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周期性低氧暴露加速阿米巴鳃病的发展。

Cyclic Hypoxia Exposure Accelerates the Progression of Amoebic Gill Disease.

作者信息

Oldham Tina, Dempster Tim, Crosbie Philip, Adams Mark, Nowak Barbara

机构信息

Institute of Marine Research, 5984 Matre, Norway.

Aquatic Animal Health Group, Institute for Marine and Antarctic Studies, University of Tasmania, Launceston, TAS 7248, Australia.

出版信息

Pathogens. 2020 Jul 22;9(8):597. doi: 10.3390/pathogens9080597.

DOI:10.3390/pathogens9080597
PMID:32707755
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7460382/
Abstract

Amoebic gill disease (AGD), caused by the amoeba , has led to considerable economic losses in every major Atlantic salmon producing country, and is increasing in frequency. The most serious infections occur during summer and autumn, when temperatures are high and poor dissolved oxygen (DO) conditions are most common. Here, we tested if exposure to cyclic hypoxia at DO saturations of 40-60% altered the course of infection with compared to normoxic controls maintained at ≥90% DO saturation. Although hypoxia exposure did not increase initial susceptibility to , it accelerated progression of the disease. By 7 days post-inoculation, amoeba counts estimated from qPCR analysis were 1.7 times higher in the hypoxic treatment than in normoxic controls, and cumulative mortalities were twice as high (16 ± 4% and 8 ± 2%), respectively. At 10 days post-inoculation, however, there were no differences between amoeba counts in the hypoxic and normoxic treatments, nor in the percentage of filaments with AGD lesions (control = 74 ± 2.8%, hypoxic = 69 ± 3.3%), or number of lamellae per lesion (control = 30 ± 0.9%, hypoxic = 27.9 ± 0.9%) as determined by histological examination. Cumulative mortalities at the termination of the experiment were similarly high in both treatments (hypoxic = 60 ± 2%, normoxic = 53 ± 11%). These results reveal that exposure to cyclic hypoxia in a diel pattern, equivalent to what salmon are exposed to in marine aquaculture cages, accelerated the progression of AGD in post-smolts.

摘要

由阿米巴原虫引起的阿米巴鳃病(AGD)已在每个主要的大西洋鲑鱼生产国造成了相当大的经济损失,且发病率正在上升。最严重的感染发生在夏季和秋季,此时温度较高且溶解氧(DO)水平较低的情况最为常见。在此,我们测试了与维持在≥90% DO饱和度的常氧对照组相比,在40 - 60% DO饱和度下暴露于周期性缺氧是否会改变感染进程。虽然缺氧暴露并未增加对[病原体名称未给出]的初始易感性,但它加速了疾病的进展。接种后7天,通过qPCR分析估计,缺氧处理组中的阿米巴原虫数量比常氧对照组高1.7倍,累积死亡率分别是常氧对照组的两倍(16 ± 4%和8 ± 2%)。然而,接种后10天,缺氧处理组和常氧处理组之间的阿米巴原虫数量、出现AGD病变的鳃丝百分比(对照组 = 74 ± 2.8%,缺氧组 = 69 ± 3.3%)或每个病变的鳃小片数量(对照组 = 30 ± 0.9%,缺氧组 = 27.9 ± 0.9%,通过组织学检查确定)均无差异。实验结束时,两种处理组的累积死亡率同样很高(缺氧组 = 60 ± 2%,常氧组 = 53 ± 11%)。这些结果表明,以相当于鲑鱼在海水养殖网箱中所经历的昼夜模式暴露于周期性缺氧,加速了后幼鲑阶段AGD的病程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1741/7460382/4115475107a2/pathogens-09-00597-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1741/7460382/49c0915ea547/pathogens-09-00597-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1741/7460382/4115475107a2/pathogens-09-00597-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1741/7460382/49c0915ea547/pathogens-09-00597-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1741/7460382/4115475107a2/pathogens-09-00597-g003.jpg

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