hosts. If the host dies in the open, the developing fly faces months of cold, dehydration, fungi, and even other parasites. If the host dies underground, the fly is sheltered and more likely to survive.

These kinds of manipulations are common in the world of parasites, many of which commandeer the brains and bodies of their hosts to ensure their own survival. There are wasps that turn caterpillars into head-banging zombie bodyguards, and fungi that make ants climb to the ideal locations for spores to grow. In this case, a fly turns a bee into a shovel.

But not all bees make equally good shovels.

In the summer of 2012, Rosemary Malfi at the University of Virginia collected three closely related species of bumblebees from a local field. She found that a quarter of them were parasitised by a single conopid species—a black, wasp-like insect called Physocephala tibialis.

The parasite forced all three species of bumblebee to dig, but with varying degrees of success. Around 70 percent of the two-spotted or common eastern bumblebees dug their own graves when infected, but only 18 percent of the brown-belted bumblebees did so.

This isn’t a case of resistance in the classical sense. Host insects often have defences that stop parasitic flies and wasps from implanting them with eggs. If that fails, their immune system can sometimes destroy the developing larva. Some species can even self-medicate (with booze, no less) to cure themselves. These countermeasures can force parasites to be very specific, to only target hosts whose defences they can overcome.

It’s possible that the brown-belted bees in Malfi’s study use one or more of these countermeasures, but they could also protect themselves by resisting manipulation. If they don’t dig their own graves, they’d make poor winter homes for a conopid maggot, and a poor choice of target for a conopid adult. Perhaps they defend themselves from parasites not by being inhospitable hosts, but by being incompetent ones.

PS: Carolyn Beans has written a good post on one of Malfi’s earlier studies on conopid flies. Check it out.

Reference: Malfi, Davis & Roulston. 2014. Parasitoid fly induces manipulative grave-digging behaviour differentially across its bumblebee hosts. Animal Behaviour. http://dx.doi.org/10.1016/j.anbehav.2014.04.005

More on parasites:

Parasites Make Their Hosts Sociable So They Get Eaten

Sexually Transmitted Virus Sterilises Insects, Turns Them On

Zombies Snipers At The Doorstep

Parasite Cuisine: Eating the Eaters

This week I took a trip to the University of Maryland to give a talk about parasites. I waxed poetic about how sophisticated parasites are in their manipulations of their hosts, and how we might do well to learn from their wisdom about how the brain works. At dinner, I sat next to David Inouye, the incoming president of the Ecological Society of America. The waiter set down plates in front of us, loaded with plants, animals and fungi–free-living organisms, in other words. As we looked at the plates, a question came up: is there a parasite you can eat?

Obviously, no one sits down to a piping hot bowl of smallpox soup. But parasites can also take the form of plants, animals and fungi–just like the plants, animals, and fungi we were eating.

Having written a book (and many articles) on parasites, I couldn’t think of a parasite that people eat. But if there’s one thing I’ve learned about parasites, it’s never to make an assumption about them, because the truth will always be weirder than I imagined.

Inouye, on the other hand, immediately thought of one: pea crabs.

Pea crabs get their names from their tiny size. They slip into the shells of mussels and oysters, where they take up residence on the gills of their hosts. They feed on the bits of food in the water that their hosts pump into the shell. Pea crabs are bad for their hosts, gradually eroding their gills that they depend on to take in oxygen. But despite their cruel way of life, they’re tasty. George Washington, Inouye informed me, was the most famous fan of pea crabs, delighting to eat them in oyster stew.

In Mexico, another parasite is a popular delicacy. Called huitlacoche, this parasitic fungus infects corn. As it feeds on an ear of corn, it balloons out into a gruesome grey bulb. But served up in a quesadilla, it’s reportedly delicious.

Later in the week, Inouye decided to present our question to an email list of ecologists. It turned out there were a lot more parasitic dishes.

Take lampreys. Lampreys belong to an ancient lineage of vertebrates, branching off on their own before the evolution of jaws. Instead, these creatures have a disk-shaped mouth ringed with rasp-like teeth. Many species of lampreys are parasites. They use their suckers to grab onto other fish. Riding along, they dig into the flesh of their host, and feed on its blood and flesh.

Despite being rather loathsome parasites, lampreys are a delicacy. Henry I, the king of England, reportedly died from eating too many lampreys. Queen Elizabeth was served a lamprey pie on her coronation day. (The Internet being the Internet, there is a whole page dedicated to the 1000-year history of the lamprey pie.)

I could imagine eating a lamprey pie (if it was diced into very small pieces), but some forms of parasite cuisine are beyond my comfort zone. The zoologist Tim Flannery describes watching someone in New Guinea gut a marsupial, remove any tapeworms from its intestines, and put the still-squirming parasites in his mouth. In 1955, a biologist doing field work in Alaska reported that Inuits liked to eat the warble fly maggots that develop in the hide of the reindeer.

And in his 2003 presidential address to the American Society of Parasitologists, Robin Overstreet discussed another delicacy of the Inuits:

These people, however, obtain an even larger parasite snack by eating Pennella balaenopterae, a poorly understood [crustacean] species that can grow to monstrous proportions. Specimens up to 30 cm long routinely embed deeply into the blubber of baleen whales, with the posterior of their bodies trailing free from the host. The plump and juicy body extremity is plucked from the host and eaten raw, and the “sweet” contents of the blood-filled neck are sucked out.

Overstreet’s whole speech was about ingesting parasites. Apparently, you cannot impeach a president for such an act. If you’re so inclined, you can read the speech here. It’s fascinating, but the quality of the photographs that accompany it is far too good for my peace of mind.

Finally, people eat parasites as medicine. Dodder is a parasite, growing on other plants and drawing out their nutrients. In the Philippines, people take dodder as a traditional treatments for aches and other ailments. Another fungus, called Cordyceps, turns ants into zombies. To keep the insides of their ant homes clean of germs, they make antibiotics. The popularity of the fungus in Chinese medicine has led to a Cordyceps boom in Tibet, the subject of this fascinating National Geographic story.

The list of parasites as food turns out to be encyclopedic. And so, when your local artisanal hipster eatery runs out of ideas, don’t be surprised if they reopen under a new name: Cafe Liver Fluke.

[Update: Thanks for all the comments. I have to pull this one up into the post itself:

How in the world did you miss the French dish Bécasse ? This gastronomic delicacy consists of an oven roasted woodcock (Scolopax rusticola) whose intestines are infested with the tiny tapeworm Amoebotaenia lumbrici. After the bird is roasted whole with the innards intact, the intestines are removed and chopped up into a pâté. The unique flavor of the pâté has always been attributed to the roasted tapeworms. After reading your first paragraph, Bécasse pâté was the first thing that I thought of.]

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Zombies Snipers At The Doorstep

Somewhere in the Brazilian rainforest, a lone carpenter ant marches out of its nest towards its doom.

The ant is infected with a fungus called Ophiocordyceps unilateralis, which has both infiltrated and commandeered its body. While it devours the ant alive, it also sends its zombified host scurrying up a plant stem. The ant walks along the underside of a leaf and vigorously locks its jaws around a vein. This is a death-grip; those jaws will never open again. In a week or so, a long stalk erupts from the ant’s head growing outwards and downwards into a bulbous capsule, which releases a rain of spores. If other ants walk underneath, they become infected.

The fungus controls its zombie host with incredible precision. The ant always climbs to around 25 centimetres above the soil—a zone with just the right temperature and humidity for the fungus to grow.

But why does the ant leave its nest in the first place?

Outside, the fungus needs to drive its host to a spot that offers the best chance of raining spores down upon passing workers. But inside the nest, there are thousands of such workers nearby. With this dense smorgasbord of new hosts to infect, why does the fungus send its current host into the great outdoors?

Perhaps these forays are the ants’ doing. Colony-living insects like ants have a kind of social immune system—they behave in ways that prevent infections from spreading through their nests. They clean each other and remove the corpses of their nestmates. Sick ants, which have been infected by killer fungi, are often shunned by their fellow workers, and sometimes leave the nest to die alone. Biologists often view these as acts of self-sacrifice, as if the ant was a six-legged Captain Oates.

But Raquel Loreto and David Hughes from Pennsylvania State University see things differently. The duo first realised what was going on when they collected carpenter ant nests, and seeded them with ants that had been freshly killed by Ophiocordyceps. The ants detected and removed around half of these remaining cadavers—a clear example of their vaunted “social immunity” at work.  But they needn’t have bothered. It turns out that the fungus simply cannot grow inside the nests of its hosts. Even if the cadavers were placed in nests that had no ants, the fungus still wouldn’t sprout.

“The best place for the sick individuals is at home!” says Hughes, who had been studying the zombifying fungi for many years. “In a naive framework, leaving the nest appears to be altruistic but it’s actually part of the fungus’ manipulation.”

So, what happens outside the nest? To find out, Loreto trekked into the same stretch of Brazilian rainforest for 20 months to study 17 specific carpenter ant nests. She ventured into the jungle at night with infrared torches to map the foraging trails that the workers walk along.

She also marked out a 200-cubic-metre zone around four of the nests nest —an area that she calls the “doorstep” of the colony. It’s the zone that all workers must pass through on their way in and out of the nest. Once a month, Loreto walked through these doorsteps and checked the underside of every single leaf within them for the zombified corpses of infected ants.

“This is important because it’s one of the few field studies of ant-parasite interactions,” says Sylvia Cremer from the Institute of Science and Technology Austria. Most people who study social immunity have exposed ants to parasites within the artificial confines of a laboratory. “It’s always good to bring some realism to these discussions,” says Hughes.

At the end of her Herculean effort, Loreto had found zombified corpses around every one of the 17 nests she studied. And she kept on finding new corpses every month around the four nests she studied in detail. The results were clear: despite the ant’s vaunted social immunity, the fungus infects close to 100 percent of the nests in the area, and does so throughout the year. It’s a permanent and omnipresent threat.

The team thinks that the fungus is so successful precisely because it sends its hosts outside the nest. Inside, the ants’ social immune system can protect them. Outside, it doesn’t work. “Over 20 months, Raquel never saw the colony disinfecting its borders,” says Hughes.

The ants also rely on the same trails, so the fungus is virtually guaranteed to find new hosts if it positions its current one in the right spot. Hughes compares it to a sniper’s alley. “The foragers come out at night and pass under the cadavers of their siblings that are now shooting spores at them,” he says.

But why wouldn’t the carpenter ants evolve a countermeasure? Over time, surely you’d expect them to start removing infected corpses from the leaves around their nests, as other species of ants do elsewhere in the world. Hughes suggests that they might not need to. Young carpenter ants stay exclusively within their nests. They only venture out to forage when they get older, so the fungus can only ever infect ants that are near the end of their lives anyway.

This strategy seems to suit both parties. The ants ensure that only their weakest members face death by zombifying fungus, and the fungus get a continually renewed supply of susceptible hosts to infect. It’s as close to a win-win as you get in evolution.

Reference: Loreto, Elliot, Freitas, Pereira & Hughes. 2014. 3D mapping of disease in ant societies reveals a strategy of a specialized parasite. BiorXiv. http://dx.doi.org/10.1101/003574

For more on surprising and counter-intuitive world of mind-controlling parasites, have a look at my TED talk:

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Sexually Transmitted Virus Sterilises Insects, Turns Them On

Why would a sterile male cricket mate with an infertile female? On the surface, this behaviour makes no sense: sex takes energy and effort, and there’s nothing in it for either of these partners. Neither one can foster the next generation.

Shelley Adamo from Dalhousie University has the answer. Her team have shown that one particular insect virus can sterilise crickets, but also change their behaviour so they continue to mate with each other. By doing so, they pass the virus on to uninfected hosts.

This virus is the latest example of parasitic mind control—a topic that I’ve covered regularly on this blog, and that I spoke about at the recent TED2014 conference.

Scientists have now documented hundreds of such manipulators. There are wasps that turn caterpillars into head-banging bodyguards, and those that take cockroaches for walks. There are tapeworms that make shrimps sociable, and those that turn sticklebacks into heat-seekers. There’s Toxoplasma gondii, which sends rodents running towards cats.

And there are viruses. The rabies virus is a classic manipulator, which occasionally makes its hosts more aggressive so they spread the virus through bites. There’s a type of baculovirus that compels caterpillars to climb into trees, so their disintegrating bodies send a rain of viral particles onto plants below. And now we have the less-than-catchily named IIV-6/CrIV—a sexually transmitted virus that acts as an aphrodisiac for infertile crickets.

Adamo’s team first noticed the virus when some of the female crickets in their lab stopped laying eggs. They dissected the uncooperative insects and found that their fat bodies—organs that store fat and make proteins—were swollen and blue. Under a microscope, these organs were loaded with viruses, which were packed into dense crystals that gave off a blue sheen.

The team identified the viruses as IIV-6/CrIV, which had been discovered in crickets just over a decade ago. It effectively sterilises any cricket that it infects. A typical female carries more than a hundred eggs in her reproductive system, but these infected ones had fewer than ten. Meanwhile, the males had plenty of sperm, but these cells couldn’t swim.

Still, the males actually became quicker to court nearby females and the females continued to mate with them. These continuing hook-ups don’t benefit the crickets. But the virus, which turned out to be sexually transmitted, gets an easy ride into fresh, uninfected hosts.

Adamo found that IIV-6/CrIV also changes the crickets’ behaviour in other subtle ways. A sick cricket will typically try to ward off an invading virus by releasing immune chemicals from its fat body. While these protective substances do their work, the cricket stops eating and trying to attract mates.

But a cricket that’s infected by IIV-6/CrIV  doesn’t show these “sickness behaviours”. The virus targets the fat bodies, preventing them from firing off their defensive salvos. It also seems to compel the insect to continue eating and courting. That makes sense: as Adamo writes, “a host that behaves as if it were sick will not attract mates” and a cricket that doesn’t mate is a dead-end for the virus.

There are almost certainly many more examples of sexually-transmitted parasites that subvert their hosts’ behaviour. There’s another virus called Hz-2v, which infects and sterilises the corn earworm moth, but also ensures that its hosts carry on mating. And Toxoplasma gondii, besides turning rats into cat-seeking missiles, also makes male rats more attractive to females.

Reference: Adamo, Kovalko, Easy & Stoltz. 2014. A viral aphrodisiac in the cricket Gryllus texensis. http://dx.doi.org/10.1242/jeb.103408

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My TED Talk on Mind-Controlling Parasites

When we think about animal behaviour, we often assume that the animals are in charge of their own actions. That’s often not the case. At the TED2014 conference in Vancouver last week, I gave a talk on the fascinating and macabre world of mind-controlling parasites, from the tapeworm that makes shrimps sociable to the wasp that takes cockroaches for walks, with special shout-outs to the NSA and Elizabeth Gilbert. Take a look.

You can also find out more information on the talk page at TED’s site, and lots of links, citations and other goodies.

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Bird Cheaters Target Teams, But Teamwork Beats Cheats

The common cuckoo is famed for its knack for mooching off the parental instincts of other birds. It lays its eggs in the nests of at least 100 other species, turning them into inadvertent foster parents for its greedy chicks. For this reason, it’s called a brood parasite.

It’s not alone. Among the birds, the full list of brood parasites includes more than 50 members of the cuckoo family, cowbirds, honeyguides, several finches, and at least one duck.

Now, William Feeney from the Australian National University has found that brand of reproductive cheating goes hand in hand with its polar opposite: cooperative breeding, where birds raise their young with help from siblings or offspring, often at the cost of the helpers’ own reproductive success.

The two strategies couldn’t be more different but Feeney found that each drives the evolution of the other. In places where one is common, the other is too. Exploitation goes hand-in-hand with cooperation.

Biologists have been exploring the origins of cooperative breeding for almost 140 years. “What I liked about the new paper is that is presents convincing evidence for an idea that wasn’t even really on the table—it is beneficial because groups reduce the risk of brood parasitism,” says Bruce Lyon from the University of California, Santa Cruz.

Similarly, scientists who study brood parasites have mostly focused on defences like spotting a cuckoo’s eggs. “For some reason the social system of the hosts was not really considered,” says Lyon.

The seeds of the discovery were planted in Australia, where Feeney’s group were studying the aptly named superb fairy-wren. It gets parasitised by Horsfield’s bronze cuckoo, but not without a fight. The team noticed that the fairy-wrens attacked incoming cuckoos with extreme prejudice, and that larger groups almost never got parasitised. They wondered if the two behaviours—cooperative breeding and brood parasitism—were connected in other parts of the world.

The answer was a resounding yes. Look at the maps below. The top one shows the global spread of cooperatively breeding passerines—the small perching birds that are the most frequent target of brood parasites. Red areas are rich in cooperative species, while white areas are devoid of them. The bottom map shows the spread of brood parasites. There’s a very strong match between the two. Even if you account for the total richness of species in a given area, places with lots of cooperative breeders also have lots of brood parasites. Africa and Australasia are particularly rich in both.

Credit: Feeney et al, 2013. Science.
Credit: Feeney et al, 2013. Science.

Of course, this connection could be due to some unrelated factor. For example, extreme parenting styles might just be more common in Africa and Australia, because these continents have harsh, variable environments. If the two strategies really are connected, then you’d expect that connection to hold within regions as well as between them.

That’s exactly what Feeney found. Even within Africa and southern Australia, brood parasites are much more likely to target cooperative breeders than other birds.

Here’s a family tree showing all the birds from southern Africa. The orange circles denote species that are cuckoo hosts, and the blue circles are the cooperative breeders. Around 28 percent of the hosts help each other out in the nest, compared to just 8 percent of the non-hosts.

Credit: Feeney et al, 2013. Science.
Credit: Feeney et al, 2013. Science.

And here are all the passerines in Australia. Again: an obvious connection. Around 53 percent of the hosts help each other out in the nest, compared to just 12 percent of the non-hosts.

Credit: Feeney et al, 2013. Science.
Credit: Feeney et al, 2013. Science.
Credit: Feeney et al, 2013. Science.

There are two possible reasons for this correlation. Brood parasites might selectively target cooperative breeders because they’d provide the best care. Alternatively, birds might resort to teamwork because they can better defend their nest against parasites.

Feeney found that both answers are right.

His team returned to the superb fairy-wren—a bird where some parents get help in the nest, but others don’t. By comparing different nests over 6 years, they showed that cuckoo chicks grow faster and survive better if they’re raised by larger groups of fairy-wrens. So cooperative breeding can foster the rise of brood parasitism.

But cuckoos rarely get to realise this benefit, because larger groups of fairy-wrens are also better at fending them off. Collectively, they’re more vigilant around the nest. If one of them spots a cuckoo, it makes a cuckoo-specific alarm call and the entire group mobs the intruder. The larger the group, the more persistently they attack. So the presence of brood parasites fosters can foster the rise of cooperative breeding.

Naomi Langmore, who led the study, thinks that the relative strength of these two effects probably changes over time. Cuckoos and other brood parasites often switch hosts. When this happens, it’s initially easier for them to reap the benefits of a larger surrogate family because the new hosts have evolved to detect or repel their infiltrators. Over time, as such defences emerge, the balance shifts. For the fairy-wrens and bronze cuckoos, “cooperation protecting against parasitism is the stronger force,” says Langmore.

Of course, there are many reasons for species to evolve cooperative breeding, and the threat of parasites is just one of them. If there aren’t enough territories to go around, or if predators are particularly rampant, it will also benefit youngsters to stay near their families rather than strike out on their own.  “Brood parasitism is not exclusive of other factors but may simply help tip the balance in favour of helping over dispersing,” says Lyon.

“The relative importance of brood parasitism in selecting for cooperative breeding is likely to vary from species to species,” says Langmore, “but our evidence suggests that, overall, it is one of the major selective forces favouring the evolution of cooperation.”

She’s not just talking about birds, either. There are also many brood parasites among the insects, including a group of over 3,000 cuckoo wasps. Many lay their eggs in the nests of other wasps, and their grubs devour the hosts’ own eggs and larvae. “The hosts of cuckoo wasps also mount highly aggressive colony attacks on the parasites,” says Langmore, “and hosts from parasitized populations have actually evolved larger bodies so they are better able to drive off the parasites.”

Reference: Feeney, Medina, Somveille, Heinsohn, Hall, Mulder, Stein, Kilner & Langmore. 2013. Brood Parasitism and the Evolution of Cooperative Breeding in Birds. Science http://dx.doi.org/10.1126/science.1240039

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New Study Upholds Reputation of Classic Parasite

I was ten years old when I first saw Trials of Life, David Attenborough’s landmark series on animal behaviour. Its twelve glorious episodes left an indelible mark in my mind, with unforgettable scenes of killer whales beaching themselves to eat sea-lions and elephant shrews bounding along carefully memorised paths.

But if you asked me to list the most memorable scenes from the series, I would tell you about the snails.

They appear in episode 7, grazing on leaves in a Danish meadow. One of them looks weird. Its slender eyestalks have transformed into swollen sacs, with green and yellow stripes, black spots, and red tips. They look like gangrenous popsicles. Something inside them is pulsating.

During an inauspicious meal, this particular snail had accidentally swallowed the eggs of a fluke—a  parasitic flatworm called Leucochloridium paradoxum. The eggs hatched, and the young flukes started taking over the snail’s body. As they matured, they sent large broodsacs, full of larvae, into the snail’s eyestalks. For some reason, the flukes usually go for the left one, but they’ll corrupt both if two of them share the same snail.

In the light, these sacs start to throb. The effect was revolting and unforgettable to my young eyes. But it’s also compelling to birds, because the sacs look very much like juicy caterpillars or grubs. In the Trials of Life, a flycatcher swoops in and devours the snail. That works for the fluke, which can only complete its life cycle in the guts of a bird.

But Attenborough claimed that the flukes did more than change the snail into a billboard. “For some reason, the presence of the parasite changes the snail’s behaviour,” he said. “As the day wears on, it does not like uninfected snails crawl back into the undergrowth out of harm’s way. Instead, it remains exposed out in the open, dangerously so.”

Attenborough isn’t the only person to make such claims. Leucochloridium has become a textbook example of a parasite that manipulates the behaviour of its host for its own ends. But Wanda Wesolowska and Tomasz Weslowski from Wroclaw University in Poland discovered that this “fact” was based on the shakiest of foundations.

Leucochloridium’s hijacking behaviour was first described in 1835. In the intervening 178 years, the only evidence that it manipulates the snails came from a German paper published in 1922. That author simply suggested that infected snails seek the well-lit upper surfaces of leaves, where they are visible to birds, and never presented any data to back up the claim.

Weslowska and Weslowski were chagrined, and they set out to Białowieza National Park in Poland to observe some of the snails. By carefully recording their behaviour, they confirmed that the infected animals behave very differently to the uninfected ones. They sat higher above the ground, kept to better-lit areas, stayed in more open spaces, moved around more, and oozed along more erratic paths. All of these traits would make them easier to spot and to attack.

Phew! Attenborough stands correct; the textbooks don’t have to be rewritten.

But wait! There’s more work to do. The only evidence that birds are attracted to the broodsacs comes from an 1874 study in which captive birds attacked the sacs. No one has checked that wild birds behave in the same way.

As Weslowska and Weslowski write, “Despite strong prevailing opinions and numerous popular accounts, there is not a single study documenting attacks of definite passerine hosts on snails with broodsacs… We think that such a situation is quite embarrassing, and thus, we would like to encourage the readers to undertake studies of this host–parasite association.”

You might think this represents nitpicking of the highest order, but the world of natural history is heaving with claims that sound right but have never been properly tested. Many of these “facts” deflate in the face of evidence. Cheetahs don’t overheat after they hunt—that’s a myth based on a 1973 experiment in which captive animals ran on treadmills. Komodo dragons don’t kill with a bacteria-laden bite—that’s a myth based entirely on speculation. And honeyguide birds do not lead honey badgers to honey—that’s a myth based on folk tales and some very unscrupulous documentary-makers.

But others check out. Thresher sharks really do slap fish with their huge tails—something that was assumed for around a century but filmed this year. Cheetahs really can run at 60 miles per hour, something that was based on a single measurement and had never been checked in the wild. And I’m personally delighted that Leuchochloridium’s manipulative streak seems to fall into this camp.

Reference: Wesołowska & Wesołowski. 2013. Do Leucochloridium sporocysts manipulate the behaviour of their snail hosts? Journal of Zoology http://dx.doi.org/10.1111/jzo.12094

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Tree-Killing Worm, Please Make Your Way To The Boarding Gate

Meet the microscopic worm that can kill forests. It’s called the pinewood nematode (Bursaphelenchus xylophilus) and though each one is barely a millimetre long, they can collectively bring down a towering pine tree.

Once it gets into a tree, the nematode spreads through the trunk, branches, and roots. It feeds on the cells lining the pine’s resin canals, causing resin to leak into other vessels that carry water around the tree. Cut off from their water supply, the pine’s needles turn yellow and brown. The change is dramatic. Within just a few months, the tree wilts and dies. This pine wilt disease has claimed millions of pines, especially in Europe and East Asia, causing huge problems for ecosystems and the forestry industry alike.

But the nematode can’t spread to new trees on its own. Instead, it hitches a ride on pine sawyer beetles—substantial, finger-sized insects with long antennae and sharp mandibles.

The nematodes hide inside the breathing tubes that carry oxygen around the beetles’ bodies. They emerge only to enter the open wounds caused when the insects nibble on pine twigs. They spread through the tree and kill it—that’s perfect for the beetles, which lay their eggs in dead or dying wood. Their larvae eat the wood until they transform into adults and fly off in search of fresh pines. And before they do, they’re boarded by nematodes.

These two partners enjoy a tight, mutually beneficial relationship. The beetle brings the nematode to fresh victims, while the nematode creates the conditions that the beetle needs to reproduce.

But timing is everything. The nematode goes through four larval stages and it can only colonise beetles in the last of these—L4. The beetles, meanwhile, can only host the nematodes as adults. Fortunately, the duo have a way of synchronising their complex life cycles.

The pine wilt nematode. Credit: USDA Forest Service Region 2, Rocky Mountain Region Archive, Bugwood.org
The pine wilt nematode. Credit: USDA Forest Service Region 2, Rocky Mountain Region Archive, Bugwood.org

Lilin Zhao from the Chinese Academy of Sciences has found that the beetles produce a chemical signal when they transform into adults. This tells the nematode that its ride will soon be ready, and that it should enter the L4 stage. It’s a molecular announcement that says the insect will soon be ready for boarding.

Zhao’s team first noticed that although the beetle grub is surrounded by nematodes inside a pine tree, very few of these worms are in the L4 stage. They only transform en masse when the insect reaches the last stages of pupation and is about to emerge as an adult.

To work out why, the team analysed the chemicals on the beetle’s surface at different life stages. They found four that are mass-produced at the end of its pupal stage. When the adults emerge, they give off waves of this chemical stew. And when Zhao dabbed the cocktail onto stage-three nematodes, they quickly transformed into stage-four.

The substances in question are all fatty acid esters—long chains of carbon and hydrogen atoms with a couple of oxygen atoms at the end. Insects commonly use these chemicals as pheromones, but the pine sawyers make four very specific ones—ethyl palmitate, ethyl stearate, ethyl oleate and ethyl linoleate—and they do so in bulk.

These signals are very specific. Similar esters don’t trigger the nematodes’ transformation, nor do those from beetles other than the pine sawyers. That’s important—many beetles bore into wood and it would be counter-productive for the nematodes to get a boarding announcement from an insect that can’t serve as its host.

It’s possible that this discovery could be used to save pine trees from the nematodes, by somehow disrupting the worms’ ability to synchronise their lives with that of their beetles. But for now, it serves as yet another example of the intimate partnerships that exist between different animals, and the signals that seal those alliances.

Reference: Zhao, Zhang, Wei, Hao, Zhang, Butcher & Sun. 2013. Chemical Signals Synchronize the Life Cycles of a Plant-Parasitic Nematode and Its Vector Beetle. Current Biology http://dx.doi.org/10.1016/j.cub.2013.08.041

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Mercenary Ants Protect Farmers With Chemical Weapons

Humans have a long history of bolstering their armies by paying mercenaries to fight on their behalf. Now, Rachelle Adams from the University of Copenhagen has found that some ants do the same.

Some ants defend their colonies with special soldiers, which are bigger and wield more formidable weapons. But others lack a proper army. Sericomyrmex ants, for example, are fungus-farmers. They bring bits of vegetation back to their nests and use these to nourish a fungus, which they then eat. They are poorly defended, and a sitting target for raiders and pirates. That’s why they rely on other ants to fight for them.

Another ant called Megalomyrmex symmetochus forms its own colonies, complete with queen and workers, inside those of Sericomyrmex colonies. This guest is present in over 80 percent of the farmers’ nests and, at first glance, it looks like a parasite. It eats the fungus that the farmers so assiduously grow, without contributing any labour of its own. Worse still, it eats some of the farmers’ larvae and clips the wings of their young queens, so they contribute to the gardening rather than flying off to start their own colonies.

But M.symmetochus doesn’t just freeload off its hosts. In some cases, it can be their salvation.

Megalomyrmex mercenary (top right) defends a fungus garden from a Gnamptogenys raider (bottom). Credit: Rachelle Adams
Megalomyrmex mercenary (top right) defends a fungus garden from a Gnamptogenys raider (bottom). Credit: Anders Illum

Sericomyrmex nests are often attacked by a third ant called Gnamptogenys hartmani—a sort of six-legged pirate. It raids the colonies of farming species, drives them out, usurps their nests and gardens, and eats any remaining larvae.

The farmers can do very little against these raiders, since they lack specialised soldiers and have mostly lost their stings. Their powerful jaws can deliver a strong bite, but at such close quarters, they risk getting stung and bitten themselves. When attacked, they’re much more likely to feign death or flee. That is, unless there’s a M.symmetochus colony living in their nests.

Back in 2011, Adams let some raiders loose upon a colony of Sericomyrmex farmers, which was already being parasitized by M.symmetochus. “To our surprise, the hosts hid and the parasites rose to the top of the garden to confront and kill the invaders,” she says.

Unlike their hosts, the parasitic ants are far from defenceless. They raise their stings and release a powerful venom directly into the air—an airborne chemical weapon that kills the raiders and befuddles any survivors. “Rather than uniting as an efficient infiltration squad they turn on each other and attack, sometimes killing their own kin,” says Adams.

M.symmetochus behaves like a colony of mercenaries. They can cause problems for the farmers during peace-time, but they provide an invaluable defence when an invading force arrives.

By pitting the three types of ants against each other, first in one-to-one battles and then in more realistic groups, Adams’ team showed that the mercenaries are much better at subduing the raiders than the farmers. It takes just two of them to overpower a single raider, while the same task requires at least eight farmers. On average, a pair of raiders can kill 70 percent of farmers in an unprotected nest, but just 10 percent of them if there are six mercenaries around.

And the raiders seem to know it. When the team gave them a choice between two nests, only one of which was defended by mercenaries, they were more likely to attack the unprotected nest. In the experiment, a wire mesh prevented the raiders from actually touching the colonies, so they were probably put off by the smell of the mercenaries’ chemical weapons. Just by living in the same colonies, the mercenaries protect the farmers by cloaking them in a defensive miasma.

The thing that clinches this incredible relationship is probably Megalomyrmex’s life cycle. They form a life-long bond with a single colony of farmers, and won’t leave to seek out a different host. They exploit their hosts but they don’t overexploit them, and if raiders attack, they mount a defence rather than abandoning the farmers to their fates.

Next, the team wants to study how this alliance varies over time and space. For example, it should be easier to find the mercenaries in the farmers’ nests in places where the raiders are more common. Similarly, a different farmer called Trachymyrmex zeteki should be relatively unbothered by raiders, since it also hosts a parasitic mercenary but in fewer than 6 percent of its nests.

For now, they very astutely compare the mercenary ants to a human disease called sickle cell anaemia. It’s an inherited genetic disease that warps the shape of red blood cells and causes a gradual building illness. The mutated gene behind the disease is common in Africa because two copies might cause sickle-cell anaemia, but one copy protects a person against malaria. Similarly, M.symmetochus is like a mild chronic disease that exerts a toll upon its host, while protecting it from an acute and more destructive infection—the Gnamptogenys raiders.

Reference: Adams, Liberti, Illum, Jones, Nasha & Boomsma. 2013. Chemically armed mercenary ants protect fungus-farming societies. PNAS http://dx.doi.org/10.1073/pnas.1311654110

Experimental manipulation of the tendon of the large jumping muscle of one hindleg

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Parasitic Bird Fights Evolutionary Arms Race… With Itself

Top row: cuckoo eggs. Bottom row: eggs from cuckoo victims. Credit: Mary Caswell Stoddard, Harvard University
Top row: cuckoo eggs. Bottom row: eggs from cuckoo victims. Credit: Mary Caswell Stoddard, Harvard University

In the image above, all the eggs in the top row are laid by cuckoos and those in the bottom row belong to their victims. These uncanny similarities help cuckoos to fob off their parental duties by laying their eggs in the nests of other species. If the hosts can’t tell the difference between their eggs and the foreign ones, they’ll end up raising the cuckoo chick as their own. And they pay a hefty price for their gullibility, since cuckoo chicks often kill or outcompete their foster siblings.

The relationship between cuckoos and their hosts is a classic example of an evolutionary arms race. Cuckoos, should evolve eggs that more closely match those of their hosts, while the hosts should evolve keener senses to discriminate between their own eggs and a cuckoo’s.

But in Africa, this classic story takes an unusual twist.

Greater honeyguide chick. Credit: Claire Spottiswoode
Greater honeyguide chick. Credit: Claire Spottiswoode

The greater honeyguide isn’t a cuckoo but uses the same tactics—it parasitises the nests of little bee-eaters by laying eggs of the same size and shape. But this mimicry doesn’t help it to fool the bee-eaters, which seem to accept any old egg no matter how different it looks. Instead, Claire Spottiswoode from the University of Cambridge has found that the parasitic honeyguides are fighting an evolutionary arms race against… each other.

Bee-eaters build their nests underground, usually within abandoned aardvark burrows. When honeyguides invade, they’ll puncture the bee-eater’s eggs before laying their own. This kills some of the eggs outright and weakens others. If any chicks survive to hatching, they’re finished off by the honeyguide chick, which stabs its foster siblings to death with a vicious hooked bill.

Greater honeyguide chick killing little bee-eater chicks. Credit: Claire Spottiswoode
Greater honeyguide chick killing little bee-eater chicks. Credit: Claire Spottiswoode

Spottiswoode filmed this brutal behaviour in 2011, and she showed that honeyguides are a huge problem. Two-thirds of the nests are parasitised, and a third of these contain eggs from more than one honeyguide. That’s important—it means that honeyguides aren’t just trying to dupe the bee-eaters, but are also competing with each other.

The honeyguide eggs are reasonably similar to those of the bee-eaters in both size and shape. But when Spottiswoode added very dissimilar eggs to the clutches, including those from doves, woodpeckers or kingfishers, the bee-eaters almost never noticed. The honeyguide eggs can’t have evolved to fool the bee-eaters, since the bee-eaters apparently have the discriminatory prowess of a brick.

Host = little bee-eater eggs. Control = little bee-eater egg from a different nest. Honeyguide = honeyguide egg. Experimental = egg from a completely different bird.
Host = little bee-eater eggs. Control = little bee-eater egg from a different nest. Honeyguide = honeyguide egg. Experimental = egg from a completely different bird.

But the honeyguides are more savvy. Whenever they visited a nest where Spottiswoode had added an extra egg, they inflicted at least twice as many punctures upon it as they did to the others. They could tell if an egg looked different to the usual bee-eater shape, and concentrated their efforts on destroying it.

Spottiswoode thinks that the honeyguides have evolved bee-eater-esque eggs to fool each other, because they go easier on such eggs than on those that feel very different. After all, honeyguides can’t puncture everything. If they go overboard, they might cause so much damage that the hosts abandon their nests altogether. So, their best play is to puncture the bee-eater eggs a little bit, enough to give their murderous chick an advantage when it hatches but not so much that the bee-eaters desert.

If a honeyguide egg was obviously different to a bee-eater’s one, it would be thoroughly destroyed by other honeyguides that arrived at the same nest. If its mimicry is good, it gets a chance at surviving.

This story reminds me of some recent discoveries in bacteria. In 2010, I wrote about how the harmless gut bacterium Escherichia coli can sometimes make us ill because disease-causing strains are better at fending off hungry amoebas. The bacteria evolve in response to the threat of predators and by complete coincidence, they also become deadlier to us. Along similar lines, the normally harmless nose bacterium Streptococcus pneumonia can become infectious when it competes with another species called Hameophilius influenzae. It defends itself against this rival by producing a thicker coat, which also happens to shield it from our immune system.

We have this knee-jerk tendency to view parasites in terms of their hosts (since we ourselves are host to legions). But as the honeyguide, E.coli and S.pneumonia show, parasites also have to compete with each other. This competition can drive their evolution just as readily as the need to outfox a host.

Reference: Spottiswoode. 2013. A brood parasite selects for its own egg traits. Biology Letters http://dx.doi.org/10.1098/rsbl.2013.0573

More on cuckoos and other brood parasites:

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Ladybird Invader Carries Deadly Parasite as Biological Weapon

When Europeans arrived in the New World, they brought devastating diseases like smallpox, which killed more native Americans than guns and other weapons. Infections go the other way too: When grey squirrels from North America arrived in the UK, they brought a squirrel pox virus that decimated the local red squirrels. Time and again, animals have invaded new regions and killed the locals by inadvertently bringing biological weapons with them.

Now, Andreas Vilcinskas from Justus-Liebig-University of Giessen has found that one the world’s most invasive insects—the harlequin ladybird—also belongs in the biological weapons club.

It hails from central Asia, but was willingly introduced to Europe, North America, and other parts of the world, by people who were seemingly undeterred by the outcomes of bringing cane toads to Australia or mongooses to Hawaii. Like those other invaders, the harlequin has brought ruin to local ladybirds, many of which have declined dramatically since its incursion.

There are probably many reasons for that. Perhaps it simply outcompete other species for food, or eats them directly. It carries a potent slew of antibacterial chemicals in its blood (or haemolymph) that makes it remarkably resistant to disease. For example, it can shrug off a deadly fungus that kills other ladybirds.

One of these antibacterials is a toxic chemical called harmonine. Many scientists suspected that this substance was poisoning other ladybirds that tried to eat the harlequin’s eggs. But Vilcinskas found that harmonine doesn’t affect native species at all. When he injected the seven-spot ladybird with high doses of the stuff, they were fine. But when he shot them up with the harlequin’s unfiltered haemolymph, they died. The invader clearly has something in its blood that’s deadly to other ladybirds, but it’s not harmonine.

Vilcinskas found the culprit by looking at harlequin haemolymph under a microscope. He found it swarming with microscporidians—a type of single-celled parasitic fungus. These parasites are found in every harlequin that the team examined, but don’t seem to do any harm. They stay in an inactive state and their genes are completely inactive. “I have worked on insect immunity for 20 years, and I had never [before] seen a haemolymph sample that was full of microsporidians that do not harm the carrier,” says Vilcinskas.

It’s possible that harmonine and other antibacterials allow the harlequin to tolerate its parasite. But the native seven-spot ladybird isn’t so well-defended. When Vilcinskas injected them with the microsporidians, they all died within two weeks.

This might be why so many native ladybirds die when the harlequin invades. Since all ladybirds eat each other’s eggs, those that chomp on the harlequin’s young could get a mouthful of lethal microsporidians.

Of course, they need to actually prove that. Helen Roy, who leads the UK Ladybird Survey, says that injecting seven-spots with microsporidians is a far cry from showing that they actually get infected in the field. For a start, she says that seven-spots very rarely eat harlequin eggs, so their chances of getting infected by microsporidians would be few and far between. Then again, seven-spots seem to be holding their own against the invaders, and are unusual among British ladybirds in showing no population declines. Perhaps other species are more wanton in their feeding habits and pay the price?

Either way, Vilcinskas’s team need to show that wild ladybirds do eat harlequin eggs, that they contract microsporidian infections, and that this contributes to their downfall. “The next steps would be to assess ecological relevance,” says Roy. “What does this mean in the real world?”

Lori Lawson Handley, who also works on the UK Ladybird Project, wonders if the microsporidians could be travelling between species through a more grisly route. Some parasitic wasps, like Dinocampus coccinellae, lay their eggs in ladybirds, and they could be spreading the parasites from the harlequin to other species. Their stings could be the equivalent of dirty needles.

A version of this piece also appears at Nature News.

Reference: Vilcinskas, Stoecker, Schmidtberg, Rohrich & Vogel.  2013. Invasive Harlequin Ladybird Carries Biological Weapons Against Native Competitors. Science http://dx.doi.org/10.1126/science.1234032