A study into the epidemiology of mud crab (Scylla serrata) shell disease

An outbreak of a previously unrecorded shell disease in the Portunid mud crab Scylla serrata from Gladstone Harbour, Port Curtis, Queensland, was investigated. The shell lesions called 'rust spots' appeared as orange coloured areas on the dorsal carapace, which in severe cases would ulcerate to expose underlying soft tissues. Through the examination of over 3000 mud crabs the disease prevalence in Port Curtis compared to a number of other locations in Queensland, was determined. Although the prevalence varied over the three successive sampling periods, the average prevalence (14.3%) in Gladstone Harbour was higher than the normal background prevalence of 5% reported for shell disease in other crustacean populations. The lesion pathology of rust spot lesions was determined to be unique compared to the described pathology of other shell diseases, where there is an external erosion of the shell primarily due to pathogenic organisms. In non-perforated rust spot lesions, however, the external shell layers remain intact, with the lesions being restricted to the endocuticle layer and adjacent muscle attachments. As this layer is fonned in the postmoult period, it is likely the lesions are due to a defect in the manufacturing of this layer rather than one of pathogenic degeneration. The histopathology was supported by observations of diseased mud crabs held over a moulting period, in which lesions were also observed to form in the postmoult phase. Although chitinoclastic bacteria are considered to be the primary causative agents of shell disease in other crustaceans, there was no evidence of an infectious or parasitic agent being associated with the internal organs or carapace lesions of the diseased mud crabs examined. Furthermore, water and inoculation transmission experiments failed to reproduce the disease in juvenile mud crabs, sand crabs (Portunus pelagicus) or prawns (Penaeus japonicus). Although the nature of transmission experiments is that failure to reproduce the disease does not necessarily mean definitively a noninfectious cause, in combination with the pathology results they suggest that the cause of rust spot shell lesions is likely to be non-infectious. Haemolympl1. assays were undertaken in an endeavour to measure the health status of diseased mud crabs. Results indicated elevated biochemical factors (two immune factors; antibacterial and phenoloxidase and one cellular enzyme; glutamate dehydrogenase) in both diseased and non-diseased crabs from Gladstone compared to the crabs from Ayr, a non-impacted site where no shell disease had been recorded. Levels in the diseased group of crabs were, however, depressed in comparison to their non-diseased cohorts from the same location, indicating a possible suppression of immune responses in diseased crabs. As shell disease had been associated with polluted environments, the metal analyses of diseased and non-diseased mud crab tissues from Gladstone were also compared with those from Ayr. Copper and zinc were elevated in mud crab hepatopancreas from Gladstone compared to Ayr in two consecutive years. Mean copper concentrations of Gladstone crabs were two to three times greater than for mud crabs sampled from other locations in Queensland. Total metal burdens were also elevated in the Gladstone mud crabs, with a high variation in the diseased mud crabs suggesting that this group may be unable to regulate metal levels. As copper and other metals have been demonstrated to cause inhibition of calcium uptake in other crustaceans, copper exposure experiments were conducted to test the hypothesis that copper could cause rust spot shell lesions by inhibiting calcium uptake in the developing postmoult cuticle. The experiment confirmed that calcium uptake into the carapace of softshelled juvenile, mud crabs was inhibited by sublethal copper exposure. The copper exposure experiments supported the pathology findings that rust spot shell lesions are likely to be caused by a defect in the manufacturing process of the endocuticle. The source of elevated copper accumulations in mud crabs, whether water or sediment borne or dietary was investigated. Water and sediments collected from mud crab burrows and analysed for metals determined that very low concentrations of metals exist in the burrows. A comparison was made between the diets of Gladstone mud crabs and those from Ayr to determine whether diet could be implicated as a source of elevated copper in the Gladstone mud crabs. Stable isotope analyses (carbon and nitrogen) of mud crab muscle was undertaken as an alternative to gut content analysis to determine the dietary sources of carbon and trophic position of crabs from the two areas. Although Gladstone and Ayr crabs had a similar trophic position the disparate delta carbon results suggests the diets of the crabs are different with a correlation established between delta carbon and copper concentration in the tissues. It is possible that diet may be a source of copper in Gladstone mud crabs through biomagnification along the food chain. Although results are preliminary, research into this poorly defined area of ecosystem health in Port Curtis should be continued.