Host-Parasite Interactions in Experimental Populations

我的长期目标是使用两个模型系统识别影响宿主-寄生虫种群动态的因素：鱼体外寄生虫和老鼠肠道线虫。寄生虫通过减少生长、繁殖和存活直接影响宿主的健康，影响到宿主人口。人们不太了解，但可能同样重要的是，受感染的宿主是否能够向其他人发出感染风险的信号。最近的结果表明，这在鱼和老鼠身上都是可能的，这对宿主-寄生虫种群动态和宿主-寄生虫共同进化的途径都有影响。在跟踪孔雀鱼感染的流行动态时，我的学生发现，对孔雀鱼群体的负面影响是由于种群中存在感染，而不是对受影响的个体。此外，当引入相对条件较高的孔雀鱼时，感染传播更快。与捕食反应释放的化学警报类似，受感染鱼类(特别是条件较差的鱼类)的表皮俱乐部细胞可能会释放化学警报，从而降低其他鱼类的易感性，并抑制感染的传播。如果是这样的话，我们的发现将扩大对恐惧化学生态的理解。 *我的学生还证明，受感染的怀孕小鼠会将信号传递给胎儿和新生儿，这些信号会损害胎儿的线性生长，并改变胎盘和胎儿大脑中的基因表达。这可能涉及到幼犬肠道微生物群的改变，以及随后的肠道与大脑的串扰。随着新生儿微生物组的变化持续存在，大脑基因表达的变化可能也会持续下去。大脑调节行为，其中一些与寄生虫传播有关，大脑影响先天免疫，如果幼崽接触寄生虫，可能会改变易感性。传播动态或易感性的改变将影响感染通过F1人群的传播。*将在宿主种群中探索感染传播风险对宿主-寄生虫种群动态的影响，并通过基于个体的研究来支持，以证明受感染的鱼释放化学警报，以及受感染的小鼠堤坝改变幼体微生物群和脑基因表达。在应用层面上，我们的发现可能有助于控制加拿大和国际上水产养殖设施的感染，并可能证明母体感染增强了后代对未来感染风险的适应能力。**

My LONG-TERM GOAL is to identify factors that impact host-parasite population dynamics using two MODEL SYSTEMS: a fish ectoparasite and a mouse intestinal nematode. Parasites directly impact host health through reduced growth, reproduction and survival with implications that extend to the host population. What is less understood, but possibly of equal importance, is whether the infected host is able to SIGNAL OTHERS OF THE RISK OF INFECTION. Recent results suggest this is possible both in fish and mice, with implications for host-parasite population dynamics and for pathways of host-parasite co-evolution.*** ***In tracking the epidemic dynamics of infection on guppies, my students found that the negative impact on guppy mass was due to presence of infection in the POPULATION but not on the affected INDIVIDUAL. Also infection spread more rapidly when introduced on a guppy of high relative condition. Similar to chemical alarms released in response to predation, epidermal club cells of infected fish (especially those of poor condition) may release chemical alarms that reduce susceptibility of other fish and dampen spread of infection. If so, our findings will extend understanding of the chemical ecology of fear.  ******My students have also shown that infected pregnant mice transfer signals to their fetus and newborn that impair linear growth and that alter gene expression in the placenta and fetal brain. This may involve alterations to the microbiome in the pup gut and subsequent gut-brain cross talk. As changes to the neonatal microbiome persist, altered brain gene expression may also persist. The brain regulates behaviors, some of which are related to parasite transmission, and the brain influences innate immunity which may alter susceptibility should the pups be exposed to the parasite. Altered transmission dynamics or susceptibility will impact transmission of infection through the F1 population. ******The consequences of communicating risk of infection on host-parasite population dynamics will be explored in host populations and supported by individual-based research to document that infected fish release chemical alarms and that infected mouse dams alter the pup microbiome and brain gene expression. At an applied level, our findings may be helpful in controlling infections in aquaculture facilities in Canada and internationally and may demonstrate that maternal infection increases the resilience of offspring to a future risk of infection. **