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Modeling Vector-Borne Diseases in a Commoditized Landscape

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Abstract

As Mandal et al. (2011) review, there is a rough hierarchy of models for vector-borne disease, focusing on malaria. These range from Ross (1911) through Macdonald (1957) to Anderson and May (1991), who present, respectively, two-, three-, and four-dimensional models. Macdonald and Anderson-May extend the Ross model to include latent periods in both human and vector. Further extensions explore the role of immune competence, superinfection, pathogen evolution, host and mosquito behavior, migration, population age structure, spatial dynamics, environmental factors, and so on, all largely variations on the Ross and Macdonald theme (Reiner et al. 2013). Yang (2000) studies a model containing ten differential equations.

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This volume compiles five papers modeling the effects of neoliberal economics on the emergence of Ebola and its aftermath. Neoliberalism is currently the world’s primary economic philosophy. It centers international relations around globalizing laissez-faire economics for multinational companies, promoting free trade, deregulating economic markets, and shifting state expenditures in favor of private property. The multidisciplinary teams represented here place both Ebola Makona, the Zaire Ebola virus variant that has infected 28,000 in West Africa, and Ebola Reston, which is currently emerging in industrial hog farms in the Philippines and China, within a multi-plank modeling framework. Using a stochastic extinction model that one group spatializes, environmental stochasticity across the ecologies in which Ebola evolves is treated as an ecosystemic prophylaxis. An agroecological logic gate is developed for epidemic control. A Black-Scholes model explicitly links economic margins across agricultural systems to success in biocontrol. This new control theory is further developed around the data-rate and rate-distortion theorems, a turbulence model, and cognitive symmetry breaking. Lastly, a model of pandemic penetrance is used to explore the domino effects of serious outbreaks amplifying through the cascades of disasters that can follow deadly pandemics. All the models presented are contextualized by socioeonomic geographies specific to outbreak locales.Together the models suggest shifts in regional agroeconomics under the neoliberal doctrine, driving deforestation and monoculture production, destroying the ecosystemic “friction” with which local forests typically disrupt Ebola transmission. The resulting collapse in such an ecological function accelerates pathogen spillover and propagation across the remaining host populations. The failure on the part of current control efforts to assimilate such a structural context may render even an efficacious vaccine dysfunctional. The authors propose an alternate science of disease and an adjunct program of interventions useful to researchers and public health officials alike.
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This article charts the diverse pathways through which austerity and other policy shifts associated with neoliberalism have come to be embodied globally in ill-health. It combines a review of research on these processes of embodiment with the development of a theory of the resulting forms of biological sub-citizenship. This theory builds on other studies that have already sought to complement and complicate the concept of biological citizenship with attention to the globally uneven experience and embodiment of bioinequalities. Focused on the unevenly embodied sequelae of austerity, the proceeding theorization of biological sub-citizenship is developed in three stages of review and conceptualization: 1) Biological sub-citizenship through exclusion and conditionalization; 2) Biological sub-citizenship through extraction and exploitation; and 3) Biological sub-citizenship through financialized experimentation. In conclusion the paper argues that the analysis of biological sub-citizenship needs to remain open-ended and relational in order to contribute to socially-searching work on the social determinants of health.
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This chapter focuses on the impacts of changing climate on arthropod vectors of disease, their relationship with the pathogens they transmit, and the implications of these phenomena for disease transmission,ceteris paribus, that is, assuming everything else stays the same. It introduces a case study that illustrates some of the complexities present when untangling the potential role of climate change on the distribution of disease vectors. Useful concepts to study impacts of climate change on insect vectors of disease are illustrated with this study on changes in the distribution of two major globally invasive vectors: Aedes albopictus and Aedes japonicus, facing the emergence of Aedes flavopictus, formerly a rare species along an altitudinal gradient in Nagasaki, Japan. The basic pattern that has been observed regarding the impact of temperature on pathogens developing inside vectors of disease is that the extrinsic incubation period (EIP).
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Urbanization and climate change are the two major environmental challenges of the 21st century. The dramatic expansion of cities around the world creates new conditions for the spread, surveillance, and control of infectious diseases. In particular, urban growth generates pronounced spatial heterogeneity within cities, which can modulate the effect of climate factors at local spatial scales in large urban environments. Importantly, the interaction between environmental forcing and socioeconomic heterogeneity at local scales remains an open area in infectious disease dynamics, especially for urban landscapes of the developing world. A quantitative and conceptual framework on urban health with a focus on infectious diseases would benefit from integrating aspects of climate forcing, population density, and level of wealth. In this paper, we review what is known about these drivers acting independently and jointly on urban infectious diseases; we then outline elements that are missing and would contribute to building such a framework.
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Mosquitoes transmit many viruses to a variety of hosts. Cycles of mosquito borne arbovirus transmission are the result of complex interactions between the mosquito, the arbovirus and the host that are influenced by genetic variations in a variety of traits in each that are all influenced by many environmental factors. R0, the basic reproduction number or mean number of individuals infected from a single infected individual, is a measure of mosquito borne arbovirus transmission. Understanding the causes for the distribution of R0 in any transmission cycle is a daunting challenge due to the lack of information on the genetic and environmental variances that influence R0. Information about the major factors influencing R0 for specific transmission cycles is essential to develop efficient and effective strategies to reduce transmission in different cycles and locations.
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The conclusion highlights the major contributions of the book both for anthropologists and for public-health practitioners. By focusing on both bodies and the urban landscapes they inhabit, I emphasize the particularities of dengue in Ciudad Sandino to understand how the regulation of human and nonhuman life produces specific forms of belonging and exclusion. I suggest that the politics of life in emerging infectious-disease complexes is as much about ecologically imagined, multispecies communities—about landscapes that include people and mosquitoes and garbage and viruses—as it is about biomedically imagined human bodies. While much of contemporary global health orients itself to the future, seeking ways to anticipate or head off pandemics, I believe that anthropology’s role should be a bit different. In order to critically examine global health, we cannot be futurists. Rather, for anthropologists, understanding dengue and diseases like it entails trailing, working from behind (or even along with) pathogens and vectors and people, gathering knowledge from the traces they—and we—leave. These traces, I argue, play a significant role in how we think of health.
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The complexity and connectedness of eco-social processes have major influence on the emergence and spread of infectious diseases amongst humans and animals. The disciplinary nature of most research activity has made it difficult to improve our understanding of interactions and feedback loops within the relevant systems. Influenced by the One Health approach, increasing efforts have recently been made to address this knowledge gap. Disease emergence and spread is strongly influenced by host density and contact structures, pathogen characteristics and pathogen population and molecular evolutionary dynamics in different host species, and host response to infection. All these mechanisms are strongly influenced by eco-social processes, such as globalization and urbanization, which lead to changes in global ecosystem dynamics, including patterns of mobility, human population density and contact structures, and food production and consumption. An improved understanding of epidemiological and eco-social processes, including their interdependence, will be essential to be able to manage diseases in these circumstances. The interfaces between wild animals, domestic animals and humans need to be examined to identify the main risk pathways and put in place appropriate mitigation. Some recent examples of emerging infectious disease are described to illustrate eco-social processes that are influencing disease emergence and spread.