The disease signs mimicked those on naturally infected fish ie erratic swimming

The disease signs mimicked those on naturally

This preview shows page 353 - 355 out of 594 pages.

1995). The disease signs mimicked those on naturally infected fish, i.e. erratic swimming and melanosis. Incidentally, the organism failed to infect red seabream. Vibrio ordalii The virulence plasmid, pJMl, has not been detected in V. ordalii (Crosa, 1980). However, a 30 kb cryptic plasmid, designated pMJlOl and which repHcates in the absence of DNA polymerase I without generating single-stranded intermediates, has been found in ah isolates of V. ordalii (Bidinost et al, 1994; 1999). Moreover, haemolysins and proteases have not been found (Kodama et al, 1984). Vibrio pelagius Infectivity experiments with rainbow trout (10 g) and turbot (5g in size) confirmed virulence, and an LD50 of 1.9 x 10^ cells/fish and 9.5 x 10^ cells/fish, respectively (Angulo et al, 1992). Subsequently, Villamil et al. (2003) published the LD50 for larval and post-larval turbot as <5 bacteria/ml and 3.9 x 10^ bacteria/ml, respec- tively. The profound virulence for larvae is clearly demonstrated. The administration of bacterial cells to head kidney macrophages resulted in a marked inhibition of the chemiluminescence response when compared with controls, i.e. untreated macro- phages, but an increase in the nitric oxide production. Additionally, in turbot larvae, the appHcation of live cells of the pathogen via i.p. injection led to a dramatic inhibition of the chemiluminescence response in one day (Villamil et al, 2003a).
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334 Bacterial Fish Pathogens Vibrio salmonicida Intraperitoneal injection and immersion of Atlantic salmon and rainbow trout with broth cultures led to clinical disease. Atlantic salmon were more susceptible than rainbow trout (Egidius et al, 1986; Hjeltnes et al, 1987). The LD50 dose ranges from 4 X 10^-1 X 10^ cells/fish (Wiik et aL, 1989). The presence of other acute diseases, such as infectious pancreatic necrosis, has exacerbated infections in Atlantic salmon caused by V. salmonicida (Johansen and Sommer, 2001). In addition, V. salmonicida has caused mortalities in cod (J0rgensen et aL, 1989). The plasmids, which are regarded as being present in all strains, do not appear to be related to virulence (Valla et aL, 1992). Using isolated macrophages from Atlantic salmon and rainbow trout with immunofluorescence techniques, the pathogen has been observed to be internahsed (Brattgjerd et aL, 1995). The pathogen demonstrated the ability to adhere to mucus from Atlantic salmon epithehal surfaces, i.e. foregut, gills, hindgut, pyloric caeca and skin (Knudsen et aL, 1999). What about the risk of disease after transferring salmon from fresh to seawater? Eggset et aL (1997) concluded that the susceptibility of Atlantic salmon to Hitra disease in seawater possibly reflected the overall quahty of the smolts. Vibrio splendidus The bacterium was pathogenic to rainbow trout and turbot, with an LD50 of 2.2 X 10"^ cells and 1.2 x lO"^ cells, respectively (Angulo et aL, 1994).
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