Development of resistance to an introduced marine pathogen by a native host
Development of resistance to an introduced marine pathogen by a native host
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DOI：
10.1357/002224012802851922
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发表时间：
2012-03-01
影响因子：
0.5
通讯作者：
Bushek, David
中科院分区：
文献类型：
--
作者：
Ford, Susan E.;Bushek, David
在1957-1959年，引入的原生生物寄生虫，单孢子虫nelsoni，杀死了特拉华州湾下游90-95%的牡蛎（Crassostrea virginica）和海湾上游约一半的牡蛎。不久之后，H。纳尔逊造成的下湾野生种群死亡率下降，接近第一代选择性养殖牡蛎的死亡率。此后近30年来，野生种群的生存没有进一步的变化，尽管通过持续的选择性育种实现了稳定的改善。野生种群的生存被认为是平稳的，因为绝大多数牡蛎居住在上湾，在那里它们受到保护，免受H。Nelsoni感染和低盐度的选择性死亡。因此，它们为海湾种群贡献了大部分后代。从1957年到1987年，H.纳尔逊流行率呈周期性变化，但总体而言，下湾的流行率很高（每年最高为60%至85%）。然而，自1988年以来，在海湾的任何地方，野生牡蛎的流行率很少超过30%，即使牡蛎在暴露时继续受到严重感染，分子证据表明，寄生虫仍然存在于整个海湾。这显然是野生牡蛎抗药性发展的“第二步”，发生在与干旱相关的H。在80年代中期进入上湾。与1957年至1959年的动物流行病相比，死亡率普遍、严重和极端。第二次动物流行病的抵抗幸存者显然已经在海湾重新定居。当与普通砧木相比时，普通菜园暴露于H。nelsoni的结果表明，在相隔近30年的两次主要选择事件之后，对MSX疾病发展的高度抗性已经在特拉华州湾的野生牡蛎种群中广泛存在。
In 1957-1959, the introduced protistan parasite, Haplosporidium nelsoni, killed 90-95% of the oysters (Crassostrea virginica) in lower Delaware Bay and about half of those in the upper bay. Shortly thereafter, H. nelsoni-caused mortality in the wild population of the lower bay declined, approximating that of first-generation selectively bred oysters. For nearly three decades thereafter no further change in survival of the wild population was evident, although steady improvement was achieved by continued selective breeding. Survival of the wild population is thought to have plateaued because the great majority of oysters inhabited the upper bay where they were protected from H. nelsoni infection and selective mortality by low salinity. Consequently, they contributed most of the offspring to the bay population. From 1957 through 1987, H. nelsoni prevalence was cyclic, but overall high (annual maxima of 60 to 85%) in the lower bay. Since 1988, however, prevalence in wild oysters has rarely exceeded 30% anywhere in the bay, even though unselected oysters continue to become heavily infected when exposed, and molecular evidence indicates that the parasite remains present throughout the bay. This apparent "second step" in the development of resistance in the wild oysters occurred after a drought-associated incursion of H. nelsoni into the upper bay in the mid-1980s. Mortalities were widespread, heavy and more extreme than during the 1957-59 epizootic. Resistant survivors of the second epizootic have apparently repopulated the bay. When compared to unselected stocks, common-garden exposure to H. nelsoni of oysters from both upbay and downbay sites indicates that a high degree of resistance to the development of MSX disease has become widespread in the wild oyster population of Delaware Bay after two major selection events separated by nearly 30 years.