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Amoebic gill diseases (AGD) caused primarily by the amphizoic Neoparamoeba spp. have been identified as significant to fish health in intensive aquaculture. These diseases have consequently received significant attention with regard to disease pathophysiology. Neoparamoeba perurans has been putatively identified as the aetiological agent in salmonids, with other species such as turbot Psetta maxima and sea bass Dicentrarchus labrax also affected. Similarly, Neoparamoeba spp. have also been identified in co-infections with other gill diseases in salmonids. While infection of the gills results in an acute multifocal hyperplastic host response, reduced gill surface area and increased mucous cell densities, ion regulation and respiration in terms of blood gasses are only marginally affected. This may be partially attributed to reserve respiratory capacity and a reduction in mucous viscosity allowing for a greater flushing of the gill, so reducing the gill mucus boundary layer. Clinical and acute infections result in significant cardiovascular compromise with increases in aortic blood pressure, and systemic vascular resistance in Atlantic salmon, Salmo salar, which are not seen in rainbow Oncorhynchus mykiss and brown trout Salmo trutta. Increases in vascular resistance appear to be due to vascular constriction potentially reducing blood flow to the heart in compromised fishes, the overall effect being to lead to a compensatory tissue remodelling and change in cardiac shape in chronically infected fishes. The combined effect of reduced gill surface area and cardiovascular compromise leads to a significant reduction in swimming performance and increases in the routine metabolic rate that lead to an increase in the overall metabolic cost of disease.