Lysiphlebus fabarum

Recently there was a widely circulated study about fruit flies consuming alcohol to fight off parasitoid infections. But there are other methods that insects employ to fight off attacks by parasitoids, and the defence employed by aphids against one of its parasitoids - Lysiphlebus fabrum - is multi-layered in more ways than one.

From the parasitoid's perspective, bigger aphids provide more resources - but they are also more dangerous to tackle. Larger aphids can deliver a mean kick against parasitoid wasps, and they also have a more well-developed innate immune system, so even if the wasp can get past the kicking limbs, her eggs may not survive even if they do make their way in. Small aphids are much easier to attack and subdue and have weaker immune systems. But, because of their smaller size, they are also more likely to die from the trauma associated with being stabbed with a wasp's ovipositor, and this would end up being a waste of time and resources for L. fabarum. Therefore, much like Goldilocks, L. fabarum usually selects for the intermediate-size aphids - not so big that they put on too much of a fight, but not so small that they might not even survive the initial infection process.

However, there's another thread weaving through this story and that thread is coevolution. The effectiveness of the aphid's immune system depends on its genetic lineage. In typical co-evolutionary arms race fashion, there is considerable genetic variation in the aphid's innate immune system and certain aphid clones are better at fighting off parasitoids. But just when you are getting comfortable with the idea of aphid resistance being based on a combination of aphid age and genotype against the adversarial wasps, it's time to throw in another factor to complicate the story - the appropriately named bacterial symbiont Hamiltonella defensa.

Some (but not all) aphids carry this protective symbiont, which acts as an internal guard dog (guard germ?) that enhances the aphid's ability to kill off parasitoids. To complicate the picture further, H. defensa itself has acquired this ability by incorporating a toxin-producing gene into its genome that originated from a virus. Not only does this toxin-producing microbe kill off the parasitoid larvae inside the aphid, they also affect the egg-depositing behaviour of the parasitoid. And much like the aphid's innate immunity, age also plays a role in modulating the defense conferred by the symbiont. Younger aphids have smaller populations of H. defensa to start off, but they increase as they got older, and the more symbionts an aphid has, the better it is at fighting off parasitoids.

So how does this affect the evolutionary pathway of L. fabarum? Researchers found that because H. defensa play such a major role in the aphid's defense, not only are the wasps locked in a coevolutionary race with the aphids, they are also engaged in an even more intense arms race with the H. defensa symbionts carried by the said aphids. Even when H. defensa do not outright kill the L. fabarum larvae, they do still incur a cost; in aphids carrying the symbiont, the wasp took longer to develop, and also emerged slightly emaciated compared with those that infected H. defensa-free aphids.

The most remarkable finding that emerged was when researchers looked specifically at the different strains of symbionts and their interactions with different lines of L. fabrum. For example, they found that one particular strain of H. defensa that they called H323 conferred protection against most lines of L. fabarum - but offered the aphid no protection against one particular line of L. fabrum. Even the star performer out of all the symbionts - strain H76 - that conferred the greatest protection on average against almost all the lines of wasp tested - had a nemesis. A different genetic line of L. fabarum was able to weather the bacterial guardian's toxins and successfully develop to maturity.

What emerges is a complex series of coevolution that is occurring not just between different genetic lines of aphids and wasps, but also between the wasps and the symbionts carried by the aphids. While superficially, it may seem like the story of a coevolutionary arms race between aphids and wasps, given the strong interactions between the wasps and the bacterial symbionts, it is much more a story of coevolution between L. fabrum versus H. defensa, being played out on an "aphid stage."

Image from figure in the paper.

Reference:

Schmid, M., Sieber, R., Zimmermann, Y-S. and Vorburger, C. (2012) Development, specificity and sublethal effects of symbiont-conferred resistance to parasitoids in aphids. Functional Ecology 26: 207-215

Acanthocephalus dirus

The word parasite has a lot of connotations associated with it, and "maternal" is certainly not one of them. To most people, the term "freeloader" comes to mind (hopefully, this blog will show you that parasitism is actually a very challenging way of life). They also have a reputation as being pretty lousy parents. In most textbooks, parasites are usually considered as "r-strategists" - which produce many, many offspring and don't take good care of them (as opposed to a K-strategist which produces fewer offspring, but invest a lot into parental care - like an elephant). But not all parasites are bad parents, and today, I am going to tell you about a study on a maternal parasite which sacrifices everything (literally) for her offspring.

Acanthocephalus dirus has a reproductive strategy that is unusual for its group - the acanthocephalans or the thorny-headed worms (Acantho = "thorns", Cephala = "head"). In fact it is unusual compared to most intestinal parasites. Unlike some tapeworms, which profligately cast off segments (each containing hundreds of eggs) into the wilderness with abandonment, A. dirus has rather different approach. The impetus that spurred on this piece of research were two separate observations: (1) fish that are infected with A. dirus do not have any worm eggs in their feces (unlike most animals infected with intestinal parasites) and (2) perfectly healthy and intact female worms were often expelled from the definitive host. What the researchers found was that instead of simply laying eggs that are expelled from the worm and from the host, a female A. dirus actually retains her eggs until she become completely bloated with them - at which point she exits gracefully from the host fish's digestive tract. Some readers might recall a nematode that has a similar reproductive strategy, and that both lineages have evolved such a reproductive strategy independently. So why has A. dirus evolved such an extreme strategy instead of just laying eggs normally like other thorny-head worms?

One reason could be that A. dirus infects creek chub - which, as its name indicates - lives in flowing creeks. The chub acquire the worm through eating infected isopods in the stream (the picture shows the light-coloured infected isopod on the right, and the darker uninfected individual on the left), which become infected when they ingest worm eggs resting on the creek bed. Acanthocephalan eggs tend to float - so if the eggs are simply expelled into the environment, they would get washed away downstream and deposited where the isopods do not occur. Whereas with A. dirus, the worm's own body can act like a weight belt which would carry the eggs down to the sediment layer, so by the time the worm herself decays, the eggs are already in the sediment where isopods can pick them up.

Furthermore, laboratory tests showed that isopods like to eat egg-filled female worms as much as their usual food - leaf litter - and the worm body itself actually enhances the infection success of the eggs. Researchers found that when exposed to fresh eggs alone, fewer than one in four isopods became infected, whereas when exposed to gravid females, over 80% became infected (natural infection comes somewhere in between those at about 60%). By making the ultimate maternal sacrifice, A. dirus gives her offspring the best possible start in life.

Image from figure in: Seidenberg (1973) Journal of Parasitology 59: 957-962

Reference:

Kopp, D.A., Elke, D.A., Caddigan, S.C., Raj, A., Rodriguez, L., Young, M.L. and Sparkes, T.C. (2011) Dispersal in the acanthocephalan Acanthocephalus dirus. Journal of Parasitology 97: 101-105

Ascarophis sp.

When I saw the reports of giant amphipods being dragged up from the Kermadec Trench off the coast of New Zealand, my immediate thought was "I wonder what parasites it has?" This promoted me to do a write-up of a paper I've read recently, which is about a parasite that infects amphipods - admittedly those that are more modestly sized. Today, we are featuring a study on Ascarophis, a nematode worm that infects an intertidal amphipod (Gammarus deubeni) in Passamaquoddy Bay, New Brunswick, Canada. Compared with related species this worm has evolved to live the simple life(-cycle), and avoids the complications that come with having a complex life-cycle.

Previously on this blog, we have featured parasites that have evolved to take short-cuts with their complicated life-cycles. When a particular host is absent, such parasites may opt to ditch that host from their life-cycle, and switch up their developmental schedule. This is the case with the fluke Coitocaecum parvum. However, while C. parvum can switch between different life-cycles depending on circumstances, Ascarophis has completely abandoned that altogether, and has evolved to make things simpler by completing its entire life-cycle within its amphipod host. Usually, parasites with complex life-cycles use different hosts for different functions - i.e., one host might merely serve as a transport and/or resources for temporary development, whereas another acts as a mating ground and/or habitat in which it reaches maturity. So how can Ascarophis get so much functionality out of a tiny little crustacean?

Nematodes normally go through 4 larval stages (L1-L4) before becoming a sexual mature "fifth stage" worm (L5). The end of each larval stage is accompanied by a molt (rather like insects). In related nematodes that have retained their complex life-cycle, the L3 worms (which are ready to infect the next host) live encapsulated in the first host, while the L4-L5 live in the digestive tract of the final host. What the researchers found with the Ascarophis they collected from New Brunswick is that L1 and L2 worms were found in the muscle tissue, and upon reaching L3 the worms begin to migrate into the body cavity where they complete their development into adulthood and start producing eggs. Now compare this with Ascarophis from the White and Baltic Seas, which also infect amphipods, but uses a species of sculpin as their final host. Those fish acquire their infection by eating amphipods infected with L3 stage nematode, and the worms develop into adults in the fish's gut.

In effect, the Ascarophis from New Brunswick gets the most out of its little crustacean host by using different parts of the amphipod's body as surrogates for different hosts - instead of being transmitted to a different host, it simply moves to occupy a different part whose function is close enough to its needs for it to complete its development. Unlike the C. parvum, it appears that Ascarophis has abandoned the fish host altogether, and has committed itself to using the amphipod as the sole host for its entire life-cycle. Even though the Ascarophis found in the White and Baltic Seas have retained their complex life-cycle, researchers of this study suggested that they are the same species as the worms they looked at, but the New Brunswick variant has simply adapted to local condition and evolved a different life-cycle. However, it must be noted that the researchers have come to this conclusion based on the worm's morphology and as we have seen before, appearance can be deceptive with nematodes.

Through all that, this plucky little New Brunswick parasite faces one last problem - getting its eggs out of its crustacean host. For worms that live in inside a fish's gut, passing eggs out into the environment is a pretty straightforward affair - the eggs simply get washed out with the poop. But there is no exit in the body cavity of an amphipod, so how is a worm supposed to cast its eggs out into the environment? Well, this thrifty nematode simply waits for the host to die, and as the body disintegrates, the eggs are released as well. Of course, it helps that these amphipods have a tendency to cannibalise the rotting bodies of their fallen comrades - this presents the perfect opportunity for the parasite to infect a new batch of hosts - yet another reason to not gnaw on any random corpses you may come across.

Image modified from figure in the paper

Reference:

Appy, R.G. and Butterworth, E.W. (2011) Development of Ascarophis sp. (Nematoda: Cystidicolidae) to maturity in Gammarus deubeni (Amphipoda). Journal of Parasitology 97: 1035-1048.

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.