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Luijckx, P.

Publications and source records attributed to Luijckx, P..

7 recordsLinked to original sources

Beyond Environmental Matching: Maternal Effects Depend on Offspring Environmental Complexity and Fitness Traits

The consequences of maternal effects for offspring fitness can depend on the environmental conditions offspring encounter and the fitness traits considered. We used a transgenerational experiment in Daphnia magna to test how maternal exposure to warming and elevated salinity influenced offspring survival, reproduction and body size across matching, mismatching and multiple-stressor environments. Maternal exposure to salinity enhanced offspring survival under matching salinity, and benefits extended to mismatching environments. In contrast, maternal exposure to warming provided no survival benefit under matching warming and reduced survival in mismatching environments, while accelerating reproduction across contexts. Multiple-stressor conditions revealed pronounced maternal effects, while contrasting responses across survival, reproduction and body size showed that benefits to one fitness trait did not extend to others. Our findings demonstrate that environmental matching alone is insufficient to predict maternal effects, whose consequences depend on offspring environmental complexity and the fitness trait considered.

ecology↗

Feeding the host reshapes virulence: nonlinear scaling in a microsporidian pathogen.

Resource availability is a central driver of ecological and evolutionary processes, yet its effects on infectious disease and virulence are not fully understood. A key limitation is that many studies consider only a narrow range of resource conditions or a limited subset of host and pathogen traits, potentially obscuring non-linear relationships. Here, we quantify how a gradient of six food levels simultaneously shapes host fitness and pathogen performance in the Daphnia magna- Ordospora colligata system. Across two laboratory experiments, we measured infection rates, pathogen burden, host fecundity, survival, and filtration rates. Increased food availability enhanced pathogen fitness, with both infection rates and spore burden increasing with provisioning. In contrast, host responses were trait-specific: while fecundity increased with food availability, pathogen-induced reductions in fecundity (i.e., virulence) peaked at intermediate resource levels, despite continued increases in pathogen load. This pattern indicates that resource availability alters host tolerance as well as pathogen growth, generating non-linear disease outcomes. Host survival was unaffected by either food provisioning or infection, further demonstrating that resource availability can simultaneously influence host and pathogen traits in different directions. Our results highlight the importance of integrating multiple fitness components across provisioning levels to understand disease dynamics and suggest that ongoing anthropogenic changes in resource availability may alter host-pathogen interactions.

zoology↗

The duration and predictability of heatwaves shape host-parasite interactions under thermal stress

Anthropogenic climate change is expected to increase not only mean temperatures but also the magnitude and pattern of thermal variability, including the frequency, duration, and predictability of extreme events. While the effects of elevated mean temperatures on disease dynamics are well studied, far less is known about how different patterns of temperature variability shape host-parasite interactions, despite clear theoretical predictions from the climate variability hypothesis. Here, we used a controlled experimental system (Daphnia magna and two microsporidian parasites, Ordospora colligata and Hamiltosporidium tvaerminnensis) to disentangle the effects of thermal variability structure from mean temperature. Across two experiments, we exposed hosts to cyclic (predictable) and random (unpredictable) heatwaves under both non-stressful and stressful mean temperature regimes. Contrary to predictions from the climate variability hypothesis, temperature variability did not uniformly increase infection risk. Instead, infection outcomes depended on the interaction between mean temperature, duration of the heatwaves, the pattern of thermal variation, and parasite identity. Under non-stressful mean temperatures, thermal variability had negligible effects on infection. In contrast, under stressful mean temperatures, parasites responded in distinct ways: H. tvaerminnensis infection was sensitive to the predictability of heat events, whereas O. colligata responded primarily to heatwave duration. These results demonstrate that climatic variability can differentially alter host-parasite interactions rather than exerting consistent directional effects on disease. By showing that parasite-specific sensitivities to the pattern of thermal variation emerge under thermal stress, our study highlights a mechanism by which increasing climatic variability may reshape parasite communities and disease outcomes in a warming world.

ecology↗

Heatwaves and cold snaps alter host-parasite population dynamics in the Daphnia magna-Ordospora colligata system

Climate change is driving more frequent and severe temperature extremes, including heatwaves and cold snaps, with growing implications for ecology and disease. Yet, our understanding of how heatwaves and cold snaps influence disease dynamics remains underexplored. Using the host Daphnia magna infected with its microsporidian microparasite Ordospora colligata, pathogen fitness and host population size were measured in experimental populations using a factorial design at four baseline temperatures (14, 17, 20 and 23{degrees}C). A heatwave or cold snap treatment with an amplitude of {+/-}6{degrees}C was administered four weeks after measurements began and lasted for ten days. The effect of heatwaves is dependent on baseline temperature but can induce long-lasting increases in burden (>4 weeks). The impact of cold snaps were also temperature-dependent, leading to short-term increases in parasite fitness at higher temperatures. Host population size also varied in response to temperature and treatment. Importantly, burden and host density were interdependent, jointly shaping infection patterns. At lower temperatures, parasite burden and host population size were positively correlated, whereas at higher temperatures, increased host population size corresponded with reduced burden. These patterns were consistent at both individual and population levels, underscoring how individual physiological responses can scale up to impact disease dynamics across populations. Thus, extreme temperature variation can have complex, context-specific outcomes on disease dynamics. As climate extremes become more frequent, understanding these nuanced responses is critical for predicting and managing disease risk in natural populations. Author SummaryWe are experiencing more extreme weather events around the world, including heatwaves and cold snaps, but we dont fully understand how these temperature extremes will affect wildlife diseases. In our study, we tested how heatwaves and cold snaps influence both parasite success and host population size using a small aquatic animal, the water flea, and its naturally occurring gut parasite. We ran experiments at four average temperatures and simulated a heatwave or cold snap by raising or lowering the temperature by 6{degrees}C for ten days. We found that heatwaves often led to long-lasting increases in parasite burden, while cold snaps caused short-term spikes in parasite fitness, especially at warmer average temperatures. These effects also depended on the baseline temperature and were linked to changes in the host population. At cooler temperatures, parasite levels increased as host populations grew, but at warmer temperatures, the opposite happened, resulting in negative density-dependence. This suggests that the impact of extreme weather on disease isnt straightforward; it depends on when and where the event occurs. As extreme temperatures become more common with climate change, understanding these complex interactions is important for predicting disease outbreaks in the wild.

ecology↗

Early warning signals do not predict a warming-induced experimental epidemic

Climate change can impact the rates at which parasites are transmitted between hosts, ultimately determining if and when an epidemic will emerge. As such, our ability to predict climate-mediated epidemic emergence will become increasingly important in our efforts to prepare for and mitigate the effects of disease outbreaks on ecological systems and human health. Theory suggests that statistical signatures termed "early warning signals" (EWS), can function as predictors of disease emergence. Here, we analyze experimental and simulated time series of disease spread within populations of the model disease system Daphnia magna-Ordospora colligata for EWS of epidemic emergence. In this system, low temperatures prevent disease emergence, while sufficiently high temperatures force the system through a critical transition to an epidemic state. We found that EWS of epidemic emergence were nearly as likely to be detected in populations maintained at a sub-epidemic temperature as they were to be detected in populations subjected to a warming treatment that induced epidemic spread. Our findings suggest that the detection of false positives may limit the reliability of EWS as predictors of climate-mediated epidemic emergence.

ecology↗

Alternate patterns of temperature variation bring about very different disease outcomes at different mean temperatures

The dynamics of host-parasite interactions are highly temperature-dependent and may be modified by increasing frequency and intensity of climate-driven heat events. Here, we show that altered patterns of temperature variance lead to an almost order-of-magnitude shift in thermal performance of host and pathogen life history traits over and above the effects of mean temperature and, moreover, that different temperature regimes affect these traits differently. We found that diurnal fluctuations of {+/-}3{degrees}C lowered infection rates and reduced spore burden compared to constant temperatures in our focal host Daphnia magna exposed to the microsporidium parasite Ordospora colligata. In contrast, a three-day heatwave (+6{degrees}C) did not affect infection rates, but increased spore burden (relative to constant temperatures with the same mean) at 16{degrees}C, while reducing burden at higher temperatures. We conclude that changing patterns of climate variation, superimposed on shifts in mean temperatures due to global warming, may have profound and unanticipated effects on disease dynamics.

ecology↗

Four QTL underlie resistance to a microsporidian parasite that may drive genome evolution in its Daphnia host

Despite its pivotal role in evolutionary and ecological processes the genetic architecture underlying host-parasite interactions remains understudied. Here we use a quantitative trait loci approach to identify regions in the Daphnia magna genome that provide resistance against its microsporidium parasite Ordospora colligata. The probability that Daphnia became infected was affected by a single locus and an interaction between two additional loci. A fourth locus influenced the number of spores that grew within the host. Comparing our findings to previously published genetic work on Daphnia magna revealed that two of these loci may be the same as detected for another microsporidium parasite, suggesting a general immune response to this group of pathogens. More importantly, this comparison revealed that two regions previously identified to be under selection coincided with parasite resistance loci, highlighting the pivotal role parasites may play in shaping the host genome.

genetics↗