Frozen Evolution. Or, that’s not the way it is, Mr. Darwin. A Farewell to Selfish Gene.

The fact that a parasite is frequently in close contact with its host provides it with an opportunity for targeted interventions in the functioning of the host organism. Manipulation hypothesis suggests that parasites are capable of modifying for their needs various traits of the host, from the morphology through regulation of metabolism and allocation of energy for the individual life functions to specific interventions in the nervous system, leading to changes in the behavior of the host. Thus, parasites are typical organisms utilizing the extended phenotype principle (Dawkins 1982) (see XVIII.6). A number of their genes have become fixed in evolution, not because they would favorably affect the traits of the parasite organism, but because, through their products, they affect the traits of the host organism. Thus, the body of the host becomes part of the extended phenotype of the parasite and a great many of its traits assist not in spreading its own genes but rather in spreading the genes of the parasite. The genes of the parasite and genes of the host frequently have quite opposing interests in relation to the traits and functioning of the host organism. As was mentioned in Section XIX.2, the genes of a parasite in the co-evolutionary battle with the genes of the host are in a more advantageous position, so that their interests frequently predominate in the attacked organism.
            An important mechanism enabling an increase in the chance of transmission of a parasite between hosts consists in inducing behavioral changes in the infected host that can positively affect the probability of transmission of a parasite from one host to another (Barnard & Behnke 1990; Moore 1984). The parasite can cause these changes in various ways. The most specific mechanisms include direct intervention in the central nervous system of the host, through which the parasite is even capable of initiating very complicated patterns of behavior. The simplest mechanisms, on the other hand, encompass unspecific pathogenic effects on the host organism that, while they reduce the vitality of the host and thus increasethe chance that the parasite will kill its host and die itself, also can be very functional for the parasite in some special cases, from the standpoint of its transmission in the host population. The types of behavioral changes that the parasite induces depend primarily on the mechanism of its transmission. It is understandable that the behavioral changes that assist in transmission from an intermediate host to the definitive host through predation are completely different from changes that increase the effectiveness of transmission of sexually transmitted parasites.
            The effect of a parasite on human behavior has been observed in a great many systems. For example, explanations have been given for the negative effect of various parasitic infections (Ascaris, Schistosoma, Toxoplasma) on intelligence and learning ability (Nokes & Bundy 1994; Piekarski 1981; Saxon et al. 1973). (Cook & Derrick 1961; Ladee, Scholten, & Meyes 1966; Robertson 1965; Flegr & Hrdy 1994; Flegr et al. 1996){13300}.
However, in most of these cases, it is difficult to decide when this is a more or less unspecific symptom of the current or recent disease and when it is a manifestation of targeted influencing ofthe host’s behavior by the parasite. It is obvious that the behavior of a sick person will differ from that of a healthy person and that prolonged sickness can even be manifested in personality changes and thus, secondarily, on the way he will act in certain situations. In addition, most results are based on monitoring the correlation between the frequency of the occurrence of a particular parasite and a certain type of behavior in the monitored persons. In these situations, it is difficult to decide whether the presence of the parasite induced the observed changes in these persons, or whether a certain type of behavior in the observed persons increased the probability of infection by this parasite. Of course, a third possibility also exists, i.e. that both the changes in behavior and the infection by the particular parasite are both caused by a third, unknown factor. If the research is based on study of a large group of persons, then it would be possible to demonstrate statistically significant correlation arising as a consequence of the indirect effect of a very weak factor.
So far, the best-documented example of the existence of manipulative activity of a parasite in humans is the effect of latent asymptomatic infection by the protozoa Toxoplasma gondii on the psychological profile of humans, which was first described by Czech parasitologists (Flegr & Hrdy 1994; Flegr et al. 1996) {13300}.In nature, Toxoplasma is transmitted from its intermediate host, mostly mice rodents, to cats, its definitive host, through predation. An infected cat excretes resistant oocysts in its faeces, which can infect a wide spectrum of intermediate host species, including mice and humans. Infected persons generally have a mild form of the disease and, without realizing it, become carriers of the latent stage of the parasite to the end of their lives. It has been estimated that 30-50% of people in the Czech Republic have suffered from toxoplasmosis, while a figure of 83% has been given for Paris, France. Comparison of the psychological profile of persons infected and not infected by the parasite has revealed statistically significant differences in a number of monitored factors, including a tendency to look for new stimuli (Fig. XIX.15). It is interesting that different factors were affected in men and women and, when the changes were related to the same psychological factor, the shift mostly occurred in the opposite direction in men and women. When changes in these factors were examined for former patients who had suffered from acute toxoplasmosis in the past, i.e. persons for which records exist of when they were infected, it was found that there is a positive correlation between the time that had expired from the infection and the level of change in the psychological factors (Fig. XIX.16). This indicates that, at least in this case, the psychological changes were caused by the infection and not the infection by a change in psychological factors. In addition, latent toxoplasmosis is asymptomatic in practically all humans, so it cannot be expected that the psychological changes would occur as a result of unspecific deterioration of the state of health of the infected persons. However, the results of four studies of correlation between latent toxoplasmosis and the risk of traffic accidents indicate that the generally accepted assumption of harmlessness of latent “symptom-free” toxoplasmosis might not be valid and that this “harmless” parasitosis could, in fact, be responsible for more human fatalities than malaria (Fig. XIX.17).