With growing environmental pressures placed on our marine habitats there is concern that the prevalence and severity of diseases affecting marine organisms will increase. Yet relative to terrestrial systems, we know little about the underlying causes of many of these diseases. Moreover, factors such as saprophytic colonizers and a lack of baseline data on healthy individuals make it difficult to accurately assess the role of specific microbial pathogens in disease states. Emerging evidence in the field of medicine suggests that a growing number of human diseases result from a microbiome imbalance (or dysbiosis), questioning the traditional view of a singular pathogenic agent. Here we discuss the possibility that many diseases seen in marine systems are, similarly, the result of microbial dysbiosis and the rise of opportunistic or polymicrobial infections. Thus, understanding and managing disease in the future will require us to also rethink definitions of disease and pathogenesis for marine systems. We suggest that a targeted, multidisciplinary approach that addresses the questions of microbial symbiosis in both healthy and diseased states, and at that the level of the holobiont, will be key to progress in this area.

BackgroundType II diabetes is a chronic health condition which is associated with skin conditions including chronic foot ulcers and an increased incidence of skin infections. The skin microbiome is thought to play important roles in skin defence and immune functioning. Diabetes affects the skin environment, and this may perturb skin microbiome with possible implications for skin infections and wound healing. This study examines the skin and wound microbiome in type II diabetes.MethodsEight type II diabetic subjects with chronic foot ulcers were followed over a time course of 10 weeks, sampling from both foot skin (swabs) and wounds (swabs and debrided tissue) every two weeks. A control group of eight control subjects was also followed over 10 weeks, and skin swabs collected from the foot skin every two weeks. Samples were processed for DNA and subject to 16S rRNA gene PCR and sequencing of the V4 region.ResultsThe diabetic skin microbiome was significantly less diverse than control skin. Community composition was also significantly different between diabetic and control skin, however the most abundant taxa were similar between groups, with differences driven by very low abundant members of the skin communities. Chronic wounds tended to be dominated by the most abundant skin Staphylococcus, while other abundant wound taxa differed by patient. No significant correlations were found between wound duration or healing status and the abundance of any particular taxa.DiscussionThe major difference observed in this study of the skin microbiome associated with diabetes was a significant reduction in diversity. The long-term effects of reduced diversity are not yet well understood, but are often associated with disease conditions.

SummaryMacroalgae are important ecosystem engineers in temperate marine waters. The function of macroalgae is intimately linked to the composition and structure of their epibiotic bacterial, communities, and evidence has emerged that bacteria can also have a negative impact on their host by causing disease. A few examples exist where bacteria have been unambiguously linked to macroalgal disease, however in many cases, pathogenicity has not been clearly separated from saprophytic behaviour or secondary colonization after disease initiation. Nevertheless, pathogenic pressure by bacteria might be substantial, as macroalgae have evolved a range of innate and induced defence mechanism that have the potential to control bacterial attacks. The presence and abundance of virulence factors in marine bacteria, which have not previously been recognized as pathogens, also represents an underappreciated, opportunistic potential for disease. Given that virulence expression in opportunistic pathogens is often dependent on environmental conditions, we predict that current and future anthropogenic changes in the marine environment will lead to an increase in the occurrence of macroalgal disease. This review highlights important areas of research that require future attention to understand the link between environmental change, opportunistic pathogens and macroalgal health in the world's oceans.

The role of diet in type 1 diabetes development is poorly understood. Metabolites, which reflect dietary response, may help elucidate this role. We explored metabolomics and lipidomics differences between 352 cases of islet autoimmunity (IA) and controls in the TEDDY (The Environmental Determinants of Diabetes in the Young) study. We created dietary patterns reflecting pre-IA metabolite differences between groups and examined their association with IA. Secondary outcomes included IA cases positive for multiple autoantibodies (mAb+). The association of 853 plasma metabolites with outcomes was tested at seroconversion to IA, just prior to seroconversion, and during infancy. Key compounds in enriched metabolite sets were used to create dietary patterns reflecting metabolite composition, which were then tested for association with outcomes in the nested case-control subset and the full TEDDY cohort. Unsaturated phosphatidylcholines, sphingomyelins, phosphatidylethanolamines, glucosylceramides, and phospholipid ethers in infancy were inversely associated with mAb+ risk, while dicarboxylic acids were associated with an increased risk. An infancy dietary pattern representing higher levels of unsaturated phosphatidylcholines and phospholipid ethers, and lower sphingomyelins was protective for mAb+ in the nested case-control study only. Characterization of this high-risk infant metabolomics profile may help shape the future of early diagnosis or prevention efforts.

There is increasing evidence to suggest that macroalgae (seaweeds) are susceptible to infectious disease. However, to date, little is known about the mechanisms that facilitate the colonization and virulence of microbial seaweed pathogens. One well-described example of a seaweed disease is the bleaching of the red alga Delisea pulchra, which can be caused by the bacterium Nautella italica R11, a member of the Roseobacter clade. This pathogen contains a unique luxR-type gene, varR, which we hypothesize controls its colonization and virulence. We show here that a varR knock-out strain is deficient in its ability to cause disease in D. pulchra and is defective in biofilm formation and attachment to a common algal polysaccharide. Moreover complementation of the varR gene in trans can restore these functions to the wild type levels. Proteomic analysis of bacterial cells in planktonic and biofilm growth highlight the potential importance of nitrogen scavenging, mobilization of energy reserves, and stress resistance in the biofilm lifestyle of N. italica R11. Moreover, we show that VarR regulates the expression of a specific subset of biofilm-associated proteins. Taken together these data suggest that VarR controls colonization and persistence of N. italica R11 on the surface of a macroalgal host and that it is an important regulator of virulence.