The extent to which the biodiversity and community composition of ecosystems affect their functions is an issue that grows ever more compelling as human impacts on ecosystems increase. We present evidence that supports a novel function of vertebrate biodiversity, the buffering of human risk of exposure to Lymedisease-bearing ticks. We tested the Dilution Effect model, which predicts that high species diversity in the community of tick hosts reduces vector infection prevalence by diluting the effects of the most competent disease reservoir, the ubiquitous white-footed mouse (Peromyscus leucopus). As habitats are degraded by fragmentation or other anthropogenic forces, some members of the host community disappear. Thus, species-poor communities tend to have mice, but few other hosts, whereas species-rich communities have mice, plus many other potential hosts. We demonstrate that the most common nonmouse hosts are relatively poor reservoirs for the Lyme spirochete and should reduce the prevalence of the disease by feeding, but rarely infecting, ticks. By accounting for nearly every host species' contribution to the number of larval ticks fed and infected, we show that as new host species are added to a depauperate community, the nymphal infection prevalence, a key risk factor, declines. We identify important ''dilution hosts'' (e.g., squirrels), characterized by high tick burdens, low reservoir competence, and high population density, as well as ''rescue hosts'' (e.g., shrews), which are capable of maintaining high disease risk when mouse density is low. Our study suggests that the preservation of vertebrate biodiversity and community composition can reduce the incidence of Lyme disease.

Vectors of infectious diseases are generally thought to be regulated by abiotic conditions such as climate or the availability of specific hosts or habitats. In this study we tested whether blacklegged ticks, the vectors of Lyme disease, granulocytic anaplasmosis and babesiosis can be regulated by the species of vertebrate hosts on which they obligately feed. By subjecting field-caught hosts to parasitism by larval blacklegged ticks, we found that some host species (e.g. opossums, squirrels) that are abundantly parasitized in nature kill 83 -96% of the ticks that attempt to attach and feed, while other species are more permissive of tick feeding. Given natural tick burdens we document on these hosts, we show that some hosts can kill thousands of ticks per hectare. These results indicate that the abundance of tick vectors can be regulated by the identity of the hosts upon which these vectors feed. By simulating the removal of hosts from intact communities using empirical models, we show that the loss of biodiversity may exacerbate disease risk by increasing both vector numbers and vector infection rates with a zoonotic pathogen.

The drivers of variable disease risk in complex multi-host disease systems have proved very difficult to identify. Here we test a model that explains the entomological risk of Lyme disease (LD) in terms of host community composition. The model was parameterized in a continuous forest tract at the Cary Institute of Ecosystem Studies (formerly the Institute of Ecosystem Studies) in New York State, U.S.A. We report the results of continuing longitudinal observations (10 years) at the Cary Institute, and of a shorter-term study conducted in forest fragments in LD endemic areas of Connecticut, New Jersey, and New York, USA. Model predictions were significantly correlated with the observed nymphal infection prevalence (NIP) in both studies, although the relationship was stronger in the longer-term Cary Institute study. Species richness was negatively, albeit weakly, correlated with NIP (logistic regression), and there was no relationship between the Shannon diversity index (H') and NIP. Although these results suggest that LD risk is in fact dependent on host diversity, the relationship relies explicitly on the identities and frequencies of host species such that conventional uses of the term biodiversity (i.e., richness, evenness, H') are less appropriate than are metrics that include species identity. This underscores the importance of constructing interaction webs for vertebrates and exploring the direct and indirect effects of anthropogenic stressors on host community composition.

Distinguishing the mechanisms responsible for the relationship between biodiversity and ecosystem services requires knowledge of (1) the functional roles played by individual species and (2) the sequence with which species are added to or lost from communities in nature (i.e., “community assembly” and “community disassembly,” respectively). Rarely, if ever, are both these issues understood with certainty in any given ecosystem. We used an empirically based simulation model to assess the degree to which the sequence of species loss from vertebrate communities influences risk of human exposure to Lyme disease, as measured by the proportion of ticks infected with the etiological agent. Dramatic differences in the shapes of the curves relating vertebrate biodiversity to disease risk (which we consider an ecosystem service) were observed. Randomized sequences of species loss resulted in a decrease in disease risk with reduced biodiversity, a result that is contradicted by both empirical observations and model results from nonrandomized sequences of species loss (i.e., specific “disassembly rules”). All potentially realistic disassembly rules resulted in increases in disease risk with decreasing biodiversity, although shapes of the curves varied considerably. Our results highlight the importance of both species identity and the order by which species are lost, in understanding the mechanisms by which biodiversity affects ecosystem functioning. Corresponding Editor: O. V. Schmitz.