|Fecundity compensation in the three-spined stickleback Gasterosteus aculeatus infected by the diphyllobothriidean cestode Schistocephalus solidus|
|Heins, D.C. (2012). Fecundity compensation in the three-spined stickleback Gasterosteus aculeatus infected by the diphyllobothriidean cestode Schistocephalus solidus. Biol. J. Linn. Soc. 106(4): 807-819. dx.doi.org/10.1111/j.1095-8312.2012.01907.x|
|In: Biological Journal of the Linnean Society. Academic Press: London. ISSN 0024-4066, more|
castration; manipulation; nutrient theft; parasitism; side effect; sterility
Causal explanations for host reproductive phenotypes influenced by parasitism fit into three broad evolutionary models: (1) non-adaptive side effect; (2) adaptive parasitic manipulation; and (3) adaptive host defence. This study demonstrates fecundity compensation, an adaptive non-immunological host defence, in the three-spined stickleback fish (Gasterosteus aculeatus) infected by the diphyllobothriidean cestode Schistocephalus solidus. Both infected and uninfected female sticklebacks produced egg clutches at the same age and size. The reproductive capacity of infected females decreased rapidly with increased parasite : host body mass ratio. Body condition was lower in infected females than uninfected females and decreased with increasing parasite : host mass ratio. Females with clutches had greater body condition than those without clutches. A point biserial correlation showed that there was a body condition threshold necessary for clutch production to occur. Host females apparently had the capacity to produce egg clutches until the prolonged effects of nutrient theft by the parasite and the drain on resources from reproduction precluded clutch formation. Clutch mass, adjusted for female body mass, did not differ significantly between infected and uninfected females. Infected females apparently maintained the same level of reproductive allotment (egg mass as proportion of body mass) as uninfected females. Infected females produced larger clutches of smaller eggs than uninfected females, revealing a trade-off between egg mass and egg number, consistent with the fecundity compensation hypothesis. The rapid loss of reproductive capacity with severity of infection probably reflects the influence of the parasite combined with a trade-off between current and future reproduction in the host. Inter-annual differences in reproductive performance may have reflected ecological influences on host pathology and/or intra-annual seasonal changes.