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Climatic and Evolutionary Drivers of Phase Shifts in the Plague

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Climatic and Evolutionary Drivers of Phase Shifts in the Plague PAPER Climatic and evolutionary drivers of phase shifts in the COLLOQUIUM plague epidemics of colonial India Joseph A. Lewnarda and Jeffrey P. Townsendb,c,d,1 aDepartment of Epidemiology of Microbial Diseases, Yale School of Public Health, New Haven, CT 06520; bDepartment of Biostatistics, Yale School of Public Health, New Haven, CT 06510; cProgram in Computational Biology and Bioinformatics, Yale University, New Haven, CT 06511; and dDepartment of Ecology and Evolutionary Biology, Yale University, New Haven, CT 06520 Edited by Alan Hastings, University of California, Davis, CA, and approved September 23, 2016 (received for review April 29, 2016) Immune heterogeneity in wild host populations indicates that environmental drivers (22). In a model system of the plankton disease-mediated selection is common in nature. However, the species Daphnia dentifera and its parasite Metschnikowia bicuspidata, underlying dynamic feedbacks involving the ecology of disease environmental factors affecting transmission intermittently alter the transmission, evolutionary processes, and their interaction with intensity of selection for resistance, in turn impacting the size and – environmental drivers have proven challenging to characterize. timing of recurrent epidemics (23 25). In a rare example from Plague presents an optimal system for interrogating such cou- vertebrates, the intensity of seasonal myxomatosis epidemics in plings: Yersinia pestis transmission exerts intense selective pres- Australia predicted year to year variationinthesusceptibilityofwild sure driving the local persistence of disease resistance among its rabbits (26) in a broader context of decades-long selection for resistance (12). wildlife hosts in endemic areas. Investigations undertaken in co- For zoonotic disease agents, knowing how environment and lonial India after the introduction of plague in 1896 suggest that, host evolution factor into transmission dynamics is of immediate only a decade after plague arrived, a heritable, plague-resistant public health relevance. Responses of the black rat (Rattus rattus)to phenotype had become prevalent among commensal rats of cities the plague-causing bacterium Yersinia pestis present one of the most undergoing severe plague epidemics. To understand the possible important and best studied cases for understanding disease-medi- evolutionary basis of these observations, we developed a mathe- ated selection of host immunity. R. rattus is encountered in sylvatic matical model coupling environmentally forced plague dynamics and urban settings, serving as a both a wildlife plague reservoir and with evolutionary selection of rats, capitalizing on extensive archi- the host that propagates bubonic plague epidemics affecting hu- val data from Indian Plague Commission investigations. Incorpo- mans. In areas of Madagascar, where sylvatic R. rattus populations rating increased plague resistance among rats as a consequence of function as the primary plague reservoir (27), variable innate sus- intense natural selection permits the model to reproduce observed ceptibility to Y. pestis infection is associated with resistance alleles changes in seasonal epidemic patterns in several cities and capture that have undergone intense selection over a century of plague experimentally observed associations between climate and flea exposure (28–30). Historical human bubonic plague epidemics have population dynamics in India. Our model results substantiate Vic- been associated with the introduction of Y. pestis to previously un- torian era claims of host evolution based on experimental obser- exposed commensal rat populations. However, little is known re- vations of plague resistance and reveal the buffering effect of such garding the dynamics and epidemiological impact of host evolution evolution against environmental drivers of transmission. Our anal- among rats during such incursions (31, 32). From a public health ysis shows that historical datasets can yield powerful insights into perspective, understanding plague ecology among commensal rats is the transmission dynamics of reemerging disease agents with which we have limited contemporary experience to guide quanti- Significance tative modeling and inference. Whereas pathogens are a well-known selective pressure on host modeling | infectious disease | vector-borne disease | zoonosis | immunity, few empirical examples illustrate the coupled dynamics immunoecology of transmission and evolution. After the arrival of plague in co- lonial India, a plague-resistant rat phenotype was reported to nnate resistance is critically advantageous to host species facing have become prevalent in the subcontinent’s hardest hit cities. Ivirulent pathogens that represent endemic or epidemic disease Capitalizing on archival data from these investigations, we iden- threats. However, the ability to mount strong immune defenses tify the evolution of resistance in rats as a driver of observed shifts can incur significant physiological costs. A central principle in of seasonal outbreaks in concert with the flea lifecycle and its disease ecology, this evolutionary tradeoff implies that envi- climatic determinants. Disentangling climatic and evolutionary — ronmental factors determining the exposure of hosts to path- forcing, our findings based on century-old observations and — ogens concurrently drive the selection—or counterselection— experiments by the Indian Plague Commission substantiate the of disease resistance (1–3). Understanding how environment rapid emergence of host heterogeneity and show how evolu- impacts the coupled dynamics of transmission and evolution is tionary responses can buffer host populations against environ- critically important amid global climatic and environmental mentally forced disease dynamics. changes affecting the distribution, emergence, and reemergence of This paper results from the Arthur M. Sackler Colloquium of the National Academy of pathogens (4, 5). Sciences, “Coupled Human and Environmental Systems,” held March 14–15, 2016, at the Numerous examples of immune heterogeneity in wild plant National Academy of Sciences in Washington, DC. The complete program and video BIOLOGY POPULATION and animal hosts document the existence of innate resistance in recordings of most presentations are available on the NAS website at www.nasonline. the context of pathogen-mediated selection (6–11). That the org/Coupled_Human_and_Environmental_Systems. physiological basis of such resistance incurs a cost is predicted by Author contributions: J.A.L. and J.P.T. designed research; J.A.L. performed research; J.A.L. ecological theory (12–15), shown in laboratory measurements and J.P.T. contributed new reagents/analytic tools; J.A.L. analyzed data; and J.A.L. and J.P.T. (16–19), and exemplified by the natural selection of susceptibility wrote the paper. in resistant host populations that have been removed from The authors declare no conflict of interest. pathogen exposure (20, 21). Despite these direct findings re- This article is a PNAS Direct Submission. garding expansion of resistance in a host population, in few in- 1To whom correspondence should be addressed. Email: [email protected]. SCIENCE stances has it been possible to provide insight into the coupled This article contains supporting information online at www.pnas.org/lookup/suppl/doi:10. SUSTAINABILITY trajectories of transmission, evolutionary dynamics, and their 1073/pnas.1604985113/-/DCSupplemental. www.pnas.org/cgi/doi/10.1073/pnas.1604985113 PNAS | December 20, 2016 | vol. 113 | no. 51 | 14601–14608 Downloaded by guest on October 1, 2021 important because of the contemporary reemergence (33) and un- A rivaled historical impact of plague: Y. pestis epidemics decimated medieval Europe and Mediterranean classical civilization (34–36), disrupted trade and geopolitics in the late Victorian British empire (37), and may have driven major population movements and ad- mixture throughout Bronze Age Eurasia (38, 39). B Endemic present day Y. pestis in most world regions radiated from China in a late nineteenth century expansion known as the third plague pandemic, which brought the disease to port cities of every continent by 1901 via maritime trade networks (40, 41). Historical investigations undertaken in the decade after the in- C troduction of plague to colonial India documented the expansion of a heritable, plague-resistant phenotype among urban R. rattus:in dose escalation studies of experimental plague infection carried out D across Indian cities, the prevalence of rats resisting plague infection increased in association with the local severity of recent plague epidemics (42, 43). Recognizing that “it would be an extraordinary coincidence if plague had visited just those places where the rats Fig. 1. Schematic of compartmental transmission and susceptibility trait were naturally most immune to the disease and spared those with ” model structure. (A) Compartmental model for plague transmission the most susceptible rat populations, Victorian era investigators among R. rattus. Uninfected rats (U) acquire infection at a rate determi- from the Indian Plague Commission suggested an evolutionary basis ned by the applicable force of infection (λ1) and their susceptibility (ξ; B for resistance patterns, reasoning that “the one per thousand or ten and C) and progress through exposed incubating (E) and infectious (I) thousand of the rat population ... which lived through a severe states, shedding infected fleas (V) in the latter state. From a total sus-
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