salmonicida Thus they reported that nearly all of the lesions normally

Salmonicida thus they reported that nearly all of the

This preview shows page 329 - 331 out of 594 pages.

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 artificially 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 confirmed such effects of fish serum on ECP. Rockey et al. (1989) pubHshed an article detailing the inhibition of haemolysin activity by salmonid serum. Sakai (1984) mentioned a decrease in, or absence of, mortahty among rainbow trout that had received ECP first treated with large volumes of rainbow trout serum prior to injection. These results indicated involvement of com- plement in the detoxification of ECP. Continuing this theme, Grisley et al. (1984) reported the presence of an a-migrating protein (a possible homologue of mammahan a2-macroglobulin) in normal rainbow trout serum. This protein apparently exerts a role in a non-specific defence function against microbial, proteolytic toxins. Ellis and
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310 Bacterial Fish Pathogens Grisley (1985) pursued the theme, concluding that normal trout serum inhibits ECP protease, but neutralisation is effected by different anti-proteases and less efficiently than trypsin. They contended that the data, to some extent, explained the potency of ECP in causing disease. Elhs 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 colonisation of different host tissues by the pathogen. It was concluded that the pathological effects resulting from infection by 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 colonisation. Generalised circulatory failure could ensue if the ECP subse- quently entered the circulatory system. Just when the role of ECP and proteases was becoming clarified, some elegant work with deletion mutants caused a fundamental re-think. It was obvious that to be sure of a specific component, eliminate the genes from the bacteria and determine the effect on the host. Using this approach, Vipond et al. (1998) confirmed that mutants lacking GCAT or serine protease (AspA) were not less virulent than the parental cell following i.p. or cohabitation challenge of Atlantic salmon.
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