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首页> 外文期刊>Frontiers in Marine Science >Stony Coral Tissue Loss Disease in Florida Is Associated With Disruption of Host–Zooxanthellae Physiology
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Stony Coral Tissue Loss Disease in Florida Is Associated With Disruption of Host–Zooxanthellae Physiology

机译:佛罗里达州的石珊瑚组织丧失疾病与宿主毒素生理的破坏有关

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Samples from eight species of corals (Colpophyllia natans, Dendrogyra cylindrus, Diploria labyrinthiformis, Meandrina meandrites, Montastraea cavernosa, Orbicella faveolata, Pseudodiploria strigosa, and Siderastrea siderea) that exhibited gross clinical signs of acute, subacute, or chronic tissue loss attributed to stony coral tissue loss disease (SCTLD) were collected from the Florida Reef Tract during 2016–2018 and examined histopathologically. The hallmark microscopic lesion seen in all eight species was focal to multifocal lytic necrosis (LN) originating in the gastrodermis of the basal body wall (BBW) and extending to the calicodermis, with more advanced lesions involving the surface body wall. This was accompanied by other degenerative changes in host cells such as mucocyte hypertrophy, degradation and fragmentation of gastrodermal architecture, and disintegration of the mesoglea. Zooxanthellae manifested various changes including necrosis (cytoplasmic hypereosinophilia, pyknosis); peripheral nuclear chromatin condensation; cytoplasmic vacuolation accompanied by deformation, swelling, or atrophy; swollen accumulation bodies; prominent pyrenoids; and degraded chloroplasts. Polyhedral intracytoplasmic eosinophilic periodic acid–Schiff-positive crystalline inclusion bodies (~1–10 μm in length) were seen only in M. cavernosa and P. strigosa BBW gastrodermis in or adjacent to active lesions and some unaffected areas (without surface lesions) of diseased colonies. Coccoidlike or coccobacilloidlike structures (Gram-neutral) reminiscent of microorganisms were occasionally associated with LN lesions or seen in apparently healthy tissue of diseased colonies along with various parasites and other bacteria all considered likely secondary colonizers. Of the 82 samples showing gross lesions of SCTLD, 71 (87%) were confirmed histologically to have LN. Collectively, pathology indicates that SCTLD is the result of a disruption of host–symbiont physiology with lesions originating in the BBW leading to detachment and sloughing of tissues from the skeleton. Future investigations could focus on identifying the cause and pathogenesis of this process.
机译:来自八种珊瑚(Colpophyllia Natans,Dendrogyra Cylindrus,Diploria Labyrinthiformis,incorastraea cavernosa,Orbicella Faveolata,Pseudodivia,令人州的Siderastrea Siderea)的样本,其表现出急性,亚急性或慢性组织损失的总临床症状归因于石珊瑚从2016 - 2018年在佛罗里达礁道收集组织丧失疾病(SCTLD),并在组织病理学上检查。在所有八种物种中看到的,在所有八种物种中看到的标志性微观病变是源自基底体壁(BBW)的胃肠杆菌和延伸到Calicodermis的多焦裂解坏死(LN),涉及表面体壁的更先进的病变。这伴随着宿主细胞的其他退行性变化,例如粘蛋白肥大,降解和胃胚胎结构的崩解和脱髓糖薄膜的崩解。 Zooxanthellae表现出各种变化,包括坏死(细胞质低血液粒细胞,Pyknosis);外周核染色质凝结;细胞质真空伴有变形,肿胀或萎缩;肿胀的积聚机构;突出的芘;和降解叶绿体。在活性病变中的M. cavernosa和P. strigosa bbw胃肠杆菌或邻近有源病变和一些未受影响的区域(没有表面病变),仅在M. cavernosa和P. stirogosa bbw胃肠杆菌中观察到多面体的嗜酸性嗜酸性周期性酸 - 席夫阳性结晶包衣体(〜1-10μm)。患病殖民地。椰子状或可口可球状结构(革兰氏体)使微生物联想到偶尔与LN病变相关,或者在患病菌落的明显健康组织中以及各种寄生虫和其他细菌中观察到,所有寄生虫也可能被认为是二次结肠剂。在显示SCTLD的粗糙病变的82个样品中,71(87%)在组织学上确认以具有LN。统称,病理学表明,SCTLD是Host-Symbiont生理的结果,其源于BBW的病变导致从骨架中脱离和剥离组织。未来的调查可以专注于确定该过程的原因和发病机制。

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