Pasteuria ramosa

Parasitic infections can severely debilitate the host in many ways, sometimes this manifests itself as the loss of some, or even all, of the host's reproductive ability. Evolutionary speaking, an organism that cannot reproduce is as good as dead. However, it's not entirely clear who (if anyone) is benefiting from this outcome - is it; (1) a survival strategy by the host to temporarily free up resources to compensate for the parasite's presence? Or is it (2) an adaptive strategy by the parasites to divert as many resources as possible to themselves without compromising the host's ability for self-maintenance and survival? Or is it (3) merely an unintended side-effect of infection? Of course, (1) and (2) are not mutually exclusive, and in the case of (3), even if it had started out as an unintended side-effect of infection, if host castration resulted in higher reproductive fitness for the parasite, then that trait will be positively selected for and become part of the its repertoire of host-exploitation strategies.

Waterfleas (Daphnia) are infected by all manner of parasites (we featured one of them during the early days of the blog: Caullerya mesnili) ; most of them are pretty nasty - they often end up castrating and/or killing the host. Pasteuria ramosa is no different - it is a spore-forming bacterium that infects waterfleas, makes them bloated, darkening their body (see the right waterflea in the photo) and castrates them in the process. While it was previously thought that any waterfleas infected by P. ramosa were permanently castrated, it turns out that some lucky Daphnia can actually recover from their infection.

So do these little crustaceans adjust their reproductive output in response to the parasites and is castration a way for them to compensate for a (potentially) temporary hiccup in their baby-making ability? To find out, a team of scientists from Norway set out to see just who benefits the most from host castration. Their logic is that if it is an adaptive strategy by the parasite, then we should see higher spore output from a permanently castrated host. Whereas, if castration is an adaptive coping mechanism by the waterflea, then there should be a jump in reproduction upon the onset of infection as the waterflea tries to make as many baby Daphnia as possible before P. ramosa put a stop to it, then store up reserves during the infection to "wait it out".

To correct for any potential sex differences (there are many documented case of sex-bias in parasitism), these scientists used only female waterfleas for the experiment. During the course of the study, about half the waterfleas they infected with P. ramosa managed to regain their reproductive capacity. In those lucky ones, the parasite produced many fewer spores than in waterfleas that had been permanently castrated. So evidently, P. ramosa benefits from having permanently castrated hosts. But what about the waterfleas themselves? Were they able to compensate by adjusting their reproductive output in the parasite's presence?

The scientists found that by far, the strongest predictor for the lifetime reproductive output of a parasitised waterflea is the age at which it becomes infected - the later that it became infected, the more time it had to churn out babies before it came down with a severe case of P. ramosa. So it's pretty much a case of "use it or lose it". They did not find evidence to suggest the waterfleas made any effort to increase their reproductive output before they are castrated by their parasites. This is unlike other systems where parasite-castration occurs. In trematode-snail systems, the infected snails are less likely to recover from their infection. The strategy which has evolved among snails in areas with high parasite prevalence is to reach sexual maturity as quickly as possible (For example: see this study) so they can eke as many baby snails as they can before they inevitably become infected and be taken over by squirming body snatchers.

It should be noted that the waterfleas used in the experiment were from Southern Finland, whereas the parasites were isolated from a pond in Northern Germany. So perhaps the reproductive strategy of the Daphnia population used in that experiment has evolved in response to their local parasite(s) population instead. Other studies have found waterfleas to be locked in a close evolutionary race with their parasites across space and time, so the outcome of any host-parasite interaction will be dependent on the genetic identity of both host and parasite.

Image credit: Jensen et al./PLoS Biology

Reference:
Magerøy, J.H., Grepperud, E.J. and Jensen, K.H. (2011) Who benefits from reduced reproduction in parasitized hosts? An experimental test using the Pasteuria ramosa-Daphnia magna system. Parasitology 138: 1910-1915

Spauligodon atlanticus

Today, we look at a paper showing how data from DNA sequences can help resolve the evolutionary relationship of different parasite species, and even find new species where we least expected it. Traditionally, parasites - like other organisms - are classified based on key characteristics of their anatomy. However, many parasites have simplified morphology (an extreme example is the parasitic snail which has evolved into nothing but a bag of genitalia) and often the few key characters that can be examined are heavily reduced. Therefore, any conclusions about relationships between different parasite species that are based upon anatomical characteristics can lead to misleading or, at best, incomplete conclusions.

Spauligodon atlanticus is a species of nematode that parasitises Gallotia, a genus of lizards living on the Canary Islands (see image). Spauligodon atlanticus was initially described in 1987 using traditional methods, i.e. based solely on its anatomical features. In the case of parasitic nematodes, the key characteristic for distinguishing different species is the shape of the genitalia and tail appendages of the male specimen (such features are too indistinct in the females across different species).

For this particular study, a group of biologist from Portugal and Spain went to the Canary Islands to collect S. atlanticus from Gallotia lizards, as well as sampling for other species of Spauligodon from lizards of southern Spain, Morocco, and Armenia. They compared the DNA sequences of the worms and found that nematodes that had been identified as S. atlanticus (based on their anatomy) actually consisted of two distinct species. While they looked the same, their molecular signature revealed two separate lineages; an eastern lineage that is specific to the lizard species Gallotia atlanticus, and the western lineage that is found in 4 different Gallotia species. They also differ in their evolutionary relationships with other nematodes in the Spauligodon genus. The eastern lineage is more closely related to nematodes in wall lizards (Podacris spp.) from southern Spain and Morocco while the western lineage is more related to worms in green lizards (Lacerta spp.) from Armenia.

These two genetically separate lineages of S. atlanticus are what are known as a cryptic species complex (something that we have previously covered on this blog). Recent studies in the last ten years have shown that some parasite species which had previously been thought to be a single generalist species infecting multiple hosts, are in fact composed of multiple specialised species in disguise.

Meanwhile, this study raises another question - how did these two genetically separate lineages, living in different lizards, evolve such similar anatomical characteristics? The authors of the paper raised the possibility that the anatomy of the two lineages had evolved to convergence due to similar conditions they encounter inside the gut of their respective lizard hosts, or that even sexual selection was responsible, since the key anatomical difference use to distinguish these nematode species is the shape of the male genitalia. But this is a question that will only be resolved with further analyses of related Spauligodon species. As the authors wrote in the title of their paper, there are "no simple answers".

Image from the Wikipedia.

Reference:
Jorge, F., Roca, V., Perera, A., Harris, D.J. and Carretero, A. (2011) A phylogenetic assessment of the colonisation patterns in Spauligodon atlanticus Astasio-Arbiza et al., 1987 (Nematoda: Oxyurida: Pharyngodonidae), a parasite of lizards of the genus Gallotia Boulenger: no simple answer. Systematic Parasitology 80:53-66

Apocephalus borealis

Many of you have heard of the very scary phenomenon called "Colony Collapse Disorder" - and if you haven't, you should, because it could be a major threat to the food we eat. CCD is when the worker honey bees abandon their hives and die, which, if widespread, can mean drastic decreases in pollination of crops. This phenomenon was first reported in the U.S. in 2006 and ever since that time, scientists have struggled to uncover what was responsible. Everything from cell phone radiation to genetically modified crops to a variety of parasites of honey bees were suggested to be the cause. Then, today, a new paper in PLoS One showed data suggesting that another kind of parasite is linked to CCD. Apocephalus borealis is a parasitoid fly that was known to attack bumblebees and paper wasps, but now has been demonstrated to also attack honeybees in the U.S. - in fact, 77% of the colonies sampled near San Francisco were parasitized by A. borealis. The authors used DNA barcoding to confirm that the flies in the honey bees were genetically indistinguishable from those parasitizing bumble bees.

The authors of the new study also found that bees that were found flying around at night (something honey bees don't normally do) were significantly more likely to be parasitized by the fly and furthermore, the sick bees also seemed disoriented. It is not currently known whether or not the tendency for the parasitized bees to fly at night away from their colonies is another example of manipulation of the host by a parasite or whether this might be an act of altruism by the bee, carrying its parasite away from its colony and thus protecting the others.

Although these new results are very exciting, many questions remain to be answered about the history and impact of A. borealis. First, when did the switch into honey bees occur? Honey bees are not native to the U.S., but since they are so well monitored and studied, the authors believe that the switch must have happened recently - otherwise it would have been noticed by apiculturists. Second, could these flies also be serving as vectors for other bee pathogens? Two known bee pathogens, Deformed Wing Virus and Nosema ceranae, a microsporidian were found in the A. borealis flies. And finally, could the invasion of honey bees by this parasite mean that CCD is going to increase? The natural hosts of A. borealis are bumble bees, which live in small colonies where only the queen herself survives the winter, but honey bee colonies have thousands of bees and their activity maintains some amount of heat, even in colder winter months. This increase in host resources and more generations per year could spell a population explosion of A. borealis...and that won't be good for those of us who depend on pollination - like all of us.

The image is from the paper. Look closely at the abdomen of the bee - that's a little parasitic fly laying eggs into it. Soon the larvae will emerge from the dead host. (You can see a photo of this in the original paper as well.)

Source: Core A, Runckel C, Ivers J, Quock C, Siapno T, et al. (2012) A New Threat to Honey Bees, the Parasitic Phorid Fly Apocephalus borealis. PLoS ONE 7(1): e29639. doi:10.1371/journal.pone.0029639.

Chipping away at the tip of the iceberg

Through out 2011, we have been featuring more weird and wonderful parasites as we have done in 2010, but on top of that we have also been featuring some of the latest pieces of research being published on all manners of parasitic and infectious organisms which may not have been covered elsewhere in the blogosphere.

Just this year we saw a molecular study that revealed the transmission pathway of a great white shark tapeworm via dolphin blubber, a koala blood parasite named after Steve Irwin, a nematode which infiltrate pine trees via borrowed genes from fungi, a parasitic plant which disperse its seeds via beetles, and a little digenean fluke which changed the face of an entire mudflat, just to name a handful out of dozens that we have featured.

So in 2011, we have gone beyond merely showing you the parasites, but also told you about the research which are being conducted behind the scene to work out how they live. At the same time, you also got a bit of insight into the scientific process, and how knowledge accumulate and grow over time.

In 2012, we will continue to bring you new and exciting research on parasites and parasitism - publications which we found interesting but might not have received their share of fanfare and press releases (as I type this up, I have at least another 4 paper waiting in line to write up. And no doubt I'll find another 4 to write about by the time I'm done with those).

Of course, research on a particular host-parasite system does not simply enter suspended animation after a single study has been published. For many lab groups, the parasite we have featured on this blog form the basis of their scientific research, and the newly published paper we have chosen to feature here merely represents a thin cross-section of their ongoing research program. So in 2012 we might also be revisiting some of the parasites that we have previously featured on the blog, and fill you in on the latest updates as they hit the press.

Of course, you can now also find us on other forms of social media where we will be posting about updates to the blog. Susan is on Twitter , and you can find myself on Google Plus.

Here's to another year of parasitism - the most common way of life on this planet!

Hematodinium sp.

Today's parasite, Hematodinium sp., infects blue crabs and causes a disease known as "bitter crab". While the name may sound just slightly nauseating for your palate, for the afflicted crabs, its symptom is down right horrific. The parasite causes the crab's hepatopancreas (equivalent of our liver and pancreas) to malfunction, it starts suffocating, and its muscles eventually dissolve within its exoskeleton. Crabs that are experimentally infected start dying about 2 weeks after initial exposure, and this deadly parasite may have even contributed to the recent decline of blue crabs in Chesapeake Bay.

Hematodinium and related species are dinoflagellates, and while most dinoflagellate are free-living, this species belongs to a group which have evolved to be parasites, with many different species infecting a wide variety of hosts. While several different stages of the parasite have been isolated from the blood of infected crabs, little is known about how they are transmitted between hosts, nor the inner life of those different stages in the hosts. Because many parasites live enclosed within the body of their hosts, it is almost impossible to directly observe how they live and grow the way you might be able to observe a fish or a bird. Ideally, if you can isolate a parasite out of its host, put in it a clear container which closely mimics the conditions found within its host, and still have it complete its life-cycle, then you can find out a lot more about how it lives.

Recently, a group of researchers from Virginia were able to successfully complete the life-cycle of Hematodinium - in vitro - which means they were able to grow it in a culture of chemical broth that sustained the parasite's every need, without any host animals involved. This was accomplished through a painstaking series of transfers, starting with isolating the parasite from infected crabs, then moving each stage into different culture mixes as it grew, all while keeping the conditions as sterile as possible. Out of the 10 isolates they attempted to grow, only 4 successfully completed their life-cycle in vitro. The researchers also found out that the parasite grows best in the dark, and indeed light exposure kills them within weeks, which makes sense given that it is pretty dark inside a crab (a variation on the Marx Brother joke).

Through this in vitro technique, they were able observe the different parasitic stages of Hematodinium directly, and view them as they would have been while floating in the blood and organs of a blue crab. They noted that when Hematodinium cells first enter the crab as "dinospores," they turn into a worm-shaped form called a "filamentous trophont" (see the accompanying photo which was from a figure in the paper). About a month after that, the cells begin transforming into clumps that are composed of multiple clones of the original infection stage. These clumps then grow into a stage called an "arachnoid trophont," which resembles a blob with numerous tendrils around its fringe (which would be embedded in the hepatopancreas of the crab). These clumps tend to merge and form larger blobs as they come into contact with each other. When those "arachnoid trophonts" fully develop, the cells in the middle of the blob start producing spores that eventually turn into the infective dinospores that escape from the crab to infect new hosts, starting the life-cycle anew.

Reference:
Li, C., Miller, T.L., Small, H.J. and Shields, J.D. (2011) In vitro culture and developmental cycle of the parasitic dinoflagellate Hematodinium sp. from the blue crab Callinectes sapidus. Parasitology 138:1924-1934.

Postscript: Three days after this post went up, I was contacted by Peter Coffey, who used to work on this species of parasite with a bit of additional information/correction: I just have one quick comment on the first sentence in your post. In blue crabs we don't see the same bitter flavor that we do in Alaskan Tanner and Snow Crabs, so we haven't been calling infections in blue crabs BCD.
Thanks Peter!

Lepeophtheirus acutus

Today, we are featuring a paper which reported on a grey reef shark (Carcharhinus amblyrhynchos) at Burger's Zoo in the Netherlands that had to be euthanized. "Wait a sec!" you think, "Isn't this supposed to be a blog about parasites? I didn't come here for dead sharks!" Well, just calm down before you close your browser tab in outrage. This particular shark actually succumbed due to a heavy infection of today's parasite - Lepeophtheirus acutus. This parasite is in the same genus as other fish lice that we have previously featured on this blog, but very little is known about this particular species. Prior to this incident, it has only been reported once from the wild, and it was found on the back of a ribbon-tailed stingray (Taeniura lymma), not a shark and certainly nothing was known about how harmful it can be to its host.

From what the staff at the aquarium could work out, this deadly little crustacean was introduced to the facility by an infected male zebra shark (Stegostoma fasciatum) collected off Cairns, Australia on the Great Barrier Reef, which appeared perfectly healthy at the time and passed quarantine. However, about 2 weeks after he was introduced into the aquaria with the other fishes, he started acting weird. At the same time, the grey reef shark mentioned at the start of this post became lethargic and ceased to eat regularly, and about a month after that, both sharks were afflicted with swollen and opaque eyes. Despite the best efforts of the staff to put the infected sharks in quarantine, filter the water with activated carbon, and give them anti-parasite drugs, they were unable to save the grey reef shark, by which time it was swimming with its mouth wide open, not eating at all, and its eyes had deteriorated even further, so the decision was made to euthanize the long-suffering shark.

A necropsy revealed the identity of the killer - a parasitic copepod - most of which were found around the shark's eyes which caused them to become swollen and covered in mucus, and the mouth which led to bleeding gums. The parasite was also found on a female zebra shark and a shovelnose ray (Glaucostegus typus) which shared the aquaria with the deceased grey reef shark. Notably, the blacktip reef shark (Carcharhinus melanopterus) and blacktip sharks (Carcharhinus limbatus) which swam in the same water alongside those infected sharks did not become infected, nor did the many different species bony fishes sharing the same tanks and water. This indicates that L. acutus does display some selectivity in the type of host it infects, with a particular preference for elasmobranchs (sharks and rays), and even then only certain species within that group.

Other than the dead grey reef shark, the other infected sharks survived and recovered fully after treatment. However, this incident shows how outbreaks of infectious diseases can be a big problem for animals in the confined conditions of captivity. In the case of L. acutus, its small size, semi-transparent body, its tendency to infect parts of the host that are difficult to inspect (for example, inside the mouth), and the fact that nothing is know about its ecology meant that the staff had not anticipated such an outbreak. It was the first documented case of infection by a parasitic copepod that led to a shark dying in captivity. This case also illustrates the importance of thorough quarantine procedures, especially when introducing new animals into any facility, as captive conditions can seriously alter the transmission dynamics and pathology of relatively harmless parasites.

Image from figure in the paper.

Reference:

Kik, M.J.L., Janse, M., Benz, G.W. (2011) The sea louse Lepeophtheirus acutus (Caligidae, Siphonostomatoida, Copepoda) as a pathogen of aquarium-held elasmobranchs. Journal of Fish Diseases 34: 793-799,

Rhinanthus minor

Many parasites can have substantial effects on their hosts, but their impact can often extend to other organisms in the environment. Today's parasite is one of the more pretty-looking ones which we have featured in a while - as opposed to the usual worms and lice, today we are featuring a flowering plant - the yellow rattle. But don't let its pretty yellow flowers fool you, Rhinanthus minor is a ruthless parasite.

It is a hemiparasite (like the mistletoe , which becomes rather popular during this time of the year). The plant overwinters as seed in the soil and germinates during spring, penetrating into the roots of its host plants where it can suck out nutrients and water from the plant's xylem tissue. The yellow rattle is a fast growing plant - it flowers 12 weeks after germination and 3 weeks after that it produces seeds that are loosely held in dry capsules, which gives the plant its name. The yellow rattle often share its host plants with a range of insects, so a group of researchers in the UK decided to look at how this hemiparasite can affect those insects. Specifically, they looked at the effects of R. minor on insects that exploit plants in different ways; the aphid that feeds on the sugary sap flowing in the plant's phloem, the spittle bug, which taps into the xylem that transports water and other nutrients, and the grasshopper, which simply chews on leaves.

The researchers predicted that over the course of its growth, the yellow rattle would affect those insects differently. They were expecting that it would negatively impact on the spittle bug, because that insect and the hemiparasite both draw their nutrients from the host's xylem. But as is often the case in science, they found something unexpected.

First of all, they found that the effect R. minor had on those insects depended upon the parasite's growth stage, and it becomes most pronounced when the yellow rattle reaches its peak biomass and begins setting seeds. However in contrast to what they were expecting, spittle bugs actually preferred plants parasitised by R. minor. But the insect that benefited the most from the hemiparasite's presence were the aphids. Not only did they prefer sharing a host plant with the yellow rattle (there were three times as many aphids on plants with R. minor compared to uninfected plants), they also tend to breed more on infected plants. What about the grasshoppers? Grasshoppers were not all that affected by the presence of the yellow rattle either way.

The mechanism behind why the yellow rattle makes its host more attractive to plant-feeding insects is currently unknown. However, it may have something to do with the hemiparasite altering the water content of the host plant, or changing the composition of the phloem sap, which makes it more nutritious to aphids. Either way, it seems that at least for some insects, sharing a plant with a hemiparasite might actually be a good thing.

Image from the Wikipedia.

Reference:

Ewald, N.C., John, E.A. and Hartley, S. (2011) Responses of insect herbivores to sharing a host plant with a hemiparasite: impacts on preference and performance differe with feeding guild. Ecological Entomology 36: 596-604.

Ophiocordyceps unilateralis

Have you ever been so intoxicated that you start walking erratically, stumble away from your friends, stagger around in circles, clamber onto things that you wouldn't normally be seen near, and the next thing you know, you are strapped down in unfamiliar surroundings, unable to extricate yourself? Well, that pretty much describe what happens to ants which become infected with the famous "zombie ant" fungus - Ophiocordyceps unilateralis.

Much has been written about this famous fungus which turns ants into zombies - it is a parasite which captures the same part of our psyche as the monstrosities of horror movies, and there is evidence to suggest that these fungi have been tormenting ants for at least tens of millions of years. But despite all that attention, few people have actually witnessed or documented the sequence of behaviour leading up to the infected ant's paralysis and death. But in a paper published this year, a group of researchers followed the behaviour of ants infected with the famous "zombie"-inducing fungus and compare them to their uninfected brethren.

They noticed a few peculiarities with the behavioural repertoire of infected ants which stood out. While healthy ants studiously stick to the usual lanes of ant traffic, climbing into the canopy to forage with all the other busy worker ants, "zombie ants" are loners which meander around in the understory by themselves, are unresponsive to most stimuli, and frequently stumble and fall from the branches they are walking on. Essentially, the ants act absolutely drunk, indeed, the researchers described the behaviour of the "zombie ants" as a "drunkard's walk" in their paper. Another weird thing that infected ants start doing is their tendency to crawl all over and bite into leaves - something which healthy ants don't tend to do. There's a good reason why the fungus steers the ant towards leaves and afflict it with this oral fixation - it is preparing it for the next step in the fungus' development.

For the fungus to successfully reproduce, the ant must die - but it must die in a particular position to maximise the viability and dispersal of the fungal spores, specifically in the humid understory, hanging from the underside of a leaf, about 25 cm (about 10 inches) above the ground. But once the fungus maneuver the ant into position, how does it get the host to comply and stay there? The researchers made fine histological cross-section of the infected ant's head and found that once the fungus has made the ant locks its mandible in place, it busily gets to work dissolving the muscles which control those mandibles, ensuring that the ant will be locked in a death grip forevermore. A few days after the ant dies while gripping onto, the fungal stalk emerges from the head of the ant, ready to spray its spores down to the soil below to create more drunken "zombie ants".

Image from the Wikipedia.

Reference:

Hughes DP, Andersen SB, Hywel-Jones NL, Himaman W, Billen J, Boomsma JJ. (2011) Behavioral mechanisms and morphological symptoms of zombie ants dying from fungal infection. BMC Ecology 11:13

Postscript: A few hours after I wrote this post, I found out that Carl Zimmer has already written about this study (why, of course! *facepalm*), so if you want to read his version instead, you can see it here.

Polypocephalus sp.

Today's parasite might be thought of as an "aquatic Toxoplasma" in that it also induces behavioral changes in its hosts. Polypocephalus is a genus of tapeworms that infects both shrimp (Litopenaeus setiferus) and then likely rays such as the Atlantic stingray, (Dasyatis sabina). The larvae of the cestode invade the neural tissue of the shrimp hosts, particularly in the abdominal ganglia. Studies recently showed that the more larval tapeworms a shrimp had, the more time these hosts spent walking on the substrate, as opposed to sitting still or swimming. Although the authors had predicted that they would see an increase in swimming behavior because that might expose them to predation more readily, perhaps just the increased activity in general is enough to promote transmission. Nonetheless, this was an exciting insight into a potentially new system for studying parasite manipulation of their hosts.

Source: Carreon, N., Z. Faulkes, and B. L. Fredensborg. 2011. Polypocephalus sp. infects the nervous system and increases activity of commercially harvested shrimp. Journal of Parasitology 97:755-759

Image from figure of that paper.

Bursaphelenchus xylophilus

Today's parasite is the nematode Bursaphelenchus xylophilus, a well-known tree-killer responsible for the devastating plant disease known as pine wilt. Originating in North America, it has since been spread over much of Asia, and has recently been introduced to Europe. This nematode is transported by longhorn beetles known as "pine sawyers", and gain initial access to the tree through the feeding wound created by that insect. So the arrival of a B. xylophilus-laden beetle pretty much amounts to a death sentence for a pine tree. While pine trees in North America have coevolved with B. xylophilus and developed resistance or tolerance for the parasite, it has caused widespread wilting and death to the pine trees of Japan. So how can such a tiny worm bring down an entire pine forest?

For B. xylophilus, or any other plant parasites for that matter, a tree is a formidable fortress - protected by walls and scaffolding of tough cellulose, and canals of deadly resin. Plant cell wall presents the main barrier to any plant parasites - it is a tough material to break down, and most animals are incapable of doing so without the aid of symbiotic microbes. In addition, the vascular tissue of many coniferous plants like pine are saturated with resin - a thick, sticky cocktail of aromatic chemicals (from which we derive many useful substances including solvents, varnishes, adhesive and perfume) which would overwhelm and kill most invaders. Yet none of those defenses seem to deter B. xylophilus - not only can it break through the thick cellulose barrier of the pine tree, it actually lives within the resin canals of its host, which is practically the most lethal place within the tree. It would be akin to living in a moat of toxic tar.

A recent study published in PLoS Pathogens on the genome of B. xylophilus offers vital clues to how this nematode exploits its pine tree host. One of the most important enzymes for plant exploitation is cellulase - it is used to break down cellulose structures and allow potential parasites to enter and navigate through the host. Bursaphelenchus xylophilus is able to produce a unique combination of 34 enzymes for breaking down cellulose and carries a diverse suite of genes for producing enzymes that detoxify the aromatic compounds found in resin. So how did this tree killer acquire the necessary molecular machinery to invade and disarm its host?

The wide range of detoxifying genes in the B. xylophilus genome appear to be multiple duplication of pre-existing genes which are also found in other nematodes, such as the well-known standard lab worm Caenorhabditis elegans - B. xylophilus just happen to have more of copies of those genes to cope with the wider array of toxins it encounters. However, the cellulase genes have a much more unusual origin. Out of the 34 cellulase enzymes produced by B. xylophilus, 11 of those enzymes are not found in any other nematode, but are most similar to those produced by fungi. So how does a nematode end up producing fungal enzymes?

The answer might be through horizontal gene transfer (HGT). The closest living relatives of B. xylophilus are fungi-eating worms which are transported by beetles to dead and dying trees. Once they reach their destination, they disembark from their beetle vectors and feed on the fungi which have colonised the dead trees. In a case of you are what you eat, the ancestors of B. xylophilus appeared to have incorporated a whole suite of useful genes from their food, allowing them to bypass the process of feeding on fungi which are growing on dead trees and just go straight to breaking down live plant tissue.

Image from figure of the paper.

Reference:

Kikuchi T, Cotton JA, Dalzell JJ, Hasegawa K, Kanzaki N, et al. (2011) Genomic Insights into the Origin of Parasitism in the Emerging Plant Pathogen Bursaphelenchus xylophilus. PLoS Pathog 7(9): e1002219. doi:10.1371/journal.ppat.1002219