Lyngbya majuscula is a toxic cyanobacterium that forms extensive and long lasting blooms. In this thesis I examine the implications of L. majuscula for green turtle (Chelonia mydas) health and foraging ecology and explore a potential role for naturally produced compounds Lyngbyatoxin A (LA) and Debromoaplysiatoxin (DAT) in the aetiology of fibropapillomatosis (FP).
To address these issues I took a broad geographical approach examining the diets of green turtle from Shoalwater Bay, Australia, over four years and also from seven sites in the Hawaiian Islands, USA, during two sampling events in 2003. My first objective was to understand the foraging ecology of these populations. Shoalwater Bay provided a case study of a seagrass dominated habitat and the Hawaiian Islands of an algal based community. In Shoalwater Bay, turtles were found to feed predominantly on seagrass with small amounts of algae, animal material and mangrove present in their diet indicating that they are opportunistic foragers. The short distance between recaptures over multiple years indicated that some turtles forage within a small region. The Hawaiian Islands provided an insight into the foraging ecology of green turtles in an algal dominated system. Here turtles fed predominantly on algae, particularly of the division rhodophyta. Diets differed in composition between sites signifying that the availability of a food source plays an important role in whether an item is consumed by the turtles. With this knowledge, and an understanding of the normal feeding ecology of turtles at these locations, I was able to address whether turtles consume L. majuscula and in what quantities. Under non-bloom conditions in both Australia and Hawaii, turtles consumed only small amounts of L. majuscula and this ingestion was suggested to be incidental. The amount of the cyanobacterium in turtle diet was positively correlated with the amount of the cyanobacterium available in the environment. However, behavioural observations of turtles during a bloom suggested that they were attempting to avoid the cyanobacterium. An analysis of diet during a bloom suggested that L. majuscula was only contributing a minor component, which indicated that the turtles may have been ingesting a substandard diet in an attempt to avoid the L. majuscula. This data was supported by blood biochemistry data that demonstrated changes in sodium, calcium and glucose plasma concentrations, which may be indicative of malnutrition. Turtles in the Hawaiian Islands were also found to consume the L. majuscula in small amounts, however, LA was found to be present in samples collected from the crop of live animals indicating that they were exposed to the tumour promoter.
The final goal of this study was to assess whether turtles were assimilating toxins produced by L. majuscula, specifically the tumour promoting compounds LA and DAT. Stranded dead and moribund turtles were collected from in and around Moreton Bay, Australia, a region where blooms of L. majuscula have been prevalent during the last decade. LA was detected in muscle, liver, small intestine and FP tissue indicating that turtles were exposed to the compound and that it is taken up in tissue.
The results from the current study indicate that blooms of L. majuscula negatively impact on green sea turtles, limiting their foraging capabilities and potentially compromising population health through decreased reproductive output. This study has also demonstrated that turtles are exposed to tumour promoting compounds produced by the cyanobacterium, providing potential for these compounds to be involved in FP. My findings indicate the need to explore further the implications of the trophic transfer of naturally produced compounds and the role of tumour promoting compounds such as LA and DAT in marine turtle FP.