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

- If a parasite is transmitted horizontally through direct contact between an infected and uninfected individual, parasitosis is generally less virulent. From the standpoint of spreading of the parasite, it would be inexpedient if it were to substantially harm the state of health of the infected host and thus limit its number of contacts with healthy individuals. To the contrary, the virulence of parasites tends to be greater for some other means of spreading parasitosis. For example, parasites spread by vectors tend to have high virulence. This is true both for parasites spread by animal vectors (Ewald 1983), such as mosquitoes (Fig. XIX.10), as well as parasites spread by abiotic vectors, for example flowing water. (Ewald 1991) (Fig. XIX.11). The infected animal can be harmed by the parasite or even immobilized, as the vector is responsible for transfer of the infection to another individual in the population. If water acts as the vector, high virulence of the parasite is also enhanced by a large size of the infection inoculum, which generally enters a single host during infection, with the related high genetic variability within the infrapopulation (see XIX.4.2.2). If the vector is an animal, its manifestations of parasitosis are generally much milder than those in the actual host. It is the role of the vector in the life cycle of the parasite to spread the infection in space and any damage to its state of health would be detrimental to this function. 
 
Parasites capable of independent active motion from one individual to another within the host population, for example, parasitic Hymenoptera or Diptera, also frequently exhibit high virulence. In this case, the parasite is very frequently converted to a parasitoid during evolution, i.e. a parasite that kills its host after a certain period of symbiosis with the infected individual.
Parasites spread alimentarily, specifically by predation, also exhibit high virulence (Ewald 1995). In these cases, the pathological manifestations of parasitosis can increase the chance that the infected individual will be caught by a predator, leading to transfer of the infection. Simultaneously, the predator is usually harmed substantially less than its prey. Otherwise, it would be a relatively easy matter for individuals to be selected in the population of predators that would learn to avoid infected individuals amongst prey when hunting. It could also be important that the definitive host often also acts as a vector and harming the vector would be detrimental to its function in the life cycle of the parasite – spreading infection in space. Simultaneously, the frequent combination of the function of a vector and definitive host need not be accidental and can have a certain importance. During spreading of parasites in space, offspring can frequently encounter conditions differing from those under which their parents lived; under these circumstances, even temporary variability, formed during multiplication through recombination and segregation, can be an advantage (see for example, XIII.3.2.2.2).
High virulence can be exhibited by sit-and-wait infections, i.e. infection transmitted through long-lived resistant stages, spores and cysts, which remain where the infected host died and then infect another host that comes some time in the future (Ewald 1995). Anthrax and smallpox are typical examples of sit-and-wait infections and their spores can remain in the environment for years or even decades. The high virulence of infection in these parasites is a result of the fact that the probability of infecting another host is proportional to the number of spores that remain at the site of death of the infected individual. Consequently, a parasite will attempt to convert as large a part of the body of its host into its own spores or cysts as fast as possible. This is, of course, mostly incompatible with the life of the host organism.