Diseases

Stewart, James E.

doi:10.1016/b978-0-12-177401-1.50013-2

Cited by 31 publications

(21 citation statements)

References 70 publications

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“…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.…”

Section: Discussionmentioning

confidence: 99%

“…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.…”

Section: Introductionmentioning

confidence: 99%

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

Comeau

Benhalima

2009

New Zealand Journal of Marine and Freshwater Research

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For the first time in decades, multiple lesions on the exoskeleton of wild caught American lobsters (Homarus americanus) were observed in eastern Canada in 2005 and 2006. These lesions were similar to those observed since the mid 1990s in the eastern United States. Of the 12 lobsters examined, 8 were males. Scanning electron microscopy showed a dense population of rod-shaped bacteria associated with the breakdown of the first layer of cuticle. However, the ability of bacteria to fully penetrate the carapace is unknown. The shell disease did not seem to be immediately fatal and was often associated with alterations in the histoarchitecture of several internal organs (i.e., testis, vas deferens, hepatopancreas, and gills). For instance, follicle cells responsible for spermatogenesis were damaged, resulting in deformed and non-viable spermatozoa in the testis and vas deferens. In contrast, the female reproductive organ did not show any abnormalities. R-cells responsible for the storage of lipids and glycogen in the hepatopancreas were severely damaged or destroyed, indicating stress and starvation. Beside necrosis and calcification of gill filaments, debris between the gill filaments was also observed that would limit ion exchange and cause metabolic exhaustion. It does not seem that shell disease was the causative agent or a vector for the pathological conditions of internal organs, but one of the symptoms of a common agent affecting the internal organs. Although shell disease was observed in several areas in eastern Canada, its prevalence M07111;

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Comeau

Benhalima

2009

New Zealand Journal of Marine and Freshwater Research

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“…Culturing of bacteria from lesions of lobsters with impoundment shell disease has predominantly identified Vibrio, Aeromonas, Beneckea and Pseudo monas spp. (Malloy 1978, Stewart 1980, Getchell 1989, Smolowitz et al 1992). Many of the aforementioned bacteria are known to be chitinoclastic (Chis to serdov et al 2005).…”

Section: Introductionmentioning

confidence: 99%

Lesion bacterial communities in American lobsters with diet-induced shell disease

Quinn¹,

Metzler²,

Tlusty³

et al. 2012

Dis. Aquat. Org.

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In southern New England, USA, shell disease affects the profitability of the American lobster Homarus americanus fishery. In laboratory trials using juvenile lobsters, exclusive feeding of herring Clupea harengus induces shell disease typified initially by small melanized spots that progress into distinct lesions. Amongst a cohabitated, but segregated, cohort of 11 juvenile lobsters fed exclusively herring, bacterial communities colonizing spots and lesions were investigated by denaturing gradient gel electrophoresis of 16S rDNA amplified using 1 group-specific and 2 universal primer sets. The Bacteroidetes and Proteobacteria predominated in both spots and lesions and included members of the orders Flavobacteriales (Bacteriodetes), Rhodo bacterales, Rhodospirillales and Rhizobiales (Alphaproteobacteria), Xanthomonadales (Gamma proteobacteria) and unclassified Gammaproteobacteria. Bacterial communities in spot lesions displayed more diversity than communities with larger (older) lesions, indicating that the lesion communities stabilize over time. At least 8 bacterial types persisted as lesions developed from spots. Aquimarina 'homaria', a species commonly cultured from lesions present on wild lobsters with epizootic shell disease, was found ubiquitously in spots and lesions, as was the 'Candidatus Kopriimonas aquarianus', implicating putative roles of these species in diet-induced shell disease of captive lobsters.

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“…homari is the causative agent of gaffkemia, a systemic disease of homarid lobsters (Homarus americanus and H. gammarus) found in the coastal waters of both North America and Europe (Wood 1965a, Stewart et al 1966, Audouin & Léglise 1971. However, it is within the commercial lobster industry where the major economic impact of gaffkemia occurs, because the disease contributes significantly to post-harvest losses (Stewart 1980). Gaffkemia was first described in dying American lobsters from a holding unit in Maine in 1947, and subsequently the bacterium A. viridans var.…”

Section: Introductionmentioning

confidence: 99%

“…homari enters the lobster through breaks in the integument caused by fighting, overcrowding and poor handling practices after capture and during transport (Stewart 1980). Typically, after the lobster's exoskeleton is breached, a fatal septicemia ensues as virulent strains of A. viridans var.…”

Section: Introductionmentioning

confidence: 99%

Genetic characterization of the lobster pathogen Aerococcus viridans var. homari by 16S rRNA gene sequence and RAPD

Greenwood

Keith²,

Despres³

et al. 2005

Dis. Aquat. Org.

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A combination of 16S rRNA sequencing and random amplified polymorphic DNA (RAPD) analysis was used to evaluate the genetic diversity within Aerococcus viridans var. homari, the causative agent of gaffkemia in lobsters. A collection of 7 A. viridans var. homari strains and 2 avirulent A. viridans-like cocci isolated from homarid lobsters harvested from different regions on the Atlantic Coast of North America were analyzed. The isolates are separated geographically and temporally between the years 1947 and 2000. Sequencing of 16S rRNA genes confirmed the inclusion of all 9 isolates in the monophyletic A. viridans clade (99.8 to 100% similarity). RAPD analysis revealed that the 9 A. viridans var. homari isolates could be separated into 2 distinct subtypes. Subtype 1 included the 7 pathogenic lobster isolates and constituted a homogeneous group regardless of their geographical, temporal or virulence differences. Subtype 2 contained the 2 avirulent A. viridans-like cocci that had distinct RAPD patterns and clustered separately with the non-marine A. viridans. RAPD analysis represented a useful method for determining molecular subtyping for the intraspecific classification and epidemiological investigations of A. viridans var. homari.

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Diseases

Cited by 31 publications

References 70 publications

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

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

Lesion bacterial communities in American lobsters with diet-induced shell disease

Genetic characterization of the lobster pathogen Aerococcus viridans var. homari by 16S rRNA gene sequence and RAPD

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