For my dissertation I’m planning on studying California killifish and Euhaplorchis californiensis, my favorite host/parasite system. The Kuris Lab has done some really excellent work on this system, providing a great foundation for future studies.
Euhaplorchis californiensis is a trematode parasite with a complex life cycle. Its life starts in the digestive tract of waterbirds, where it remains for only a short time before being defecated. Shitty way to start off, huh?
The horn snails, the parasite’s next host, aren’t especially perceptive and consume E. californiensis while grazing along the bed of the estuary. Once infected, the parasites castrate their snail host and turn the snail into a parasite-making factory. After a few parasite generations, a significant portion of the snail’s mass will be E. californiensis offspring. When the parasite has completed development, it burrows out of the snail and swims into the water column.
The picture on the left is of a deshelled, parasitized horn snail. If you click on the picture to enlarge it, you’ll notice that much of its back half is white and it almost looks like it’s filled with small grains of white rice. It’s actually filled with a bunch of trematode parasites (though in this case it isn’t E. californiensis).
The parasite’s next target is the California killifish (Fundulus parvipinnis). When a killifish is unfortunate enough to run into the parasite, the parasite will burrow inside and make its way up to the fish’s brain. Research on closely related species suggests that the parasites find a nerve and follow it up to the brain.
This is where it gets cool.
Jenny Shaw and her collaborators looked at how neurotransmitters in killifish brains change as parasites accumulate (the paper can be found here). They found significant changes in the concentrations of two neurotransmitters, dopamine and serotonin, and found that these changes were more pronounced as parasite density increased.
One striking finding was that the parasites were suppressing a common stress response. When vertebrates are stressed, a part of the brain known as the raphe nuclei increases its rate of serotonin metabolism, which essentially means serotonin levels decrease in this part of the brain. In infected killifish, serotonin levels decreased much less, indicating that the parasites are affecting their host’s responses to stressful situations. As encounters with a predator are clearly stressful, this may be an important mechanism used by the parasites to get the killifish eaten by its next host.
This poses an interesting possibility – are the parasites altering killifish behavior to make them more likely to be eaten by a particular animal?
The answer is yes, infected killifish do exhibit strange behaviors that make them significantly more likely to be comsumed by waterbirds, the definite host (that is, the host in which the parasite reaches maturity) of E. californiensis. Lafferty and Morris 1996 observed that infected killifish frequently engaged in behaviors that made them quite conspicuous, including quick trips up to the water surface (which could make the killifish into a quick meal for an awaiting waterbird). They then set up outdoor enclosures containing killifish that they knew to be infected and those that were uninfected. Waterbirds were capable of accessing the fish in the enclosure and twenty days after the enclosures were set up the researchers returned to see who was left.
The results were staggering. Infected killifish were 30 times more likely to have been consumed by waterbirds than the uninfected fish! This is immensely strong evidence that the parasites are adaptively manipulating their hosts.
Much remains to be learned about this system, but parasites like E. californiensis which are capable of behavioral manipulation may tell us important things about how our brain works and perhaps even provide insight into treatments for certain behavioral disorders. Many behavioral disorders including depression and bipolar disorder are thought to be associated with inappropriate concentrations of neurotransmitters such as dopamine and serotonin in the brain. Understanding how parasites manipulate the concentrations of these chemicals may teach us how we can alter them as well.
At the moment, we don’t know how parasites are changing neurotransmitter concentrations in the brain. They could either be secreting the chemicals themselves or they could be manipulating the brain into doing it for them. If they’re manipulating the brain, then the method that they use to do this could provide us with new treatment ideas.
Here comes the fun, wild speculation part. If the technology for nanobots ever gets off the ground then we could use parasites as a model for how to make small-scale changes to neurotransmitters as a way to control behavioral disorders. Alternatively, I wonder if we could create genetically modified parasites capable of altering the concentration of a particular neurotransmitter in specific parts of the brain. Parasites already know how to get to the brain on their own and we know that controling the number of parasites controls the intensity of the changes in neurotransmitters. So why not give it a shot (in animal models first, of course)?