If you would like to listen to this blog rather than reading it, please click on this link!)
Parasites and pathogens often have very obvious effects on the their hosts. Some parasites (like tapeworms, for example) basically steal a percentage of their host organism’s food and, thus, reduce the energy available to the host for growth, movement, or reproduction. In mildly competitive environments a parasitized individual may function quite well, while in more intensely competitive (and stressful) environments, the parasitized individual may perish. It is in the parasite’s great short-term interest to preserve the host in which it resides: parasites don’t “want” to kill their hosts right out. They “want” to use them as a habitat and an energy source for as long as possible unless, of course, the continued existence of the host presents a barrier to the parasite’s reproduction or dispersal. Pathogens, on the other hand, seem less concerned with the preservation of their hosts possibly because of their already extremely well developed (and very efficient) mechanisms of dispersal.
Parasites and pathogens (and the variations of reactions to them by individuals in a host species’ population) can be very powerful forces for population control and also for evolution. In a population under assault by a particular parasite or pathogen any individual that even has a slight resistance to infection or disability would logically be more likely to survive and reproduce and pass along those resistance traits to their offspring. So, exposure of a population to a parasite or pathogen over evolutionary time would be expected to result in that population becoming less and less vulnerable to these maladies.
This evolutionary logic sets up some very interesting interactions when a species enters a new environment. For example, some invasive species carry parasites or pathogens to which they have evolved significant resistance. Native species that are similar to these invasive organisms, though, may have very weak resistances to the invader’s parasites or pathogens. The North American gray squirrel, for example carries, with few health consequences, a parapoxvirus. When the gray squirrel was introduced into Great Britain it encountered the British red squirrel which occupied a very similar ecological niche. The red squirrel, though, had no evolutionary history of exposure and adaptation to the parapoxvirus, and , as a consequence, was weakened by infection and then decimated by subsequent competition with the healthy, vigorous gray squirrel.
Similar “parasite/pathogen” aided species invasions have been seen in Asian cyprinid fish that oust native fish from streams in Europe, in garlic mustard plants deploying their toxic mycorrhizal fungi against potential competing plants throughout North America, and in invasive American bullfrogs spreading their self-tolerated fungus (Batrachochytrium) to almost all other native (and highly vulnerable) amphibian species. Introduced pheasants in the United Kingdom also carried a fungus (Heterakis gallinarum) to which they were evolutionarily adapted but to which the U.K. native partridges, much to their great detriment, were not.
Sometimes an invasive species does not bring the parasite or pathogen with them, though. Sometimes the invader is just naturally more resistant to a native parasite or pathogen than the native species are. The possible mechanism for this may involve prior evolutionary exposure of the invader to similar pathogens, but it may just be a consequence of chance. For example, vineyards in California are being overwhelmed by invasive, grapevine-damaging leaf hoppers that are resistant to the native parasites and parasitoids that keep native leaf hopper populations under control. The native leaf hoppers, then, are being extirpated from their habitats, and the grape crops are being severely damaged as a consequence of this ecological imbalance.
In another example, invasive, often intentionally introduced, European brown trout aggressively push native fish species into warmer, lower current flow sections of their streams. This exposes the native species to higher levels of parasite exposures and higher levels of debilitation and mortality. Similar patterns are seen in the invasion of South African mussel beds by trematode resistant Mediterranean mussels, and in the red introduced fire ants in the American South that are unaffected by the parasitoid wasps that greatly reduce the activity of many native ant species. Numerous invasive grasses and weeds are also able to flourish in their new environments because of their innate (and maybe serendipitous) resistance to some controlling virus or fungus that regulates populations of native plants.
There are some examples of the opposite, regulatory serendipity, too. Some invading species turn out to be more sensitive to controlling parasites or pathogens than native species. Red invasive fire ants, for example, may be unaffected by native parasitoid wasps but they are much more sensitive to an exotic parasitoid than are native ants. This observation suggests a possible program of biological control for the southern U. S. through the introduction of these exotic parasitoids. In another example, the North American eastern white pine has turned out to be exquisitely sensitive to the European endemic blister rust fungus. Introduction of the eastern white pine into Europe, then, has not been possible nor has there been any invasion of European forests by the eastern pine occurred because of this sensitivity.
Parasites and pathogens may also alter host organisms’ behaviors often to allow the parasite or pathogen to continue on its life cycle. There are some anecdotal accounts of humans that are infected with viral pathogens tending to be more social and more likely to be clustered together with other (possibly un-infected) humans. This tendency is ascribed to the “need” of the virus to escape its infected host and find a fresh human environment in which it can proliferate. Happy flu season, everyone!
There are also some scientifically rigorous studies that have shown that rodents infected with Toxoplasma gondii (a protozoan parasite) are less vigilant around predators (like cats) and are even, in fact, drawn to cats (and the scent of cat urine). These reactions suggest a level of control by the parasitic T. gondii (that “wants” to get into the body of the cat so that it can carry out its reproductive life cycle) over the T. gondii carrying rodent host (that presumably does not really “want” to get eaten!).
This idea that a parasite can control the behavior of its host even to the detriment and death of the host itself expresses itself in many other parasite-host systems. For example, hairworms (Nematomorpha) cause infected crickets to seek bodies of water into which they can plunge themselves and drown. The hairworm is then able to leave the dead cricket’s body, find a mate in the body of water, reproduce and start a new life cycle. Bad for the cricket but very good for the hairworm.
Another example of parasite control over a host was recently published in the Proceedings of the National Academy of Science by a group of Penn State researchers. They looked at the interaction of a fungal parasite (Ophiocordyceps unilateris) with a carpenter ant (either Camponotus castaneus or Camponotus americanus). The infected ants are referred to as “zombie ants” due to their predilection to stagger up onto vegetation overhanging their colony, clamp their mandibles on the underside of a leaf or twig and then hang there until they die. Then, out of their dead bodies a fungal stalk arises from which spores are released. The spores rain down on the ant colony below and infect new individuals. Using some very elegant imaging techniques the Penn State team found that the fungus forms a dense network of cells throughout the ant’s body. These fungal cells especially wrap themselves around the ant’s muscles and take over their control (“like a puppeteer controlling a marionette,” as one researcher put it). The ant had little control over its activities by the time the fungal cellular system was fully developed. The ants were “a fungus in ant’s clothing,” according to another one of the researchers.
Parasitism is an incredibly common strategy of life! There are theories that our reflexive revulsion to parasites is, in fact, an evolutionary adaptation by which we, as potential hosts, avoid them! So wash your hands and cook your food! That’s about the best that you can do!