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

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 ‚ÄövÑvÆ 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.