279
Aer. salmonicida were probably caused by the ECP released by the pathogen. Thus,
the leucocytolytic component might act against leucocytes, eventually resulting in
leucopenia, and preventing the destruction of the bacterial colonies, thus allowing
microbes to be transmitted to other organs via the circulatory system where they
may initiate the development of more colonies. It was further submitted by these
authors that lesions and mortalities are due to the collagenolytic activity of the ECP
(this is one of the notable features of furunculosis), with haemorrhaging resulting in
the vicinity of bacterial colonization. Generalised circulatory failure could ensue if
the ECP subsequently entered the circulatory system.
Just when the role of ECP and proteases was becoming clarifi ed, some elegant
work with deletion mutants caused a fundamental re-think. It was obvious that to be
sure of the role of a specifi c component, eliminate the genes from the bacteria and
determine the effect on the host. Using this approach, Vipond et al. ( 1998 ) confi rmed that mutants lacking GCAT or serine protease (AspA) were not less virulent
than the parental cell following i.p. of cohabitation challenge of Atlantic salmon.
Finally, it is appropriate to recall the words of Munn et al. ( 1982 ), who commented that the interrelationships of ECP suggest that the pathogen exerts its toxic
effects in vivo by means of multiple factors that interact synergistically.
Scavenging for Iron
A current theme, which has prompted some excellent work, concerns the ability of
Aer. salmonicida cells to successfully scavenge for iron in iron-limited conditions.
These would be created in the host, and function as a defence mechanism against
invasion by pathogens. Indeed, there is evidence that IROMP are produced in vivo
(Ellis et al. 1997 ). Thus, free iron would be bound to proteins, such as transferrin,
resulting in iron-restricted conditions in the host. Initially, Chart and Trust ( 1983 )
demonstrated that typical strains of Aer. salmonicida were capable of sequestering
iron. Then, Kay et al. ( 1985 ) determined that the A-layer was implicated as a component of an iron-uptake mechanism. The conclusion was that the A-layer functioned as the initial stage of iron-uptake, being a binding site for porphyrins, i.e.
haemin and protoporphyrin. The difference between typical and atypical isolates
was reinforced by the conclusion that there was a fundamental difference in the
mechanism of utilisation of non-haem bound sources of iron. Hirst et al. ( 1991 ) and
Hirst and Ellis ( 1996 ) described an inducible siderophore (these are soluble low
molecular weight iron-chelators)-dependent iron-chelating system in typical strains
and an unidentifi ed siderophore-independent system in atypical Aer. salmonicida.
Among Aer. salmonicida subsp. salmonicida (17 isolates from Scotland and Spain
were examined), the siderophore is regarded as homogeneous (Fernandez et al.
1998 ).
Six genes have been studied that showed similarity with haem uptake genes of
other Gram-negative bacteria, and other genes of unknown function. Mutation of
hutB, which encodes a periplasmic haemin-binding protein led to a marked effect on
the ability of the pathogen to use haemin as a source of iron. Mutation of hutB ,
Aeromonas salmonicida
Aer. salmonicida were probably caused by the ECP released by the pathogen. Thus,
the leucocytolytic component might act against leucocytes, eventually resulting in
leucopenia, and preventing the destruction of the bacterial colonies, thus allowing
microbes to be transmitted to other organs via the circulatory system where they
may initiate the development of more colonies. It was further submitted by these
authors that lesions and mortalities are due to the collagenolytic activity of the ECP
(this is one of the notable features of furunculosis), with haemorrhaging resulting in
the vicinity of bacterial colonization. Generalised circulatory failure could ensue if
the ECP subsequently entered the circulatory system.
Just when the role of ECP and proteases was becoming clarifi ed, some elegant
work with deletion mutants caused a fundamental re-think. It was obvious that to be
sure of the role of a specifi c component, eliminate the genes from the bacteria and
determine the effect on the host. Using this approach, Vipond et al. ( 1998 ) confi rmed that mutants lacking GCAT or serine protease (AspA) were not less virulent
than the parental cell following i.p. of cohabitation challenge of Atlantic salmon.
Finally, it is appropriate to recall the words of Munn et al. ( 1982 ), who commented that the interrelationships of ECP suggest that the pathogen exerts its toxic
effects in vivo by means of multiple factors that interact synergistically.
Scavenging for Iron
A current theme, which has prompted some excellent work, concerns the ability of
Aer. salmonicida cells to successfully scavenge for iron in iron-limited conditions.
These would be created in the host, and function as a defence mechanism against
invasion by pathogens. Indeed, there is evidence that IROMP are produced in vivo
(Ellis et al. 1997 ). Thus, free iron would be bound to proteins, such as transferrin,
resulting in iron-restricted conditions in the host. Initially, Chart and Trust ( 1983 )
demonstrated that typical strains of Aer. salmonicida were capable of sequestering
iron. Then, Kay et al. ( 1985 ) determined that the A-layer was implicated as a component of an iron-uptake mechanism. The conclusion was that the A-layer functioned as the initial stage of iron-uptake, being a binding site for porphyrins, i.e.
haemin and protoporphyrin. The difference between typical and atypical isolates
was reinforced by the conclusion that there was a fundamental difference in the
mechanism of utilisation of non-haem bound sources of iron. Hirst et al. ( 1991 ) and
Hirst and Ellis ( 1996 ) described an inducible siderophore (these are soluble low
molecular weight iron-chelators)-dependent iron-chelating system in typical strains
and an unidentifi ed siderophore-independent system in atypical Aer. salmonicida.
Among Aer. salmonicida subsp. salmonicida (17 isolates from Scotland and Spain
were examined), the siderophore is regarded as homogeneous (Fernandez et al.
1998 ).
Six genes have been studied that showed similarity with haem uptake genes of
other Gram-negative bacteria, and other genes of unknown function. Mutation of
hutB, which encodes a periplasmic haemin-binding protein led to a marked effect on
the ability of the pathogen to use haemin as a source of iron. Mutation of hutB ,
Aeromonas salmonicida