Relationship between Southern Bluefin Tuna, Thunnus maccoyii, melanomacrophage centres and Cardicola spp. (Trematoda: Aporocotylidae) infection.

Southern Bluefin Tuna (SBT), Thunnus maccoyii, is ranched off Port Lincoln, South Australia and is Australia's second largest economic finfish aquaculture industry. The biggest threats to SBT health identified by the industry are the blood flukes Cardicola forsteri and C. orientalis (Trematoda: Aporocotylidae). Melanomacrophage centres (MMCs) are aggregations of pigmented macrophage like cells present in spleen, kidney and liver of teleost fish. The aim of this study was to quantify MMCs in SBT anterior kidney, liver and spleen to investigate changes in relation to Cardicola spp. Infection. Samples were collected at the end of ranching from pontoons where SBT were treated with PZQ and pontoons with untreated SBT. SBT MMC percentage of surface area cover was highest in SBT spleen and lowest in the liver. Significant positive correlations were identified between SBT MMC area and SBT size in all three organs (p < 0.05). MMC area and parasite infection showed significant positive correlations in the kidney and spleen for Cardicola spp. gill egg counts, and in the kidney for C. forsteri DNA from SBT hearts and gills (p < 0.05). MMCs area increased with increased intensity of Cardicola spp. Infection and MMCs have the potential to be used as an indicator to assess health effects that Cardicola spp. have on SBT.

Experimentally induced marine flexibacteriosis in Atlantic salmon smolts Salmo salar. II. Pathology.

The fish disease marine flexibacteriosis is characterised by necrotic lesions on the body, head, fins, and occasionally gills, with erosive lesions on the external surface as the prominent clinical sign. In Australia, the main species affected are Atlantic salmon Salmo salar and rainbow trout Oncorhynchus mykiss in sea-cage culture in Tasmania. Using a dose-dependent trial to determine pathology, 2 forms of the disease were noted in Atlantic salmon. The acute form occurs within 2 to 3 d after inoculation at high doses (1 x 10(8) cells ml(-1)) and is characterised by the disintegration of the epithelium. The chronic form of the disease began as small superficial blisters of the epidermis, which develop into ulcerative lesions that leave musculature exposed. The predominant lesion sites were the dorsum and pectoral fins. Jaws were commonly affected, and gill necrosis was also noted. Behaviour of Atlantic salmon as well as the conditions under which they were kept contribute to the size and distribution of lesions observed. Lack of an inflammatory response in pathology and rapid and destructive mortalities observed in higher inoculum doses suggested a role of toxins in the pathogenesis of Tenacibaculum maritimum. This is the first study to examine the development of marine flexibacteriosis lesions and to utilise immunohistochemistry to verify that the bacteria observed in histology was T. maritimum.

Experimentally induced marine flexibacteriosis in Atlantic salmon smolts Salmo salar. I. Pathogenicity.

Tenacibaculum maritimum causes marine flexibacteriosis in many cultured fish species, including Atlantic salmon Salmo salar in Tasmania, Australia. Several aspects of the pathogenicity of this bacterium were investigated in naive Atlantic salmon smolts using different isolates, growth conditions and doses to produce a model of infection. We found that T. maritimum is pathogenic to Atlantic salmon using either marine Shieh's or marine Ordal's culture medium. The use of aeration in broth culture produced a dose effect in challenge due to a 'clumping' of the bacteria during culture. The virulence of a strain appears to be connected with this 'clumping'; the more adherent the cells, the more pathogenic the strain. Differences in virulence between 3 strains was apparent, with 1 of the strains (89/4747) being non-pathogenic and unable to produce disease in the host. The 2 other strains (89/4762, 00/3280) were highly virulent, resulting in 100% mortalities within 3 d. A reproducible model of infection has been established in the present study using strain 89/4762. Results from the present study provide a better insight into the nature of the disease.

Experimental induction of gill disease in Atlantic salmon Salmo salar smolts with Tenacibaculum maritimum.

An experimentally induced bacterial infection of marine Atlantic salmon Salmo salar smolt gills was developed using strains of Tenacibaculum maritimum originally isolated from disease outbreaks in Tasmania. The gills of salmon were inoculated with a high concentration of bacteria (4 x 10(11) cells per fish) of either strain 00/3280 or 89/4747 T. maritimum. Gentle abrasion of the gills was used to enhance the progression of gill disease. One strain (00/3280) was highly pathogenic, causing morbidity and mortality within 24 h post-inoculation, and produced acute focal branchial necrosis associated with significant increases in plasma osmolality and lactate concentration compared with controls (non-inoculated) or strain 89/4747-inoculated fish. There were no differences in the whole body net ammonium flux between control (non-inoculated) and strain 00/3820-inoculated fish. Gill abrasion resulted in acute telangiectasis and focal lamellar hyperplasia in all fish regardless of bacterial inoculation. This work provides the basis of a challenge model suitable for investigating the pathophysiological processes associated with acute branchial necrosis in marine fish, suggesting that osmoregulatory and possibly respiratory dysfunction are the primary consequences of infection.