Resilience of Coral-Associated Bacterial Communities Exposed to Fish Farm Effluent

10.1371/journal.pone.0007319PLoS ONE410

Vignette 14: Eelgrass Wasting Disease

Rising seawater temperatures can increase the risk of disease outbreaks in many taxa. Pathogens are potentially the ultimate keystone species in that their small biomass can have massive impacts that ripple through ecosystems. Disease outbreaks can be particularly damaging when they affect ecosystem engineers, such as seagrasses. Outbreaks of wasting disease in seagrasses are one of a myriad of stressors associated with declining temperate and tropical seagrass meadows around the globe. Levels of eelgrass wasting disease are high in the San Juan Islands and Puget Sound. These increasing levels of disease are a threat to sustainability of eelgrass meadows, our most valuable marine habitat

Cellular Responses in Sea Fan Corals: Granular Amoebocytes React to Pathogen and Climate Stressors

BACKGROUND: Climate warming is causing environmental change making both marine and terrestrial organisms, and even humans, more susceptible to emerging diseases. Coral reefs are among the most impacted ecosystems by climate stress, and immunity of corals, the most ancient of metazoans, is poorly known. Although coral mortality due to infectious diseases and temperature-related stress is on the rise, the immune effector mechanisms that contribute to the resistance of corals to such events remain elusive. In the Caribbean sea fan corals (Anthozoa, Alcyonacea: Gorgoniidae), the cell-based immune defenses are granular acidophilic amoebocytes, which are known to be involved in wound repair and histocompatibility. METHODOLOGY/PRINCIPAL FINDINGS: We demonstrate for the first time in corals that these cells are involved in the organismal response to pathogenic and temperature stress. In sea fans with both naturally occurring infections and experimental inoculations with the fungal pathogen Aspergillus sydowii, an inflammatory response, characterized by a massive increase of amoebocytes, was evident near infections. Melanosomes were detected in amoebocytes adjacent to protective melanin bands in infected sea fans; neither was present in uninfected fans. In naturally infected sea fans a concurrent increase in prophenoloxidase activity was detected in infected tissues with dense amoebocytes. Sea fans sampled in the field during the 2005 Caribbean Bleaching Event (a once-in-hundred-year climate event) responded to heat stress with a systemic increase in amoebocytes and amoebocyte densities were also increased by elevated temperature stress in lab experiments. CONCLUSIONS/SIGNIFICANCE: The observed amoebocyte responses indicate that sea fan corals use cellular defenses to combat fungal infection and temperature stress. The ability to mount an inflammatory response may be a contributing factor that allowed the survival of even infected sea fan corals during a stressful climate event

Impacts of aspergillosis on sea fan coral demography: modeling a moving target

Little is known about how epizootics in natural populations affect vital rates and population structure, or about the process of recovery after an outbreak subsides. We investigated the effects of aspergillosis, an infectious disease caused by the fungal pathogen Aspergillus sydowii, on the demography of a gorgonian coral, Gorgonia ventalina. Caribbean sea fans were affected by a seven-year epizootic, marked by an initial period in 1994 of high infection prevalence, high mortality rates, and almost complete reproductive failure of infected fans. Post epizootic, in 2005, host populations were relatively healthy, with low disease prevalence. Using longitudinal data from populations on coral reefs in the Florida Keys (USA) and the Yucatán Peninsula (Mexico), we documented changes in the epidemiology of sea fan aspergillosis over the course of the epizootic. We developed an "integral projection model" that scales disease impacts from individual to population levels using direct estimates of vital rates. Within-colony lesion growth rate and host mortality were higher during the peak of the epizootic. Effects on individuals and populations changed substantially post-epizootic; recruitment increased, mortality of infected adults decreased, and the size dependence of infection was reduced. Elasticity analysis indicated that population growth is more sensitive to changes in the growth and survival of established colonies than to recruitment, due to slow colony growth and the longevity and fecundity of large adults. Disease prevalence in our monitored populations decreased from ∼50% in 1997 to <10% by 2003 and <1% in 2007 and was accompanied by very high mortality during the early stages of the epizootic. The population model suggested that host evolution (due to selection for higher disease resistance through differential mortality) could proceed quickly enough to explain the observed changes in prevalence and in the size independence of infection risk. Our model indicates that the time required for population recovery following an outbreak is largely determined by the percentage of healthy tissue lost from the population. However, recovery following an especially severe outbreak (i.e., 80% or more tissue loss) is much faster if the affected population receives an external supply of recruits from unaffected areas

Deeper habitats and cooler temperatures moderate a climate-driven seagrass disease

Eelgrass creates critical coastal habitats worldwide and fulfills essential ecosystem functions as a foundation seagrass. Climate warming and disease threaten eelgrass, causing mass mortalities and cascading ecological impacts. Subtidal meadows are deeper than intertidal and may also provide refuge from the temperature-sensitive seagrass wasting disease. From cross-boundary surveys of 5761 eelgrass leaves from Alaska to Washington and assisted with a machine-language algorithm, we measured outbreak conditions. Across summers 2017 and 2018, disease prevalence was 16% lower for subtidal than intertidal leaves; in both tidal zones, disease risk was lower for plants in cooler conditions. Even in subtidal meadows, which are more environmentally stable and sheltered from temperature and other stressors common for intertidal eelgrass, we observed high disease levels, with half of the sites exceeding 50% prevalence. Models predicted reduced disease prevalence and severity under cooler conditions, confirming a strong interaction between disease and temperature. At both tidal zones, prevalence was lower in more dense eelgrass meadows, suggesting disease is suppressed in healthy, higher density meadows. These results underscore the value of subtidal eelgrass and meadows in cooler locations as refugia, indicate that cooling can suppress disease, and have implications for eelgrass conservation and management under future climate change scenarios

Growth anomalies on the coral genera Acropora and Porites are strongly associated with host density and human population size across the Indo-Pacific

Growth anomalies (GAs) are common, tumor-like diseases that can cause significant morbidity and decreased fecundity in the major Indo-Pacific reef-building coral genera, Acropora and Porites. GAs are unusually tractable for testing hypotheses about drivers of coral disease because of their pan-Pacific distributions, relatively high occurrence, and unambiguous ease of identification. We modeled multiple disease-environment associations that may underlie the prevalence of Acropora growth anomalies (AGA) (n = 304 surveys) and Porites growth anomalies (PGA) (n = 602 surveys) from across the Indo-Pacific. Nine predictor variables were modeled, including coral host abundance, human population size, and sea surface temperature and ultra-violet radiation anomalies. Prevalence of both AGAs and PGAs were strongly host density-dependent. PGAs additionally showed strong positive associations with human population size. Although this association has been widely posited, this is one of the first broad-scale studies unambiguously linking a coral disease with human population size. These results emphasize that individual coral diseases can show relatively distinct patterns of association with environmental predictors, even in similar diseases (growth anomalies) found on different host genera (Acropora vs. Porites). As human densities and environmental degradation increase globally, the prevalence of coral diseases like PGAs could increase accordingly, halted only perhaps by declines in host density below thresholds required for disease establishment

Improving marine disease surveillance through sea temperature monitoring, outlooks and projections

International audienceTo forecast marine disease outbreaks as oceans warm requires new environmental surveillance tools. We describe an iterative process for developing these tools that combines research, development and deployment for suitable systems. The first step is to identify candidate host–pathogen systems. The 24 candidate systems we identified include sponges, corals, oysters, crustaceans, sea stars, fishes and sea grasses (among others). To illustrate the other steps, we present a case study of epizootic shell disease (ESD) in the American lobster. Increasing prevalence of ESD is a contributing factor to lobster fishery collapse in southern New England (SNE), raising concerns that disease prevalence will increase in the northern Gulf of Maine under climate change. The lowest maximum bottom temperature associated with ESD prevalence in SNE is 128C. Our seasonal outlook for 2015 and long-term projections show bottom temperatures greater than or equal to 128C may occur in this and coming years in the coastal bays of Maine. The tools presented will allow managers to target efforts to monitor the effects of ESD on fishery sustainability and will be iteratively refined. The approach and case example highlight that temperature-based surveillance tools can inform research, monitoring and management of emerging and continuing marine disease threats