not all of these OMPs are involved in initial host pathogen interactions

Not all of these omps are involved in initial host

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not all of these OMPs are involved in initial host-pathogen interactions (Skirpstunas and Baldwin, 2003). Saeed (1983) showed that cells are highly piHated, and inferred that the pili might be associated with virulence. By means of intragastric intubation and a comparatively high dose of 1 x 10^ cells, Edw. ictaluri crossed the intestinal mucosa of channel catfish in 15 min (Baldwin and Newton, 1993). Using 1x10^ cells/ ml and an application directly into the olfactory organs of channel catfish, light and electron microscopy revealed damage after Ih (Morrison and Plumb, 1994). Certainly, it has been firmly established that channel catfish are highly susceptible to the organism, with an injected dose of 1.5 x 10^ cells capable of killing the host within 10 days at a water temperature of 26°C (Plumb and Sanchez, 1983). It does not appear that the organism produces abundant exo-enzymes, which would function as exotoxins in fish. It has been argued that both gut and nares are primary sites for the invasion o^ Edw. ictaluri in natural outbreaks of disease (Shotts et al, 1986). Fluor- escence microscopy evidence pointed to the localisation of the organism on the gill
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314 Bacterial Fish Pathogens within 5 min and within gill epithelia after 45 min and to the kidney within 4 h of a waterborne route (Nusbaum and Morrison, 2002); the outcome was a bacteraemia within 24 h (Wise et al, 1997). By 72 h, the pathogen was recoverable from the blood. Then by 216 h, there was evidence of the pathogen clearing from the blood, with all survivors developing agglutinating antibodies to Edw. ictaluri. Entry, survival (many organisms were present in vacuoles) and repHcation in head kidney macrophages of channel catfish has been observed microscopically. Opsonisation with normal serum led to even greater internahsation o^ Edw. ictaluri at 0 h, but did not affect replication once internalised (Booth et al, 2006). Uptake of the pathogen into host (epithehal) cells may well involve actin polymerisation and receptor-mediated endocytosis (Skirpstunas and Baldwin, 2002). The infection process was accompanied by shed- ding of the pathogen into the water, a process contributing to transmission of the disease (Wise et ai, 1997). It does not appear that the level of dietary iron affected antibody production and thereby influenced the course of an infection (Sealey et al, 1997). Edwardsiella tarda To date, the disease has been recorded in a diverse array of fish species, including Chinook salmon (Amandi et ai, 1982), channel catfish (Meyer and Bullock, 1973), mullet (Kusuda et ai, 1976b), carp (Sae-Oui et ai, 1984), eels (Wakabayashi and Egusa, 1973), tilapia (Kubota et al, 1981), olive flounder (Han et al, 2006) and flounder (Nakatsugawa, 1983; Mekuchi et al, 1995a; Pakingking et al, 2003). From laboratory-based experiments, pathogenicity has also been demonstrated in steelhead and rainbow trout (Amandi et ai, 1982), yellowtail (Nakatsugawa, 1983) and loach (Park et ai, 1983). Co-infection of Edw. tarda with aquabirnavirus has led to higher mortalities in Japanese flounder (Pakingking et al., 2003).
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