The fate of Lernaeocera branchialis (L.) (Crustacea; Copepoda) in Atlantic cod, Gadus morhua L.

Lernaeocera branchialis, a copepod crustacean parasite of gadoids, represents a potential threat to both wild and farmed cod, Gadus morhua. The pathological changes associated with the early stages of experimental infection have previously been reported in detail, and this article describes the lesions associated with later chronic stages of experimental infection. Chronic infection is characterised by extravascular granuloma formation and proliferation of fibrovascular tissue around intact and fragmented, degenerate parasites within both the gill arch and cardiac region. The majority of parasite granulomas are located within connective tissues of the gill arch or pericardium; however, low numbers are present within the wall of large vessels. The intraluminal parasites and thrombi of early stage infection are largely absent in these later lesions. We propose that organisation and incorporation of the parasite thrombus into the vessel wall with subsequent granuloma formation and extrusion into the surrounding connective tissue leads to the elimination of the parasite from the vascular system. Thus, rather than being a negative consequence of infection thrombosis is protective, allowing the host to survive the substantial initial vascular insult.

The pathology of chronic erosive dermatopathy in Murray cod, Maccullochella peelii peelii (Mitchell).

Chronic erosive dermatopathy (CED) is a disease of intensively farmed Murray cod in Australia that has been reported in association with the use of groundwater (mechanically extracted from shallow boreholes) supplies. CED results in focal ulceration of the skin overlying sensory canals of the head and flanks. Trials were conducted at an affected fish farm to study the development of the condition, both in Murray cod and in goldfish, and also to assess the reported recovery of lesions when affected fish were transferred to river water. Grossly, lesions began after 2-3 weeks with degeneration of tissue at the periphery of pores communicating with the sensory canals. Widening of these pores along the axis of the canals resulted from a loss of tissue covering the canal. Histopathologically, hyperplasia of the canal epithelial lining was seen after 3 weeks in borehole water and subsequent necrosis and sloughing of this tissue resulted in the loss of the canal roof. Canal regeneration occurred when fish were transferred from borehole water into river water. The lack of lesions in other organs and the pattern of lesion development support exposure to waterborne factors as the most likely aetiology.