Effects of Coralliophila violacea on tissue loss in the scleractinian corals Porites spp. depend on host response.
Effects of Coralliophila violacea on tissue loss in the scleractinian corals Porites spp. depend on host response.
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Coralliophila violacea 对石珊瑚滨珊瑚 (Porites spp) 组织损失的影响。
DOI：
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发表时间：
2016
影响因子：
1.4
通讯作者：
PL Lozada
中科院分区：
文献类型：
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作者：
LJ Raymundo;TM Work;RL Miller;PL Lozada
我们研究了珊瑚腹足类Coralliophila violacea和它的首选宿主滨珊瑚之间的相互作用。我们的目标是通过实验确定组织损失是否可以在Porites的进展过程中或之后Coralliophila捕食珊瑚和没有组织损失和组织学文件蜗牛捕食。在64%的喂养疤痕，组织再生3周内，没有留下捕食的痕迹。然而，在大约28%的瘢痕中，病变进展为类似白色综合征的亚急性组织缺损。在喂养实验中，以前喂养患病组织的蜗牛的疤痕发生进行性组织损失的频率是以前喂养健康组织的蜗牛疤痕的两倍。以前健康喂养的蜗牛的疤痕愈合的可能性是以前生病喂养的蜗牛的3倍。组织学显示，宿主对蜗牛的反应存在显著差异;柱螺表现出强烈的炎症反应，具有较少的次级定植生物，如藻类，海绵和蠕虫，而P.罗斯没有表现出明显的炎症和更多的次级定植。我们的结论是，与珊瑚虫相关的病变进展可能与二次殖民的珊瑚组织损伤的捕食者引起的创伤和坏死。重要的是，在解释受捕食等现象影响的珊瑚宿主反应的种间差异时，应考虑细胞水平的变化。
We investigated interactions between the corallivorous gastropod Coralliophila violacea and its preferred hosts Porites spp. Our objectives were to experimentally determine whether tissue loss could progress in Porites during or after Coralliophila predation on corals with and without tissue loss and to histologically document snail predation. In 64% of feeding scars, tissue regenerated within 3 wk, leaving no trace of predation. However, in roughly 28% of scars, lesions progressed to subacute tissue loss resembling white syndrome. In feeding experiments, scars from snails previously fed diseased tissue developed progressive tissue loss twice as frequently as scars from snails previously fed healthy tissue. Scars from previously healthy-fed snails were 3 times as likely to heal as those from previously diseased-fed snails. Histology revealed marked differences in host responses to snails; P. cylindrica manifested a robust inflammatory response with fewer secondary colonizing organisms such as algae, sponges, and helminths, whereas P. rus showed no evident inflammation and more secondary colonization. We conclude that lesion progression associated with Coralliophila may be associated with secondary colonization of coral tissues damaged by predator-induced trauma and necrosis. Importantly, variation at the cellular level should be considered when explaining interspecific differences in host responses in corals impacted by phenomena such as predation.