278
correlation between virulence and the leucocytolytic properties. Therefore according to Cipriano et al. ( 1981 ), leucocytolytic factors could not be considered as a
principal virulence mechanism. Alternatively, the activity may not solely relate to
the attack on leucocytes. Instead, Cipriano and colleagues suggested that the leucocytolytic factor, contained within fraction II of the ECP, contributed to virulence not
only by way of its leucocytolytic properties, but also through its role as a generalised cytotoxin capable of generating pathological changes. Indeed, these investigators recorded that intramuscular injection of fraction II (produced by a virulent
isolate) into brook trout caused haemorrhaging at the mouth, base of the fi ns and site
of inoculation. Death occurred within 24 h. Such deleterious changes did not ensue
in fi sh that received fraction II derived from an avirulent isolate.
It must be emphasised that the lack of a leucocytic response, apparent in the
majority of salmonids with furunculosis, has not been substantiated in infections of
coarse fi sh. In one example, a chronic leucocytosis was observed in goldfi sh
(Mawdesley-Thomas 1969 ).
Ellis et al. ( 1981 ) outlined a hypothesis for the role of ECP in pathology.
Moreover, they highlighted some of the diffi culties involved in reaching a complete
understanding of the pathogenic process. Importantly, they emphasised that in many
respects furunculosis is an inconsistent disease, insofar as a variety of lesions have
been associated with invasion of the aetiological agent. Yet, virtually none of the
symptoms may be considered as unique to the disease (Wolke 1975 ). Consequently,
it is hardly surprising that inconsistencies have resulted in confl icting opinions over
the pathogenicity mechanisms. Ellis and co-workers formulated a tentative explanation for the lesions caused by Aer. salmonicida. Thus, they reported that nearly all
of the lesions normally associated with the disease may be achieved by i.p. or i.m.
injection of ECP. However, it would appear that artifi cially high doses are required
to accomplish such lesions. Munro et al. ( 1980 ) suggested that the presence of an
a-globulin in normal trout serum may have the ability to neutralise ECP activities.
Indeed, other workers have confi rmed such effects of fi sh serum on ECP. Rockey
et al. ( 1989 ) published an article detailing the inhibition of haemolysin activity by
salmonid serum. Sakai ( 1984 ) mentioned a decrease in, or absence of, mortality
among rainbow trout that had received ECP fi rst treated with large volumes of rainbow trout serum prior to injection. These results indicated involvement of complement in the detoxifi cation of ECP. Continuing this theme, Grisley et al. ( 1984 )
reported the presence of an a-migrating protein (a possible homologue of mammalian a 2 -macroglobulin) in normal rainbow trout serum. This protein apparently
exerts a role in a non-specifi c defence function against microbial proteolytic toxins.
Ellis and Grisley ( 1985 ) pursued the theme, concluding that normal trout serum
inhibits ECP protease but neutralisation is effected by different antiproteases and
less effi ciently than trypsin. They contended that the data, to some extent, explained
the potency of ECP in causing disease. Ellis et al. ( 1981 ) assumed that in natural
infections lesions would be produced after the ECP had exhausted any inhibiting
factors, either locally or systemically. They thought that the various symptoms of
furunculosis were explained by the colonization of different host tissues by the
pathogen. It was concluded that the pathological effects resulting from infection by
5 Aeromonadaceae Representative (Aeromonas salmonicida)
correlation between virulence and the leucocytolytic properties. Therefore according to Cipriano et al. ( 1981 ), leucocytolytic factors could not be considered as a
principal virulence mechanism. Alternatively, the activity may not solely relate to
the attack on leucocytes. Instead, Cipriano and colleagues suggested that the leucocytolytic factor, contained within fraction II of the ECP, contributed to virulence not
only by way of its leucocytolytic properties, but also through its role as a generalised cytotoxin capable of generating pathological changes. Indeed, these investigators recorded that intramuscular injection of fraction II (produced by a virulent
isolate) into brook trout caused haemorrhaging at the mouth, base of the fi ns and site
of inoculation. Death occurred within 24 h. Such deleterious changes did not ensue
in fi sh that received fraction II derived from an avirulent isolate.
It must be emphasised that the lack of a leucocytic response, apparent in the
majority of salmonids with furunculosis, has not been substantiated in infections of
coarse fi sh. In one example, a chronic leucocytosis was observed in goldfi sh
(Mawdesley-Thomas 1969 ).
Ellis et al. ( 1981 ) outlined a hypothesis for the role of ECP in pathology.
Moreover, they highlighted some of the diffi culties involved in reaching a complete
understanding of the pathogenic process. Importantly, they emphasised that in many
respects furunculosis is an inconsistent disease, insofar as a variety of lesions have
been associated with invasion of the aetiological agent. Yet, virtually none of the
symptoms may be considered as unique to the disease (Wolke 1975 ). Consequently,
it is hardly surprising that inconsistencies have resulted in confl icting opinions over
the pathogenicity mechanisms. Ellis and co-workers formulated a tentative explanation for the lesions caused by Aer. salmonicida. Thus, they reported that nearly all
of the lesions normally associated with the disease may be achieved by i.p. or i.m.
injection of ECP. However, it would appear that artifi cially high doses are required
to accomplish such lesions. Munro et al. ( 1980 ) suggested that the presence of an
a-globulin in normal trout serum may have the ability to neutralise ECP activities.
Indeed, other workers have confi rmed such effects of fi sh serum on ECP. Rockey
et al. ( 1989 ) published an article detailing the inhibition of haemolysin activity by
salmonid serum. Sakai ( 1984 ) mentioned a decrease in, or absence of, mortality
among rainbow trout that had received ECP fi rst treated with large volumes of rainbow trout serum prior to injection. These results indicated involvement of complement in the detoxifi cation of ECP. Continuing this theme, Grisley et al. ( 1984 )
reported the presence of an a-migrating protein (a possible homologue of mammalian a 2 -macroglobulin) in normal rainbow trout serum. This protein apparently
exerts a role in a non-specifi c defence function against microbial proteolytic toxins.
Ellis and Grisley ( 1985 ) pursued the theme, concluding that normal trout serum
inhibits ECP protease but neutralisation is effected by different antiproteases and
less effi ciently than trypsin. They contended that the data, to some extent, explained
the potency of ECP in causing disease. Ellis et al. ( 1981 ) assumed that in natural
infections lesions would be produced after the ECP had exhausted any inhibiting
factors, either locally or systemically. They thought that the various symptoms of
furunculosis were explained by the colonization of different host tissues by the
pathogen. It was concluded that the pathological effects resulting from infection by
5 Aeromonadaceae Representative (Aeromonas salmonicida)