Abstract
Shell disease is a common affliction in marine crustaceans. It manifests as necrotic lesions on the exoskeleton that are caused by bacteria producing extracellular enzymes capable of degrading crustacean cuticle. Prior to 1998, shell disease was not reported in the Florida spiny lobster, Panulirus argus. Since that time it has been seen in P. argus in the Florida Keys. In 1999, an outbreak of severe shell disease occurred in the American lobster, Homarus americanus. Shell disease has been reported in this species for almost a century. To determine if shell disease etiology is the same between the species, a comparative study was undertaken. Healthy and shell-diseased cuticle was sampled in P. argus and H. americanus to determine if a consistent culturable bacterial flora exists on the exoskeleton, and if it the same flora found in lesions. Bacteria were identified by 16S ribosomal DNA sequencing. At least 600 bases of the ribosomal RNA gene were aligned with sequences of identified marine bacteria and phylogenetic relationships were determined. Seven groups of bacteria, six of which are in the gamma proteobacteria, emerged consistently on healthy and diseased cuticle. No primary pathogen was isolated from either species. Six of the groups were isolated from both lobster species and one group was isolated only from P. argus. The association of the bacterial groups with both healthy and shell-diseased cuticle suggests that the normal bacterial flora is in part responsible for shell disease lesions. For each lobster species, histological, scanning electron microscope, and transmission electron microscope observations were made of lesions. In both species, Gram-negative rods were the predominant bacterial morphology present, but cocci and pleomorphic bacteria were also seen. The pathology of the disease appeared to be very different between the lobster species. In P. argus, lesions appear to spread laterally via formation of an extracellular matrix that encapsulates the bacteria. The bacteria seem to secrete degradative enzymes into the matrix, which breaks down surrounding cuticle. Many lesions appeared to be initiated by trauma in P. argus. In H. americanus, the lesions appear to spread by direct bacterial contact with and degradation of the cuticle.
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