Therefore it is suggested that the pathogenicity mechanism involves proteases

Therefore it is suggested that the pathogenicity

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ally very active, but most isolates attack proteins (gelatin) and lipids (Tween 80). Therefore, it is suggested that the pathogenicity mechanism involves proteases and lipases. There is no evidence for the presence of an extracellular layer in virulent
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Pathogenicity 327 isolates as occurs in Aer. salmonicida. There is some evidence of species-based susceptibility to Sekiten-byo, with Japanese eels seemingly more prone to the disease than European eels. It is speculative whether or not this infers that the organism may be more common in and around European eels (or may have originated with this species). A comparative observation is that brown trout are more susceptible than rainbow trout to furunculosis caused by Aer. salmonicida. Certainly, Ps. anguilliseptica is capable of infecting a greater range of species than represented by the genus Anguilla. Thus, experimental infections have been achieved in ayu, bluegill, carp, goldfish and loach (Muroga, et al., 1975). The organism is only of low pathogenicity to rainbow trout (Lonnstrom et al., 1994). The presence of sublethal concentrations of copper (100-250 mg/1) in water exacerbates the disease (Mushiake et al., 1984). Evidence points to a reduction in lymphocytes and granulocytes, which leads to lowered phagocytosis (Mushiake et al., 1985). Pseudomonas chlororaphis The isolates from Amago trout and the neotype culture of Ps. chlororaphis were pathogenic to carp, eels and trout, following challenge by i.m. injection. Total mortalities occurred within 48 h at a water temperature of 22° C, with disease symp- toms paralleling those on the naturally infected fish. However, the pathogenicity mechanism is unknown (Hatai et al, 1975). Pseudomonas fluorescens Following invasion of the fish, extracellular proteases are probably responsible for the ensuing damage (Li and Fleming, 1967; Li and Jordan, 1968). Sakai et al. (1989a) reported the LD50 for rainbow trout as 4.2 x 10^ cells at 18°C and 1.1 x 10^ cells at 12°C. Pseudomonas plecoglossicida During surveys of dead ayu (with bloody ascites) in Japan during 1999 and 2001, with the exception of one isolate all the others were non-motile. Moreover, non-motile cells were injected intramuscularly into ayu leading to the recovery of both motile and non-motile cells from the kidney. However, motile cells were recovered after the injection of motile cultures (Park et al., 2002). By use of GFP-labelled cells, the pathogen has been observed to adhere predominantly to the site of microscopic injuries in the fins and skin (Sukenda and Wakabayashi, 2001). Pseudomonas pseudoalcaligenes Injection of 10^ cells by i.p. or i.m. injection into rainbow trout (average weight = 12 g), held at 15°C, resulted in total mortahties within 7 days. Moribund fish revealed the presence of haemorrhaging (internal and around the vent) and ascitic fluid in the peritoneal cavity (Austin and Stobie, 1992b).
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328 Bacterial Fish Pathogens Vibrionaceae representatives Vibrio alginolyticus Lee (1995) revealed that the organism produced ECP, which was lethal at 0.52 |ig/g of fish. The ECP contained a 44 kDa toxic protease, for which the minimum lethal dose was 0.17 |ig/g of fish. In comparison, the LD50 for ECP to silver sea bream was reported as 0.92 |ig/g offish, with haemolysins and proteases featuring in pathogen-
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