Infectious diseases are emerging globally at an unprecedented rate while global food demand is projected to increase sharply by 2100. Here, we synthesize the pathways by which projected agricultural expansion and intensification will influence human infectious diseases and how human infectious diseases might likewise affect food production and distribution. Feeding 11 billion people will require substantial increases in crop and animal production that will expand agricultural use of antibiotics, water, pesticides and fertilizer, and contact rates between humans and both wild and domestic animals, all with consequences for the emergence and spread of infectious agents. Indeed, our synthesis of the literature suggests that, since 1940, agricultural drivers were associated with >25% of all -and >50% of zoonotic -infectious diseases that emerged in humans, proportions that will likely increase as agriculture expands and intensifies. We identify agricultural and disease management and policy actions, and additional research, needed to address the public health challenge posed by feeding 11 billion people.
Despite awareness that disease emergence may be related to ecological change, few studies have rigorously analyzed the underlying environmental drivers of the dynamics of disease emergence. This may be due to the fact that ecological change and disease emergence are often mediated through complex and large‐scale processes that are not amenable to traditional reductionist approaches to causal inference. Here, we suggest strategies assembled from diverse disciplines, including ecology, epidemiology, and the social sciences, to analyze complex relationships, promote cooperation, increase efficiency, and minimize bias when investigating the ecological drivers of disease emergence. These techniques, which complement traditional hypothesis testing, include epidemiologic causal criteria, strong inference, causal diagrams, model selection, and triangulation. We also present several examples from recent emerging infectious disease investigations, including Hendra virus, Nipah virus, coral diseases, and avian influenza, where these techniques were successfully applied. Here, we outline some of the barriers to advancing our understanding of causation in disease ecology and offer some solutions for investigating large‐scale ecological drivers, such as global warming, pollution, and land‐use change.
Eliminating human parasitic disease often requires interrupting complex transmission pathways. Even when drugs to treat people are available, disease control can be difficult if the parasite can persist in nonhuman hosts. Here, we show that restoration of a natural predator of a parasite’s intermediate hosts may enhance drug-based schistosomiasis control. Our study site was the Senegal River Basin, where villagers suffered a massive outbreak and persistent epidemic after the 1986 completion of the Diama Dam. The dam blocked the annual migration of native river prawns (Macrobrachium vollenhoveni) that are voracious predators of the snail intermediate hosts for schistosomiasis. We tested schistosomiasis control by reintroduced river prawns in a before-after-control-impact field experiment that tracked parasitism in snails and people at two matched villages after prawns were stocked at one village’s river access point. The abundance of infected snails was 80% lower at that village, presumably because prawn predation reduced the abundance and average life span of latently infected snails. As expected from a reduction in infected snails, human schistosomiasis prevalence was 18 ± 5% lower and egg burden was 50 ± 8% lower at the prawn-stocking village compared with the control village. In a mathematical model of the system, stocking prawns, coupled with infrequent mass drug treatment, eliminates schistosomiasis from high-transmission sites. We conclude that restoring river prawns could be a novel contribution to controlling, or eliminating, schistosomiasis.
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