265
the relevance of dissociation of Aer. salmonicida colonies and the relationship to
virulence was not made apparent until the work of Udey ( 1977 ), almost 40 years
later. Early studies provided tentative evidence for a variety of possible pathogenic
mechanisms, but there is no doubt that progress in the understanding of Aer. salmonicida pathogenesis and virulence has been accelerated by rapid advances in the
knowledge of cell biology and the development of sophisticated biochemical techniques. It is the application of such techniques that continues to yield considerable
new information about the manner in which Aer. salmonicida may effect its disease
processes in fi sh.
Pathogenicity – The Value of Intraperitoneal Chambers
An intriguing and signifi cant development concerned the description of intraperitoneal chambers, which could be implanted into fi sh (Garduño et al. 1993a ). These
chambers could be fi lled with pathogens – or for that matter a range of other objects
-, implanted into fi sh, and measurements made with time. Garduño and colleagues
placed Aer. salmonicida into a chamber, and studied its fate in the peritoneal cavity
of rainbow trout. In one set of investigations, these workers observed that when the
pathogen was contained in the chamber killing occurred rapidly as a result of hostderived lytic activity (in the peritoneal fl uid). In contrast, free cells had a better
chance of survival (Garduño et al. 1993a ). Moreover, within the peritoneal chamber,
Aer. salmonicida produced novel antigens, as determined by western blots (Thornton
et al. 1993 ). In another publication using the peritoneal chamber, evidence was presented that the capsular layer around Aer. salmonicida permitted the pathogen to
resist host-mediated bacteriolysis, phagocytosis and oxidative killing (Garduño
et al. 1993b ).
Pathogenicity – Cell-Associated Versus Extracellular Components
A variety of pathogenicity mechanisms and virulence factors have been proposed
for diseases caused by Aer. salmonicida, namely possession of an extracellular (A)
layer (= the surface or “S” layer), a type III secretion system (e.g. Dacanay et al.
2006 ) and the production of ECP, with the latter involved with the effects on macrophages (Ewart et al. 2008 ), although there is confusion and even contradiction
about the relative merits of the various components in pathogenicity (see Ellis et al.
1988b ). Yet, ironically fi sh may mount an antibody response during infection
(Hamilton et al. 1986 ). Indeed, complement and non-a 2 m-antiprotease activity have
been considered important host defence mechanisms against Aer. salmonicida
(Marsden et al. 1996c ).
Munro ( 1984 ) has grouped the virulence/pathogenicity factors into cellassociated 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:
Aeromonas salmonicida
the relevance of dissociation of Aer. salmonicida colonies and the relationship to
virulence was not made apparent until the work of Udey ( 1977 ), almost 40 years
later. Early studies provided tentative evidence for a variety of possible pathogenic
mechanisms, but there is no doubt that progress in the understanding of Aer. salmonicida pathogenesis and virulence has been accelerated by rapid advances in the
knowledge of cell biology and the development of sophisticated biochemical techniques. It is the application of such techniques that continues to yield considerable
new information about the manner in which Aer. salmonicida may effect its disease
processes in fi sh.
Pathogenicity – The Value of Intraperitoneal Chambers
An intriguing and signifi cant development concerned the description of intraperitoneal chambers, which could be implanted into fi sh (Garduño et al. 1993a ). These
chambers could be fi lled with pathogens – or for that matter a range of other objects
-, implanted into fi sh, and measurements made with time. Garduño and colleagues
placed Aer. salmonicida into a chamber, and studied its fate in the peritoneal cavity
of rainbow trout. In one set of investigations, these workers observed that when the
pathogen was contained in the chamber killing occurred rapidly as a result of hostderived lytic activity (in the peritoneal fl uid). In contrast, free cells had a better
chance of survival (Garduño et al. 1993a ). Moreover, within the peritoneal chamber,
Aer. salmonicida produced novel antigens, as determined by western blots (Thornton
et al. 1993 ). In another publication using the peritoneal chamber, evidence was presented that the capsular layer around Aer. salmonicida permitted the pathogen to
resist host-mediated bacteriolysis, phagocytosis and oxidative killing (Garduño
et al. 1993b ).
Pathogenicity – Cell-Associated Versus Extracellular Components
A variety of pathogenicity mechanisms and virulence factors have been proposed
for diseases caused by Aer. salmonicida, namely possession of an extracellular (A)
layer (= the surface or “S” layer), a type III secretion system (e.g. Dacanay et al.
2006 ) and the production of ECP, with the latter involved with the effects on macrophages (Ewart et al. 2008 ), although there is confusion and even contradiction
about the relative merits of the various components in pathogenicity (see Ellis et al.
1988b ). Yet, ironically fi sh may mount an antibody response during infection
(Hamilton et al. 1986 ). Indeed, complement and non-a 2 m-antiprotease activity have
been considered important host defence mechanisms against Aer. salmonicida
(Marsden et al. 1996c ).
Munro ( 1984 ) has grouped the virulence/pathogenicity factors into cellassociated 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:
Aeromonas salmonicida