Zoonotic pathogens are significant burdens on global public health. Because they are transmitted to humans from non-human animals, the transmission dynamics of zoonoses are necessarily influenced by the ecology of their animal hosts and vectors. The 'dilution effect' proposes that increased species diversity reduces disease risk, suggesting that conservation and public health initiatives can work synergistically to improve human health and wildlife biodiversity. However, the meta-analysis that we present here indicates a weak and highly heterogeneous relationship between host biodiversity and disease. Our results suggest that disease risk is more likely a local phenomenon that relies on the specific composition of reservoir hosts and vectors, and their ecology, rather than patterns of species biodiversity.

Lyme disease is the most common tick-borne disease in temperate regions of North America, Europe and Asia, and the number of reported cases has increased in many regions as landscapes have been altered. Although there has been extensive work on the ecology and epidemiology of this disease in both Europe and North America, substantial uncertainty exists about fundamental aspects that determine spatial and temporal variation in both disease risk and human incidence, which hamper effective and efficient prevention and control. Here we describe areas of consensus that can be built on, identify areas of uncertainty and outline research needed to fill these gaps to facilitate predictive models of disease risk and the development of novel disease control strategies. Key areas of uncertainty include: (i) the precise influence of deer abundance on tick abundance, (ii) how tick populations are regulated, (iii) assembly of host communities and tick-feeding patterns across different habitats, (iv) reservoir competence of host species, and (v) pathogenicity for humans of different genotypes of Filling these knowledge gaps will improve Lyme disease prevention and control and provide general insights into the drivers and dynamics of this emblematic multi-host-vector-borne zoonotic disease.This article is part of the themed issue 'Conservation, biodiversity and infectious disease: scientific evidence and policy implications'.

The developmental timing of Ixodes pacficus Cooley & Kohls, the primary vector of the Lyme disease spirochete and the agent of human granulocytic ehrlichiosis in the far-western United States, was determined under field and laboratory conditions. During their seasonal peaks of abundance, each of the three parasitic stages of L. pacificus, both fed and unfed, was placed inside silk-screen packets. These packets were apportioned between four topographic exposures of two hilltop sites in northwestern California. The sites differed in vegetational composition and elevation: the first (elevation 390 m) was dominated by woodland-grass, the second (elevation 914 m) by chaparral. The timing of oviposition, larval eclosion, molting, and mortality were recorded in the field every 2-3 wk for 2.5 yr. Microenvironmental temperatures were measured on all four exposures at both sites. Accelerated developmental rates of all three stages were correlated with warmer soil temperatures and the time of placement in the field. In the laboratory, replete female I. pacificus maintained under uniform environmental conditions sustained constant preovipositional and prehatch periods independent of date-of-feeding. In the field, all unfed stages survived through one active feeding season with most larvae and nymphs remaining in behavioral diapause between late summer and early spring. No life stage survived through two active feeding periods which suggests that cohorts do not overlap. We concluded that I. pacificus takes a minimum of 3 yr to complete its life cycle in northwestern California.

This is the first confirmation of human disease associated with the SFGR 364D, which was likely transmitted by D. occidentalis. Although the patients described here presented with a single cutaneous eschar as the principal manifestation, the full spectrum of illness associated with 364D has yet to be determined. Possible infection with 364D or other SFGR should be confirmed through molecular techniques in patients who present with "spotless" Rocky Mountain spotted fever or have serum antibodies to R. rickettsii with group-specific assays.