It is said that one hall mark of good SF is that it predicts Science
Fact.
With the sequel to The Mote in God’s Eye, Larry Niven is still very much on
the ball as the discoverer of a new parasitic contraceptive,
Professor Chris Arme (CBiol
FIBiol), shows.
I never read science fiction, or at least not until now. This late conversion arises from reading extracts from The Moat Around Murcheson’s Eye in which an explosion of alien population growth is described. The problem was solved when the Blaine Institute engineered a C -L (Contraceptive-Longevity) worm from a parasitic organism similar to parasitic flatworms found on earth. The C-L worm produces a male sex-hormone, which is the basis for its contraceptive effect. The organisms are able to live in alien body cavities and one C-L is just as effective as several.
This story is remarkable because it reflects current research on an earthly flatworm, a tapeworm named Ligula intestinalis. This parasite lives as an immature stage in the body cavity of fish of the carp family. There are several pathological effects associated with infection and the most striking of these is that infected fish never breed. Even when only one worm is present, the effect on fish reproduction is the same as in multiple infections. The sex organs of both males and females remain undeveloped, irrespective of season or fish age, and they never contain ripe eggs or sperm. Since this effect has been known since the 1940’s, it is clear that, in this case, the science egg came first.
It is not parasitic castration, since the sex organs are not destroyed. Instead, their development is inhibited in infected fish, so that only the very earliest stages of egg and sperm development are present. Normally, these early stages would be stimulated by hormones produced by the pituitary gland to produce ripe eggs and sperm. It therefore seemed appropriate to examine the pituitary gland in parasitised and non-parasitised fish, to determine whether infection was associated with changes here, as well as in the sex organs. It was! In the pituitary gland it is possible, using staining techniques, to detect those cells that produce the hormones responsible for stimulating egg and sperm development. In normal fish, there are many of these cells, and their levels of activity change with season, in a way that can be correlated with the breeding cycle. In marked contrast, in parasitised fish there appear to be fewer such cells, and they remain small and inactive at all times of the year. This strongly suggests that the sex organs in infected fish do not develop because the tapeworm stops hormone production by the pituitary gland.
It is not competition for food because even one tapeworm in a relatively large fish can induce the contraceptive effect. We think that there is an intimate physiological interaction between the parasite and the fish reproductive hormonal system, presumably mediated by some chemical(s) produced by the tapeworm. Current studies are focused on hormones produced in the fish brain, called gonadotrophin-releasing hormones (GnRHs). These are the main stimulus for the pituitary gland to produce and release its hormones which, as noted above, go on to induce development of eggs and sperm. Molecular studies have shown that there are two main GnRHs, and the genes that are responsible for directing the production of these have been characterised. We are now determining whether there are differences in the GnRH production in parasitised and normal fish and there is some evidence that this is the case.
Some might contend that suggesting that a platyhelminth is able to disrupt the complex mechanisms controlling reproduction in a vertebrate, at the level of gene expression borders on science fiction. And yet, the more we understand about the amazingly intimate relationships that exist between some parasites and their hosts, the more credible the proposal seems. For example, there is another tapeworm species, Spirometra mansonoides, that mimics the effect of growth hormone so that parasitised rats and mice grow at a much faster rate that their parasite-free siblings. And in insects, there are very many examples of parasites influencing reproduction.
One can only speculate on the possible advantages to the worm of its contraceptive effect on fish. Reproduction is a major cause of mortality in fish. The longer the infected fish can be kept alive, the greater the chance of the parasite completing its life cycle, which involves the infected fish being eaten by a fish-eating bird, with the adult tapeworm developing and producing eggs in the bird gut. It is also worth noting that the behaviour of infected fish is changed in ways that facilitate this transmission. In summer, non-infected mature fish will shoal in deep waters of lakes to reproduce. In contrast, parasitised fish tend to stay in shallow inshore waters, where they are readily preyed upon by birds.
The hormonal systems controlling reproduction are very similar in all vertebrates, from fish to mammals. It is therefore likely that effects brought about by the parasite in the fish may also occur in other vertebrate classes. There is some evidence that this is the case in amphibians, which are not normal hosts for Ligula intestinalis. When the South African Clawed Toad (Xenopus laevis) was artificially infected with the tapeworm, changes occurred in the cells of the toad pituitary gland that closely resembled those found in fish. Is it going too far then to speculate that reproduction in humans and domesticated animals might also be controlled using a tapeworm, contraceptive? I think not. Of course, this would not involve trying to genetically engineer the parasite so that it could infect humans. Rather it is a quest for the chemicals produced by the worm, which could be administered by injection or orally. A totally novel method of contraception may be just around the corner, and one which could be equally effective in males and females. Does anyone know the telephone number of the Blaine Institute?
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