Aeromonas salmonicida has been recognized as a pathogen of fish for over 100 years. Emmerich and Weibel (1894) made the first authentic report of its isolation during a disease outbreak at a Bavarian brown trout hatchery, the manifestations of the disease including furuncle-like swelling and, at a later stage, ulcerative lesions on infected trout. Since that time a number of subspecies of A. salmonicida have been recognized, although the taxonomy of the species is far from settled. Aeromonas salmonicida is one of the most studied fish pathogens, because of its widespread distribution, diverse host range and economically devastating impact on cultivated fish, particularly the Salmonids.
Furunculosis, caused by the bacterium Aeromonas salmonicida subsp. salmonicida (A. salm), is one of the most serious infectious diseases of wild and farmed salmonids throughout the world, except South America (Ellis, 1997). Furunculosis was, for a long time, regarded as a disease occurring exclusively in salmonids. However, during the last decade several cases of A. salm infections have been reported in non-salmonids. In most cases these non-salmonids had some form of contact to salmonid populations with clinical outbreaks or as latent carrier of the causative agent (Bernoth, 1997). Furunculosis is an acute to chronic condition, with a variety of clinical signs (Hastings, 1988). The disease generally appears to develop as a septicaemia and is often fatal. Affected fish often show darkening of skin, lethargy and inappetence. Haemorrhages may occur at the bases of fins and the abdominal walls, heart and liver. Enlargement of the spleen and inflammation of the lower intestine are common features of chronic infections, but in acute outbreaks fish may die rapidly with few signs. The disease is named after the raised liquefactive muscle lesions (furuncles) which sometimes occur in chronically infected fish (Munro & Hastings, 1993).
The major route of transmission appears to be via infected fish and contaminated water (Hastings, 1988). Although the disease causes mortality of all ages, the most serious losses occurs during spring-autumn in the sea water farms. An important aspect of furunculosis is the carrier state, which is often established after the fish have been exposed to A. salm. Clinical outbreaks and mortality appear to be triggered by stress factors such as crowding, poor water quality, fright, high temperature and physical trauma (Ellis, 1997).
As a general rule, both clinical and covert Furunculosis caused by the pathogen: Aeromonas salmonicida is more likely to occur in smolting and spawning fish with the onset of higher water temperatures in spring or during periods of rapid temperature change. However, it is important to keep in mind that Furunculosis outbreaks can also occur in very young (alevin and fry) and at temperatures as low as 2°-4°C (Drinan, 1985).
Aeromonas salmonicida subsp. salmonicida is a Gram-negative, facultatively anaerobic, non-motile rod. The size is 1.3-2.0 by 0.8-1.3 mm (Munro & Hastings 1993).
The pathogenicity of A. salm is dependent on an external surface layer to the outer cell membrane called A-layer (Udey & Fryer, 1978). A-layer is mainly composed of a 50 kD protein called A-protein (Kay et al., 1981; Evenberg & Lugtenberg, 1982). The A-layer provides A. salm with a protective barrier against the defence mechanism of fish hosts (Wistreich & Lechtmann, 1988).
Lipopolysaccharide (LPS), another major cell envelope antigen is composed of three moieties: lipid A, a core oligosaccharide and an O-polysaccharide (O-antigen) which is exposed at the cell surface. Like the A-protein, the O-antigen appears to assist A. salm to resist the host’s normal bactericidal mechanisms (Munn et al., 1982). Evidence for further polysaccharide (PS) antigen, distinct from LPS, has also been reported (Evenberg et al., 1985). While cell surface antigens are important in enabling A. salm. to survive within fish, much of the pathology of furunculosis is attributable to extracellular products (ECP) released during bacterial growth and multiplication (Ellis et al., 1981; Klontz et al., 1966).
The ECPs of typical strains of A. salm. comprise at least 25 proteins, including a number of enzymes and toxins, as well as other factors. Many ECP components have yet to be identified and characterised, including the lethal toxin (Ellis et al., 1988).