The first authentic report of furunculosis was described as early as 1894 in a brown trout hatchery in Bavaria, Germany and was characterised by furuncle-like swellings and ulcerative lesions on infected trout. The causative agent is Aeromonas salmonicida a non-motile, gram-negative aerobic bacillus, typically 1µm x 2µm. Morphologically the bacterium varies from almost coccoid in freshly isolated cultures to distinct rods in cultures maintained on media. Furunculosis was generally considered a disease of salmonids, but many other species have been shown to be susceptible including eel, bass, perch, carp, cod, turbot and wrasse. However, the description below concentrates on furunculosis of salmonids.
The peracute form is normally restricted to young fish and clinical signs are limited to slight exophthalmia, darkening of the skin and tachybranchia.
Acute infections are characterised by the darkening of the skin, lethargy, tachybranchia and small haemorrhages at the base of fins.
Subacute infections will be characterised by a slight darkening of the skin, lethargy, congested blood vessels at the base of fins, slight exophthalmia and may have furuncles on the flank or dorsal surfaces. In addition, hyperaemia of serosal surfaces, punctate haemorrhage on the abdominal walls, viscera and heart are recorded. There is the presence of a soft liquefied kidney, enlarged spleen and pale liver with subcapsular haemorrhage. There may also be the presence of haemorrhagic pathces along the body side or raised furuncles in the dermis.
Chronically infected fish show visceral congestion, multiple haemorrhage in the muscle and liver, splenomegaly, necrosis of the kidney, adhesions of the viscera and intestinal inflammation. There will also be necrosis and the classical haemorrhagic furuncle involving muscle tissue.
In sub acute/chronic infections the heart and spleen are often the most infected organs; microcolonies occur in vascular endothelia with massive destruction of spleen ellipsoids, resulting in vascular collapse; damage to spleen ellipsoids that may be accompanied by reticular cell proliferation and lymphocyte accumulation. There is degeneration of cardiac ventral epicardium and toxic cardiac necrosis, especially of the atrial lining with damage to spleen and heart.