Please use this identifier to cite or link to this item: http://hdl.handle.net/1893/23260
Appears in Collections:Aquaculture Journal Articles
Peer Review Status: Refereed
Title: The fate of Lernaeocera branchialis (L.) (Crustacea; Copepoda) in Atlantic Cod, (Gadus morhua (L.))
Author(s): Baily, J E
Baily, Johanna
Wootten, Rodney
Sommerville, Christina
Contact Email: j.l.baily@stir.ac.uk
Keywords: cardiovascular system
chronic pathology
cod
copepod
host–parasite interaction
Lernaeocera
Issue Date: Feb-2011
Date Deposited: 1-Jun-2016
Citation: Baily JE, Baily J, Wootten R & Sommerville C (2011) The fate of Lernaeocera branchialis (L.) (Crustacea; Copepoda) in Atlantic Cod, (Gadus morhua (L.)). Journal of Fish Diseases, 34 (2), pp. 139-147. https://doi.org/10.1111/j.1365-2761.2010.01222.x
Abstract: 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.
DOI Link: 10.1111/j.1365-2761.2010.01222.x
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