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1 Boston University Marine Program, Woods Hole, MA
2 Marine Biological Laboratory, Woods Hole, MA
* Corresponding author: rsmol{at}mbl.edu
The American lobster, Homarus americanus, represents an important fishery for much of the New England coast as well as several coastal provinces in Canada. Yet during the past decade, New England has reported dramatic decreases in the catch value in this lucrative industry (1). Shell disease is the deterioration of the crustacean exoskeleton by chitinoclastic organisms occurring in both marine and freshwater environments (2). In the past 6 years, the prevalence and severity of shell disease has markedly increased (K. Castro, Rhode Island Sea Grant, pers. comm). Predominately occurring in areas from Buzzard’s Bay (Massachusetts) to eastern Long Island Sound (New York), it has been termed epizootic lobster shell disease (ELSD). Recently ELSD lobsters have been observed in Cape Cod Bay (Massachusetts), Kittery (Maine), and in offshore waters of New England (1).
For the present study, carapace lesions from wild-caught specimens of H. americanus were examined for the etiological agent responsible for ELSD. Although previous studies on lobster shell disease have used histology and molecular techniques to define the organisms involved in lesions (3, 4) no study has used scanning electron microscopy (SEM) to observe the progression of lesion development. For this study, SEM was used to produce three-dimensional views of ELSD development from geographically distinct areas along the New England coast for site comparisons.
During 2002–2003, lobsters with lesions (n = 22) and without lesions (n = 14) were collected. The sites sampled were the inshore waters of eastern Long Island Sound (n = 4), Rhode Island (n = 13), Buzzards Bay (n = 7), Cape Cod Bay (n = 3), and Maine (n = 4), and the offshore waters of New Hampshire (n = 5). Animals were defined as "healthy" or "infected" depending on the presence of noticeable lesions on the cephalothorax. Carapace pieces were collected, fixed in 10% formalin in sterile seawater (5), and dehydrated in increasing concentrations of ethanol on ice. Samples were trimmed, critical-point-dried, and sputter-coated with gold palladium (6). The surface of cuticle lesions in early disease phases and the deeper interface between lesions and normal cuticle (leading edge of lesions) were compared and analyzed. To compare the presence of morphologically distinct bacteria identified in lesions, images were analyzed using SigmaScan 4.0 (Jandel Scientific).
Gross examination of carapace pieces showed that the carapaces of healthy animals showed no degradation, while samples from infected animals were severely eroded. Microscopic analysis of healthy carapace revealed minimal bacterial buildup (Fig. 1A). In contrast, carapace lesions of infected lobsters were covered with bacterial cells. Setal cores and natural abrasions were consistently filled with bacteria embedded in the cuticle at the lesion surface (Fig. 1B). Additionally, bacteria were abundant at the leading edge of the lesions (Fig. 1C). Overall, healthy carapace samples had substantially fewer bacteria on the carapace surface. These observations were consistent for all sampling sites.
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Five morphologically distinct bacterial types were observed on both healthy and infected animals. The majority of cells were either rods (1 x 0.4 µm), coccoid rods (0.8 x 0.5 µm), or cocci (0.5 x 0.45 µm). Segmented rod links (each piece 1.5 x 0.5 µm) and coccoid links (each piece 1.5 x 1.0 µm) were less abundant and found on infected animals only. Most bacterial types were found on animals from all geographical areas, but coccoid links were observed only on infected Rhode Island and Cape Cod Bay samples, indicating that they may be secondary invaders.
Bacteria are ubiquitous in the marine environment, so identifying the causative agents in a disease can be difficult. Examination of the interface between healthy and necrotic tissue provided the evidence necessary to identify bacteria as the disease-initiating organisms. Scanning electron microscopic imagery cannot speciate bacteria, so additional techniques such as those used in molecular biology are needed to identify the bacteria responsible for ELSD. Findings from the present study revealed the complexity of this disease in its progression and development and demonstrated the necessity for further molecular strides, including bacterial speciation and infection studies, in ELSD research.
Literature Cited
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