Parasitic castration is a fairly common means of affecting the physiology of a host organism. In some cases, this occurs more or less incidentally; the parasite first consumes the tissues and organs that are not essential for the life of the host (Wilson & Denison 1980). However, in other cases, this is a targeted effect, brought about, for example, by the production of certain hormones. For example, in Biomphalaria glabrata snails infected with Schistosoma mansoni fluke worms, there is a substantial reduction in the level of biogenic monoamines (serotonin (5-HT), dopamine (DA) and L-dopa) in the plasma and in the central nervous system; the 5-HT level in snails is closely correlated with egg production (Manger et al. 1996). A different kind of fluke worm, Prosorhynchus squamatus, which parasitizes on marine mussels (Mytilus edulis), increases the level of the factor that reduces the intensity of division of future gametes (Coustau et al. 1991). Through temporary or permanent castration of its host, the parasite achieves a change in energy fluxes in the particular organism and specifically redirects that part of the energy, that the host would normally devote to its reproduction, towards growth and regeneration (Wilson & Denison 1980). In this way, it actually increases the viability of the host organism at the expense of reducing its fertility (Fig. XIX.13). While the host is concerned to optimize the ratio of energy invested into reproduction and into the other life functions, a parasite is usually primarily concerned with the length of survival of the infected individual, but not with its reproduction. It has been found, for example, that water snails of the Lymnaea truncatula species, infected and castrated by larvae of the fluke worm Fasciola hepatica, grow to as much as twice the weight of control snails (Wilson & Denison 1980). However, in some systems, castration of snails is only a side effect of parasitism and occurs through the effect of any kind of physiological stress.
The feminization of male mice apparently has a somewhat different purpose; this is caused by the larvae of Taenia crassiceps tapeworms through an approximately ten-fold reduction in the testosterone level and an approximately two-hundred-fold increase in the estradiol level in the serums of infected animals. It is known that mouse females are far less resistant against the infection than males and that, following hormonal feminization, the sensitivity of the two sexes (tendency to tolerate the growth and reproduction of tapeworms) is more or less equal. Some lymphokins (IL-6?), whose production is dependent primarily on the sex hormone level, are apparently of key importance here (Larralde et al. 1995).