Explore the vast range of titles available.

Despite the growing awareness that larval competition can influence adult mosquito life history traits including susceptibility to pathogens, the net effect of larval competition on human risk of exposure to mosquito-borne pathogens remains poorly understood. We examined how intraspecific larval competition affects dengue-2 virus (DENV-2) extrinsic incubation period and vectorial capacity of its natural vector Aedes albopictus. Adult Ae. albopictus from low and high-larval density conditions were orally challenged with DENV-2 and then assayed for virus infection and dissemination rates following a 6, 9, or 12-day incubation period using real-time quantitative reverse transcription PCR. We then modeled the effect of larval competition on vectorial capacity using parameter estimates obtained from peer-reviewed field and laboratory studies. Larval competition resulted in significantly longer development times, lower emergence rates, and smaller adults, but did not significantly affect the extrinsic incubation period of DENV-2 in Ae. albopictus. Our vectorial capacity models suggest that the effect of larval competition on adult mosquito longevity likely has a greater influence on vectorial capacity relative to any competition-induced changes in vector competence. Furthermore, we found that large increases in the viral dissemination rate may be necessary to compensate for small competition-induced reductions in daily survivorship. Our results indicate that mosquito populations that experience stress from larval competition are likely to have a reduced vectorial capacity, even when susceptibility to pathogens is enhanced.

Parasite transmission is thought to depend on both parasite exposure and host susceptibility to infection; however, the relative contribution of these two factors to epidemics remains unclear. We used interactions between an aquatic host and its fungal parasite to evaluate how parasite exposure and host susceptibility interact to drive epidemics. In six lakes, we tracked the following factors from pre-epidemic to epidemic emergence: (1) parasite exposure (measured observationally as fungal spores attacking wild-caught hosts), (2) host susceptibility (measured experimentally as the number of fungal spores required to produce terminal infection), (3) host susceptibility traits (barrier resistance and internal clearance, both quantified with experimental assays), and (4) parasite prevalence (measured observationally from wildcaught hosts). Tracking these factors over 6 months and in almost 7,000 wild-caught hosts provided key information on the drivers of epidemics. We found that epidemics depended critically on the interaction of exposure and susceptibility; epidemics only emerged when a host population’s level of exposure exceeded its individuals’ capacity for recovery. Additionally, we found that host internal clearance traits (the hemocyte response) were critical in regulating epidemics. Our study provides an empirical demonstration of how parasite exposure and host susceptibility interact to inhibit or drive disease in natural systems and demonstrates that epidemics can be delayed by asynchronicity in the two processes. Finally, our results highlight how individual host traits can scale up to influence broad epidemiological patterns.

Background The guts of blood-sucking insects host a community of bacteria that can shift dramatically in response to biotic and abiotic factors. Identifying the key factors structuring these microbial communities has important ecological and epidemiological implications. Methods We used the yellow fever mosquito, Aedes aegypti , to investigate the impact of mixed blood meals on gut microbiota of vector mosquitoes. Adult females were experimentally fed on sugar or blood from chicken, rabbit or a mixture of chicken and rabbit blood, and their gut microbiota were characterized using 16S rRNA gene amplification and MiSeq sequencing. Results The gut bacterial communities of mosquitoes fed on the three blood meal treatments clustered separately, suggesting that host species identity and mixed blood-feeding are key determinants of gut bacterial community composition in mosquitoes. Mixed blood meal had a synergistic effect on both operational taxonomic unit (OTU) richness and the Shannon diversity index, suggesting that mixed blood-feeding can offset the nutritional deficit of blood meals from certain host species. The microbial communities observed in this study were distinct from those identified from similarly fed Ae. aegypti from our previous study. Conclusions These findings demonstrate that vector host-feeding preferences can influence gut microbial composition and diversity, which could potentially impact pathogen acquisition and transmission by the vector. The results also demonstrate that different microenvironmental conditions within the laboratory may play an important role in structuring the microbial communities of independently reared mosquito colonies. Graphical Abstract

Parasite fitness depends on a successful journey from one host to another. For parasites that are transmitted environmentally, abiotic conditions might modulate the success of this journey. Here we evaluate how light, a key abiotic factor, influences spatiotemporal patterns of zooplankton disease where light varies seasonally, across lakes, and with depth in a lake. In an in situ experiment using those three sources of variation, we tested sensitivity of spores of two parasites to ambient light. Infectivity of both parasites was lower when exposed to ambient light in comparison to parasites exposed to otherwise similar conditions in the dark. The more sensitive parasite (the fungus, Metschnikowia) was damaged even under lower ambient light during late fall (November). With this differential sensitivity established, we evaluated links between light environment and natural outbreaks in lakes. Consistent with the incubations, epidemics of the less sensitive parasite (the bacterium, Pasteuria) started earlier in the fall (under higher ambient light), and both parasites had smaller outbreaks in more transparent lakes. Overall, light environment may impact the timing and size of disease outbreaks. Outbreaks could thus become exacerbated by human activities that darken waters, including lake browning associated with climate change and eutrophication.

Host susceptibility may be critical for the spread of infectious disease, and understanding its basis is a goal of ecological immunology. Here, we employed a series of mechanistic tests to evaluate four factors commonly assumed to influence host susceptibility: parasite exposure, barriers to infection, immune responses, and body size. We tested these factors in an aquatic host–parasite system (Daphnia dentifera and the fungal parasite, Metschnikowia bicuspidata) using both laboratory-reared and field-collected hosts. We found support for each factor as a driver of infection. Elevated parasite exposure, which occurs through consumption of infectious fungal spores, increased a host’s probability of infection. The host’s gut epithelium functioned as a barrier to infection, but in the opposite manner from which we predicted: thinner anterior gut epithelia were more resistant to infectious spores than thick epithelia. This relationship may be mediated by structural attributes associated with epithelial cell height. Fungal spores that breached the host’s gut barrier elicited an intensity-dependent hemocyte response that decreased the probability of infection for some Daphnia. Although larger body sizes were associated with increased levels of spore ingestion, larger hosts also had lower frequencies of parasite attack, less penetrable gut barriers, and stronger hemocyte responses. After investigating which mechanisms underlie host susceptibility, we asked: do these four factors contribute equally or asymmetrically to the outcome of infection? An information-theoretic approach revealed that host immune defenses (barriers and immune responses) played the strongest roles in mediating infection outcomes. These two immunological traits may be valuable metrics for linking host susceptibility to the spread of infectious disease.

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.

We examined how larvae of Culex restuans mosquito influences the bacterial abundance, composition and diversity in simulated container aquatic habitats. The microbiota of Cx. restuans larvae were also characterized and compared to those of their larval habitats. The presence of Cx. restuans larvae altered the bacterial community composition and reduced the bacterial abundance, diversity and richness. Azohydromonas sp., Delftia sp., Pseudomonas sp., Zooglea sp., unclassified Enterobacteriaceae and unclassified Bacteroidales were suppressed while Prosthecobacter sp., Hydrogenaphaga sp., Clostridium sp., unclassified Clostridiaceae and Chryseobacterium sp. were enhanced in the presence of Cx. restuans larvae. Cx. restuans larvae harbored distinct and less diverse bacterial community compared to their larval habitats. These findings demonstrate that Cx. restuans larvae play a key role in structuring the microbial communities in container aquatic habitats and may lower the nutritional quality and alter the decomposition process and food web dynamics in these aquatic systems. The findings also demonstrate that mosquito larvae are highly selective of the bacterial taxa from the larval environment that colonize their bodies. These findings provide new opportunities for more focused studies to identify the specific bacterial taxa that serve as food for mosquito larvae and those that could be harnessed for disease control.

Parasites steal resources that a host would otherwise direct toward its own growth and reproduction. We use this fundamental notion to explain resource‐dependent virulence in a fungal parasite (Metschnikowia)–zooplankton host (Daphnia) system and in a variety of other disease systems with invertebrate hosts. In an experiment, well‐fed hosts died faster and produced more parasites than did austerely fed ones. This resource‐dependent variation in virulence and other experimental results (involving growth and reproduction rate/timing of hosts) readily emerged from a model based on dynamic energy budgets. This model follows energy flow through the host, from ingestion of food, to internal energy storage, to allocation toward growth and reproduction or to a parasite that consumes these reserves. Acting as a consumer, the parasite catalyzes its own extinction, persistence with an energetically compromised host, or death of the host. In this last case, more resources for the host inadvertently fuels faster parasite growth, thereby accelerating the demise of the host (although the opposite result arises with different resource kinetics of the parasite). Thus, this model can explain how resource supply drives variation in virulence. This ecological dependence of virulence likely rivals and/or interacts with genetic mechanisms that often garner more attention in the literature on disease.

Background The process by which populations evolve to become new species involves the emergence of various reproductive isolating barriers (RIB). Despite major advancements in understanding this complex process, very little is known about the order in which RIBs evolve or their relative contribution to the total restriction of gene flow during various stages of speciation. This is mainly due to the difficulties of studying reproductive isolation during the early stages of species formation. This study examines ecological and non-ecological RIB within and between Daphnia pulex and Daphnia pulicaria, two recently diverged species that inhabit distinct habitats and exhibit an unusual level of intraspecific genetic subdivision. Results We find that while ecological prezygotic barriers are close to completion, none of the non-ecological barriers can restrict gene flow between D. pulex and D. pulicaria completely when acting alone. Surprisingly, we also identified high levels of postzygotic reproductive isolation in ‘conspecific’ interpopulation crosses of D. pulex . Conclusions While the ecological prezygotic barriers are prevalent during the mature stages of speciation, non-ecological barriers likely dominated the early stages of speciation. This finding indicates the importance of studying the very early stages of speciation and suggests the contribution of postzygotic isolation in initiating the process of speciation.