DOES SPATIAL HETEROGENEITY AND GENETIC-VARIATION IN POPULATIONS OF THE XANTHID CRAB RHITHROPANOPEUS HARRISII (GOULD) INFLUENCE THE PREVALENCE OF AN INTRODUCED PARASITIC CASTRATOR

Potential differences between two populations of the xanthid crab, Rhi thropanopeus harrisii (Gould), in susceptibility to infection by an in troduced (exotic) parasite, the sacculinid barnacle, Loxothylacus pano paei (Gissler) were investigated. The frequency of L. panopaei infecti on, which causes castration of the crab host, has risen to 80% during the last 4 yr in one population, while the second population has never been parasitized. Using eggs collected from females of both infected and uninfected populations, broods of larval crabs were reared through metamorphosis, and then placed in field enclosures at the site of the infected population where they were exposed to ambient levels of infe ctive stages of the parasite. We used differences in infection levels among sibling hosts from each population to estimate the heritability (h(2)) of susceptibility to parasite infection. Comparisons of infecti on levels between populations showed no significant differences, nor w ere there significant differences in parasitism levels among families within a population. The estimate of heritability for susceptibility t o parasitic castration was low (h(2) = 0.10), and not significantly di fferent from zero, suggesting little additive genetic variance. In a s econd experiment, we examined how levels of parasite infection within a single population were affected by the spatial distribution of the c rab population. We placed susceptible juvenile R. harrisii in enclosur es either 0.1, 1.0, or 10.0 m from experimental aggregations of infect ed crabs, which acted as a potential source of infective parasite larv ae. The spatial distribution significantly influenced levels of parasi tic castration with significantly more infected juvenile crabs in encl osures nearest to experimental aggregations (0.1 m) than in enclosures 1.0 m and 10.0 m away. The lack of differences in susceptibility amon g populations, as well as families within populations, may be explaine d by several mechanisms including significant gene flow between popula tions and insufficient time for a measurable response to selection. Th e data are also consistent with the idea that equivalent generation ti mes of host and parasite may allow the parasite to evolve infectivity as fast as the host can evolve resistance. The significant influence o f the spatial distribution of the host population on the prevalence of the parasite suggests that both the rate of spatial spread and preval ence of this parasite in Chesapeake Bay may be influenced by the dista nce between aggregations of the host population.