Adams M B, Nowak B F
School of Aquaculture, Aquafin CRC, Tasmanian Aquaculture and Fisheries Institute, Launceston, Tasmania, Australia.
J Fish Dis. 2004 Mar;27(3):163-73. doi: 10.1111/j.1365-2761.2004.00531.x.
Freshwater bathing is essential for control of amoebic gill disease (AGD) during the marine phase of the Tasmanian Atlantic salmon production cycle, a practice that is costly, production limiting and increasing in frequency. Although the pathogenesis of gill infection with Neoparamoeba sp. in naïve Atlantic salmon, Salmo salar, is now understood, the progression of re-infection (post-treatment) required elucidation. Here, we describe the weekly histopathological progression of AGD from first to second freshwater bath. Halocline cessation and increased water temperature appeared to drive the rapid onset of initial infection prior to bathing. Freshwater bathing cleared lesions of attached trophozoites and associated cellular debris. Subsequent gill re-infection with Neoparamoeba sp. was evident at 2 weeks post-bath and had significantly increased (P < 0.001), in severity by 4 weeks post-bath. No significant difference in gross pathology was observed until 4 weeks post-bath (P < 0.05). The re-infective progression of AGD was characterized by localized host tissue responses juxtaposed to adhered trophozoites (epithelial oedema, hypertrophy and hyperplasia), non-specific inflammatory cell infiltration (macrophages, neutrophils and eosinophilic granule cells) and finally advanced hyperplasia with epithelial fortification. During the post-bath period, non-AGD lesions including haemorrhage, necrosis and regenerative hyperplasia were occasionally observed, although no evidence of secondary colonization of these lesions by Neoparamoeba sp. was noted. We conclude that pathogenesis during the inter-bath period was identical to initial infection although the source of re-infection remains to be established.
在塔斯马尼亚大西洋鲑鱼生产周期的海水养殖阶段,淡水浴对于控制阿米巴鳃病(AGD)至关重要,这一做法成本高昂、限制产量且频率不断增加。尽管现在已经了解了幼稚大西洋鲑鱼(Salmo salar)感染新帕拉变形虫(Neoparamoeba sp.)导致鳃部发病的机制,但再感染(治疗后)的进展情况仍需阐明。在此,我们描述了从第一次到第二次淡水浴期间AGD的每周组织病理学进展。盐跃层停止和水温升高似乎促使洗浴前初始感染迅速发生。淡水浴清除了附着的滋养体和相关细胞碎片的病变。洗浴后2周,鳃部再次感染新帕拉变形虫明显可见,到洗浴后4周,病情严重程度显著增加(P < 0.001)。直到洗浴后4周才观察到大体病理学上的显著差异(P < 0.05)。AGD的再感染进展特征为与附着的滋养体并列的局部宿主组织反应(上皮水肿、肥大和增生)、非特异性炎症细胞浸润(巨噬细胞、中性粒细胞和嗜酸性粒细胞),最终是伴有上皮强化的晚期增生。在洗浴后期间,偶尔会观察到包括出血、坏死和再生性增生在内的非AGD病变,尽管未发现新帕拉变形虫对这些病变进行二次定植的证据。我们得出结论,洗浴间隔期的发病机制与初始感染相同,尽管再感染的来源仍有待确定。