Infectious diseases are common in marine environments, but the effects of a changing climate on marine pathogens are not well understood. Here we review current knowledge about how the climate drives host-pathogen interactions and infectious disease outbreaks. Climate-related impacts on marine diseases are being documented in corals, shellfish, finfish, and humans; these impacts are less clearly linked for other organisms. Oceans and people are inextricably linked, and marine diseases can both directly and indirectly affect human health, livelihoods, and well-being. We recommend an adaptive management approach to better increase the resilience of ocean systems vulnerable to marine diseases in a changing climate. Land-based management methods of quarantining, culling, and vaccinating are not successful in the ocean; therefore, forecasting conditions that lead to outbreaks and designing tools/approaches to influence these conditions may be the best way to manage marine disease.

Infectious marine diseases can decimate populations and are increasing among some taxa due to global change and our increasing reliance on marine environments. Marine diseases become emergencies when significant ecological, economic or social impacts occur. We can prepare for and manage these emergencies through improved surveillance, and the development and iterative refinement of approaches to mitigate disease and its impacts. Improving surveillance requires fast, accurate diagnoses, forecasting disease risk and real-time monitoring of disease-promoting environmental conditions. Diversifying impact mitigation involves increasing host resilience to disease, reducing pathogen abundance and managing environmental factors that facilitate disease. Disease surveillance and mitigation can be adaptive if informed by research advances and catalysed by communication among observers, researchers and decision-makers using information-sharing platforms. Recent increases in the awareness of the threats posed by marine diseases may lead to policy frameworks that facilitate the responses and management that marine disease emergencies require.

Between 1996 and 2006, the US Centers for Disease Control reported that the only category of food-borne infections increasing in frequency were those caused by members of the genus Vibrio. The Gram-negative bacterium Vibrio vulnificus is a ubiquitous inhabitant of estuarine waters, and is the number one cause of seafood-related deaths in the US. Many V. vulnificus isolates have been studied, and it has been shown that two genetically distinct subtypes, distinguished by 16S rDNA and other gene polymorphisms, are associated predominantly with either environmental or clinical isolation. While local genetic differences between the subtypes have been probed, only the genomes of clinical isolates have so far been completely sequenced. In order to better understand V. vulnificus as an agent of disease and to identify the molecular components of its virulence mechanisms, we have completed whole genome shotgun sequencing of three diverse environmental genotypes using a pyrosequencing approach. V. vulnificus strain JY1305 was sequenced to a depth of 33×, and strains E64MW and JY1701 were sequenced to lesser depth, covering approximately 99.9% of each genome. We have performed a comparative analysis of these sequences against the previously published sequences of three V. vulnificus clinical isolates. We find that the genome of V. vulnificus is dynamic, with 1.27% of genes in the C-genotype genomes not found in the E- genotype genomes. We identified key genes that differentiate between the genomes of the clinical and environmental genotypes. 167 genes were found to be specifically associated with environmental genotypes and 278 genes with clinical genotypes. Genes specific to the clinical strains include components of sialic acid catabolism, mannitol fermentation, and a component of a Type IV secretory pathway VirB4, as well as several other genes with potential significance for human virulence. Genes specific to environmental strains included several that may have implications for the balance between self-preservation under stress and nutritional competence.

Marine aggregates are naturally forming conglomerations of larvacean houses, phytoplankton, microbes, and inorganics adhered together by exocellular polymers. In this study, we show in vitro that the bacterial pathogen Vibrio vulnificus can be concentrated into laboratory-generated aggregates from surrounding water. We further show that environmental (E-genotype) strains exhibit significantly more integration into these aggregates than clinical (C-genotype) strains. Experiments where marine aggregates with attached V. vulnificus cells were fed to oysters (Crassostrea virginica) resulted in greater uptake of both C and E types than nonaggregated controls. When C-and E-genotype strains were cocultured in competitive experiments, the aggregated E-genotype strains exhibited significantly greater uptake by oyster than the C-genotype strains. Vibrio vulnificus is a Gram-negative, halophilic bacterium capable of causing gastroenteritis, wound infections, and fatal septicemia in humans (1-3). It is routinely found in waters of estuarine environments as part of the normal microflora, as well as in oysters and other shellfish inhabiting those estuaries (3). V. vulnificus infection is the leading cause of seafood-borne deaths in the United States, usually resulting from the consumption of raw or undercooked oysters (3). Infections caused by ingestion commonly result in primary septicemia, almost always require hospitalization, and have a fatality rate of greater than 50% (3, 4). Wound infections usually result from exposure of open wounds to seawater containing the bacterium and can progress to fatal necrotizing fasciitis (5, 6).V. vulnificus exhibits high genotypic and phenotypic variation (3) and is divided into two genotypes, a difference originally discovered by randomly amplified polymorphic DNA PCR analysis of strains from both clinical and environmental sources (7). In this classification system, a gene designated vcg (virulence-correlated gene) was found to have two variations (8). One allele (vcgC) correlates highly with strains obtained from clinical sources and is designated the C genotype, while the other (vcgE) is correlated with environmentally isolated strains and is designated the E genotype (7,8).Over 95% of infections resulting in septicemia caused by V. vulnificus involve the consumption of raw oysters, with the remainder arising from ingestion of steamed oysters and clams (3). While millions of people in the United States eat raw oysters (9), if a consumer is afflicted with a predisposing condition, such as liver impairment or immune system dysfunction (10), the risk for infection increases 80-fold (11). Even considering these two facts, it is surprising that there are only ca. 40 primary septicemia cases reported per year (10). Usually, oysters predominately contain the E-genotype strains of V. vulnificus, which is likely a factor in the low number of infections (12-18).A study comparing the population dynamics of the V. vulnificus genotypes revealed an interesting phenomenon. While Warner and Oliver (...

Sea level rise and the anthropogenic warming of the world's oceans is not only an environmental tragedy, but these changes also result in a significant threat to public health. Along with coastal flooding and the encroachment of saltwater farther inland comes an increased risk of human interaction with pathogenic Vibrio species, such as Vibrio cholerae, V. vulnificus and V. parahaemolyticus. This minireview examines the current literature for updates on the climatic changes and practices that impact the location and duration of the presence of Vibrio spp., as well as the infection routes, trends and virulence factors of these highly successful pathogens. Finally, an overview of current treatments and methods for the mitigation of both oral and cutaneous exposures are presented.