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Journal Article

Idiopathic muscle necrosis in the Norway lobster, Nephrops norvegicus (L.): aetiology, pathology and progression to bacteraemia

I D Ridgway; G D Stentiford; A C Taylor; R J A Atkinson; T H Birkbeck; D M Neil
Journal of Fish Diseases · Vol. 30, Issue 5 · pp. 279-292 · 2007

Abstract

The pathology and progression of idiopathic muscle necrosis (IMN) in Nephrops norvegicus and possible aetiologies have been investigated. Trawl capture, aerial exposure and handling initiate IMN, and the condition can be induced through periods of aerial exposure alone, in the absence of trawling. Within 24–48 h after trawl capture IMN progresses to a multi‐species bacterial septicaemia, with moribund animals exhibiting clinical signs. The aetiology of this condition has been examined using molecular (16S rRNA gene sequencing) and biochemical (standard taxonomic assays, Biolog TM ) criteria to characterize bacterial isolates from moribund and healthy animals. Histopathology of the IMN phase reveals a loss of sarcomeric structure with necrotic lesions containing pyknotic nuclei, fragments of myofibrils and connective tissue elements. In the bacterial phase there is extensive loss of abdominal muscle structure, and the presence of rod‐shaped Gram‐negative bacteria in the degrading tissues. The results demonstrate that the IMN condition is connected to stressful conditions imposed on N. norvegicus , but involves no pathogenic agents. This is followed by an opportunistic bacterial infection that causes further tissue spoilage. It is believed that the primary cause of both IMN and bacteraemia is imposed stress, but they are expressed in different time courses.

Bibliographic Information

JournalJournal of Fish Diseases
PublisherWiley
Publication Date2007-05-01
Publication Year2007
Volume30
Issue5
Pages279-292
Document TypeJournal Article
Print ISSN0140-7775
eISSN1365-2761
DOI10.1111/j.1365-2761.2007.00812.x
SubjectGeneral Aquaculture, Fisheries & Fish Science

Access Information

NARA Access Coverage1997-01-01~Current
Journal Homepagehttps://onlinelibrary.wiley.com/loi/13652761
Publisher PageOpen Publisher Page
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