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ABSTRACT Infectious diseases remain a major cause of global mortality, yet basic questions concerning the relationship between within-host processes governing pathogen burden (pathogen replication, immune responses) and population-scale (epidemiological) patterns of mortality remain obscure. We use a structured literature review to leverage the extensive biomedical data generated by controlled host infections to address the epidemiological question of whether infection-induced mortality is constant, accelerating, or follows some other pattern of change and to infer the within-host mechanistic basis of this pattern. We show that across diverse lethal infection models, the risk of death increases approximately exponentially in time since infection, in a manner phenomenologically similar to the dynamics of all-cause death. We further show that this pattern of accelerating risk is consistent with multiple alternate mechanisms of pathogen growth and host-pathogen interaction, underlining the limitations of current experimental approaches to connect within-host processes to epidemiological patterns. We review critical experimental questions that our work highlights, requiring additional non-invasive data on pathogen burden throughout the course of infection.IMPORTANCEHere, we ask a simple question: what are the dynamics of pathogen-induced death? Death is a central phenotype in both biomedical and epidemiological infectious disease biology, yet very little work has attempted to link the biomedical focus on pathogen dynamics within a host and the epidemiological focus on populations of infected hosts. To systematically characterize the dynamics of death in controlled animal infections, we analyzed 209 data sets spanning diverse lethal animal infection models. Across experimental models, we find robust support for an accelerating risk of death since the time of infection, contrasting with conventional epidemiological models that assume a constant elevated risk of death. Using math models, we show that multiple processes of growth and virulence are consistent with accelerating risk of death, and we end with a discussion of critical experiments to resolve how within-host biomedical processes map onto epidemiological patterns of disease. 

Abstract Individual animals in natural populations tend to host diverse parasite species concurrently over their lifetimes. In free‐living ecological communities, organismal life histories shape interactions with their environment, which ultimately forms the basis of ecological succession. However, the structure and dynamics of mammalian parasite communities have not been contextualized in terms of primary ecological succession, in part because few datasets track occupancy and abundance of multiple parasites in wild hosts starting at birth. Here, we studied community dynamics of 12 subtypes of protozoan microparasites ( Theileria spp.) in a herd of African buffalo. We show that Theileria communities followed predictable patterns of succession underpinned by four different parasite life history strategies. However, in contrast to many free‐living communities, network complexity decreased with host age. Examining parasite communities through the lens of succession may better inform the effect of complex within host eco‐evolutionary dynamics on infection outcomes, including parasite co‐existence through the lifetime of the host. 

Abstract Temperature and biodiversity changes occur in concert, but their joint effects on ecological stability of natural food webs are unknown. Here, we assess these relationships in 19 planktonic food webs. We estimate stability as structural stability (using the volume contraction rate) and temporal stability (using the temporal variation of species abundances). Warmer temperatures were associated with lower structural and temporal stability, while biodiversity had no consistent effects on either stability property. While species richness was associated with lower structural stability and higher temporal stability, Simpson diversity was associated with higher temporal stability. The responses of structural stability were linked to disproportionate contributions from two trophic groups (predators and consumers), while the responses of temporal stability were linked both to synchrony of all species within the food web and distinctive contributions from three trophic groups (predators, consumers, and producers). Our results suggest that, in natural ecosystems, warmer temperatures can erode ecosystem stability, while biodiversity changes may not have consistent effects. 

Abstract The measurement of uncharacterized pools of biological molecules through techniques such as metabarcoding, metagenomics, metatranscriptomics, metabolomics, and metaproteomics produces large, multivariate datasets. Analyses of these datasets have successfully been borrowed from community ecology to characterize the molecular diversity of samples ( ɑ -diversity) and to assess how these profiles change in response to experimental treatments or across gradients ( β -diversity). However, sample preparation and data collection methods generate biases and noise which confound molecular diversity estimates and require special attention. Here, we examine how technical biases and noise that are introduced into multivariate molecular data affect the estimation of the components of diversity (i.e., total number of different molecular species, or entities; total number of molecules; and the abundance distribution of molecular entities). We then explore under which conditions these biases affect the measurement of ɑ - and β -diversity and highlight how novel methods commonly used in community ecology can be adopted to improve the interpretation and integration of multivariate molecular data.