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Infectious disease burdens vary from country to country and year to year due to ecological and economic drivers. Recently, Murray et al. (Murray CJ et al 2012 Lancet380, 2197-2223. (doi:10.1016/S0140-6736(12)61689-4)) estimated country-level morbidity and mortality associated with a variety of factors, including infectious diseases, for the years 1990 and 2010. Unlike other databases that report disease prevalence or count outbreaks per country, Murray et al. report health impacts in per-person disability-adjusted life years (DALYs), allowing comparison across diseases with lethal and sublethal health effects. We investigated the spatial and temporal relationships between DALYs lost to infectious disease and potential demographic, economic, environmental and biotic drivers, for the 60 intermediate-sized countries where data were available and comparable. Most drivers had unique associations with each disease. For example, temperature was positively associated with some diseases and negatively associated with others, perhaps due to differences in disease agent thermal optima, transmission modes and host species identities. Biodiverse countries tended to have high disease burdens, consistent with the expectation that high diversity of potential hosts should support high disease transmission. Contrary to the dilution effect hypothesis, increases in biodiversity over time were not correlated with improvements in human health, and increases in forestation over time were actually associated with increased disease burden. Urbanization and wealth were associated with lower burdens for many diseases, a pattern that could arise from increased access to sanitation and healthcare in cities and increased investment in healthcare. The importance of urbanization and wealth helps to explain why most infectious diseases have become less burdensome over the past three decades, and points to possible levers for further progress in improving global public health.This article is part of the themed issue 'Conservation, biodiversity and infectious disease: scientific evidence and policy implications'.

Understanding the effects of anthropogenic disturbance on zoonotic disease risk is both a critical conservation objective and a public health priority. Here, we evaluate the effects of multiple forms of anthropogenic disturbance across a precipitation gradient on the abundance of pathogen-infected small mammal hosts in a multi-host, multi-pathogen system in central Kenya. Our results suggest that conversion to cropland and wildlife loss alone drive systematic increases in rodent-borne pathogen prevalence, but that pastoral conversion has no such systematic effects. The effects are most likely explained both by changes in total small mammal abundance, and by changes in relative abundance of a few high-competence species, although changes in vector assemblages may also be involved. Several pathogens responded to interactions between disturbance type and climatic conditions, suggesting the potential for synergistic effects of anthropogenic disturbance and climate change on the distribution of disease risk. Overall, these results indicate that conservation can be an effective tool for reducing abundance of rodent-borne pathogens in some contexts (e.g. wildlife loss alone); however, given the strong variation in effects across disturbance types, pathogen taxa and environmental conditions, the use of conservation as public health interventions will need to be carefully tailored to specific pathogens and human contexts.This article is part of the themed issue 'Conservation, biodiversity and infectious disease: scientific evidence and policy implications'.

Populations of large wildlife are declining on local and global scales. The impacts of this pulse of size-selective defaunation include cascading changes to smaller animals, particularly rodents, and alteration of many ecosystem processes and services, potentially involving changes to prevalence and transmission of zoonotic disease. Understanding linkages between biodiversity loss and zoonotic disease is important for both public health and nature conservation programs, and has been a source of much recent scientific debate. In the case of rodent-borne zoonoses, there is strong conceptual support, but limited empirical evidence, for the hypothesis that defaunation, the loss of large wildlife, increases zoonotic disease risk by directly or indirectly releasing controls on rodent density. We tested this hypothesis by experimentally excluding large wildlife from a savanna ecosystem in East Africa, and examining changes in prevalence and abundance of Bartonella spp. infection in rodents and their flea vectors. We found no effect of wildlife removal on per capita prevalence of Bartonella infection in either rodents or fleas. However, because rodent and, consequently, flea abundance doubled following experimental defaunation, the density of infected hosts and infected fleas was roughly twofold higher in sites where large wildlife was absent. Thus, defaunation represents an elevated risk in Bartonella transmission to humans (bartonellosis). Our results (i) provide experimental evidence of large wildlife defaunation increasing landscape-level disease prevalence, (ii) highlight the importance of susceptible host regulation pathways and host/vector density responses in biodiversity-disease relationships, and (iii) suggest that rodent-borne disease responses to large wildlife loss may represent an important context where this relationship is largely negative.

Infectious disease risk is often influenced by host diversity, but the causes are unresolved. Changes in diversity are associated with changes in community structure, particularly during community assembly; therefore, by incorporating change over time, host community assembly may provide a framework to resolve causation. In turn, community assembly can be driven by many processes, including resource enrichment. To test the hypothesis that community assembly causally links host diversity to future disease, we experimentally manipulated host diversity and resource supply to hosts, then allowed communities to assemble for 2 years (surveyed 2012–2014). Initially, host diversity increased disease. Subsequently, host diversity did not directly alter disease. However, host diversity determined the trajectory of host community assembly, altering colonisation by exotic host species and richness‐independent host phylogenetic diversity, which together reversed the initial increase in disease. Ultimately, incorporating the temporal dimension of community assembly revealed novel mechanisms linking host diversity to future disease. [ABSTRACT FROM AUTHOR]

Species introductions are a dominant component of biodiversity change but are not explicitly included in most discussions of biodiversity–disease relationships. This is a major oversight given the multitude of effects that introduced species have on both parasitism and native hosts. Drawing on both animal and plant systems, we review the competing mechanistic pathways by which biological introductions influence parasite diversity and prevalence. While some mechanisms – such as local changes in phylogenetic composition and global homogenization – have strong explanatory potential, the net effects of introduced species, especially at local scales, remain poorly understood. Integrative, community-scale studies that explicitly incorporate introduced species are needed to make effective predictions about the effects of realistic biodiversity change and conservation action on disease. [ABSTRACT FROM AUTHOR]

Understanding the effects of anthropogenic disturbance on zoonotic disease risk is both a critical conservation objective and a public health priority. Here, we evaluate the effects of multiple forms of anthropogenic disturbance across a precipitation gradient on the abundance of pathogen-infected small mammal hosts in a multi-host, multi-pathogen system in central Kenya. Our results suggest that conversion to cropland and wildlife loss alone drive systematic increases in rodent-borne pathogen prevalence, but that pastoral conversion has no such systematic effects. The effects are most likely explained both by changes in total small mammal abundance, and by changes in relative abundance of a few high-competence species, although changes in vector assemblages may also be involved. Several pathogens responded to interactions between disturbance type and climatic conditions, suggesting the potential for synergistic effects of anthropogenic disturbance and climate change on the distribution of disease risk. Overall, these results indicate that conservation can be an effective tool for reducing abundance of rodent-borne pathogens in some contexts (e.g. wildlife loss alone); however, given the strong variation in effects across disturbance types, pathogen taxa and environmental conditions, the use of conservation as public health interventions will need to be carefully tailored to specific pathogens and human contexts. This article is part of the themed issue ‘Conservation, biodiversity and infectious disease: scientific evidence and policy implications’.

Control of human infectious disease has been promoted as a valuable ecosystem service arising from the conservation of biodiversity. There are two commonly discussed mechanisms by which biodiversity loss could increase rates of infectious disease in a landscape. First, loss of competitors or predators could facilitate an increase in the abundance of competent reservoir hosts. Second, biodiversity loss could disproportionately affect non-competent, or less competent reservoir hosts, which would otherwise interfere with pathogen transmission to human populations by, for example, wasting the bites of infected vectors. A negative association between biodiversity and disease risk, sometimes called the "dilution effect hypothesis," has been supported for a few disease agents, suggests an exciting win-win outcome for the environment and society, and has become a pervasive topic in the disease ecology literature. Case studies have been assembled to argue that the dilution effect is general across disease agents. Less touted are examples in which elevated biodiversity does not affect or increases infectious disease risk for pathogens of public health concern. In order to assess the likely generality of the dilution effect, we review the association between biodiversity and public health across a broad variety of human disease agents. Overall, we hypothesize that conditions for the dilution effect are unlikely to be met for most important diseases of humans. Biodiversity probably has little net effect on most human infectious diseases but, when it does have an effect, observation and basic logic suggest that biodiversity will be more likely to increase than to decrease infectious disease risk. [ABSTRACT FROM AUTHOR]

Many studies have suggested that ecosystem conservation protects human and wildlife populations against infectious disease. We tested this hypothesis using data on primates and their parasites. First, we tested for relationships between species' resilience to human disturbance and their parasite richness, prevalence and immune defences, but found no associations. We then conducted a meta-analysis of the effects of disturbance on parasite prevalence, which revealed no overall effect, but a positive effect for one of four types of parasites (indirectly transmitted parasites). Finally, we conducted intraspecific analyses of malaria prevalence as a function of mammalian species richness in chimpanzees and gorillas, and an interspecific analysis of geographic overlap and parasite species richness, finding that higher levels of host richness favoured greater parasite risk. These results suggest that anthropogenic effects on disease transmission are complex, and highlight the need to define the conditions under which environmental change will increase or decrease disease transmission. [ABSTRACT FROM AUTHOR]