Glossary Critical thermal limits (CTL): CTLs are a suite of commonly used measures of the maximum and minimum temperatures at which organisms can viably function. Individuals are exposed to either static stressful temperatures or gradually ramping temperatures and observed for physiological failure; e.g., uncoordinated movement, heat coma, or death [1]. Typically, either the duration of exposure or the temperature at which loss of viability is observed is recorded as the thermal limit. Fecundity: The total number of offspring an individual can produce across a set interval or lifetime. Fertility: The ability of an organism to produce viable offspring. Fertility can be measured in a number of ways but always reaches its lower limit when conditions prevent an individual from producing any offspring (i.e. sterility). Hardening: Increased thermal tolerance shown by organisms after a short period of exposure to a stressful but non-lethal temperature within the same life stage. Hardening tests are one component of a species plastic response when exposed to stressful temperatures [2]. Sterility: Describes an individual that cannot produce any offspring over a defined period, and thus is synonymous with complete infertility. Thermal fertility limits (TFL): Outlined here for the first time, TFLs refer to a level and duration of thermal stress that renders individuals unable to reproduce. For populations and species this can be defined as the temperature at which a given proportion of individuals are qualitatively sterile and it includes both higher (TFMAX) and lower (TFMIN) thermal stress

This is a repository copy of Temperatures that sterilize males better match global species distributions than lethal temperatures.

Infectious diseases dynamics are affected by both spatial and temporal heterogeneity in their environments. Our ability to quantify and predict how this heterogeneity impacts risks of infection and disease emergence is the key to successful disease prevention efforts. Here, we review the literature on infectious diseases from human, agricultural, and wildlife ecosystems to describe the rapid ecological and evolutionary responses in pathogens to environmental heterogeneity, with expected impacts on their epidemiology. To date, the underlying network structures through which disease transmission proceeds have been notoriously difficult to quantify because of this variation. We show that with recent advances in statistical methods and genomic approaches, it is now more feasible than ever to trace disease transmission networks, the molecular underpinning of infection, and the environmental variation relevant to disease dynamics. We end by identifying major new opportunities and challenges in understanding disease dynamics in an ever-changing world.

Many micro-organisms employ a parasitic lifestyle and, through their antagonistic interactions with host populations, have major impacts on human, agricultural and natural ecosystems. Most pathogens are likely to host parasites of their own, that is, hyperparasites, but how nested chains of parasites impact on disease dynamics is grossly neglected in the ecological and evolutionary literature. In this minireview we argue that the diversity and dynamics of micro-hyperparasites are an important component of natural host–pathogen systems. We use the current literature from a handful of key systems to show that observed patterns of pathogen virulence and disease dynamics may well be influenced by hyperparasites. Exploring these factors will shed light on many aspects of microbial ecology and disease biology, including resistance–virulence evolution, apparent competition, epidemiology and ecosystem stability. Considering the importance of hyperparasites in natural populations will have applied consequences for the field of biological control and therapeutic science, where hyperparastism is employed as a control mechanism but not necessarily ecologically understood.

Heritable microbial symbionts have profound impacts upon the biology of their arthropod hosts. Whilst our current understanding of the dynamics of these symbionts is typically cast within a framework of vertical transmission only, horizontal transmission has been observed in a number of cases. For instance, several symbionts can transmit horizontally when their parasitoid hosts share oviposition patches with uninfected conspecifics, a phenomenon called superparasitism. Despite this, horizontal transmission, and the host contact structures that facilitates it, have not been considered in heritable symbiont epidemiology. Here, we tested for the importance of host contact, and resulting horizontal transmission, for the epidemiology of a male-killing heritable symbiont (Arsenophonus nasoniae) in parasitoid wasp hosts. We observed that host contact through superparasitism is necessary for this symbiont’s spread in populations of its primary host Nasonia vitripennis, such that when superparasitism rates are high, A. nasoniae almost reaches fixation, causes highly female biased population sex ratios and consequently causes local host extinction. We further tested if natural interspecific variation in superparasitism behaviours predicted symbiont dynamics among parasitoid species. We found that A. nasoniae was maintained in laboratory populations of a closely related set of Nasonia species, but declined in other, more distantly related pteromalid hosts. The natural proclivity of a species to superparasitise was the primary factor determining symbiont persistence. Our results thus indicate that host contact behaviour is a key factor for heritable microbe dynamics when horizontal transmission is possible, and that ‘reproductive parasite’ phenotypes, such as male-killing, may be of secondary importance in the dynamics of such symbiont infections.