In this note, we registered the occurrence of shell diseases and carapace abnormalities in a natural population of Neohelice granulata from a tropical mangrove forest, in South America, as a part of a wide ecological study. The occurrence of 32 adult crabs (1.77%) with black or brown spotted shells, or deformities on the carapace was registered, collected in the autumn and winter seasons. The low prevalence of shell diseases and abnormalities in this natural population is considered normal and probably caused by injuries occurring during the moult period of crabs.

Brown ring disease (BRD) in Ruditapes philippinarum and Ruditapes decussatus is a shell disease caused by Vibrio tapetis. This disease has begun in 1987 in clams beds in Brittany (France) and then has spread along the European Atlantic coast. Since about fifteen years, research on BRD has progress a lot and the purpose of this review is to give a short description of BRD in clams in retrospect and in addition of recent and pertinent results. Diagnosis including isolation, biochemical, serological and molecular characterization has been developed to identify and detect the pathogen. Therefore, Vibrio tapetis-like strains has been detected in other host specie, in cultured fishes during mortalities, such as the wrasse, Symphodus melops in Norway and the halibut, Hippoglossus hippoglossus in Scotland. Mechanisms of host-pathogen interactions modulated by environmental factors were studied using in vivo bacterial challenge and in vitro bio-assays. According to these studies, adherence and cytotoxic factors have been yet identified as virulence factors; identification and characterization of virulence genes are in progress. Field and experimental studies confirmed the significant effect of temperature on the development of BRD and on clam defense related activities. A significant increase in temperature over 21 °C may have a preventive effect on the development of the disease.

A programme of zoosanitary survey of the populations of black-lip pearl oyster (P. margaritifera) has been developed in French Polynesia during 1996 and 1997. Based on histological and ultrastructural examinations, the study of pearl oysters sampled in several pearl farms from the Society Islands, Tuamotu Atolls and Gambier Archipelago, has been particularly turned to enzootic pathological problems. Particular attention has been given to the shell disease and to the necrosis of the adductor muscle, symptoms that had accompanied the mass mortality in 1985.Virus–like particles, about 40 nm in diameter, were detected in membrane bound vesicles from the necrosized muscle tissue. A new Rickettsia-like organism found in epithelial cells of the digestive tubules was described, while parasites previously reported, such as cestodes and gregarines, were recognized in some animals. Apart from the pathology, a thorough study of ‘parasite-like bodies’ discovered in the pearl sack epithelium showed dysfunction in the periostracal secretion.

Juvenile oyster disease (JOD) in the eastern oyster, Crassostrea virginica, is characterized by a conchiolin deposit on the inner surface of the valves. Similarities to pathological syndromes affecting other oysters (pearl oyster mortality) and clams (brown ring disease), has suggested an infectious origin and a possible bacterial etiology. Bacteriological analysis (Total Heterotrophic Bacteria, THB and Total Vibrio sp., TVS) of oyster soft tissues, shell fluid and inner shell surfaces were monitored during the course of JOD onset and development. A significant increase in THB (but not TVS) occurred in shell fluid and at thesurface of the inner shell of JOD affected oysters. At the same time, changes in cytometric parameters (Total Hemocyte Counts, THC; Differential Hemocyte Counts, DHC) in hemolymph and shell fluid were documented in symptomatic oysters. THC in the shell fluid showed a decrease in late-stage JOD oysters. The disease was also correlated with altered cell ratios in both hemolymph and shell fluid, resulting in an increase in the percentage of the granulocytes in both locations. Our results have showed that main pathological changes associated with JOD occurred in extrapallial region rather than in the soft tissues. The disease was transmitted in the laboratory by extracts from diseased oysters: anomalous conchiolin developed within 4 weeks and the prevalence was higher when two inoculations were performed rather than one. A number of bacterial strains were found at high levels in diseased oysters and isolated. However, none produced the JOD deposit when injected into asymptomatic oysters. The bacterial etiology hypothesis for JOD should be explored further, expanded beyond the family Vibrionaceae, and should include consideration of a multiple etiology.

A description is provided of the anomalous conchiolin deposits which are formed by Pinctada maxima and which are associated with unusual mortalities. Comparisons are made with brown ring disease found in Ruditapes philippinarum and juvenile Crassostrea virginica. In P. maxima, the deposits are not organized into a ring but rather are broad-based and result in retraction of the mantle with the deposits lying outside the edge of the mantle. Vibrio sp. have been implicated in causing the diseases of P. maximaand R. philippinarum whereas the etiological agent of the disease in C. virginica is unknown. It is suggested that the coccoid bodies formed in the mantle of C. virginica, but not in affected P. maxima and R. philippinarum, are sequestered portions of cytoplasm formed as a result autophagocytosis. Stimuli which could be responsible for inducing sequestration are discussed. The ultrastructure of the presumptive autophagosomes is described and compared to similar bodies found in C. gigas infected with a herpes-like virus.