Collaborative Research: How do predators spread disease? Tests of five ecological and eco-evolutionary mechanisms with disease in the plankton

疾病生态学家的一个实际目标是找到阻止或减缓感染在宿主之间传播的方法。一个流行的观点是，捕食者通过杀死受感染的猎物来控制疾病的爆发，这些猎物较弱，因此更容易捕获。然而，该提案警告说，捕食者有时可能会在宿主种群中传播疾病。研究人员将利用生活在湖泊中的生物来测试捕食者传播疾病的五种方式。这些观点是：捕食者：（1）在捕食猎物时，通过物理方式将寄生虫传播到猎物栖息地;（2）可以增加猎物的食物供应，更多的食物可以导致感染宿主体内寄生虫的产量增加;（3）可以将猎物种群的组成向更容易感染的年龄和大小转移;（4）可以杀死控制疾病的其他物种;（5）可引起猎物种群的遗传变化，使它们更容易受到疾病生物的影响。该项目将重点关注水蚤（宿主），一种致命的真菌寄生虫和一种昆虫捕食者，以测试这些可能性。该研究使用这些生物作为模型系统：这种真菌的爆发可以在湖泊中取样，在湖泊和实验室中的实验中创建，并且可以使用数学模型来理解。这些新想法一旦在实验室中得到彻底测试并在自然界中得到验证，将有助于管理人员就如何控制野生和家养动物种群中的疾病爆发做出谨慎的决定。该项目将培训许多学生，并侧重于让那些代表性不足的群体参与进来。该项目结合了三种方法。首先，它将在40个湖泊的水蚤宿主中进行真菌流行病调查。这项大型调查的数据将用于生成复杂的统计模型，以测试上述前四种机制（想法）。其次，它使用受控实验。一个实验将测试机制（2）-（4）与捕食性昆虫和“竞争稀释剂”（其他水蚤物种吃寄生虫繁殖）的因子操作。第二个实验将研究机制（1）-（3）的细节。第三个实验研究了宿主的克隆基因型之间的权衡;更好地逃避捕食的基因型更容易受到寄生虫的影响。假设是捕食者将通过快速进化转移宿主种群，通过这种权衡走向更大的流行病。第三，该项目开发了一套新的参数化数学（动态）模型，旨在单独和共同评估每个机制。

A practical goal of disease ecologists is to find ways to stop or slow the spread of infection from host to host. A popular idea is that predators control disease outbreaks by killing infected prey which are weaker and thereby easier to capture. However, this proposal warns that predators may sometimes spread disease in host populations. The researchers will use organisms living in lakes to test five ways in which predators could spread disease. These ideas are that predators: (1) while eating prey, physically spread parasites into prey habitat; (2) can increase food supply for prey, and more food can cause higher parasite production within infected hosts; (3) can shift the composition of prey populations towards certain ages and sizes that get infected more easily; (4) can kill other species that control disease; and (5) can cause genetic changes to prey populations, making them more susceptible to disease organisms. The project will focus on water fleas (the hosts), a deadly fungal parasite, and an insect predator to test these possibilities. The research uses these organisms as a model system: outbreaks of this fungus can be sampled in lakes, created in experiments within lakes and in the lab, and can be understood using mathematical models. These new ideas, once tested thoroughly in the lab and verified in nature, will help managers make prudent decisions on how to control disease outbreaks in wild and domestic animal populations. The project will train many students, and focus on engaging those in underrepresented groups. This project integrates three approaches. First, it will invest in a survey of fungal epidemics in water flea hosts in 40 lakes. The data from this large survey will be used to generate complex statistical models that test the first four mechanisms (ideas) given above. Second, it uses controlled experiments. One experiment will test mechanisms (2)-(4) with factorial manipulation of predatory insects and "competitor-diluters" (other water flea species which eat parasite propagules). A second experiment will investigate details of mechanisms (1)-(3). A third experiment investigates a tradeoff among clonal genotypes of the host; genotypes which better escape predation are more vulnerable to parasites. The hypothesis is that predators will shift host populations, via rapid evolution, towards bigger epidemics via this tradeoff. Third, this project develops a new suite of parameterized, mathematical (dynamical) models, designed to evaluate each of the mechanisms separately and together.