Any depth of understanding of biology and ecology is accompanied by this inevitable conclusion: parasites rule the world.
They’re the “man behind the curtain” as fans of Oz would put it. They are the directors and stage managers of the grand production that is life on this Earth, nature’s finest puppeteers, and that we think we have any modicum of control over any species’ physiology in comparison (including our own) is downright laughable.
The latest reminder of our inadequacy when it comes to manipulating biology comes from a fresh paper in Proceedings of the Royal Society B. In it, scientists describe how the parasitoid wasp, Dinocampus coccinellae, is able to manipulate its host, the ladybug Coleomegilla maculata: it uses another parasite, a never-before seen RNA virus.
Our world is quite literally lousy with parasites. We are hosts to hundreds of them, and they are so common that in some ecosystems, the total mass of them can outweigh top predators by 20 fold. Even parasites have parasites. It’s such a good strategy that over 40% of all known species are parasitic. They steal genes from their hosts, take over other animals’ bodies, and generally screw with their hosts’ heads. But there’s one thing that we believed they couldn’t do: stop being parasites. Once the genetic machinery set the lifestyle choice in motion, there’s supposed to be no going back to living freely. Once a parasite, always a parasite.
Unless you’re a mite.
“Oh, beauty is a beguiling call to death, and I’m addicted to the sweet pitch of its siren.” – Johnny Quid, RocknRolla
Glinting in shimmering shades of blue and green, the emerald cockroach wasp is surely a thing of beauty, but its shimmering exterior masks its cruel nature. The emerald cockroach wasp is one nature’s most impressive neurochemists. At its core, it is a parasite. The female wasp lays her eggs on a cockroach host, and when they hatch, the larvae eat the creature from the inside out. You’d think the cockroach would be opposed to this idea, but instead the insect patiently awaits its fate while the larvae mature. Cockroaches are much larger than even a full grown wasp, and certainly could put up a fight, but that is where the wasps’ ingenious manipulation of neurochemistry comes in. When she encounters a potential host, the female cockroach wasp first stings the cockroach in its abdomen, temporarily paralyzing its front legs and allowing the wasp to perch precisely on its head. She then stings the roach again, this time delivering venom directly into a part of the roach’s brain called the sub-esophageal ganglia. This doesn’t kill the roach. Instead, it puts the roach in a zombie-like trance. The roach is less fearful and loses the will to flee. It allows the wasp to lead it by its antennae, like a dog on a leash, to the wasp’s burrow where the roach will play the martyr for the wasp’s unborn children. Even though the roach is fully capable of locomotion during the week to month that passes from when the wasp stings the its brain until the hungry brood finish eating it alive, the zombified insect doesn’t move. Emerald cockroach wasps have elevated neural manipulation to an art form to create perfect living incubators.
But, though the roach has been rendered harmless, the wasp-to-be is threatened by other organisms. Humans aren’t the only species that have to worry about their food spoiling—so do emerald cockroach wasps. Cockroaches truly are dirty creatures, and their insides are home to a suite of bacteria that can harm the wasp’s vulnerable larvae. One of these potential threats is Serratia marcescens, a vile sort of Gram negative bacteria found in cockroach bodies. It’s the same bacteria responsible for a number of human urinary tract infections and the weird pink stains that form in our toilets and showers. In insects, its effects are much more deadly. The bacteria possess a suite of protein-degrading enzymes that cut apart fragile larval cells. The larvae aren’t entirely defenseless, though—as a new study published today in the Proceedings of the National Academy of Sciences reveals, larval wasps sterilize their food by secreting antimicrobial compounds.
For many parasitic wasps, microorganisms are a serious concern. Studies on another wasp, Microplitis croceip, found that contamination with Serratia marcescens can lead to a 25% reduction in successful parasite emergence, and even the young that do survive can be infected. When adults are exposed to the bacteria, almost 80% die. The emerald cockroach wasp must defend against this mortal enemy, or pay the ultimate price.
But how do you protect yourself against bacteria that live inside your food? Well, you do what we do to foods that house potentially harmful pathogens: you sterilize them.
Gudrun Herzner and a team from the University of Regensburg in Germany noticed that larval wasps secrete droplets from their mouths that they disperse around before they feed on their cockroach meal. They suspected these secretions kill off potentially deadly bacteria, allowing the larvae to eat in peace. The researchers tested the antimicrobial activity of the oral secretions to see if they were right.
When added to bacterial cultures from the cockroach, the droplets killed off a wide variety of bacteria, including the potentially deadly Serratia marcescens. But the team wanted to know more: exactly what in the droplets killed off bacteria? So, the researchers isolated the secretions and ran them through gas chromatography–mass spectrometry to determine the nature of the substances in them. They found nine compounds previously unknown from the wasps or the cockroaches. In particular, the secretions contained a large percentage of two compounds, a kind of mellein called (R)-(-)-mellein, and micromolide, a natural product that may hold the key to treating drug-resistant tuberculosis. Both compounds showed broad-spectrum antibacterial activity, and the combination of the two was particularly effective.
As a final test, they extracted parasitized and unparasitized cockroaches and looked for these compounds. From the parasitized cockroaches, the same antimicrobial mixture could be extracted, but not from unparasitized ones. Thus, the scientists were confident that the wasp larvae produce and use these compounds to sterilize their food from the inside out.
“We found clear evidence that A. compressa larvae are capable of coping with antagonistic microbes inside their P. americana hosts by using a mixture of antimicrobials present in their oral secretion,” write the authors. While both compounds used by the larvae have been found in other animals, never before has the combination been discovered, in insects or otherwise.
The broad-spectrum nature of these antimicrobials may be key to the wasps’ success. “Food hygiene may be of vital importance, especially to the vulnerable early developmental stages of insects,” explain the authors. “The range of microbes that A. compressa larvae may encounter during their development in their hosts is unpredictable and may encompass all different kinds of microbes, such as various Gram-positive and Gram-negative bacteria, mycobacteria, viruses, yeasts, and ?lamentous fungi.” It would be vital, then, that the antimicrobial compounds produced by the wasps are able to fend off a wide variety of potential contaminants. “The secretion of a blend of antimicrobials with broad-spectrum activity seems to represent an essential frontline defense strategy.”
These beguiling wasps not only have mastered neurochemistry, they have aced microbiology to become proficient parasites. Already, this tiny wasp has given us great insights into brains through the study of its particularly effective zombification strategy. Now, it is shedding light on another field of science. This study is one of the first to suggest that larval parasites possess the ability to protect themselves against microbial pathogens, but the authors suspect many species of insects may have similar strategies. These small creatures may prove a vital new resource for natural products to fight against human diseases. Who knows what other pharmaceutical secrets are being kept by insects like the emerald cockroach wasp, and what ailments we might be able to treat with their chemical arsenal.
Citation: Herzner G., Schlecht A., Dollhofer V., Parzefall C., Harrar K., Kreuzer A., Pilsl L. & Ruther J. (2013). Larvae of the parasitoid wasp Ampulex compressa sanitize their host, the American cockroach, with a blend of antimicrobials. PNAS Early Edition, DOI: 10.1073/pnas.1213384110
We human beings are very attached to our brains. We’re proud of them – of their size and their complexity. We think our brains set us apart, make us special. We scare our children with tales of monsters that eat them, and obsessively study how they work, even when these efforts are often fruitless. So, of course, we are downright offended that a simple, single-celled organism can manipulate our favorite organ, influencing the way we think and act.
Toxoplasma gondii is arguably the most interesting parasite on the planet. In the guts of cats, this single-celled protozoan lives and breeds, producing egg-like cells which pass with the cats bowel movements. These find their way into other animals that come in contact with cat crap. Once in this new host, the parasite changes and migrates, eventually settling as cysts in various tissues including the host’s brain, where the real fun begins. Toxoplasma can only continue its life cycle and end up a happy adult in a cat’s gut if it can find its way into a cat’s gut, and the fastest way to a cat’s gut, of course, is to be eaten by a cat. Incredibly, the parasite has evolved to help ensure that this occurs. For example, Toxoplasma infection alters rat behavior with surgical precision, making them lose their fear of (and even become sexually aroused by!) the smell of cats by hijacking neurochemical pathways in the rat’s brain.
Of course, rats aren’t the only animals that Toxoplasma ends up in. Around 1/3 of people on Earth carry these parasites in their heads. Since Toxoplasma has no trouble affecting rats, whose brains are similar in many ways to our own, scientists wonder how much the parasite affects the big, complex brains we love so much. For over a decade, researchers have investigated how this single-celled creature affects the way we think, finding that indeed, Toxoplasma alters our behavior and may even play a role in cultural differences beween nations.
The idea that this tiny protozoan parasite can influence our minds is old news. Some of the greatest science writers of our time have waxed poetic about how it sneaks its way into our brains and affects our personalities. Overall, though, the side effects of infection are thought to be minor and relatively harmless. Recently, however, evidence has been mounting that suggests the psychological consequences of infection are much darker than we once thought.
In 2003, E. Fuller Torrey of the Stanley Medical Research Institute in Bethesda, Maryland his colleagues noted a link between Toxoplasma and schizophrenia – specifically, that women with high levels of the parasite were more likely to give birth to schizophrenics-to-be. The hypothesis given for this phenomenon is that while for most people who are infected, Toxoplasma has minor effects, for some, the changes are much more pronounced. The idea has gained traction – a later paper found, for example, that anti-psychotics worked just as well as parasite-killing drugs in restoring normal behaviors in infected rats, affirming the similarities between psychological disorders and Toxoplasma infection.
Continuing to work with mental patients, scientists later discovered a link between suicide and parasite infection. But, of course, this link was in people who already have mental illness. Similarly, a study found that countries with high Toxoplasma infection rates also had high suicide rates – but the connection between the two was weak, and there was no direct evidence that the women who committed suicide were infected.
What scientists really wanted to understand is whether Toxoplasma affects people with no prior disposition to psychological problems. They were in luck: in Denmark, serum antibody levels for Toxoplasma gondii were taken from the children of over 45,000 women as a part of a neonatal screening study to better understand how the parasite is transmitted from mother to child. Since children do not form their own antibodies until three months after birth, the antibody levels reflect the mother’s immune response. Thus the scientists were both able to passively screen women not only for infection status, but degree of infection, as high levels of antibodies are indicative of worse infections. They were then able to use the Danish Cause of Death Register, the Danish National Hospital Register and the Danish Psychiatric Central Research Register to investigate the correlation between infection and self-directed violence, including suicide.
The results were clear. Women with Toxoplasma infections were 54% more likely to attempt suicide – and twice as likely to succeed. In particular, these women were more likely to attempt violent suicides (using a knife or gun, for example, instead of overdosing on pills). But even more disturbing: suicide attempt risk was positively correlated with the level of infection. Those with the highest levels of antibodies were 91% more likely to attempt suicide than uninfected women. The connection between parasite and suicide held even for women who had no history of mental illness: among them, infected women were 56% more likely to commit self-directed violence.
While these results might seem frightening, they make sense when you think about how Toxoplasma is known to affect our personalities. In 2006, researchers linked Toxoplasma infection to neuroticism in both men and women. Neuroticism – as defined by psychology – is the “an enduring tendency to experience negative emotional states,” including depression, guilt and insecurity. The link between neuroticism and suicide is well established, thus if the parasite does make people more neurotic, it’s not surprising that it influences rates of self-violence.
How does a parasite affect how we think? The authors suggest that our immune system may actually be to blame. When we are infected with a parasite like Toxoplasma gondii, our immune system goes on the offensive, producing a group of molecules called cytokines that activate various immune cell types. The trouble is, recent research has connected high levels of cytokines to depression and violent suicide attempts. The exact mechanism by which cytokines cause depression and other mental illnesses is poorly understood, but we do know they are able to pass the blood-brain barrier and alter neurotransmitters like serotonin and dopamine in the brain.
But the authors caution that even with the evidence, correlation is not causation. “Is the suicide attempt a direct effect of the parasite on the function of the brain or an exaggerated immune response induced by the parasite affecting the brain? We do not know,” said Teodor T. Postolache, the senior author and an associate professor of psychiatry and director of the Mood and Anxiety Program at the University of Maryland School of Medicine, in a press release. “We can’t say with certainty that T. gondii caused the women to try to kill themselves.”
“In fact, we have not excluded reverse causality as there might be risk factors for suicidal behavior that also make people more susceptible to infection with T. gondii,” Postolache explained. But given the strong link between the two, there is real potential for therapeutic intervention. “If we can identify a causal relationship, we may be able to predict those at increased risk for attempting suicide and find ways to intervene and offer treatment.” The next step will be for scientists to affirm if and how these parasites cause negative thoughts. Not only could such research help target at-risk individuals, it may help scientists understand the dark neurological pathways that lead to depression and suicide that the sinister protozoan has tapped into. But even more disconcerting is that scientists predict that Toxoplasma prevalence is on the rise, both due to how we live and climate change. The increase and spread of this parasitic puppeteer cannot be good for the mental health of generations to come.
Citation: Pedersen, M.G., Mortensen, P.B., Norgaard-Pedersen, B. & Postolache, T.T.
Photos: Toxoplasma gondii parasites in rat ascitic fluid from the CDC’s Public Health Image Library; Brain MRI Scan in Patient with Toxoplasma Encephalitis from the University of Washington’s HIV Web Study
Rafflesia cantleyi, perhaps better known as the corpse flower for its pungent scent, steals everything from its host. Though each blossom can be in excess of three feet across, the massive buds cannot support themselves, and have no leaves, stalks or true roots. Instead, they rely entirely upon their vine host, Tetrastigma rafflesiae, for survival. Harvard researchers have now discovered that food and water aren’t the only things the corpse flowers steal – over the course of evolutionary history, Rafflesia has also stolen Tetrastigma‘s genes.
The corpse flower and its host have a very intimate relationship. From the start, Rafflesia burrows into the Tetrastigma‘s tissues, growing as thread-like strands in direct contact with the surrounding vine’s cells. They are so dependant on their host that the corpse flowers have even lost the ability to make chlorophyll, a requirement for photosynthesis, and thus defy the very nature of being a plant by being unable to produce food from sunlight. These parasites feed off their host vines, growing and growing until they finally erupt, dramatically if briefly, into large, rubbery flowers that stink like rotting flesh.
Somehow, after generations and generations of intimate contact between parasite and host, Rafflesia has ended up with more than the usual parasitic spoils. As a new study published today in BMC Genomics reveals, the parasite expresses dozens of genes that it has co-opted from its host.
The passage of genes from distant lineages, such as the corpse flower and its vine host, is known as horizontal gene transfer. Though common in bacteria (e.g. the transfer of antibiotic resistance), it is much rarer in plants and animals, and we still don’t fully understand how it occurs.
Scientists were first alerted that something was a little off with Rafflesia several years ago. At that time, they were looking at a much bigger picture – the overall evolution of parasitism in plants – when they noticed something a little odd in their data. For one of the genes, Rafflesia and similarly deeply-embedded parasites didn’t appear to be related to their closest kin, and instead, appeared to be cousins of their hosts. They hypothesized that such a strange evolutionary relationship could only have evolved in one way: if the parasites had stolen that gene.
Now, the Harvard team has sequenced all of the active genes of both the corpse flower and its host to determine how many genes were stolen. Researchers found that 49 of the proteins expressed by Rafflesia – 2% of its transcribed genome – are bootlegged.
“We found that several dozen actively transcribed genes likely originated from the flower’s host,” said Zhenxiang Xi, first author and a graduate student at Harvard University. They also found that most of these genes were incorporated into the parasites own DNA, even replacing similar genes, and another third of Rafflesia‘s own genes have evolved to look more like the vine’s.
The genes that were stolen perform a wide variety of cellular functions, including roles in respiration, metabolism, mitochondrial translation, and protein turnover. Their active expression suggests that they play a key role in the parasite’s survival, but the researchers hope that future research will determine exactly how important these genes are and whether they help the parasite evade detection by the host’s immune system. “These findings might reflect a sort of genomic camouflage, or genomic mimicry for the parasite,” says Charles Davis, co-author and head of the lab at Harvard. A bacterial pathogen of citrus trees, for example, produces a hijacked protein which limits the victim’s ability to detect and remove the intruder.
What’s truly remarkable about this study is that the rate of gene transfer between the vine and its parasitic corpse flower is as high as rates of lateral gene transfer seen in bacteria. Never before have scientists thought that horizontal gene transfer could play such a pivotal role in the evolution of plants and animals, let alone in parasite-host relationships. Given that parasites make up for an astounding 40% of the species on Earth, these findings are bound to transform our understanding of evolutionary processes and how we ended up with the diversity of life we see today.
Reference: Xi, Z. & et al, (2012). Horizontal transfer of expressed genes in a parasitic flowering plant, BMC Genomics, 13 DOI: 10.1186/1471-2164-13-227
Rafflesia Image provided by BMC Genomics
Weighing in at only 40 grams, brown mouse lemurs are one of the smallest species of primate in the world. Their diminutive size as well as their nocturnal, tree-dwelling lifestyle makes them difficult to track and observe. It would have been completely understandable if Sarah Zohdy, a graduate student at the University of Helsinki, had simply given up her quest to understand the social structure of these elusive creatures — but she didn’t. Instead, she and her colleagues came up with an ingenious way to study the interactions of these small lemurs: they followed their lice.
For as long as there have been mammals, there have been lice. Though it’s hard to find lice in the fossil record, scientists have estimated that the group originated at least 130 million years ago, feeding off feathered dinosaurs, though they now live on just about all species of birds and mammals. Lice tend to be very host-specific, meaning they only live and feed on one species or a set of closely related species. Furthermore, lice can only survive a limited time without their hosts, and must quickly find a new one if they leave or are forcibly removed. This means that for lice to reproduce and spread, their hosts have to be in fairly close contact (like, as many parents know, kids in a kindergarden classroom). In wild species, lice rarely switch hosts unless the animals interact physically, whether through wrestling, nesting together or mating.
It was that requirement for close contact that made Zohdy and her colleagues think they might be an ideal proxy for investigating social interactions that can’t be viewed directly. They had already been collecting data on the mouse lemur populations in Madagascar using traps to monitor their movement. But while the researchers knew certain lemurs spent a lot of time together if they were caught together in traps, the researchers figured they were probably missing a good amount of social interaction. So, they decided to follow the lemur’s lice as well.
Mouse lemurs are parasitized by a particular species of louse, Lemurpediculus verruculosus, which feed off the lemurs’ blood. The researchers were able to track the transfer of these lice between lemurs by tagging lice with a unique color code using nail polish, so they could tell what lemur each louse started on. Over time, they continued to trap lemurs and look at their lice to see if any of the tagged ones had switched hosts.
In total, they tracked 76 transfers between 14 animals — all males — over the course of a month, which happened to be during the breeding season. The researchers hypothesized that the male-only transfers likely occurred during fights over females. But perhaps more interestingly, the lice data only supported 8 of the 28 expected social interactions predicted by trapping data, and found 13 new ones, suggesting the louse marking technique was able to uncover lemur social activity that the researchers have never observed. They also found that some animals shared more lice than others. Sarah Zohdy explained, “The youngest male in the study had the worst louse infestation, but only donated one louse, indicating a low number of interactions, while the eldest male, who also had a heavy infestation, appeared to be more sociable, collecting lice from many donors. Other males appeared to be ‘superspreaders’ donating but not collecting lice.”
The lice also revealed that lemurs travel more than the researchers had thought. “Most of the louse transfers occurred between lemurs over 100 m from each other, and one transfer spanned over 600 m,” the authors write. “The transfers therefore demonstrate a degree of lemur ranging far greater than anticipated.”
Overall, these data provide new insights into the social interaction of mouse lemurs as well as the relationship between the lice and their hosts. This isn’t the first study that used lice to look at a bigger scientific picture. Because of their host-specific nature, scientists have used them to map ancient speciation events, and even determine when humans first wore clothes. But never before have lice been used to study behavior in a living wild species, though the team hopes their study shows the usefulness of this technique. “The approach developed here has potential for application in any species parasitized by sucking lice, including the many trappable species of cryptic, nocturnal, subterraneous or otherwise elusive mammals in which host social contact and parasite exchange data are difficult to obtain.”
Reference: Zohdy S., Kemp A.D., Durden L.A., Wright P.C. & Jernvall J. (2012). Mapping the social network: tracking lice in a wild primate (Microcebus rufus) population to infer social contacts and vector potential., BMC ecology, PMID: 22449178
153 years ago on November 24th a naturalist named Charles Darwin published a book with a rather long and cumbersome title. It was called On the Origin of Species by Means of Natural Selection, or the Preservation of Favoured Races in the Struggle for Life (for its sixth edition in 1872, the title was cut short to simply The Origin of Species, which was found to be much more manageable to say in conversation). It was inspired by an almost five year journey around the world on a ship named for a small, floppy eared canine during which Darwin did his best to catalog and understand geology and the diversity of life he found.
It’s incomprehensible, now, to think of someone writing a single volume that could equally change science as we know it. The two simple ideas that Darwin fleshed out in his first publication were earth shattering at the time. He has since been called both a genius and a heretic for these two theories – both titles equally deserved. But whatever you call him, his vision has changed the world irrevocably. Today, on what would have been his 203 birthday, we celebrate the life and scientific contributions of this man. In honor of the occasion, I am reposting my first Darwin Day post ever, from way back in 2009. Enjoy!
If I ask you what group of organisms is an exhibition of evolution at its finest, what would you say? Most people, I think, would say human beings, or at least apex predators. After all, we have staggering intellect compared to our prey items and clearly dominate the planet, eat what we will, etc. Not only that, we’re insanely complex. Ask some scientists, and they might give you any number of answers. Cockroaches are likely to exist long after we do, as are rodents, so maybe they get the title. Or, being scientists, they might be biased to whatever organism they study. Maybe algae and plants, as the sustenance for all other life. But all of you, in my humble opinion, are wrong. That is, unless you choose parasites.
It’s ok if you don’t believe me yet. Darwin wouldn’t have, either. He and his contemporaries viewed parasites as degenerates who, at best, violated the progressive nature of evolution. Even in The Origin of Species, Darwin refers to parasites as regressive instead of progressive. But truly, no group of species is a better choice for evolution’s finest.
Soybean Nematode and Egg
First off, let’s talk numbers. Parasitism is the most popular lifestyle on earth – over 40% of all known species are parasitic, and the number of parasitic species rises daily1. Sure, you might say, but they tend to be small. In that case, let’s talk biomass – weight, just to be clear. One group of parasites, the flukes, have been found to be equal in weight to fish in estuarine habitats, and three to nine times the weight of the top predators, the birds – estimates which are thought to be conservative for the earth as a whole2. Though they’re largely ignored when we study food webs, they’ve been estimated to be involved in over 75% of inter-species interactions1. Clearly, by the numbers, they are the most prolific and successful organisms on earth.
But even that is not why I would argue they are evolution’s finest. They, more than any other group out there, both exhibit extreme evolutionary adaptations and spur them onward in other species.
No matter how complex or how impressive any other species may be, it has parasites. We do – lots, actually. Every species we might hold as a masterpiece of evolutionary complexity cannot out maneuver their parasites. Not one. Even parasites, marvelous as some are, have parasites – like a crazy russian doll. They have evolved amazing abilities to survive host defense systems, manipulate host behavior and boost heir own reproductive success. They’ve even been implicated in major cultural differences in people. It turns out that a rat parasite, Toxoplasma gondii, needs to be eaten by a cat to complete its lifestyle. Somehow it developed a trick to make rats unafraid of cat smells. When it accidentally ends up in people, it does the same kind of mind-altering, making people more guilty and insecure, even more frugal, mild-tempered, and complacent3. Other parasites do far more intricate manipulations of behavior, turning males into females, creating walking zombies, even forcing suicide. If parasites can not only break into and survive the most complex assortments of systems available, even with modern medicine fighting against them, and manipulate those complex organisms to slave to their bidding, how can we not credit them as masters at what they do?
left: Malaria and red blood cells.
© National Geographic
But even more impressively, I would argue, is that no other group has so dramatically impacted how other species have evolved. They don’t just affect their hosts immune systems, either. If you read much into evolutionary theory, you realize it’s riddled with parasites. Why are some birds very colorful? Oh, because if they’ve got a lot of parasites they can’t be, so it’s a signal of a healthy male4. Why are we attracted to certain people? Because their immune genes are different from ours, giving our children the best chance to fight off the next generation of parasites. Almost everywhere you look, evolutionary changes are spurred on by parasites. It’s even suggested that sex itself evolved as a response to parasites. It’s a way of better shuffling our genes so that we have better odds at fighting off parasites.
Even we, as “ideal” or “complex” as we are, owe much to parasites. Some even argue that we are worse off without them. The argument, as it goes, is that our immune system evolved in the presence of unkillable parasites, particularly the parasitic worms. These worms, or Helminths as they are called as a group, were too costly to try and eradicate. Attacking foreign invaders, after all, is energetically expensive, and always runs the risk of over-activating our immune system, leading to self-inflicted injuries and diseases. So the best strategy, instead, was to have an immune system that functioned optimally against other issues, like the fatal viruses or bacteria, despite the mostly benign worm infections5. Since worms secrete anti-inflammatory compounds to fight off our defenses, we were better off with systems that overcompensated for that. Now, since we have drugs which kill them off, our immune system is out of balance. Many cite the rising rates of auto-immune and inflammatory diseases like allergies, arthritis, irritable bowel, type 1 diabetes, and even cancer in developed nations as evidence that ridding ourselves of helminths has damaged our health6. They’re backed up with multiple studies that show unexpected results, like that mice genetically predisposed to diabetes never develop it if infected with flukes at an early enough age.7
Parasites are uniquely capable of out-evolving their hosts and adapting to whatever changes go on in them. Simply put, they evolve better. They change their genes faster and keep up with a barrage of host defense systems, often like it’s effortless, spurring onward dramatic changes in other species. If Darwin had only known how amazingly complex the barriers these creatures have to overcome and the extent to which they have affected the species he’d encountered on his travels, he would not have labeled them “degenerates”.
As far as evolution is concerned, no group of species demonstrates it, causes it, and is so capable of it as the parasites. While disgusting or even cruel, they are truly evolutionary masterpieces. So while you may find them vile or detestable, you have to admit they’re good at it. Can you really argue that some other group is more deserving of the title of Evolution’s Finest?Cited:
1. A. Dobson, K. D. Lafferty, A. M. Kuris, R. F. Hechinger, W. Jetz (2008). Colloquium Paper: Homage to Linnaeus: How many parasites? How many hosts? Proceedings of the National Academy of Sciences, 105 (Supplement_1), 11482-11489 DOI: 10.1073/pnas.0803232105
2. Armand M. Kuris, Ryan F. Hechinger, Jenny C. Shaw, Kathleen L. Whitney, Leopoldina Aguirre-Macedo, Charlie A. Boch, Andrew P. Dobson, Eleca J. Dunham, Brian L. Fredensborg, Todd C. Huspeni, Julio Lorda, Luzviminda Mababa, Frank T. Mancini, Adrienne B. Mora, Maria Pickering, Nadia L. Talhouk, Mark E. Torchin, Kevin D. Lafferty (2008). Ecosystem energetic implications of parasite and free-living biomass in three estuaries Nature, 454 (7203), 515-518 DOI: 10.1038/nature06970
3. Kevin D. Lafferty (2006). Can the common brain parasite, Toxoplasma gondii, influence human culture? Proceedings of the Royal Society B: Biological Sciences, 273 (1602), 2749-2755 DOI: 10.1098/rspb.2006.3641
4. Jesús Martínez-Padilla, François Mougeot, Lorenzo Pérez-Rodríguez, Gary R. Bortolotti (2007). Nematode parasites reduce carotenoid-based signalling in male red grouse Biology Letters, 3 (2), 161-164 DOI: 10.1098/rsbl.2006.0593
5. Joseph A. Jackson, Ida M. Friberg, Susan Little, Janette E. Bradley (2009). Review series on helminths, immune modulation and the hygiene hypothesis: Immunity against helminths and immunological phenomena in modern human populations: coevolutionary legacies? Immunology, 126 (1), 18-27 DOI: 10.1111/j.1365-2567.2008.03010.x
6. Joel V. Weinstock, David E. Elliott (2009). Helminths and the IBD hygiene hypothesis Inflammatory Bowel Diseases, 15 (1), 128-133 DOI: 10.1002/ibd.20633
7. Anne Cooke (2009). Review series on helminths, immune modulation and the hygiene hypothesis: How might infection modulate the onset of type 1 diabetes? Immunology, 126 (1), 12-17 DOI: 10.1111/j.1365-2567.2008.03009.x
“The purpose of man’s life…is to become an abject zombie who serves a purpose he does not know, for reasons he is not to question.” – Ayn Rand
Of all the cryptic, creepy and cruel creatures that emerge each Halloween, few captivate our imaginations like the living dead. Sure, they look dreadful, smell bad, and have the conversational skills of a well-adjusted slug, but despite their bad manners and constant lust for our brains, zombies have clawed their way into our hearts. It just wouldn’t be Halloween without them.
Like any good monster, the legend of the zombie is based in truth. According to Voodoo traditions, powerful spiritual men called Bokors have the power to kill a man and then raise him from the dead, turning him into a zombi, a mindless slave to the Bokor who created him. As outsiders began to look into the myths, they discovered that these sinister sorcerers use a chemical cocktail, including the deadly poison tetrodotoxin, to mimic the physiological signs of death. This zombi juice doesn’t just slow the victim’s heart rate – the toxic mix has lasting effects on the human brain including memory loss and delirium, making them ideal slaves. Once the target is declared dead and buried, the Bokor can dig up the grave and claim his zombi.
While Bokors have been tinkering with brain chemistry to make the perfect zombie for hundreds of years, there are others that have been perfecting the art of zombification for much longer. Parasites are the Victor Frankensteins of the natural world. These mini-neuroscientists turn other creatures into mindless slaves, serving only to further the master’s selfish goals. They do that voodoo better than we do, and they have for eons.
In all of the cases I’m about to present, once the host is infected, they are the living dead. They have no hope of recovery, no chance for redemption. They will perform their acts as needed by their parasitic Bokor, and only once their bodies have served their function will the zombie be released into the sweet arms of eternity.
The zombie, it stings
While they might lack the lust for brains, parasitic wasps are the masters of neurological zombification. The emerald cockroach wasp, for example, turns its cockroach host into an ill-fated nanny. With carefully placed stings which inject a venom cocktail into the roach’s brain, the wasp puts the roach into a zombie-like state where it happily follows its attacker to a dark chamber underground. The wasp then lays her eggs in the complacent roach and seals it in its tomb. Soon enough, the eggs hatch, eat, pupate, and emerge while the cockroach sits and waits for its body to be consumed.
But perhaps it is the parasitic wasp Cotesia glomerata that most deserves the title of master. Females lay their eggs in unsuspecting caterpillars. When the larvae hatch, they literally eat their host from the inside out. But even more incredible is the caterpillar’s reaction to such usury: the hapless host transforms into an undead bodyguard, protecting the young wasps even after they have gorged themselves on the caterpillar’s internal organs. The mostly-eaten victim will even spin a silk web over the pupated wasps which just feasted on its flesh, a final act of devotion to its Bokors, before it dies. What chemical spell the larvae cast on their host to instill such loyalty remains a mystery.
Fly me to the grave
They might look like fruit flies, but Phorid flies are more than just a harmless pest – at least to the ants which serve as host for the fly’s larvae. Phorid flies are the ideal Hollywood zombie parasite, complete with a hunger for neurological tissue. Gruesome as they might be, you gotta give the flies points for style.
Phorid fly larvae hatching from an
ant's head, from National Geographic
First, the momma fly injects her eggs into the body cavity of the ant host. Once they hatch, the larvae make their way to the ant’s head, where they feed on hemolymph (ant blood), muscle, and nervous tissue (aka brraaaaaiiiiiinnnnssss). The larval flies will spend weeks inside the head of their host, controlling its behavior while snacking on its brains until they have completely emptied the ant’s head. The ant, meanwhile, wanders around in a zombie-like state. When the young fly decides it is ready to pupate, it releases an enzyme which decapitates the ant by dissolving the membrane which attaches its head to its body. The larva pupates in the ant’s disembodied head for about two more weeks, then emerges as a full-grown adult, ready to mate and find its own zombie host.
Other flies turn wasps into murderous zombie queens. Xenos vesparum larvae wait patiently until a wasp lands close by. When it senses its victim, the larva leaps onto the wasp and burrows through its exoskeleton into its abdomen, and begins feasting on the wasp’s blood. As it grows, the larva starts to mess with the wasp’s mind. The normally social wasp withdraws from its colony, and starts to act recklessly. Then, in early summer, the infected wasp just leaves its colony behind, and as if under some spell, travels to a meeting place. Soon, other parasitized wasps arrive, and the parasites begin to mate. The male flies emerge from the wasps and seek out the females which remain in their zombie hosts, granting the men access to the only part needed for reproduction.
The wasps which were lucky enough to be infected by male flies die. Those infected with females, though, are still under the control of their parasites. They begin to act like wasp queens, gathering food and gaining weight. They then travel to sites where queens gather in the fall, and spend the winter in the lap of luxury among other wasp royalty. When the seasons change and the wasps emerge, the zombie queens go back to their colonies, carrying their deadly load of fly larvae. Everywhere they travel, larvae are left behind, waiting for the next unsuspecting wasp to land.
Rosemary’s baby barnacle
Most parasites are really, really small. But not all zombifying parasites are itsy-bitsy. Take, for example, the Rhizocephalans – the parasitic barnacles.
Yes, I did just say parasitic barnacle, although they don’t look much like barnacles as adults. The adult parasites look like a sac where a female crab would have eggs. It’s classified as a barnacle, however, due to its larval forms, specifically the cypris larvae, which neatly place it in the class Cirripedia.
The barnacle’s strategy is simple: find a crab. Stop her from shedding so she can’t get rid of you. Tap into her nervous and circulatory systems and get comfortable. Grow. Sterilize her, so nothing competes for your living space. As you get too big to fit inside, pretend to be an egg sac. Have her bathe you in water, take gentle care of you, and feed you nutrients because she thinks she’s pregnant. She’ll even help you spread your larvae like they’re her own eggs by fanning them into the water.
However, there is an obvious problem. Not every crab is female, and thus predisposed to tending its eggs. So what does the parasite do when it accidentally infects a male crab instead? Well, it’s simple, really. It makes it act like a woman.
That’s right – the parasite turns male crabs into transvestites.
By altering hormones in the male crab’s neurophysiology, it causes the male crab to act like a female one. Its abdomen flattens and widens, and it starts taking on the behavioral traits of a pregnant female. The male goes through the same process of nurturing and caring for its wee little parasite babies that the female would. The big boy will continue to love, adore and feed its little parasitic baby until he dies, just like a girl crab would.
Swimming with the fishes
Spinochordodes tellinii, also known as a hairworm, are free-living aquatic organisms as adults, who, as nematodes, eek out an existence in the mud. Their young, though, thrive on the flesh of crickets. Problem is, crickets don’t always hang around wet places, and if the nematode were to leave its host when it’s somewhere high and dry, it would die. What better way to ensure that it ends up where it wants to be than to drive the unwitting cricket host to suicide by drowning?
How exactly the worm control the cricket’s brain is unknown, but theories suggest that the parasite has developed a way to mimic natural chemical signals in the bug’s brain. Analysis of the compounds of infested brains reveals heightened levels of neurotransmitters and chemicals responsible for movement and orientation, particularly with relation to gravity. These proteins are similar to the ones produced by the insect, but are not naturally occurring, suggesting that the parasite is able to produce and excrete its own chemical signals to screw with the cricket’s mind. The end result of which, much to the parasite’s joy, is that the cricket seeks out water and hops right in. More often than not, the act is fatal – crickets are terrible swimmers, and most who leap into the cool depths drown. This assisted suicide gives the parasite the chance to break free and wiggle its way easily down to the mud, where it continues its life cycle.
More than a fluke
Trematodes, or flukes, are known for their complex life cycles which involve multiple hosts. Often, switching from host to host is facilitated by predatory interactions. Dicroelium dentriticum, a trematode which lives in the livers of sheep, is no exception. The trouble is, its intermediate host is an ant, and sheep aren’t generally known for their hunger for ants. So how does a parasitic fluke get from an ant to a sheep?
Well, actually, it starts with a snail. The snail accidentally eats the fluke’s eggs while going along its merry snail way, and the parasite hatches and develops in the snail’s gonads. Eventually, the fluke is excreted in the snail’s slime, which is conveniently eaten by an ant. This is where things get weird. Once infected, the ant continues about its business as normal – for the most part. By day the ant acts like an ant. But as the sun goes down, the parasite takes over. Every night, the zombie ant will leave its colony behind and search for a blade of grass. When it finds one, it climbs to the top, bites down, and waits until sunrise. Night after night, the ant will dutifully wait atop its blade until it gets accidentally eaten by a grazing sheep, thus completing its enslaver’s life cycle.
Who said zombies aren’t fungis?
Even microscopic fungi get in on the zombifying trend. The fungus Ophiocordyceps unilateralis is yet another zombifying parasite targeting ants (they really get the short end of the zombie stick). It’s all well and good to target ants, but a bit of a dilemma for the fungus arose from its choice of host: the fungus needs the perfect combination of light, humidity and temperature to survive, and those conditions don’t exist on the ground. Ants generally live on the ground, and thus shouldn’t be good housing for Ophiocordyceps. Not to worry, though – the fungus has engineered a mind-altering solution.
Ants infected with Ophiocordyceps unilateralis find themselves compelled to amble far from their homes, climb trees or sprouts, and end up on the bottom side of a leaf where they clamp down their jaws and wait while the fungus eats them from the inside out. What’s incredible is the precision with which these zombied ants choose their final resting place: they all choose to die on the vein on the bottom of a north-facing leaf approximately 25 cm above the ground in an area with 94 to 95 percent humidity and between 20 and 30 degrees Celsius – perfect conditions for the fungus to grow. After a few weeks, spores fall from the now fully eaten corpse to infect other ants and continue the fungus’ life cycle.