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Pathology of amoebic gill disease in Atlantic Salmon (Salmo salar L.)

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Adams, Mark (2003) Pathology of amoebic gill disease in Atlantic Salmon (Salmo salar L.). PhD thesis, University of Tasmania.

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Abstract

Although AGD has affected the Tasmanian salmonid industry for nearly 20 years,
several fundamental questions regarding the pathology of this condition remain
unanswered. This thesis elucidates the requirements for AGD outbreaks and how
AGD progresses within the commercial culture environment.
Atlantic salmon Salmo salar L. gills, affected with amoebic gill disease, were
analysed by routine histology to identify lesion morphology and distribution patterns.
Interlamellar cyst (or vesicle) function was hypothesised as a host defence mechanism
leading to entrapment of trophozoites and clearance from hyperplastic tissues by host
cellular processes.
The degree of conformity between clinical signs and histological lesions was
investigated in commercially reared Atlantic salmon. Micro-stereoscopic analysis
showed that grossly affected tissue regions correspond to areas of hyperplastic
lamellae fusion generally in association with attached amoebae. Agreement between
gross signs of AGD and histopathological diagnosis, as indicated by Kappa, was
moderate to good (0.52 — 0.74). Stage of disease development, lesions derived from
other pathogens, assessor interpretation / experience, sampling methods, histological
technique and/or experience all featured as potential factors leading to individual case
disagreement. The causal mechanisms for AGD lesion development and the primary role of
Neoparamoeba sp. were investigated. AGD only occurred when fish were exposed to
viable trophozoites. A progressive host response and significant increases (P<0.001)
in the numbers of attached amoebae was apparent over the 48 h duration. Attachment
of Neoparamoeba sp. to damaged gill filaments was significantly lower than upon
damaged filaments (P<0.05) by 48 h post exposure. Histopathological observations of AGD from smolts, sampled weekly,
following transfer to estuarine/marine sites were investigated. Results suggest that
AGD progression was linked to retraction of the estuarine halocline and increases in
water temperature. The host response to gill infection with Neoparamoeba sp. is
characterized by a focal fortification strategy concurrent with a migration of irnmunoregulatory
cells to lesion affected regions.
Subsequently, the progression of re-infection (post-treatment) was investigated
using a similar sequential investigation. 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. During the post-bath period, non AGD lesions including haemorrhage,
necrosis and regenerative hyperplasia were occasionally observed though 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.
Together, these data have addressed the need for an improved understanding
of AGD associated pathology during commercial culture of Atlantic salmon in
Tasmania primarily by defining an improved pathological model of AGD. This work
forms the basis for not only differential diagnosis per se but also a foundation and/or
reference for future research dependent upon histopathological outcomes as an
evaluative endpoint.

Item Type: Thesis (PhD)
Keywords: Paramoebidae, Atlantic salmon, Atlantic salmon
Copyright Holders: The Author
Copyright Information:

Copyright 2003 the Author - The University is continuing to endeavour to trace the copyright
owner(s) and in the meantime this item has been reproduced here in good faith. We
would be pleased to hear from the copyright owner(s).

Additional Information:

Thesis (Ph.D )--University of Tasmania, 2004. Includes bibliographical references

Date Deposited: 25 Nov 2014 00:53
Last Modified: 11 Mar 2016 05:54
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