INTRODUCTION

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).

ETIOLOGY

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).