Branchial mechanical injury does not accelerate the progression of experimentally induced amoebic gill disease (AGD) in Atlantic salmon Salmo salar L
It remains unclear whether the pathological severity of AGD can be exacerbated by injury to the branchialepithelium; a circumstance that may arise in situ due to contact with harmful water-borne agents. Here,results from an experimental laboratory infection are given, testing the assertion that bran...
| Published in: | Aquaculture |
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| Main Authors: | , , |
| Format: | Article in Journal/Newspaper |
| Language: | English |
| Published: |
Elsevier Science Bv
2009
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| Subjects: | |
| Online Access: | https://doi.org/10.1016/j.aquaculture.2009.02.007 http://ecite.utas.edu.au/60124 |
| Summary: | It remains unclear whether the pathological severity of AGD can be exacerbated by injury to the branchialepithelium; a circumstance that may arise in situ due to contact with harmful water-borne agents. Here,results from an experimental laboratory infection are given, testing the assertion that branchial injury wouldaccelerate the pathological development of AGD. The lamellar epithelium of the left and right, first andsecond, anterior hemibranchs of Atlantic salmon were damaged by physical abrasion and subsequentlyexposed to Neoparamoeba perurans. Control groups of non damaged/infected and damaged/non-infectedfish were synchronously maintained for 32 days. Further undamaged fish were selected for mechanicaldamage at day 16, following the onset of AGD. Gills were collected from each group and processed for routinehistology at 2, 4, 8, 16, 24 & 32 days post-exposure to Neoparamoeba spp. Mechanical injury initially resultedin oedema, telangiectasis, haemorrhaging and leucocytic infiltration. During subsequent recovery, thelamellae were fused with undifferentiated cells, mucous cells and leucocytes. The degree of lamellar fusion(due to mechanical injury) had dissipated substantially by the conclusion of the trial. Trophozoites ofN. perurans were largely undetected upon mechanically injured portions of the gills for the duration of theexperiment. Concurrently, there was no significant difference between injured and control fish in terms ofAGD development over time, neither was there a significant difference within fish when comparing damagedand undamaged hemibranchs. Together, these data suggest mechanical injury does not present an enhancedopportunity for attachment and/or colonization of the gill epithelium in Atlantic salmon duringexperimental infection with N. perurans. 2009 Elsevier B.V. All rights reserved. |
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