Host-Parasite Interactions in Experimental Populations

我的长期目标是使用两个模型系统来确定影响宿主-寄生虫种群动态的因素：鱼类体外寄生虫和小鼠肠道线虫。 寄生虫通过降低生长、繁殖和存活率直接影响宿主健康，并影响到宿主人口。 受感染的宿主是否能够向其他人发出感染风险的信号，这一点不太清楚，但可能同样重要。 最近的研究结果表明，这在鱼类和小鼠中都是可能的，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，我的学生发现孔雀鱼群的负面影响是由于群体中存在感染，而不是受影响的个体。 此外，感染传播更迅速时，介绍了高相对条件的孔雀鱼。 与捕食反应中释放的化学警报类似，受感染鱼类（特别是那些条件差的鱼）的表皮俱乐部细胞可能会释放化学警报，降低其他鱼类的易感性，抑制感染的传播。 如果是这样的话，我们的发现将扩展对恐惧的化学生态学的理解。 * 我的学生还表明，受感染的怀孕小鼠将信号传递给胎儿和新生儿，损害线性生长，改变胎盘和胎儿大脑中的基因表达。 这可能涉及幼犬肠道中微生物组的改变以及随后的肠-脑串扰。随着新生儿微生物组的变化持续存在，大脑基因表达的改变也可能持续存在。 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，这可能会改变幼鼠暴露于寄生虫的易感性。 传播动力学或易感性的改变将影响F1代群体的感染传播。** 将在宿主种群中探索感染风险对宿主-寄生虫种群动态的影响，并得到基于个体的研究的支持，以记录受感染的鱼类释放化学警报，受感染的小鼠母体改变幼仔微生物组和大脑基因表达。在应用层面上，我们的研究结果可能有助于控制加拿大和国际水产养殖设施的感染，并可能表明母体感染增加了后代对未来感染风险的恢复力。 **

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. **