Professional Education


  • Doctor of Philosophy, Indiana University (2016)
  • Bachelor of Arts, Bard College (2009)

Stanford Advisors


All Publications


  • Temperature explains broad patterns of Ross River virus transmission. eLife Shocket, M. S., Ryan, S. J., Mordecai, E. A. 2018; 7

    Abstract

    Thermal biology predicts that vector-borne disease transmission peaks at intermediate temperatures and declines at high and low temperatures. However, thermal optima and limits remain unknown for most vector-borne pathogens. We built a mechanistic model for the thermal response of Ross River virus, an important mosquito-borne pathogen in Australia, Pacific Islands, and potentially at risk of emerging worldwide. Transmission peaks at moderate temperatures (26.4°C) and declines to zero at thermal limits (17.0 and 31.5°C). The model accurately predicts that transmission is year-round endemic in the tropics but seasonal in temperate areas, resulting in the nationwide seasonal peak in human cases. Climate warming will likely increase transmission in temperate areas (where most Australians live) but decrease transmission in tropical areas where mean temperatures are already near the thermal optimum. These results illustrate the importance of nonlinear models for inferring the role of temperature in disease dynamics and predicting responses to climate change.

    View details for DOI 10.7554/eLife.37762

    View details for PubMedID 30152328

  • Temperature Drives Epidemics in a Zooplankton-Fungus Disease System: A Trait-Driven Approach Points to Transmission via Host Foraging AMERICAN NATURALIST Shocket, M. S., Strauss, A. T., Hite, J. L., Sljivar, M., Civitello, D. J., Duffy, M. A., Caceres, C. E., Hall, S. R. 2018; 191 (4): 435–51

    Abstract

    Climatic warming will likely have idiosyncratic impacts on infectious diseases, causing some to increase while others decrease or shift geographically. A mechanistic framework could better predict these different temperature-disease outcomes. However, such a framework remains challenging to develop, due to the nonlinear and (sometimes) opposing thermal responses of different host and parasite traits and due to the difficulty of validating model predictions with observations and experiments. We address these challenges in a zooplankton-fungus (Daphnia dentifera-Metschnikowia bicuspidata) system. We test the hypothesis that warmer temperatures promote disease spread and produce larger epidemics. In lakes, epidemics that start earlier and warmer in autumn grow much larger. In a mesocosm experiment, warmer temperatures produced larger epidemics. A mechanistic model parameterized with trait assays revealed that this pattern arose primarily from the temperature dependence of transmission rate (β), governed by the increasing foraging (and, hence, parasite exposure) rate of hosts (f). In the trait assays, parasite production seemed sufficiently responsive to shape epidemics as well; however, this trait proved too thermally insensitive in the mesocosm experiment and lake survey to matter much. Thus, in warmer environments, increased foraging of hosts raised transmission rate, yielding bigger epidemics through a potentially general, exposure-based mechanism for ectotherms. This mechanistic approach highlights how a trait-based framework will enhance predictive insight into responses of infectious disease to a warmer world.

    View details for DOI 10.1086/696096

    View details for Web of Science ID 000428287200004

    View details for PubMedID 29570399

  • Rapid evolution rescues hosts from competition and disease but-despite a dilution effect-increases the density of infected hosts PROCEEDINGS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES Strauss, A. T., Hite, J. L., Shocket, M. S., Caceres, C. E., Duffy, M. A., Hall, S. R. 2017; 284 (1868)
  • Allocation, not male resistance, increases male frequency during epidemics: a case study in facultatively sexual hosts ECOLOGY Hite, J. L., Penczykowski, R. M., Shocket, M. S., Griebel, K. A., Strauss, A. T., Duffy, M. A., Caceres, C. E., Hall, S. R. 2017; 98 (11): 2773–83

    Abstract

    Why do natural populations vary in the frequency of sexual reproduction? Virulent parasites may help explain why sex is favored during disease epidemics. To illustrate, we show a higher frequency of males and sexually produced offspring in natural populations of a facultative parthenogenetic host during fungal epidemics. In a multi-year survey of 32 lakes, the frequency of males (an index of sex) was higher in populations of zooplankton hosts with larger epidemics. A lake mesocosm experiment established causality: experimental epidemics produced a higher frequency of males relative to disease-free controls. One common explanation for such a pattern involves Red Queen (RQ) dynamics. However, this particular system lacks key genetic specificity mechanisms required for the RQ, so we evaluated two other hypotheses. First, individual females, when stressed by infection, could increase production of male offspring vs. female offspring (a tenant of the "Abandon Ship" theory). Data from a life table experiment supports this mechanism. Second, higher male frequency during epidemics could reflect a purely demographic process (illustrated with a demographic model): males could resist infection more than females (via size-based differences in resistance and mortality). However, we found no support for this resistance mechanism. A size-based model of resistance, parameterized with data, revealed why: higher male susceptibility negated the lower exposure (a size-based advantage) of males. These results suggest that parasite-mediated increases in allocation to sex by individual females, rather than male resistance, increased the frequency of sex during larger disease epidemics.

    View details for DOI 10.1002/ecy.1976

    View details for Web of Science ID 000414242600004

    View details for PubMedID 28766698

  • Detecting the impact of temperature on transmission of Zika, dengue, and chikungunya using mechanistic models. PLoS neglected tropical diseases Mordecai, E. A., Cohen, J. M., Evans, M. V., Gudapati, P., Johnson, L. R., Lippi, C. A., Miazgowicz, K., Murdock, C. C., Rohr, J. R., Ryan, S. J., Savage, V., Shocket, M. S., Stewart Ibarra, A., Thomas, M. B., Weikel, D. P. 2017; 11 (4)

    Abstract

    Recent epidemics of Zika, dengue, and chikungunya have heightened the need to understand the seasonal and geographic range of transmission by Aedes aegypti and Ae. albopictus mosquitoes. We use mechanistic transmission models to derive predictions for how the probability and magnitude of transmission for Zika, chikungunya, and dengue change with mean temperature, and we show that these predictions are well matched by human case data. Across all three viruses, models and human case data both show that transmission occurs between 18-34°C with maximal transmission occurring in a range from 26-29°C. Controlling for population size and two socioeconomic factors, temperature-dependent transmission based on our mechanistic model is an important predictor of human transmission occurrence and incidence. Risk maps indicate that tropical and subtropical regions are suitable for extended seasonal or year-round transmission, but transmission in temperate areas is limited to at most three months per year even if vectors are present. Such brief transmission windows limit the likelihood of major epidemics following disease introduction in temperate zones.

    View details for DOI 10.1371/journal.pntd.0005568

    View details for PubMedID 28448507