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The surface array matrix, i.e. theS-layer,has been considered to influence the interaction between the bacterial cell and its environment (Esteveet al,2004). A major function is beheved to be the provision of physical protection from lytic components, including serum proteins and bacteriophages (Dooleyet ai,1988). Work also links the presence of an S-layer with invasive disease in humans and mice (but not fish!) (Murrayet ai,1988). As a result of studying one isolate, i.e. TF7 (isolated from a lesion on trout in Quebec), it was determined that the S-layer did not confer any increase in surface hydrophobicity or any enhanced association with macrophages, and did not specifically bind porphyrin or immunoglobulin (Murray et ai,1988). Nevertheless, inAer. salmonicidathe S-layer has indeed been shown to be a prerequisite for virulence, by increasing hydrophobicity and enhancing macro-phage association (Murrayet al,1988). The detailed structure of the S-layer has been revealed in an excellent series of publications (Dooleyet al,1986, 1988; Dooley and Trust, 1988). After studying eight isolates of a serogroup with a high virulence to fish, Dooley and Trust (1988) concluded that the S-layer was tetragonally arrayed. SDS-PAGE revealed a protein of 52kDa molecular weight, which was the major surface (protein) antigen. This protein effectively masked the underlying OMP. Ascencioet al.(1991) investigated extracellular matrix protein binding toAer hydrophila.In particular, binding of ^^^I-labelled collagen, fibronectin and laminin is common to isolates from diseased fish. Moreover, the binding property was specific, with cultural conditions influencing expression of the bacterial cell surface-binding structures. Experiments showed that calcium (in the growth medium) enhanced expression of the bacterial extracellular matrix protein surface receptors. The con-clusion was reached that success in infecting/colonising a host depended on the abihty of the pathogen to bind to specific cell surface receptors of the mucus layer, epithelial cells and subepitheHal basement membranes. 'Adhesins'' It appears that the pathogen has the ability to attach to selected host cells, e.g. erythrocytes, and tissue proteins, i.e. collagen, fibronectin, serum proteins and glyco-proteins, via the action of "adhesins" (Trustet al.,1980a, b,c; Toranzoet al.,1989; Ascencioet al.,1991; Leeet al.,1997; Fanget al.,2004) and become internahsed (Tan et al.1998). The adhesins, of which a 43kDa (AHAl) adhesin has been cloned and shown to have high homology to two OMPs (Fanget al,2004), appear to be extremely selective, recognising D-mannose and L-fucose side chains on polymers located on the surface of the eukaryotic cells. The specificity was further highlighted by the observation that human isolates ofAer. hydrophilafailed to bind (or bound poorly) to fish tissue culture cells (Krovaceket al.,1987). Indeed, using tissue culture cells from rainbow trout liver and chinook salmon embryo, Krovaceket al.(1987) demonstrated that some(~33%)isolateso^ Aer. hydrophilafrom fish adhered to the tissue culture cells and glass surfaces coated with rainbow trout mucus. Adhesion and
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