Cyclic Hypoxia Exposure Accelerates the Progression of Amoebic Gill Disease

Amoebic gill disease (AGD), caused by the amoeba Neoparamoeba perurans, 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...

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Published in:Pathogens
Main Authors: Tina Oldham, Tim Dempster, Philip Crosbie, Mark Adams, Barbara Nowak
Format: Text
Language:English
Published: Multidisciplinary Digital Publishing Institute 2020
Subjects:
Online Access:https://doi.org/10.3390/pathogens9080597
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spelling ftmdpi:oai:mdpi.com:/2076-0817/9/8/597/ 2023-08-20T04:05:18+02:00 Cyclic Hypoxia Exposure Accelerates the Progression of Amoebic Gill Disease Tina Oldham Tim Dempster Philip Crosbie Mark Adams Barbara Nowak agris 2020-07-22 application/pdf https://doi.org/10.3390/pathogens9080597 EN eng Multidisciplinary Digital Publishing Institute Immunological Responses and Immune Defense Mechanisms https://dx.doi.org/10.3390/pathogens9080597 https://creativecommons.org/licenses/by/4.0/ Pathogens; Volume 9; Issue 8; Pages: 597 Salmo salar Atlantic salmon aquaculture dissolved oxygen Paramoeba/Neoparamoeba perurans stress Text 2020 ftmdpi https://doi.org/10.3390/pathogens9080597 2023-07-31T23:48:30Z Amoebic gill disease (AGD), caused by the amoeba Neoparamoeba perurans, 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 N. perurans compared to normoxic controls maintained at ≥90% DO saturation. Although hypoxia exposure did not increase initial susceptibility to N. perurans, 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. Text Atlantic salmon Salmo salar MDPI Open Access Publishing Pathogens 9 8 597
institution Open Polar
collection MDPI Open Access Publishing
op_collection_id ftmdpi
language English
topic Salmo salar
Atlantic salmon
aquaculture
dissolved oxygen
Paramoeba/Neoparamoeba perurans
stress
spellingShingle Salmo salar
Atlantic salmon
aquaculture
dissolved oxygen
Paramoeba/Neoparamoeba perurans
stress
Tina Oldham
Tim Dempster
Philip Crosbie
Mark Adams
Barbara Nowak
Cyclic Hypoxia Exposure Accelerates the Progression of Amoebic Gill Disease
topic_facet Salmo salar
Atlantic salmon
aquaculture
dissolved oxygen
Paramoeba/Neoparamoeba perurans
stress
description Amoebic gill disease (AGD), caused by the amoeba Neoparamoeba perurans, 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 N. perurans compared to normoxic controls maintained at ≥90% DO saturation. Although hypoxia exposure did not increase initial susceptibility to N. perurans, 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.
format Text
author Tina Oldham
Tim Dempster
Philip Crosbie
Mark Adams
Barbara Nowak
author_facet Tina Oldham
Tim Dempster
Philip Crosbie
Mark Adams
Barbara Nowak
author_sort Tina Oldham
title Cyclic Hypoxia Exposure Accelerates the Progression of Amoebic Gill Disease
title_short Cyclic Hypoxia Exposure Accelerates the Progression of Amoebic Gill Disease
title_full Cyclic Hypoxia Exposure Accelerates the Progression of Amoebic Gill Disease
title_fullStr Cyclic Hypoxia Exposure Accelerates the Progression of Amoebic Gill Disease
title_full_unstemmed Cyclic Hypoxia Exposure Accelerates the Progression of Amoebic Gill Disease
title_sort cyclic hypoxia exposure accelerates the progression of amoebic gill disease
publisher Multidisciplinary Digital Publishing Institute
publishDate 2020
url https://doi.org/10.3390/pathogens9080597
op_coverage agris
genre Atlantic salmon
Salmo salar
genre_facet Atlantic salmon
Salmo salar
op_source Pathogens; Volume 9; Issue 8; Pages: 597
op_relation Immunological Responses and Immune Defense Mechanisms
https://dx.doi.org/10.3390/pathogens9080597
op_rights https://creativecommons.org/licenses/by/4.0/
op_doi https://doi.org/10.3390/pathogens9080597
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