280
which encodes the outer membrane haemin receptor, led to an initial reduction in
the ability to grow on haemin as a sole source of iron, but after 24 h there was a
recovery to that of the parental strain (Najimi et al. 2008 ).
In summary, a variety of cell-associated and extracellular factors have been
investigated in order to determine their role in virulence and pathogenicity of diseases of Aer. salmonicida aetiology. Unfortunately, the overview that emerges for
the current understanding of pathogenicity mechanisms is confused. Much of the
evidence, about the various factors suspected to be involved with virulence, is contradictory, or is based solely upon in vitro studies. Thus, although the presence of an
A-layer is fi rmly believed to be a primary determinant of virulence, reports of avirulent isolates with A-layer (Udey 1978) raises further questions. Conversely, ECP
contain such a diverse array of different factors implicated with virulence and
pathogenicity, that to pin-point the function of each in vivo has proved diffi cult.
Hence, a defi nitive assessment of the role of the various haemolysins, proteases and
leucocidins in the natural disease process still eludes us. However, it is conceded
that substantial progress has been made in the isolation, purifi cation and biochemical characterisation of the ECP. Moreover, strong evidence exists that the ECP are
capable of eliciting a pathology reminiscent of the natural disease (Cipriano et al.
1981 ; Ellis et al. 1981 ). However, the interrelationships between the various subcomponents remain unclear. Thus, Cipriano et al. ( 1981 ) believed that the leucocytolytic and proteolytic activities were dual expressions of a component, i.e. the
chromatographic fraction II; a notion which requires more information for confi rmation. This group opined that the generalised cytotoxicity for rainbow trout gonad
cell lines by ECP was a better indicator of virulence. There was, however, agreement with the suggestion of Sakai ( 1977 ) that proteases constituted the most pathogenic element of the ECP. Yet, it is apt to recall the warnings of Sheeran et al.
( 1984 ), who emphasised that it is vital to establish the levels of the proteolytic
enzymes in naturally infected fi sh tissues. Until this can by done, even conclusions
drawn from in vivo experiments remain speculative. Results from some investigations
have demonstrated that there is some degree of variation in the quantities of potential virulence factors produced by different isolates of Aer. salmonicida. Thus, there
may be some variation in the precise mode of pathogenesis (Hastings and Ellis
1985 ). Yet, Titball and Munn ( 1985b ) did not fi nd any appreciable differences in the
levels of ECP between virulent and avirulent isolates. Nevertheless, these authors
admitted that this did not exclude a role for the substances as aggressins, although it
was paradoxical that a delayed release of ECP by A-layer
+ strains was observed. As
a possible explanation, the disadvantage of late release of toxic material may be
counterbalanced by the role of A-layer in conferring resistance to host defence
mechanisms (Munn et al. 1982 ). In yet another comment, Hackett et al. ( 1984 ) proposed that in peracute or acute forms of furunculosis, virulence is independent of
the presence of protease and haemolysin. Accordingly, these workers suggested that
death of the fi sh may result from organ dysfunction, due principally to massive
growth of the pathogen. Alternatively, it was speculated that there may be involvement by an as yet unidentifi ed component of the ECP.
5 Aeromonadaceae Representative (Aeromonas salmonicida)
which encodes the outer membrane haemin receptor, led to an initial reduction in
the ability to grow on haemin as a sole source of iron, but after 24 h there was a
recovery to that of the parental strain (Najimi et al. 2008 ).
In summary, a variety of cell-associated and extracellular factors have been
investigated in order to determine their role in virulence and pathogenicity of diseases of Aer. salmonicida aetiology. Unfortunately, the overview that emerges for
the current understanding of pathogenicity mechanisms is confused. Much of the
evidence, about the various factors suspected to be involved with virulence, is contradictory, or is based solely upon in vitro studies. Thus, although the presence of an
A-layer is fi rmly believed to be a primary determinant of virulence, reports of avirulent isolates with A-layer (Udey 1978) raises further questions. Conversely, ECP
contain such a diverse array of different factors implicated with virulence and
pathogenicity, that to pin-point the function of each in vivo has proved diffi cult.
Hence, a defi nitive assessment of the role of the various haemolysins, proteases and
leucocidins in the natural disease process still eludes us. However, it is conceded
that substantial progress has been made in the isolation, purifi cation and biochemical characterisation of the ECP. Moreover, strong evidence exists that the ECP are
capable of eliciting a pathology reminiscent of the natural disease (Cipriano et al.
1981 ; Ellis et al. 1981 ). However, the interrelationships between the various subcomponents remain unclear. Thus, Cipriano et al. ( 1981 ) believed that the leucocytolytic and proteolytic activities were dual expressions of a component, i.e. the
chromatographic fraction II; a notion which requires more information for confi rmation. This group opined that the generalised cytotoxicity for rainbow trout gonad
cell lines by ECP was a better indicator of virulence. There was, however, agreement with the suggestion of Sakai ( 1977 ) that proteases constituted the most pathogenic element of the ECP. Yet, it is apt to recall the warnings of Sheeran et al.
( 1984 ), who emphasised that it is vital to establish the levels of the proteolytic
enzymes in naturally infected fi sh tissues. Until this can by done, even conclusions
drawn from in vivo experiments remain speculative. Results from some investigations
have demonstrated that there is some degree of variation in the quantities of potential virulence factors produced by different isolates of Aer. salmonicida. Thus, there
may be some variation in the precise mode of pathogenesis (Hastings and Ellis
1985 ). Yet, Titball and Munn ( 1985b ) did not fi nd any appreciable differences in the
levels of ECP between virulent and avirulent isolates. Nevertheless, these authors
admitted that this did not exclude a role for the substances as aggressins, although it
was paradoxical that a delayed release of ECP by A-layer
+ strains was observed. As
a possible explanation, the disadvantage of late release of toxic material may be
counterbalanced by the role of A-layer in conferring resistance to host defence
mechanisms (Munn et al. 1982 ). In yet another comment, Hackett et al. ( 1984 ) proposed that in peracute or acute forms of furunculosis, virulence is independent of
the presence of protease and haemolysin. Accordingly, these workers suggested that
death of the fi sh may result from organ dysfunction, due principally to massive
growth of the pathogen. Alternatively, it was speculated that there may be involvement by an as yet unidentifi ed component of the ECP.
5 Aeromonadaceae Representative (Aeromonas salmonicida)