The interactions between a parasite and its host are not completely understood. Though conventional wisdom of parasitology and medicine suggests the net effect of a parasite on its host (virulence) to be little or none, recent data suggest there may be many possible coevolutionary outcomes. These outcomes, as outlined by Andrew J. Karter and Catherine A. Toft, include the settlement of virulence to intermediate levels, high levels, or zero.
According to Karter and Toft settlement of virulence to intermediate levels is more readily accepted due to the fact that the best-documented cases of coevolution are primarily of virulence settling to intermediate levels. One such case includes the introduction of avian malaria to Hawaii, in which native birds became extinct upon introduction of the disease. As time progressed, however, some native birds evolved resistant to avian malaria; therefore, reducing the virulence of Plasmodium.
Given other factors such as vectors, however, virulence may potentially rise to high levels. One argument for potential high virulence is that vector-borne parasites are able to increasingly exploit their hosts without penalty. Such parasites include the acute Plasmodium strain that infects humans, in which immobilization due to the host immune response allows the parasite to be transmitted through a feeding arthropod vector. In this case, if the host’s immune system is unable to counter the parasite, then the parasite’s virulence would have increased significantly.
When virulence is zero, the parasite and its host are considered to be in a commensal relationship. Commensalism, in this case, does not imply a peaceful coexistence, but rather a stand-off between parasite attack and host counterattack. It is, therefore, evolutionarily possible for either the host or the parasite to overcome the other at any time. Examples include the evolution of eukaryotes relative to mitochondria and chloroplasts.
Karter and Toft suggests that anyone of these outcomes may occur at anytime. In African trypanosomiasis, for example, one “species”, Trypanosma brucei, is able to infect a variety of mammals and cause varying degrees of diseases. Tryanosoma brucei brucei is non-infective to humans, but T. b. gambiense and T. b. rhodiense causes chronic and acute forms of the disease, respectively. Conventional wisdom suggests that the resistance of humans to the brucei strain occurred earlier on in evolutionary history, and that the acute strain occurred later. Though this may be conventionally reasonable, enzymatic and molecular techniques have proven otherwise, suggesting a different order of evolutionary history. Based solely on symptoms and geographical locations, it is difficult to determine what constitutes a species in T. brucei. This is due to the fact that all strains of T. brucei are morphologically indistinguishable.
As stated, Karter and Toft suggests three outcomes pertaining to the interactions between parasite and host. There is currently no sufficient evidence to suggest any sole outcome as the correct one. To further evaluate the coevolution of virulence between two interacting species it is important to gather more empirical data on the parasite-host association.
Toft, C.A., Karter, A.J. (1990). Parasite-host coevolution. Trends in Ecology & Evolution, 5(10), 326-329.