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Theory has shown that the effects of demographic stochasticity on communities may depend on the magnitude of fitness differences between species. In particular, it has been suggested that demographic stochasticity has the potential to significantly alter competitive outcomes when fitness differences are small (nearly neutral), but that it has negligible effects when fitness differences are large (highly non‐neutral). Here we test such theory experimentally and extend it to examine how demographic stochasticity affects exclusion frequency and mean densities of consumers in simple, but non‐neutral, consumer–resource communities. We used experimental microcosms of protists and rotifers feeding on a bacterial resource to test how varying absolute population sizes (a driver of demographic stochasticity) affected the probability of competitive exclusion of the weakest competitor. To explore whether demographic stochasticity could explain our experimental results, and to generalize beyond our experiment, we paired the experiment with a continuous‐time stochastic model of resource competition, which we simulated for 11 different fitness inequalities between competiting consumers. Consistent with theory, in both our experiments and our simulations we found that demographic stochasticity altered competitive outcomes in communities where fitness differences were small. However, we also found that demographic stochasticity alone could affect communities in other ways, even when fitness differences between competitors were large. Specifically, demographic stochasticity altered mean densities of both weak and strong competitors in experimental and simulated communities. These findings highlight how demographic stochasticity can change both competitive outcomes in non‐neutral communities and the processes underlying overall community dynamics.

The β-null deviation measure, developed as a null model for β-diversity, is increasingly used in empirical studies to detect the underlying structuring mechanisms in communities (e.g. niche versus neutral and stochastic versus deterministic). Despite growing use, the ecological interpretation of the presence/absence and abundance-based versions of the β-null diversity measure have not been tested against communities with known assembly mechanisms, and thus have not been validated as an appropriate tool for inferring assembly mechanisms. Using a mechanistic model with known assembly mechanisms, we simulated replicate metacommunities and examined β-null deviation values 1) across a gradient of niche (species-sorting) to neutrally structured metacommunities, 2) through time, and 3) we compared the effect of changes in assembly mechanism on the performance of the β-null deviation measures. The impact of stochasticity on assembly outcomes was also considered. β-null deviation measures proved to be interpretable as a measure of niche or neutral assembly. However, the presence/absence version of the β-null deviation measure could not differentiate between niche and neutral metacommunities if demographic stochasticity were present. The abundance-based β-null deviation measure was successful in distinguishing between niche and neutral metacommunities and was robust to the presence of stochasticity, changes through time, and changing assembly mechanisms. However, we suggest that it is not robust to changing abundance evenness distributions or sampling of communities, and so its interpretation still requires some care. We encourage the testing of the assumptions behind null models for ecology and care in their application.

Despite the ubiquity of bilateral symmetry among animals, a long-standing mystery centers on why parasites that infect paired organs often do so non-randomly. Examples from diverse host and parasite taxa continue to accumulate, yet little is known about their causes or implications for host – parasite fi tness. We combined fi eld surveys, experimental infections, and parasite choice assays to evaluate both competing explanations for – and consequences of – asymmetric infections of amphibian kidneys by echinostome trematodes, which are widespread and potentially pathogenic infections of larval amphibians. Samples from 6001 hosts representing 26 species indicated that echinostome infections exhibit a consistent, right-kidney bias, with ∼ 62% of parasites in the right kidney. Th is pattern could not be explained by variation in kidney size or total infection. Experimental infections of three anuran species reproduced this pattern, with 64% of infections in the right kidney, and indicated it was not the result of diff erential host or parasite mortality. Based on sequential infection experiments and parasite choice assays, we further showed that earlier infections did not aff ect the distribution of subsequently colonizing parasites and that echinostome cercariae followed host-derived cues rather than exhibiting congenital ‘ sidedness ’ . We advance the hypothesis that variation in the position of the right kidney along the anterior – posterior axis controls cue strength in the right nephric duct and thus determines parasite encystment. Correspondingly, anatomical measurements from a subset of larval amphibian hosts revealed that the relative position of the right kidney explained 83% of the variation in infection bias, with no additional contributions associated with kidney volume or host size. We also show that the degree of right-kidney bias associated positively with host growth in experiments. Morphological asymmetries could therefore function as a unique form of tolerance to mitigate the consequences of infection, despite the oft-cited costs of asymmetry for mate selection and enemy vulnerability.