et al 1988b Yet ironically fish may mount an antibody response during infection

Et al 1988b yet ironically fish may mount an antibody

This preview shows page 317 - 319 out of 594 pages.

et al, 1988b). Yet, ironically, fish may mount an antibody response during infection (Hamilton et al, 1986). Indeed, complement and non-a2 m-antiprotease activity have been con- sidered important host defence mechanisms against Aer. salmonicida (Marsden et al., 1996c). Munro (1984) has grouped the virulence/pathogenicity factors into cell- associated and extracellular components, a division which is convenient for the purpose of this narrative. The best-studied cell-associated factor is the additional layer, external to the cell wall, termed the A-layer. The A-layer The A-layer is now thought to be the product of a single chromosomal gene (Belland and Trust, 1985), is produced in vivo (Ellis et al., 1997) and contributes to survival in macrophages (Daly et al., 1996). The virulence array protein gene A {vapA), which encodes the A-protein has been sequenced, and differences noted in the amino acids between typical and atypical isolates, with homogeneity among the former, but heterogeneity with the latter. These differences undoubtedly lead to antigenic
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298 Bacterial Fish Pathogens differences among atypical isolates (Lund and Mikkelsen, 2004). First reported by Udey and Fryer (1978), and resulting from detailed electron-microscopic studies, the A-layer was determined to be correlated with virulence (e.g. Madetoja et al, 2003a). Thus, it was observed that virulent strains possessed the A-layer, whereas avirulent isolates did not. In addition, the presence of the A-layer was found to correspond with strong auto-agglutinating properties of the organism, and to the adhesion to fish tissue culture cells. The auto-agglutination trait has been found to be influenced by temperature, with weak and strong auto-agglutination at 25 and 15-20°C, respec- tively (Moki et al, 1995). The presence of the A-layer may confer protection against phagocytosis and thus destruction by macrophages (Olivier et al, 1986; Graham et ai, 1988). Essentially, these workers noted that avirulent cells, i.e. those without an A-layer, were phagocytosed and destroyed when virulent cells with an A-layer were more resistant. Moreover, the bacteriocidal activity of macrophages was stimulated by prior exposure to low doses of Ren. salmoninarum, but inhibited by high amounts of living or dead renibacterial cells or the p57 antigen (Siegel and Congleton, 1997). Interestingly, it was deduced that living and formalised virulent cells, in the absence of serum, attracted macrophages more readily than avirulent cells after a period of 90min (Weeks-Perkins and Ellis, 1995). The surface layer may inhibit growth at 30°C, enhance cell filamentation at 37°C, and enhance uptake of the hydrophobic antibiotics streptonigrin and chloramphenicol (Garduno et al, 1994). Following the intravenous injection of purified A-layer protein into Atlantic salmon, the protein located to the epithelial cells in renal proximal tubules of the head kidney (Stensvag et aL, 1999).
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