Biology subjects

Shocket, M. S.

Publications and source records attributed to Shocket, M. S..

6 recordsLinked to original sources

bioRxiv2024

Mean daily temperatures can predict the thermal limits of malaria transmission better than rate summation

Temperature shapes the distribution, seasonality, and magnitude of mosquito-borne disease outbreaks. Mechanistic models predicting transmission often use mosquito and pathogen thermal responses from constant temperature experiments. However, mosquitoes live in fluctuating environments. Rate summation (nonlinear averaging) is a common approach to infer performance in fluctuating environments, but its accuracy is rarely validated. We measured three mosquito traits that impact transmission (bite rate, survival, fecundity) in a malaria mosquito (Anopheles stephensi) across temperature gradients with three diurnal temperature ranges (0, 9 and 12{degrees}C). We compared thermal suitability models with temperature-trait relationships observed under constant temperatures, fluctuating temperatures, and those predicted by rate summation. We mapped results across An. stephenesis native Asian and invasive African ranges. We found: 1) daily temperature fluctuation significantly altered trait thermal responses; 2) rate summation partially captured decreases in performance near thermal optima, but also incorrectly predicted increases near thermal limits; and 3) while thermal suitability characterized across constant temperatures did not perfectly capture suitability in fluctuating environments, it was more accurate for estimating and mapping thermal limits than predictions from rate summation. Our study provides insight into methods for predicting mosquito-borne disease risk and emphasizes the need to improve understanding of organismal performance under fluctuating conditions.

ecology↗

bioRxiv2022

Thermal acclimation to warmer temperatures can protect host populations from both further heat stress and the potential invasion of pathogens

Phenotypic plasticity in response to shifts in temperature, known as thermal acclimation, is an essential component of the ability of a species to cope with environmental change. Not only does this process potentially improve an individuals thermal tolerance, it will also act simultaneously on various fitness related traits that determine whether a population increases or decreases in size. In light of global change, thermal acclimation therefore has consequences for population persistence that extend beyond simply coping with heat stress. This particularly important when we consider the additional threat of parasitism associated with global change, as the ability of a pathogen to invade a host population depends on both its capacity to proliferate within a host and spread between hosts, and thus the supply of new susceptible hosts in a population. Here, we use the host Daphnia magna and its bacterial pathogen Pasteuria ramosa to investigate how thermal acclimation may impact various aspects of host and pathogen performance at the scale of both an individual and the population. We independently test the effect of maternal thermal acclimation and direct thermal acclimation on host thermal tolerance, measured as knockdown times, as well as host fecundity and lifespan, and pathogen infection success and spore production. We find that direct thermal acclimation enhances host thermal tolerance and intrinsic rates of population growth, despite a decline observed for host fecundity and lifespan. Pathogens, on the other hand, faired consistently worse at warmer temperatures at the within-host scale, and also in their potential to invade a host population. Our results suggest that hosts could benefit more from warming than their pathogens, but highlight that considering both within- and between-host thermal performance, including thermal tolerance and fitness traits, is needed to fully appreciate how increasing thermal variability will impact host and pathogen populations.

ecology↗

bioRxiv2021

A paradox of parasite resistance: Disease-driven trophic cascades increase the cost of resistance, selecting for lower resistance with parasites than without them

Most evolutionary theory predicts that, during epidemics, hosts will evolve higher resistance to parasites that kill them. Here, we provide an alternative to that typical expectation, with an explanation centered on resource feedbacks. When resistance is costly, hosts evolve decreasing resistance without parasites, as expected. But with parasites, hosts can evolve lower resistance than they would in the absence of parasites. This outcome arises in an eco-evolutionary model when four conditions are met: first, resistance has a fecundity cost (here, via decreased foraging/exposure rate); second, resources increase during epidemics via trophic cascades; third, increased resources magnify the benefit of maintaining a fast foraging rate, thereby magnifying the cost of evolving a slower foraging/exposure rate (i.e., resistance); fourth, that amplification of the cost outweighs the benefit of resistance. When these conditions are met, hosts evolve lower resistance than without parasites. This phenomenon was previously observed in a mesocosm experiment with fungal parasites, zooplankton hosts, and algal resources. Re-analyzing this experiment produced evidence for our models mechanism. Thus, both model and experiment indicate that, via resource feedbacks, parasites can counterintuitively select against resistance.

ecology↗

bioRxiv2020

Virulent disease epidemics can increase host density by depressing foraging of hosts

All else equal, parasites that harm host fitness should depress densities of their hosts. However, parasites that alter host traits may increase host density via indirect ecological interactions. Here, we show how depression of infected host foraging rate can produce such a hydra effect. Using a foraging assay, we quantified reduced foraging rates of a zooplankton host infected with a virulent fungal parasite. We then parameterized a dynamical model of hosts, parasites, and resources with this foraging function, showing how foraging depression can create a hydra effect. Mathematically, the hydra arose when increased resource productivity exceeded any increase in resource consumption per host. Therefore, the foraging-mediated hydra effect more likely emerged (1) for hosts which strongly control logistic-like resources and (2) during larger epidemics of moderately virulent parasites. We then analyzed epidemics from 13 fungal epidemics in nature. We found evidence for a foraging-mediated hydra effect: large outbreaks depressed foraging rate and correlated with increased densities of both algae and hosts. Therefore, depression of foraging rate of infected hosts can produce higher host densities even during epidemics of parasites that increase host mortality. Such hydras might prevent collapse of host populations but also could produce higher densities of infected hosts.Competing Interest StatementThe authors have declared no competing interest.View Full Text

ecology↗

bioRxiv2019

Transmission of West Nile virus and other temperate mosquito-borne viruses occurs at lower environmental temperatures than tropical diseases

The temperature-dependence of many important mosquito-borne diseases has never been quantified. These relationships are critical for understanding current distributions and predicting future shifts from climate change. We used trait-based models to characterize temperature-dependent transmission of 10 vector-pathogen pairs of mosquitoes (Culex pipiens, Cx. quinquefascsiatus, Cx. tarsalis, and others) and viruses (West Nile, Eastern and Western Equine Encephalitis, St. Louis Encephalitis, Sindbis, and Rift Valley Fever viruses), most with substantial transmission in temperate regions. Transmission is optimized at intermediate temperatures (23-26{degrees}C) and often has wider thermal breadths (due to cooler lower thermal limits) compared to pathogens with predominately tropical distributions (in previous studies). The incidence of human West Nile virus cases across US counties responded unimodally to average summer temperature and peaked at 24{degrees}C, matching model-predicted optima (24-25{degrees}C). Climate warming will likely shift transmission of these diseases, increasing it in cooler locations while decreasing it in warmer locations.

ecology↗

bioRxiv2018

Temperature explains broad patterns of Ross River virus transmission across Australia

Temperature impacts the physiology of ectotherms, including vectors that transmit disease. While thermal biology predicts nonlinear effects of temperature on vector and pathogen traits that drive disease transmission, the empirical relationship between temperature and transmission remains unknown for most vector-borne pathogens. We built a mechanistic model to estimate the thermal response of Ross River virus, an important mosquito-borne pathogen of humans in Australia, the Pacific Islands, and potentially emerging worldwide. Transmission peaks at moderate temperatures (26.4{degrees}C) and declines to zero at low (17.0{degrees}C) and high (31.5{degrees}C) temperatures. The model predicted broad patterns of disease across Australia. First, transmission is year-round endemic in the tropics and sub-tropics but seasonal in temperate zones. Second, nationwide human cases peak seasonally as predicted from population-weighted seasonal temperatures. These results illustrate the importance of nonlinear, mechanistic models for inferring the role of temperature in disease dynamics and predicting responses to climate change.

ecology↗