Nicothoë astaci

The parasite we are featuring today is Nicothoë astaci, the "lobster louse." Despite its name, it is not a "louse" (true lice are insects) as such, but rather a copepod (a type of crustacean), just like the salmon lice we have previously featured on this blog. But whereas salmon lice are well-studied due to their economic impact on salmonid fisheries (especially on farmed fishes), far less is know about the lobster louse. Despite having been recorded on the European lobster (Homarus gammarus) since the 1950s, to this day there is very little known about this parasite, including the type of pathology it causes, its complete life-cycle, or even what the male of the species looks like (parasitic copepods often have cryptic or dwarf males which are very elusive).

The paper we are looking at today is taking the first step to rectifying that situation. The photo (from the paper itself) depicts larval stages of N. astraci, with the arrows indicating the oral cone,the structure this parasite uses (along with its front pairs of legs) to attach itself to the host's gill filament and feed on its blood. While the larval stage looks like a rather ordinary copepod, as it matures into an adult, it morphs into what looks like a miniature boomerang with a pair of stretched out "wings" on either side, and a pair of bulbous egg sacs dangling from its rear end. The attachment and feeding activity of the lobster louse can cause pronounced physical damage to the lobster's gill filaments.

As with any kind of infection, you would expect to see some kind of cellular response. While the innate immune systems of invertebrates like lobsters are not as sophisticated as the adaptive immune system of vertebrate animals such as ourselves, they can present a formidable challenge to any would-be intruder (to see an example of what the cellular defence of a crustacean can do to a parasite, click here). Basically, the crustacean's equivalent of blood cells wrap themselves around the parasite or pathogen and initiate the process of melanization, where the intruder becomes entombed in a hardened capsule of melanin (the pigment which determines our skin colour). The researcher did find signs of melanization and other cellular disruption throughout the gills of infected lobsters, but none of it was near the lobster louse's attachment point.

So the lobster's immune system recognizes the presence of an intruder, but is unable to pinpoint and focus its wrath on the parasite. The authors of this paper suggest that this indicates the lobster louse is able to somehow interfere with the lobster's defensive mechanism so that it can blood-feed in peace. The mechanism through which the lobster louse disrupts this particular aspect of host physiology is yet to be uncovered, along with much of the parasite's ecology and life-cycle. Hopefully, with further research on this host-parasite system, this situation will change in the future.

Image from the paper.

Reference:

Wootton EC, Pope EC, Vogan CL, Roberts EC, Davies CE, Rowley AF. (2011) Morphology and pathology of the ectoparasitic copepod, Nicothoë astaci ('lobster louse') in the European lobster, Homarus gammarus. Parasitology 138:1285-1295.

Maritrema subdolum

This is a story about two little crustaceans and a parasitic fluke. Corophium volutator and Corophium arenarium are amphipods that make a living tunneling in the mudflats on the coast of the Danish Wadden Sea. They are also host to many species of parasitic flukes, and one of them is the parasite we are featuring today - Maritrema subdolum. Last year, we featured a related species from New Zealand - M. novaezealandensis - and much like its Kiwi cousin, M. subdolum is the bane of the local crustacean population. However, M. subdolum does not affect all of its crustacean hosts equally and this has some important ecological consequences.

Out on the Danish mudflats, C. volutator is king. Of the two Corophium species, it is the stronger competitor, reaching much higher abundances and generally making life difficult for C. arenarium. But along comes M. subdolum, which evens out the playing field. Living alongside those little crustaceans are mud snails, and during early spring they can become extremely abundant, with over 25000 snails per square metre. By summer, almost half of those snails are infected with M. subdolum, which turn them into little parasite factories, each cloning a massive reserve of parasite larval stages call cercariae that are then unleashed into the environment to infect the amphipods. The main trigger for releasing these cercariae is high temperature, and during 1990 there was a bout of unusually high temperature during summer that has been linked to North Atlantic Oscillation (NAO), a phenomenon that plays a major role in determining climatic conditions in the northern hemisphere.

All of this combined into a perfect storm that devastated the C. volutator population. Triggered by high temperature, all the infected snails released their payload of parasites into the surrounding waters. Each infected snail can release hundreds of cercariae, and with thousands of snails per square metre, the shallow waters of the mudflats turned into a seething parasite soup. To the amphipod, this amounted to being in a shooting range, as each cercaria is armed with glands of digestive enzymes and a scalpel-like organ call a stylet with that they use to puncture the amphipod's exoskeleton. For many C. volutator, the outcome of being attacked by a swarm of these little horrors was terminal, and this resulted in a dramatic decline in their population. However, for some reason we still don't know, the C. arenarium population was able to weather the M. subdolum storm unscathed, either because they tolerated the parasite swarm, or because they were simply not the preferred target. Either way, with the collapse of the C. volutator population, in the next season, C. arenarium was able to succeed them and become the dominant amphipod species on the Danish mudflat.

And this dramatic ecological change was ultimately brought about by a little parasite.

Photo by Kim Mouritsen

Reference:

Larsen, M.H., Jensen, K.T. and Mouritsen, K.M. (2011) Climate influences parasite-mediated competitive release. Parasitology 138: 1436-1441

Metarhizium acridum

The locust in the photo is covered in a fine layer of green mold - that is because it was killed by the parasite we're featuring today, Metarhizium acridum. Metarhizium acridum is a pathogenic fungus which specifically infects and kills grasshoppers, locust and other insects in the Orthoptera order. Because of the pest status of some orthopterans (think locust plagues), M. acridum is mass-produced as type of environmentally-friendly, biological alternative to most insecticide. But while M. acridum only targets locust and grasshoppers, its close relative, M. robertsii, is far less picky, capable of infecting hundreds of different insect species.

So why is M. acridum so picky while its close relative is so indiscriminate? Amazingly, it appears to come down to a single gene call Mest1 - a gene present in M. robertsii, but is absent in M. acridum. To find out the function of this gene, a group of researchers in China created a mutant M. robertsii strain which has a non-functioning copy of Mest1. This mutant lost its ability to infect most insects - except grasshoppers and locusts - which happens to be the speciality of M. acridium. In parallel, the researchers also inserted functional copies of Mest1 into M. acridum. The insertion of this single gene allowed M. acridium to infect a wider range of insects.

What is so special about Mest1? In M. robertsii, Mest1 is expressed during spore germination, and plays an important role in initiating the infection process. Mest1 expression can be triggered by a range of stimuli including nutrient poor conditions or contact with insect cuticle. Metarhizium acridium has other genes playing the role of Mest1, but they are triggered by substances which are present only in the waxy coating of grasshoppers and locusts. So if its spores land on other insects such as caterpillars which have a different type of coating, M. acridum fails to germinate because the appropriate stimuli are absent. Thus, the insertion of Mest1 into M. acridium allows the fungus to bypass those usual stimuli and begin germinating under a wider range of conditions

Host specificity is one of the central question in the evolutionary biology of parasitic organisms. In this case, we can see how a single gene can changed this otherwise specialist pathogen into a broad-spectrum generalist.

Image from the Wikipedia.

Wang S, Fang W, Wang C, St. Leger RJ (2011) Insertion of an Esterase Gene into a Specific Locust Pathogen (Metarhizium acridum) Enables It to Infect Caterpillars. PLoS Pathog 7(6): e1002097. doi:10.1371/journal.ppat.1002097