It was assigned to a new genus and species (13) with the type strain LF-89 (1, 17)

It was assigned to a new genus and species (13) with the type strain LF-89 (1, 17). levels against the pathogen. Documentation also exist that there is correlation between antibody titers and protection against mortality. Future vaccination regimes will likely also include live-attenuated vaccines or other technologies such as DNA vaccination. So far, there is no documentation available for live vaccines and, for Timonacic DNA vaccines, studies have been unsuccessful under laboratory conditions. (3). Similar disease outbreaks have later been diagnosed in Ireland and Scotland (4), Norway (5), and the Atlantic and Pacific coasts of Canada (6). SRS still causes major losses in salmon farming in Chile, and current annual losses are estimated at 250 million USD and the infection results in a high consumption of antibiotics toward the end of the production cycle (7). Disease outbreaks Timonacic are seen in all salmonid species farmed in Chile, Chinook salmon (L.) (7), and also in other species like Sakura salmon (C Atlantisk laksCanada C Atlantic ocean(4, Timonacic Timonacic 5, 66, 67)NorwayIrelandScotlandPink salmonCanada C Pacific Ocean(68)Chinook salmonC Atlantic salmonCoho salmonChile(2, 8, 69)rainbow troutChinook salmonC Atlantic salmonMasu salmonC White sea bassUSA(70)GrouperTaiwan(11) Open in a separate window Etiology in cell-free media (14C16). The bacterium is classified into a new family in the phylum Proteobacteria, class (1). It was assigned to a new genus and species (13) with the type strain LF-89 (1, 17). It can infect a wide variety of cells lines, such as RTG-2, CHSE-214, RTS-11, and also Sf-21 cells (18), the latter being an insect cell line that yields high titer (19). The understanding is that replicates within membrane-bound cytoplasmic vacuoles by binary fission (12, 20), and survives and multiplies in macrophages (21). In Chile, the disease normally occurs 6C12?weeks after introduction to seawater, but it is seen throughout the production cycle, resulting in high losses of larger fish. Moribund fish appear dark, anorexic or lethargic, and swim near the surface or edges of the cage (1, 17). Some fish may also present skin lesions: hemorrhages, petecchiae, nodules, and ulcers of varying size (20). Brain infection also occurs and the bacterium is also able to form biofilm under given conditions (22). Pathology Salmonid rickettsial septicemia in Atlantic salmon is often found with liver changes characterized by multifocal, necrotic areas of the hepatic parenchyma (Figure ?(Figure1).1). Histologically, the typical tissue response to infection is the formation of granulomas, often with central Timonacic suppuration and changes are seen in liver, spleen, and kidney (23), for this reason, the changes have been classified into the broad category of necrosis and inflammation but the principal changes are those of a granulomatous response that are more or less organized (5). At early stage of infection, granulomas typically consist of macrophages and a large number of neutrophils, often with central necrosis or suppuration (5) (Figure ?(Figure2).2). Older granulomas consist of a central necrosis surrounded by FGF18 connective tissue and fewer inflammatory cells. Perivascular infiltration of macrophages is also a typical finding (5). Open in a separate window Figure 1 Macroscopic changes in Atlantic salmon infected with infection is not understood. Pathogenesis of Infection The exact sequence of infection has not been clarified (23), but several studies indicate that the bacterium is able to penetrate through intact skin and gills followed by systemic invasion. Invasion through the oral and/or intestinal routes has also been suggested (24). To what extent the bacterium will survive passage through the stomach and the foregut is not known. Understanding infection routes are important for optimizing immunization protocols and will.