This chapter explores how changes in land use, climate, and the function of ecosystems may act synergistically to alter exposure to infectious disease and natural disasters and curtail access to food, clean air, and clean water – basic components of the public’s health. It focuses on the greatest emerging threats from climate and large-scale, anthropogenic changes to landscapes and natural systems for ecosystem services: food production and clean water provision. These 2 are difficult to study using traditional approaches as they are multi-factoral and complex and often occur over very large scales. Ample evidence exists regarding alterations to disease transmission; most but not all show increases. Mechanisms by which changes occur include: changes in the density or presence of disease-related organisms; changes in exposure pathways; and changes in community species composition. Food and water scarcity combined with greater vulnerability to natural disasters may lead to much higher morbidity and mortality e.g. from malnutrition and chronic hunger, particularly in SSA and parts of SE Asia experiencing ecological constraints to local food production due to soil degradation and water scarcity. Water is also needed for drinking, sanitation, hygiene, and food preparation - inadequate access causes millions of deaths. Climate change is expected to worsen water scarcity. Depletion of ecosystem services might impact health only when resources are very constrained and a threshold is reached. Vulnerability to natural disasters (fires, floods, storms, tidal waves, landslides) influences how changing environmental conditions may impact human health. Vulnerability differs by socioeconomic status and by gender (especially women) and age. This summary is not an official abstract. Users should refer to the original published version of the material for the full abstract
There has been, to date, little discussion about the defining features and measures of wildlife health in the literature or legislation. Much wildlife health work focuses on the detection and response to infectious or parasitic diseases; this perspective has been reinforced by the focus of the One Health initiative on wildlife as sources of emerging infections. The definition of health as ‘‘the absence of disease’’ lags 70 yr behind modern concepts of human health and emerging concepts of wildlife health in terms of vulnerability, resilience, and sustainability. Policies, programs, and research that focus on the integration of wildlife health with natural resource conservation, ecosystem restoration, and public health need a working definition of health that recognizes the major threats to fish and wildlife are the result of many other drivers besides pathogens and parasites, including habitat loss, globalization of trade, land-use pressure, and climate change. A modern definition of wildlife health should emphasize that 1) health is the result of interacting biologic, social, and environmental determinants that interact to affect capacity to cope with change; 2) health cannot be measured solely by what is absent but rather by characteristics of the animals and their ecosystem that affect their vulnerability and resilience; and 3) wildlife health is not a biologic state but rather a dynamic social construct based on human expectations and knowledge.
Infectious diseases of humans, wildlife, and domesticated species are increasing worldwide, driving the need to understand the mechanisms that shape outbreaks. Simultaneously, human activ- ities are drastically reducing biodiversity. These concurrent pat- terns have prompted repeated suggestions that biodiversity and disease are linked. For example, the dilution effect hypothesis posits that these patterns are causally related; diverse host communities inhibit the spread of parasites via several mecha- nisms, such as by regulating populations of susceptible hosts or interfering with parasite transmission. However, the generality of the dilution effect hypothesis remains controversial, especially for zoonotic diseases of humans. Here we provide broad evidence that host diversity inhibits parasite abundance using a meta- analysis of 202 effect sizes on 61 parasite species. The magnitude of these effects was independent of host density, study design, and type and specialization of parasites, indicating that dilution was robust across all ecological contexts examined. However, the magnitude of dilution was more closely related to the frequency, rather than density, of focal host species. Importantly, observa- tional studies overwhelmingly documented dilution effects, and there was also significant evidence for dilution effects of zoonotic parasites of humans. Thus, dilution effects occur commonly in nature, and they may modulate human disease risk. A second analysis identified similar effects of diversity in plant–herbivore systems. Thus, although there can be exceptions, our results in- dicate that biodiversity generally decreases parasitism and herbiv- ory. Consequently, anthropogenic declines in biodiversity could increase human and wildlife diseases and decrease crop and forest production.
HIV/AIDS can present a significant economic, medical, and psychological shock to households in sub-Saharan Africa, and can considerably alter household livelihood behavior. While there is speculation that household impoverishment related to HIV-affliction and the onset of AIDS can drive households into greater dependence on their local, natural environment for food, medicine, fuel, construction materials, and other products, evidence is limited. This study queried the 2008-2009 Kenyan Demographic Health Survey Database for associations at the national level between household HIV-affliction and three natural resource use variables: primary household fuel type, drinking water source, and presence in the household of an adult self-reporting as a subsistence fisheries or agricultural worker. Manual, step-wise binomial and multinomial logistic regression models (N=4000+ households) were constructed to examine these associations while controlling for geographic and socio-demographic factors. Model results demonstrated that HIV- afflicted households were 40-70% less likely than un-afflicted households to use natural fuels compared to processed fuels, and 30% less likely (weighted model, only) to rely on surface water sources compared to purchased or engineered water
sources. No difference was detected between HIV-afflicted versus un-afflicted households regarding presence of an adult engaged in subsistence fishery or agricultural work. While a cross-sectional analysis limits discussion of causality, possible explanations include household adaptation to labor loss and/or increased exposure to HIV infection of communities with access to infrastructure. The results of this study caution against case study bias in the existing HIV-environment literature, and highlight the need for randomized, longitudinal studies on this topic.
Habitat overlap can increase the risks of anthroponotic and zoonotic pathogen transmission be- tween humans, livestock, and wild apes. We collected Escherichia coli bacteria from humans, livestock, and mountain gorillas (Gorilla gorilla beringei) in Bwindi Impenetrable National Park, Uganda, from May to Au- gust 2005 to examine whether habitat overlap influences rates and patterns of pathogen transmission between humans and apes and whether livestock might facilitate transmission. We genotyped 496 E. coli isolates with repetitive extragenic palindromic polymerase chain reaction fingerprinting and measured susceptibility to 11 antibiotics with the disc-diffusion method. We conducted population genetic analyses to examine genetic differ- ences among populations of bacteria from different hosts and locations. Gorilla populations that overlapped in their use of habitat at high rates with people and livestock harbored E. coli that were genetically similar to E. coli from those people and livestock, whereas E. coli from gorillas that did not overlap in their use of habitats with people and livestock were more distantly related to human or livestock bacteria. Thirty-five percent of isolates from humans, 27% of isolates from livestock, and 17% of isolates from gorillas were clinically resistant to at least one antibiotic used by local people, and the proportion of individual gorillas harboring resistant isolates declined across populations in proportion to decreasing degrees of habitat overlap with humans. These patterns of genetic similarity and antibiotic resistance among E. coli from populations of apes, humans, and livestock indicate that habitat overlap between species affects the dynamics of gastrointestinal bacterial transmission, perhaps through domestic animal intermediates and the physical environment. Limiting such transmission would benefit human and domestic animal health and ape conservation.
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.
We detected Cryptosporidium sp. by direct immunofluorescence in fecal samples from greater bamboo lemurs (Prolemur simus) and eastern rufous mouse lemurs (Microcebus rufus) inhabiting the Ranomafana National Park, Madagascar. This is the first report of an occurrence of these potentially zoonotic parasites in free-ranging lemurs in the rain forest of Madagascar.
The Millennium Ecosystem Assessment and other commentators have warned about the impacts that biodiversity decline will have on human health. There is no doubting that the natural world provides mankind with the majority of the resources required to sustain life and health. Many species provide food, fuel, medicines; with the potential for many more (as of yet) undiscovered uses for various species. Despite this, there have been very few attempts to actually investigate relationships between biodiversity (i.e. number of species, rather than the ability of specific species to provide health benefits) and human health. This paper reviews the available evidence and demonstrates that while the links between biodiversity and health seem intuitive, they are very difficult to prove. Socio- economics has a huge influence on health status and the exploitation of natural resources (leading to eventual biodiversity loss) tends to have a positive economic effects. More direct effects of biodiversity on health include the diversity of the internal microbiome, the effect of natural diversity on our mental health and well-being (although this has large social aspects with many people feeling fearful in very diverse environments). Still to be elucidated are the tipping points where the level of global biodiversity loss is such that human health can no longer be sustained.
Background: After many years of general neglect, interest has grown and efforts came under way for the mapping, control, surveillance, and eventual elimination of neglected tropical diseases (NTDs). Disease risk estimates are a key feature to target control interventions, and serve as a benchmark for monitoring and evaluation. What is currently missing is a georeferenced global database for NTDs providing open-access to the available survey data that is constantly updated and can be utilized by researchers and disease control managers to support other relevant stakeholders. We describe the steps taken toward the development of such a database that can be employed for spatial disease risk modeling and control of NTDs.
Methodology: With an emphasis on schistosomiasis in Africa, we systematically searched the literature (peer-reviewed journals and ‘grey literature’), contacted Ministries of Health and research institutions in schistosomiasis-endemic countries for location-specific prevalence data and survey details (e.g., study population, year of survey and diagnostic techniques). The data were extracted, georeferenced, and stored in a MySQL database with a web interface allowing free database access and data management.
Principal Findings: At the beginning of 2011, our database contained more than 12,000 georeferenced schistosomiasis survey locations from 35 African countries available under http://www.gntd.org. Currently, the database is expanded to a global repository, including a host of other NTDs, e.g. soil-transmitted helminthiasis and leishmaniasis.
Conclusions: An open-access, spatially explicit NTD database offers unique opportunities for disease risk modeling, targeting control interventions, disease monitoring, and surveillance. Moreover, it allows for detailed geostatistical analyses of disease distribution in space and time. With an initial focus on schistosomiasis in Africa, we demonstrate the proof-of- concept that the establishment and running of a global NTD database is feasible and should be expanded without delay.
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.
Despite increasing control measures, numerous parasitic and infectious diseases are emerging, re-emerging or causing recurrent outbreaks particularly in Asia and the Pacific region, a hot spot of both infectious disease emergence and biodiversity at risk. We investigate how biodiversity affects the distribution of infectious diseases and their outbreaks in this region, taking into account socio-economics (population size, GDP, public health expenditure), geography (latitude and nation size), climate (precipitation, temperature) and biodiversity (bird and mammal species richness, forest cover, mammal and bird species at threat). We show, among countries, that the overall richness of infectious diseases is positively correlated with the richness of birds and mammals, but the number of zoonotic disease outbreaks is positively correlated with the number of threatened mammal and bird species and the number of vector-borne disease outbreaks is negatively correlated with forest cover. These results suggest that, among countries, biodiversity is a source of pathogens, but also that the loss of biodiversity or its regulation, as measured by forest cover or threatened species, seems to be associated with an increase in zoonotic and vector-borne disease outbreaks.
Accelerating rates of species extinctions and disease emergence underscore the importance of understanding how changes in bio- diversity affect disease outcomes. Over the past decade, a growing number of studies have reported negative correlations between host biodiversity and disease risk, prompting suggestions that biodiversity conservation could promote human and wildlife health. Yet the generality of the diversity–disease linkage remains conjectural, in part because empirical evidence of a relationship between host competence (the ability to maintain and transmit infections) and the order in which communities assemble has proven elusive. Here we integrate high-resolution field data with multi-scale experiments to show that host diversity inhibits transmission of the virulent pathogen Ribeiroia ondatrae and reduces amphibian disease as a result of consistent linkages among species richness, host composition and community competence. Surveys of 345 wetlands indi- cated that community composition changed nonrandomly with species richness, such that highly competent hosts dominated in species-poor assemblages whereas more resistant species became progressively more common in diverse assemblages. As a result, amphibian species richness strongly moderated pathogen transmission and disease pathology among 24,215 examined hosts, with a 78.4% decline in realized transmission in richer assemblages. Laboratory and mesocosm manipulations revealed an approxi- mately 50% decrease in pathogen transmission and host pathology across a realistic diversity gradient while controlling for host density, helping to establish mechanisms underlying the diversity–disease relationship and their consequences for host fitness. By revealing a consistent link between species richness and community competence, these findings highlight the influence of biodiversity on infection risk and emphasize the benefit of a community-based approach to understanding infectious diseases.
Understanding why some human populations remain persistently poor remains a significant challenge for both the social and natural sciences. The extremely poor are generally reliant on their immediate natural resource base for subsistence and suffer high rates of mortality due to parasitic and infectious diseases. Economists have developed a range of models to explain persistent poverty, often characterized as poverty traps, but these rarely account for complex biophysical processes. In this Essay, we argue that by coupling insights from ecology and economics, we can begin to model and understand the complex dynamics that underlie the generation and maintenance of poverty traps, which can then be used to inform analyses and possible intervention policies. To illustrate the utility of this approach, we present a simple coupled model of infectious diseases and economic growth, where poverty traps emerge from nonlinear relationships determined by the number of pathogens in the system. These nonlinearities are comparable to those often incorporated into poverty trap models in the economics literature, but, importantly, here the mechanism is anchored in core ecological principles. Coupled models of this sort could be usefully developed in many economically important biophysical systems—such as agriculture, fisheries, nutrition, and land use change—to serve as foundations for deeper explorations of how fundamental ecological processes influence structural poverty and economic development.
This report provides an evaluation of challenges presented by interactions between environment, agriculture and infectious diseases of public health importance. It explores the benefits and limitations of a more systems-based approach to conceptualizing and investigating this problem.
The authors conclude that development of such an approach necessitates stronger and harmonized strategic alliances between all organizations, sectors and institutions concerned with development, environment and social justice, including public health. They argue that the agenda for public health research and practice on infectious diseases can no longer be confined to itemized and vertically differentiated approaches to their prevention, control and (perhaps) eradication. Instead, it must also encompass the large-scale environmental, demographic and social changes that characterize today's world. This will require new types and levels of understanding, situation analyses, and interdisciplinary research and intersectoral actions to monitor and assess emerging trends and relationships.
We are at a key juncture in history where biodiversity loss is occurring daily and accelerating in the face of population growth, climate change, and rampant development. Simultaneously, we are just beginning to appreciate the wealth of human health benefits that stem from experiencing nature and biodiversity. Here we assessed the state of knowledge on relationships between human health and nature and biodiversity, and prepared a comprehensive listing of reported health effects. We found strong evidence linking biodiversity with production of ecosystem services and between nature exposure and human health, but many of these studies were limited in rigor and often only correlative. Much less information is available to link biodiversity and health. However, some robust studies indicate that exposure to microbial biodiversity can improve health, specifically in reducing certain allergic and respiratory diseases. Overall, much more research is needed on mechanisms of causation. Also needed are a re- envisioning of land-use planning that places human well-being at the center and a new coalition of ecologists, health and social scientists and planners to conduct research and develop policies that promote human interaction with nature and biodiversity. Improvements in these areas should enhance human health and ecosystem, community, as well as human resilience.
On a floodplain of the River Saale near Jena, Germany, grassland plants are naturally bombarded by spores of pathogenic fungi. But whether or not those fungi cause infection turns out to be largely about the neighborhood: Plants on highly diverse experimental plots have much lower levels of infection than plants grown in monoculture (1) (see the photos). The pathogens, it appears, are less likely to encounter their optimal host on the more diverse plots, which reduces disease prevalence and incidence. This protective effect of diversity has been found in many studies, not just for plants but also for diseases afflicting humans and wildlife. It has remained unclear, however, whether this observation holds generally (2, 3). In a recent paper, Civitello et al.addressed this question in a rigorous meta-analysis of diversity-disease relationships (4).
Infectious disease is listed among the top five causes of global species extinctions. However, the majority of available data supporting this contention is largely anecdotal. We used the IUCN Red List of Threatened and Endangered Species and literature indexed in the ISI Web of Science to assess the role of infectious disease in global species loss. Infectious disease was listed as a contributing factor in <4% of species extinctions known to have occurred since 1500 (833 plants and animals) and as contributing to a species’ status as critically endangered in <8% of cases (2852 critically endangered plants and animals). Although infectious diseases appear to play a minor role in global species loss, our findings underscore two important limitations in the available evidence: uncertainty surrounding the threats to species survival and a temporal bias in the data. Several initiatives could help overcome these obstacles, including rigorous scientific tests to determine which infectious diseases present a significant threat at the species level, recognition of the limitations associated with the lack of baseline data for the role of infectious disease in species extinctions, combining data with theory to discern the circumstances under which infectious disease is most likely to serve as an agent of extinction, and improving surveillance programs for the detection of infectious disease. An evidence-based understanding of the role of infectious disease in species extinction and endangerment will help prioritize conservation initiatives and protect global biodiversity.
The role and significance of wildlife–livestock interfaces in disease ecology has largely been neglected, despite recent interest in animals as origins of emerging diseases in humans. Scoping review methods were applied to objectively assess the relative interest by the scientific community in infectious diseases at interfaces between wildlife and livestock, to characterize animal species and regions involved, as well as to identify trends over time. An extensive liter- ature search combining wildlife, livestock, disease, and geographical search terms yielded 78,861 publications, of which 15,998 were in- cluded in the analysis. Publications dated from 1912 to 2013 and showed a continuous increasing trend, including a shift from para- sitic to viral diseases over time. In particular there was a significant increase in publications on the artiodactyls–cattle and bird–poultry interface after 2002 and 2003, respectively. These trends could be traced to key disease events that stimulated public interest and re- search funding. Among the top 10 diseases identified by this review, the majority were zoonoses. Prominent wildlife–livestock interfaces resulted largely from interaction between phylogenetically closely related and/or sympatric species. The bird–poultry interface was the most frequently cited wildlife–livestock interface worldwide with other interfaces reflecting regional circumstances. This review pro- vides the most comprehensive overview of research on infectious diseases at the wildlife–livestock interface to date.
ecent reviews have argued that disease control is among the ecosystem services yielded by biodiversity. Lyme disease (LD) is commonly cited as the best exam- ple of the ‘diluting’ effect of biodiversity on disease transmission, but many studies document the opposite relationship, showing that human LD risk can increase with forestation. Here, we unify these divergent perspec- tives and find strong evidence for a positive link between biodiversity and LD at broad spatial scales (urban to suburban to rural) and equivocal evidence for a negative link between biodiversity and LD at varying levels of biodiversity within forests. This finding suggests that, across zoonotic disease agents, the biodiversity–disease relationship is scale dependent and complex.
The increasing number of zoonotic diseases spilling over from a range of wild animal species represents a particular concern for public health, especially in light of the current dramatic trend of biodiversity loss. To understand the ecology of these multi-host pathogens and their response to environmental degradation and species extinctions, it is necessary to develop a theoretical framework that takes into account realistic community assemblages. Here, we present a multi-host species epidemiological model that includes empirically determined patterns of diversity and composition derived from com- munity ecology studies. We use this framework to study the interaction between wildlife diversity and directly transmitted pathogen dynamics. First, we demonstrate that variability in community compo- sition does not affect significantly the intensity of pathogen transmission. We also show that the consequences of community diversity can differentially impact the prevalence of pathogens and the number of infectious individuals. Finally, we show that ecological interactions among host species have a weaker influence on pathogen circulation than inter-species transmission rates. We conclude that integration of a community perspective to study wildlife pathogens is crucial, especially in the context of understanding and predicting infectious disease emergence events.