Disease caused by Nemesis robusta (van Beneden, 1851) (Eudactylinidae: Siphonostomatoida: Copepoda) infections on gill filaments of thresher sharks (Alopias vulpinus (Bonnaterre, 1758)), with notes on parasite ecology and life history

Abstract

Thresher shark gill filaments infected with the copepod Nemesis robusta exhibited a diseased state. Tissue erosion seemingly associated with the rasping effects of various copepod appendages and feeding activity was evident. Host response to parasites was grossly seen as swollen and blanched zones about infected regions. Histologically the host response consisted of proliferated epithelial and underlying connective tissue layers surrounding the efferent branchial arterioles at the gill filaments' free distal tips. Copepod attachment close to secondary lamellae was associated with proliferation of both respiratory epithelium and epithelium between the secondary lamellae. Tissue proliferation partially or completely occluded interlamellar water channels and probably compromised respiratory efficiency by blocking water passage between secondary lamellae. The abnormal thickness of affected secondary lamellae probably further reduced respiratory ion exchange.