Since the identification and imprisonment of "Typhoid Mary", a woman who infected at least 47 people with typhoid in the early 1900s, epidemiologists have recognized that "superspreading" hosts play ...a key role in disease epidemics. Such variability in transmission also exists among species within a community and among habitat patches across a landscape, underscoring the need for an integrative framework for studying transmission heterogeneity, or the differences among hosts or locations in their contribution to pathogen spread. Here, we synthesize literature on human, plant, and animal diseases to evaluate the relative influence of host, pathogen, and environmental factors in producing highly infectious individuals, species, and landscapes. We show that host and spatial heterogeneity are closely linked and that quantitatively assessing the contribution of infectious individuals, species, or environmental patches to overall transmission can aid management strategies. We conclude by posing hypotheses regarding how pathogen natural history influences transmission variability and highlight emerging frontiers in this area of study.
Pathogen transmission responds differently to host richness and abundance, two unique components of host diversity. However, the heated debate around whether biodiversity generally increases or ...decreases disease has not considered the relationships between host richness and abundance that may exist in natural systems. Here we use a multi-species model to study how the scaling of total host community abundance with species richness mediates diversity-disease relationships. For pathogens with density-dependent transmission, non-monotonic trends emerge between pathogen transmission and host richness when host community abundance saturates with richness. Further, host species identity drives high variability in pathogen transmission in depauperate communities, but this effect diminishes as host richness accumulates. Using simulation we show that high variability in low richness communities and the non-monotonic relationship observed with host community saturation may reduce the detectability of trends in empirical data. Our study emphasizes that understanding the patterns and predictability of host community composition and pathogen transmission mode will be crucial for predicting where and when specific diversity-disease relationships should occur in natural systems.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
The effect of global climate change on infectious disease remains hotly debated because multiple extrinsic and intrinsic drivers interact to influence transmission dynamics in nonlinear ways. The ...dominant drivers of widespread pathogens, like West Nile virus, can be challenging to identify due to regional variability in vector and host ecology, with past studies producing disparate findings. Here, we used analyses at national and state scales to examine a suite of climatic and intrinsic drivers of continental-scale West Nile virus epidemics, including an empirically derived mechanistic relationship between temperature and transmission potential that accounts for spatial variability in vectors. We found that drought was the primary climatic driver of increased West Nile virus epidemics, rather than within-season or winter temperatures, or precipitation independently. Local-scale data from one region suggested drought increased epidemics via changes in mosquito infection prevalence rather than mosquito abundance. In addition, human acquired immunity following regional epidemics limited subsequent transmission in many states. We show that over the next 30 years, increased drought severity from climate change could triple West Nile virus cases, but only in regions with low human immunity. These results illustrate how changes in drought severity can alter the transmission dynamics of vector-borne diseases.
•Recent outbreaks of Zika, dengue, and chikungunya have occurred in West Africa•Recently introduced Aedes albopictus is implicated in multiple arbovirus outbreaks•Arbovirus outbreaks have occurred in ...major urban centers in West Africa•Diverse factors play a role in the emergence of Aedes-borne disease in West Africa•There is urgent need for improved disease surveillance and diagnostic capacity
Arboviruses transmitted by Aedes mosquitoes are a growing global concern; however, there remain large gaps in surveillance of both arboviruses and their vectors in West Africa. We reviewed over 50 years of data including outbreak reports, peer-reviewed literature, and prior data compilations describing Zika, dengue, and chikungunya, and their vectors in West Africa. Large outbreaks of dengue, Zika, and chikungunya have recently occurred in the region with over 27,000 cases of Aedes-borne disease documented since 2007. Recent arboviral outbreaks have become more concentrated in urban areas, and Aedes albopictus, recently documented in the region, has emerged as an important vector in several areas. Seroprevalence surveys suggest reported cases are a gross underestimate of the underlying arboviral disease burden. These findings indicate a shifting epidemiology of arboviral disease in West Africa and highlight a need for increased research and implementation of vector and disease control. Rapid urbanization and climate change may further alter disease patterns, underscoring the need for improved diagnostic capacity, and vector and disease surveillance to address this evolving health challenge.
Aedes-borne disease occurrence in West Africa. Arboviral disease occurrences were extracted from previous compilations, systematic review of literature, and outbreak reports. Data are organized by timing of outbreak with panels showing oldest (bottom panel) to most recent (top panel) observations Display omitted .
Frontiers in climate change–disease research Rohr, Jason R.; Dobson, Andrew P.; Johnson, Pieter T.J. ...
Trends in ecology & evolution (Amsterdam),
06/2011, Letnik:
26, Številka:
6
Journal Article
Recenzirano
Odprti dostop
The notion that climate change will generally increase human and wildlife diseases has garnered considerable public attention, but remains controversial and seems inconsistent with the expectation ...that climate change will also cause parasite extinctions. In this review, we highlight the frontiers in climate change–infectious disease research by reviewing knowledge gaps that make this controversy difficult to resolve. We suggest that forecasts of climate-change impacts on disease can be improved by more interdisciplinary collaborations, better linking of data and models, addressing confounding variables and context dependencies, and applying metabolic theory to host–parasite systems with consideration of community-level interactions and functional traits. Finally, although we emphasize host–parasite interactions, we also highlight the applicability of these points to climate-change effects on species interactions in general.
Multi‐species experiments are critical for identifying the mechanisms through which climate change influences population dynamics and community interactions within ecological systems, including ...infectious diseases. Using a host–parasite system involving freshwater snails, amphibians and trematode parasites, we conducted a year‐long, outdoor experiment to evaluate how warming affected net parasite production, the timing of infection and the resultant pathology. Warming of 3 °C caused snail intermediate hosts to release parasites 9 months earlier and increased infected snail mortality by fourfold, leading to decreased overlap between amphibians and parasites. As a result, warming halved amphibian infection loads and reduced pathology by 67%, despite comparable total parasite production across temperature treatments. These results demonstrate that climate–disease theory should be expanded to account for predicted changes in host and parasite phenology, which may often be more important than changes in total parasite output for predicting climate‐driven changes in disease risk.
Biodiversity loss sometimes increases disease risk or parasite transmission in humans, wildlife and plants. Some have suggested that this pattern can emerge when host species that persist throughout ...community disassembly show high host competence – the ability to acquire and transmit infections. Here, we briefly assess the current empirical evidence for covariance between host competence and extirpation risk, and evaluate the consequences for disease dynamics in host communities undergoing disassembly. We find evidence for such covariance, but the mechanisms for and variability around this relationship have received limited consideration. This deficit could lead to spurious assumptions about how and why disease dynamics respond to community disassembly. Using a stochastic simulation model, we demonstrate that weak covariance between competence and extirpation risk may account for inconsistent effects of host diversity on disease risk that have been observed empirically. This model highlights the predictive utility of understanding the degree to which host competence relates to extirpation risk, and the need for a better understanding of the mechanisms underlying such relationships.
Although the presence of intermediate snails is a necessary condition for local schistosomiasis transmission to occur, using them as surveillance targets in areas approaching elimination is ...challenging because the patchy and dynamic quality of snail host habitats makes collecting and testing snails labor-intensive. Meanwhile, geospatial analyses that rely on remotely sensed data are becoming popular tools for identifying environmental conditions that contribute to pathogen emergence and persistence.
In this study, we assessed whether open-source environmental data can be used to predict the presence of human Schistosoma japonicum infections among households with a similar or improved degree of accuracy compared to prediction models developed using data from comprehensive snail surveys. To do this, we used infection data collected from rural communities in Southwestern China in 2016 to develop and compare the predictive performance of two Random Forest machine learning models: one built using snail survey data, and one using open-source environmental data.
The environmental data models outperformed the snail data models in predicting household S. japonicum infection with an estimated accuracy and Cohen's kappa value of 0.89 and 0.49, respectively, in the environmental model, compared to an accuracy and kappa of 0.86 and 0.37 for the snail model. The Normalized Difference in Water Index (an indicator of surface water presence) within half to one kilometer of the home and the distance from the home to the nearest road were among the top performing predictors in our final model. Homes were more likely to have infected residents if they were further from roads, or nearer to waterways.
Our results suggest that in low-transmission environments, leveraging open-source environmental data can yield more accurate identification of pockets of human infection than using snail surveys. Furthermore, the variable importance measures from our models point to aspects of the local environment that may indicate increased risk of schistosomiasis. For example, households were more likely to have infected residents if they were further from roads or were surrounded by more surface water, highlighting areas to target in future surveillance and control efforts.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Climate change may shift the timing and consequences of interspecific interactions, including those important to disease spread. Because hosts and pathogens may respond differentially to climate ...shifts, however, predicting the net effects on disease patterns remains challenging. Here, we used field data to guide a series of laboratory experiments that systematically evaluated the effects of temperature on the full infection process, including survival, penetration, establishment, persistence, and virulence of a highly pathogenic trematode (Ribeiroia ondatrae), and the development and survival of its amphibian host. Our results revealed nonlinearities in pathology as a function of temperature, which likely resulted from changes in both host and parasite processes. Both hosts and parasites responded strongly to temperature; hosts accelerated development while parasites showed enhanced host penetration but reduced establishment (encystment) and survival outside the host. While there were no differences in host survival among treatments, we observed a mid‐temperature peak in parasite‐induced deformities (63% at 20 °C), with the lowest frequency of deformities (12%) occurring at the highest temperature (26 °C). This nonlinear effect could result from temperature‐driven changes in parasite burden owing to shifts in host penetration and/or clearance, reductions in host vulnerability owing to faster development, or both. Furthermore, despite strong temperature‐driven changes in parasite penetration, survival, and establishment, the opposing nature of these effects lead to no difference in tadpole parasite burdens shortly after infection. These findings suggest that temperature‐driven changes to the disease process may not be easily observable from comparison of parasite burdens alone, but multi‐tiered experiments quantifying the responses of hosts, parasites and their interactions can enhance our ability to predict temperature‐driven changes to disease risk. Climate‐driven changes to disease patterns will therefore depend on underlying shifts in host and parasite development rates and the timing of their interactions.
The global community has adopted ambitious goals to eliminate schistosomiasis as a public health problem, and new tools are needed to achieve them. Mass drug administration programs, for example, ...have reduced the burden of schistosomiasis, but the identification of hotspots of persistent and reemergent transmission threaten progress toward elimination and underscore the need to couple treatment with interventions that reduce transmission. Recent advances in DNA sequencing technologies make whole-genome sequencing a valuable and increasingly feasible option for population-based studies of complex parasites such as schistosomes. Here, we focus on leveraging genomic data to tailor interventions to distinct social and ecological circumstances. We consider two priority questions that can be addressed by integrating epidemiological, ecological, and genomic information: (1) how often do non-human host species contribute to human schistosome infection? and (2) what is the importance of locally acquired versus imported infections in driving transmission at different stages of elimination? These questions address processes that can undermine control programs, especially those that rely heavily on treatment with praziquantel. Until recently, these questions were difficult to answer with sufficient precision to inform public health decision-making. We review the literature related to these questions and discuss how whole-genome approaches can identify the geographic and taxonomic sources of infection, and how such information can inform context-specific efforts that advance schistosomiasis control efforts and minimize the risk of reemergence.
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