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

In a great many cases, the pathogenic manifestations of parasitization tend to be caused by the defense mechanism of the host rather than the actual parasite activity. It is no exception for a host to die as a result of hyperactivity or autoreactivity of its immune system, while individuals with partial immunosuppression overcome the infection without difficulties. In most cases, it is apparently only a matter of failure of the relevant defense mechanisms, which are optimized for defense against certain species of parasites and that function disproportionately and counter-productively in defense against other parasites. However, it is also possible that, in at least some cases, this is an evolutionary adaptation on the part of the host, permitting elimination of infected individuals from the population and thus reducing the potential for spreading the parasite.
It is evident that a similar ability to “commit suicide” can emerge only through group or species or also kin selection. If an infected individual were occasionally capable under normal conditions of recovering and reproducing, then the strength of individual selection acting against the emergence of suicidal behavior would be so strong that the probability of its evolutionary formation would seem negligible. However, in some situations, the conditions for the formation of similar behavior are far more favorable. For example, populations of butterflies bound to food coming from a rare plant survive at a single site for a long time, so that the individuals are very closely related. In this case, a caterpillar can increase its inclusive fitness if it commits suicide following attack by a parasite or parasitoid, e.g. in that it would let itself be caught by a bird (Trail 1980). This kind of behavior has actually been observed for caterpillars of the butterfly Harris' Checkerspot (Chlosyne harrisii).
            In eusocial insects, the nonsexual casts do not participate at all in reproduction and express all their fitness in assisting sexual individuals. Here cases are also known that can be interpreted as voluntary suicide of parasitized individuals. Amongst bumble bees of the Bombus genus, individuals infected by parasitic flies of the Conopidae family stay out of the nest, both reducing the probability of transmission of the infection inside the nest and also increasing the probability that they will die (Poulin 1992; Muller & Schmidhempel 1992). However, according to some authors, the lower temperature outside the nest retards the development of the parasite and thus prolongs the survival time of the infected individual; for details, see (Poulin 1995a). Superinfection and virulence- The possibility of optimizing (and thus also of reducing) the rate of reproduction and the pathogenicity of a parasite is not limited only by the formation of genetic variability directly within the infrapopulation of parasites. It is limited even further by the possibility of multiple infection of a single host by genetically unrelated strains of parasites, i.e. the possibility of superinfection (Fig. XIX.8). In both cases, the genetic variability increases in the infrapopulation and systematic selection of “selfish” individuals multiplying at a greater rate than would be optimal from the viewpoint of the entire population (Bonhoeffer & Nowak 1994).
An increase in the growth rate within an infrapopulation and the related increase in the pathogenicity of the relevant parasitosis as a consequence of superinfection is of great importance from the standpoint of epidemiology. If, for example, a suitable epidemiological intervention manages to reduce the incidence of infection, i.e. the number of individuals infected per time unit, not only is the prevalence of infection, i.e. the number (percent) of infected individuals in the population, reduced, but also, as a consequence of reducing the frequency of superinfection, there is usually also a reduction in the pathogenicity of the relevant parasite. The trends in intestinal bacterial infections in countries where good water purification has been introduced are a typical example. This step was taken in the U.S.A. in the first quarter of the 20^th century; in the 1930’s the “virulent” (i.e. highly pathogenic) strains Shigella dysenteriae had already been replaced by less pathogenic strains S. flexneri; again, in the 1950’s these were replaced by even more benign strains of S. sonnei. Waste water treatment plants were introduced and the pathogenicity of dysentery decreased sooner in England, while both the introduction of waste water treatment and decrease in the pathogenicity of dysentery occurred later in Poland. Similar developments were also observed for Salmonella typhi and Vibrio cholerae.
            An increase in the probability of superinfection connected with increased genetic diversity of the parasite population is apparently the main reason for the great danger presented by hospital infections (Ewald 1994). In the U.S.A., infections acquired in a hospital, i.e. nosocomial infections, are the fourth most common cause of death. For example, at the present time, salmonellosis acquired outside a hospital environment is practically never fatal. However, salmonellosis acquired in a hospital is a cause of death in approximately one of seven infected patients and this can increase to one in three in some epidemics. Similarly, Staphylococcus aureus bacteria normally infect about 40% of the population but are not particularly harmful to their carriers. However, the prevalence of these bacteria reaches approximately 70% in hospitals and infection is accompanied by highly pathogenic symptoms that are frequently fatal to patients.
            There is a substantial increase in the virulence of parasitosis during military conflicts. Wars are frequently accompanied by the concentration and movement of large numbers of persons and a general decrease in hygiene standards. In some cases, there have been enormous concentrations of sick people at a single place and thus the creation of ideal conditions for selection of especially virulent strains of parasites. For example, during the I^st World War, an evacuation hospital in France had 340 beds for patients with respiratory diseases; as many as 824 people passed through per day, and a total of 34,000 people passed through over a three month period. The influenza epidemic that broke out in 1918 three months before the end of the war and which lasted approximately half a year had approximately a 10-fold higher fatality rate than influenzas in times of peace. During this period, 20 – 40 million people died, i.e. far more than those that died directly as a result of the I^st World War. After about three years, the death rate from influenza returned to normal, i.e. to a value of less than 0.1%. Similarly, during the American Civil War, 3% of those infected died from diseases with diarrhoea in the first year. Towards the end of the war, the fatality rate from diarrhoeal diseases increased to 20%. Simultaneously, this was apparently not a consequence of the reduced resistance of soldiers following from suffering during the war because, for example, the fatality rate from malaria was the same throughout this period. Basically, up to the II^nd World War, far more people died from infectious diseases during military conflicts (in recent times, primarily typhus and epidemic typhus) than as a result of war wounds. For example, it has been estimated that 10-20 times more soldiers died from parasitic diseases than in battle during the American War of Independence (Ewald 1994).