Pathologic Cuticular Changes of Winter Impoundment Shell Disease Preceding and During Intermolt in the American Lobster, Homarus americanus

Abstract

Cuticular lesions from twenty-four market sized lobsters (Homarus americanus) with winter impoundment shell disease were examined. Histological descriptions of cuticular lesions were correlated with the substage of molt for each lobster, because cuticle components and inflammatory mechanisms vary in each. A lesion severity grading system was developed and applied to four specific substages of the five-stage (A-E) molting cycle. Lesions present in substage C4, in which the membranous layer is deposited, and D0 (passive premolt) were divided into five grades, ranging from mild erosions (Grade I) to severe ulceration (Grade V) of the cuticle. Cuticular lesions from lobsters in C4/D0 were compared with cuticular lesions from lobsters in substages C2/C3. Defensive mechanisms exhibited by animals in all substages were epicuticle deposition, melanization, inflammatory cell infiltration, and pseudomembrane formation. In addition, animals in C4 and D0 showed proliferation of the membranous layer in affected foci. The lesion grading scheme presented in this paper can be used to describe and compare both inter- and intraspecies crustacean shell lesions.

Internal organ pathology of wild American lobster (Homarus americanus) from eastern Canada affected with shell disease

“…Although shell disease results from bacterial invasion of the carapace (hess 1937;Rosen 1970;Malloy 1978;Stewart 1980;Getchell 1989;Smolowitz et al 1992Smolowitz et al ,2002Smolowitz et al ,2005Chistoserdov et al 2005), reasons for the increased ability of bacteria to penetrate the carapace are unknown. our results show that there is no evidence that the destruction of the cuticle leads to systematic infection by organisms associated with the cuticular lesion.…”

“…It is characterised by an erosion of the cuticle surface (Fisher et al 1978;Malloy 1978;Stewart 1980;Getchell 1989;Young 1991;Smolowitz et al 1992Smolowitz et al , 2002 and progressive chitinolysis and necrosis of the exoskeleton (Rosen 1970;Getchell 1989;Sindermann 1989). Histo-pathologic symptoms of shell diseases are necrotic lesions with bacteria first penetrating and breaking down the first layer of the exoskeleton (epicuticle), followed by necrosis of underlying tissue.…”

Shell disease in Crangon crangon (Linnaeus, 1758): The interaction of temperature and stress response

“…Shell disease is a common term for many different melanization of necrotic lesions, erosions, and disintegrations in crustaceans such as classical or endemic shell disease (Smolowitz et al, 1992;Sindermann, 1979) and epizootic shell disease (Shields, 2013;Smolowitz et al, 2005). The proximate causes are thereby a dysbiosis of different chitinolytic and lipolytic bacteria such as Plesiomonas, Vibrio and Aquimarina (Cipriani et al, 1980;Feinmann et al, 2017;Getchell, 1989;Meres et al, 2012;Rosen, 1967).…”

“…The proximate causes are thereby a dysbiosis of different chitinolytic and lipolytic bacteria such as Plesiomonas, Vibrio and Aquimarina (Cipriani et al, 1980;Feinmann et al, 2017;Getchell, 1989;Meres et al, 2012;Rosen, 1967). These pathogens are common in marine environments Fisher et al, 1978;Hock, 1940;Malloy, 1978;Smolowitz et al, 1992) and are also present on the cuticle of healthy crustaceans (Rosen, 1967), in this case without any impact on the host. Under stressful environmental conditions (ultimate causes e.g.…”

Shell disease of Neoepisesarma mederi crabs and its associated secondary infections

“…Although the disease is not believed to be fatal in its initial stages, death is known to result from adhesion of successive moult shells at lesion sites leading to incomplete withdrawal from exuviate at moult (Smolowitz et al, 1992). Alterations in immune reactivity within invertebrates have been shown in response to various external and artificial stimuli, including changes in temperature and salinity, pollutants (Le Moullac and Haffner, 2000), and natural or artificially induced infections (Ford et al, 1993).…”