Evidence for Autoinduction and Quorum Sensing in White Band Disease-Causing Microbes on Acropora cervicornis.

Coral reefs have entered a state of global decline party due to an increasing incidence of coral disease. However, the diversity and complexity of coral-associated bacterial communities has made identifying the mechanisms underlying disease transmission and progression extremely difficult. This study explores the effects of coral cell-free culture fluid (CFCF) and autoinducer (a quorum sensing signaling molecule) on coral-associated bacterial growth and on coral tissue loss respectively. All experiments were conducted using the endangered Caribbean coral Acropora cervicornis. Coral-associated microbes were grown on selective media infused with CFCF derived from healthy and white band disease-infected A. cervicornis. Exposure to diseased CFCF increased proliferation of Cytophaga-Flavobacterium spp. while exposure to healthy CFCF inhibited growth of this group. Exposure to either CFCF did not significantly affect Vibrio spp. growth. In order to test whether disease symptoms can be induced in healthy corals, A. cervicornis was exposed to bacterial assemblages supplemented with exogenous, purified autoinducer. Incubation with autoinducer resulted in complete tissue loss in all corals tested in less than one week. These findings indicate that white band disease in A. cervicornis may be caused by opportunistic pathogenesis of resident microbes.

Experimentally induced marine flexibacteriosis in Atlantic salmon smolts Salmo salar. II. Pathology.

The fish disease marine flexibacteriosis is characterised by necrotic lesions on the body, head, fins, and occasionally gills, with erosive lesions on the external surface as the prominent clinical sign. In Australia, the main species affected are Atlantic salmon Salmo salar and rainbow trout Oncorhynchus mykiss in sea-cage culture in Tasmania. Using a dose-dependent trial to determine pathology, 2 forms of the disease were noted in Atlantic salmon. The acute form occurs within 2 to 3 d after inoculation at high doses (1 x 10(8) cells ml(-1)) and is characterised by the disintegration of the epithelium. The chronic form of the disease began as small superficial blisters of the epidermis, which develop into ulcerative lesions that leave musculature exposed. The predominant lesion sites were the dorsum and pectoral fins. Jaws were commonly affected, and gill necrosis was also noted. Behaviour of Atlantic salmon as well as the conditions under which they were kept contribute to the size and distribution of lesions observed. Lack of an inflammatory response in pathology and rapid and destructive mortalities observed in higher inoculum doses suggested a role of toxins in the pathogenesis of Tenacibaculum maritimum. This is the first study to examine the development of marine flexibacteriosis lesions and to utilise immunohistochemistry to verify that the bacteria observed in histology was T. maritimum.

Effect of an acute necrotic bacterial gill infection and feed deprivation on the metabolic rate of Atlantic salmon Salmo salar.

In this study, experiments were conducted to examine the effect of an acute necrotic bacterial gill infection on the metabolic rate (M(O2)) of Atlantic salmon Salmo salar. Fed and unfed Atlantic salmon smolts were exposed to a high concentration (5 x 10(12) CFU ml(-1)) of the bacteria Tenacibaculum maritimum, their routine and maximum metabolic rates (M(O2rout) and M(O2max), respectively) were measured, and relative metabolic scope determined. A significant decrease in metabolic scope was found for both fed and unfed infected groups. Fed infected fish had a mean +/- standard error of the mean (SEM) decrease of 2.21 +/- 0.97 microM O2 g(-1) h(-1), whilst unfed fish a mean +/- SEM decrease of 3.16 +/- 1.29 microM O2 g(-1) h(-1). The decrease in metabolic scope was a result of significantly increased M(O2rout) of both fed and unfed infected salmon. Fed infected fish had a mean +/- SEM increase in M(O2rout) of 1.86 +/- 0.66 microM O2 g(-1) h(-1), whilst unfed infected fish had a mean +/- SEM increase of 2.16 +/- 0.72 microM O2 g(-1) h(-1). Interestingly, all groups maintained M(O2max) regardless of infection status. Increases in M(O2rout) corresponded to a significant increase in blood plasma osmolality. A decrease in metabolic scope has implications for how individuals allocate energy; fish with smaller metabolic scope will have less energy to allocate to functions such as growth, reproduction and immune response, which may adversely affect the efficiency of fish growth.