Philometroides paralichthydis

Philometroides paralichthydis is a filarial nematode that parasitises the southern flounder. The fish becomes infected by eating copepods carrying the larval stage of the parasite and the adult female worm lives embedded in the inclinator muscles at the base of the dorsal and anal fins. There she feeds on blood and produces larvae that are released into the surrounding waters. The physical presence of P. paralichthydis lodged in that part of the host can lead to muscular degeneration, especially when the parasite becomes bloated with baby worms.

photo of Philometroides paralichthydis from here.

The inclinator muscles, where adult P. paralichthydis are found, usually act as pulleys that control the side-to-side motion of the flounder's fins, which in turn affect the fish's swimming performance. So it would make intuitive and common sense that a parasite that damages muscles controlling an animal's movement would cause the host to become physically impaired. For example, Curtuteria australis (a parasite that I have worked with) is a fluke that has larval stages that lodge themselves in the foot muscle of the New Zealand cockle and by doing so they impair the bivalve's burrowing ability.

But, mere common sense is not science and whatever our expectations might be, they must be tested against the real world. To find out just what effects this muscle-dwelling parasite can have, researchers collected a group of flounders from estuaries in South Carolina and put them through a series of physical exercises in a custom-built swim track and an aquarium filled with sand and water. It was a blinded experiment; the researchers did not know the parasite load of the flounders before or during the trials, so they would not be subconsciously biased about the outcome one way or the other. During the trials, they observed and recorded the flounders' ability to perform actions that are key to their survival - swimming, accelerating, and burying themselves in sand - all of which require the use of the dorsal and anal fins.

After those physical trials, they counted the number of worms found in each flounder and in contrary to what "common sense" may lead us to believe, the presence of P. paralichthydis did not seem to make much difference. Regardless of where they are located in the host, they did not compromise the flounder's ability to accelerate, or cover themselves with sand. The parasite was found to have some affect on swimming speed, but only in smaller juvenile fish and not adult fish. On average, juvenile fish with P. paralichthydis swum thirty percent slower than uninfected fish of the same size class.

So why does this parasite only affect juveniles? Perhaps fully-grown fish are better able to compensate for any pathology incurred by the parasite simply by being larger, which provides a buffer against any damage caused by the parasite. It seems that once they are large enough, the flounders are fairly safe from the damaging effects of this muscle parasite. Juvenile fish are generally more vulnerable to the injurious effects of parasites which can contribute significantly to juvenile mortality in fish and affect recruitment by making them more vulnerable to predators or simply through the pathology they can cause (see this post on how juvenile reef fish run the parasite gauntlet before settling down.)

There are two caveats to this study that we need to consider before drawing any final conclusions. It is possible that the researchers had only collected those fish that had managed to survive well enough despite having the parasite, and fish with greater morbidity from P. paralichthydis had naturally died from starvation or predation and were not represented in the sample. Also, none of the flounders in the trial were infected with more than twelve nematodes. Maybe there was simply not enough worms to have a noticeable affects on the flounder's behaviour. Even with Curtuteria australis, there needs to be a critical number of larval flukes in the cockle's foot before its burrowing ability is impaired.

Reference:
Umberger, C. M., de Buron, I., Roumillat, W. A., & McElroy, E. J. (2013). Effects of a muscle‐infecting parasitic nematode on the locomotor performance of their fish host. Journal of Fish Biology 82: 1250–1258

Asobara japonica

Drosophila suzukii is a fruit fly like no other. Native to Asia, it is related to that common lab workhorse(fly) Drosophila melanogaster, but unlike most Drosophila, which lay their eggs on overripe and rotting fruit, D. suzukii has a saw-like ovipositor that allows it to lay its eggs in fruits that are still ripening. Recently D. suzukii has been spreading its wings over the American and European continents, earning the title of being a pest species as it attacks a wide range of soft-skinned fruits including strawberries, cherries, grapes, nectarines, pears, and peaches.

The usual adversary of fruit flies is Leptopilina heterotoma, a parasitoid wasp that can devaste Drosophila maggots. It is such a threat that some maggots resort to imbibing alcohol to stave off this parasitoid. But while L. heterotoma is a menace to most fruit fly maggots, the maggots of D. suzukii is the first Drosophila found to stop that wasp in its tracks. The secret lies in the fly's blood. Insects and other invertebrates have blood cells called hemocytes that patrol their bodies, clotting wounds and entombing foreign invaders in hardened capsules. Leptopilina heterotoma disables those defensive cells by unleashing a virus that destroys them.

Asobara japonica photo from here 

However, this feat of biological warfare doesn't seem to work on D. suzukii. In the study we are featuring today, researchers exposed a group of D. suzukii to some L. heterotoma that were eager to lay their eggs in some suitable victims. But while the wasps readily injected their eggs into D. suzukii as they would with any other fruit flies, most of the eggs ended up being trapped in hemocyte coffins and none of the parasitic larvae ever made it out of a D. suzukii maggot alive. When they looked at the blood of D. suzukii, they found that it has five to ten-fold more hemocytes than D. melanogaster, making it a tough adversary for any would be parasite. Furthermore, not only were the hemocytes of D. suzukii not destroyed by L. heterotoma's "pet" virus, their numbers actually increased in response.

But D. suzukii is by no mean invincible; it has its own parasitoid to watch out for and it is also the species we are featuring today - the parasitic wasp Asobara japonica. This wasp is one nasty customer; it would have to be seeing as it has coevolved with D. suzukii. When the researchers unleashed egg-bearing A. japonica upon both D. suzukii and D. melanogaster, the exposed D. suzukii were able to entomb very few of the A. japonica eggs - a quarter of them at most. In comparison, D. melanogaster did not stand a chance - none them were able to entomb the A. japonica eggs that had been laid inside them.

While both L. heterotoma and A. japonica are both parasitic wasps of fruit flies, they have very different methods for subduing their host's immune system. Whereas Leptopilina heterotoma wages biological warfare on its host, A. japonica is a chemical warfare specialist. It injects at first glance what appears to be a peculiar cocktail into its host; a deadly venom and its antidote. Yet this mixture allows A. japonica to manipulate the host's physiology, but only when both serums are injected in combination. The venom alone will disrupt the host's immune system, and then induce paralysis, which is followed by death. But A. japonica also injects the antidote along with it which mitigates some of the venom's effects - it keeps the host alive, but at the same time allows the immune system to be ravaged. So in effect this wasp brings its host to the edge of death, enough to disable its defences, then cures it - but only so that it can then act as a living incubator for its babies.

Reference:
Poyet, M. et al. (2013). Resistance of Drosophila suzukii to the larval parasitoids Leptopilina heterotoma and Asobara japonica is related to haemocyte load. Physiological Entomology. 38: 45-53.