Manipulation of the seagrass-associated microbiome reduces disease severity.

Host-associated microbes influence host health and function and can be a first line of defence against infections. While research increasingly shows that terrestrial plant microbiomes contribute to bacterial, fungal, and oomycete disease resistance, no comparable experimental work has investigated marine plant microbiomes or more diverse disease agents. We test the hypothesis that the eelgrass (Zostera marina) leaf microbiome increases resistance to seagrass wasting disease. From field eelgrass with paired diseased and asymptomatic tissue, 16S rRNA gene amplicon sequencing revealed that bacterial composition and richness varied markedly between diseased and asymptomatic tissue in one of the two years. This suggests that the influence of disease on eelgrass microbial communities may vary with environmental conditions. We next experimentally reduced the eelgrass microbiome with antibiotics and bleach, then inoculated plants with Labyrinthula zosterae, the causative agent of wasting disease. We detected significantly higher disease severity in eelgrass with a native microbiome than an experimentally reduced microbiome. Our results over multiple experiments do not support a protective role of the eelgrass microbiome against L. zosterae. Further studies of these marine host-microbe-pathogen relationships may continue to show new relationships between plant microbiomes and diseases.

Warming and pollutants interact to modulate octocoral immunity and shape disease outcomes.

Warming environments can alter the outcome of host-parasite relationships with important consequences for biodiversity. Warming often increases disease risk, and interactions with other environmental factors can intensify impacts by modifying the underlying mechanisms, such as host immunity. In coastal ecosystems, metal pollution is a pervasive stressor that influences disease and immunity in many organisms. Despite the crisis facing coral reefs, which stems in part from warming-associated disease outbreaks, the impacts of metal pollutants on scleractinian and octocoral disease are largely unknown. We investigated how warming oceans and copper pollution affect host immunity and disease risk for two diseases of the abundant Caribbean octocoral, the sea fan Gorgonia ventalina. Field surveys across a sediment copper concentration gradient in Puerto Rico, USA revealed that cellular immunity of sea fans increased by 12.6% at higher sediment copper concentrations, while recovery from multifocal purple spots disease (MFPS) tended to decrease. MFPS severity in the field increased at warmer sites. In a controlled laboratory experiment, sea fans were inoculated with live cultures of a labyrinthulid parasite to test the interactive effects of temperature and copper on immune activation. As in the field, higher copper induced greater immunity, but the factorial design of the experiment revealed that copper and temperature interacted to modulate the immune response to the parasite: immune cell densities increased with elevated temperature at lower copper concentrations, but not with high copper concentrations. Tissue damage was also greater in treatments with higher copper and warmer temperatures. Field and lab evidence confirm that elevated copper hinders sea fan immune defenses against damaging parasites. Temperature and copper influenced host-pathogen interactions in octocorals by modulating immunity, disease severity, and disease recovery. This is the first evidence that metal pollution affects processes influencing disease in octocorals and highlights the importance of immune mechanisms in environmentally mediated disease outbreaks. Although coral conservation efforts must include a focus on global factors, such as rapid warming, reducing copper and other pollutants that compromise coral health on a local scale may help corals fight disease in a warming ocean.

Increases and decreases in marine disease reports in an era of global change.

Outbreaks of marine infectious diseases have caused widespread mass mortalities, but the lack of baseline data has precluded evaluating whether disease is increasing or decreasing in the ocean. We use an established literature proxy method from Ward and Lafferty (Ward and Lafferty 2004 PLoS Biology2, e120 (doi:10.1371/journal.pbio.0020120)) to analyse a 44-year global record of normalized disease reports from 1970 to 2013. Major marine hosts are combined into nine taxonomic groups, from seagrasses to marine mammals, to assess disease swings, defined as positive or negative multi-decadal shifts in disease reports across related hosts. Normalized disease reports increased significantly between 1970 and 2013 in corals and urchins, indicating positive disease swings in these environmentally sensitive ectotherms. Coral disease reports in the Caribbean correlated with increasing temperature anomalies, supporting the hypothesis that warming oceans drive infectious coral diseases. Meanwhile, disease risk may also decrease in a changing ocean. Disease reports decreased significantly in fishes and elasmobranchs, which have experienced steep human-induced population declines and diminishing population density that, while concerning, may reduce disease. The increases and decreases in disease reports across the 44-year record transcend short-term fluctuations and regional variation. Our results show that long-term changes in disease reports coincide with recent decades of widespread environmental change in the ocean.

Host size and proximity to diseased neighbours drive the spread of a coral disease outbreak in Hawai'i.

Understanding how disease risk varies over time and across heterogeneous populations is critical for managing disease outbreaks, but this information is rarely known for wildlife diseases. Here, we demonstrate that variation in host and pathogen factors drive the direction, duration and intensity of a coral disease outbreak. We collected longitudinal health data for 200 coral colonies, and found that disease risk increased with host size and severity of diseased neighbours, and disease spread was highest among individuals between 5 and 20 m apart. Disease risk increased by 2% with every 10 cm increase in host size. Healthy colonies with severely diseased neighbours (greater than 75% affected tissue) were 1.6 times more likely to develop disease signs compared with colonies with moderately diseased neighbours (25-75% affected tissue). Force of infection ranged from 7 to 20 disease cases per 1000 colonies (mean = 15 cases per 1000 colonies). The effective reproductive ratio, or average number of secondary infections per infectious individual, ranged from 0.16 to 1.22. Probability of transmission depended strongly on proximity to diseased neighbours, which demonstrates that marine disease spread can be highly constrained within patch reefs.

Octocoral co-infection as a balance between host immunity and host environment.

Co-infection is the reality in natural populations, but few studies incorporate the players that matter in the wild. We integrate the environment, host demography, two parasites, and host immunity in a study of co-infection to determine the drivers of parasite interactions. Here, we use an ecologically important Caribbean sea fan octocoral, Gorgonia ventalina, that is co-infected by a copepod and a labyrinthulid protist. We first expanded upon laboratory studies by showing that immune suppression is associated with the labyrinthulid in a natural setting. Histological analyses revealed that immune cells (amoebocytes) were significantly suppressed in both labyrinthulid infections and co-infections relative to healthy sea fans, but remained unchanged in copepod infections. However, surveys of natural coral populations demonstrated a critical role for the environment and host demography in this co-infection: the prevalence of copepod infections increased with sea fan size while labyrinthulid prevalence increased with water depth. Although we predicted that immune suppression by the labyrinthulid would facilitate copepod infection, the two parasites did not co-occur in the sea fans more often than expected by chance. These results suggest that the distinct ecological drivers for each parasite overwhelm the role of host immune suppression in determining the distribution of parasites among hosts. This interplay of the environment and parasite-mediated immune suppression in sea fan co-infection provides insights into the factors underlying co-occurrence patterns in wild co-infections. Moving forward, simultaneous consideration of co-occurring parasites, host traits, and the environmental context will improve the understanding of host - parasite interactions and their consequences.

Densovirus associated with sea-star wasting disease and mass mortality.

Populations of at least 20 asteroid species on the Northeast Pacific Coast have recently experienced an extensive outbreak of sea-star (asteroid) wasting disease (SSWD). The disease leads to behavioral changes, lesions, loss of turgor, limb autotomy, and death characterized by rapid degradation ("melting"). Here, we present evidence from experimental challenge studies and field observations that link the mass mortalities to a densovirus (Parvoviridae). Virus-sized material (i.e., <0.2 µm) from symptomatic tissues that was inoculated into asymptomatic asteroids consistently resulted in SSWD signs whereas animals receiving heat-killed (i.e., control) virus-sized inoculum remained asymptomatic. Viral metagenomic investigations revealed the sea star-associated densovirus (SSaDV) as the most likely candidate virus associated with tissues from symptomatic asteroids. Quantification of SSaDV during transmission trials indicated that progression of SSWD paralleled increased SSaDV load. In field surveys, SSaDV loads were more abundant in symptomatic than in asymptomatic asteroids. SSaDV could be detected in plankton, sediments and in nonasteroid echinoderms, providing a possible mechanism for viral spread. SSaDV was detected in museum specimens of asteroids from 1942, suggesting that it has been present on the North American Pacific Coast for at least 72 y. SSaDV is therefore the most promising candidate disease agent responsible for asteroid mass mortality.

Impacts of biodiversity on the emergence and transmission of infectious diseases.

Current unprecedented declines in biodiversity reduce the ability of ecological communities to provide many fundamental ecosystem services. Here we evaluate evidence that reduced biodiversity affects the transmission of infectious diseases of humans, other animals and plants. In principle, loss of biodiversity could either increase or decrease disease transmission. However, mounting evidence indicates that biodiversity loss frequently increases disease transmission. In contrast, areas of naturally high biodiversity may serve as a source pool for new pathogens. Overall, despite many remaining questions, current evidence indicates that preserving intact ecosystems and their endemic biodiversity should generally reduce the prevalence of infectious diseases.

Plant characteristics associated with widespread variation in eelgrass wasting disease.

Seagrasses are ecosystem engineers of essential marine habitat. Their populations are rapidly declining worldwide. One potential cause of seagrass population declines is wasting disease, which is caused by opportunistic pathogens in the genus Labyrinthula. While infection with these pathogens is common in seagrasses, theory suggests that disease only occurs when environmental stressors cause immunosuppression of the host. Recent evidence suggests that host factors may also contribute to disease caused by opportunistic pathogens. In order to quantify patterns of disease, identify risk factors, and investigate responses to infection, we surveyed shoot density, shoot length, epiphyte load, production of plant defenses (phenols), and wasting disease prevalence in eelgrass Zostera marina across 11 sites in the central Salish Sea (Washington state, USA), a region where both wasting disease and eelgrass declines have been documented. Wasting disease was diagnosed by the presence of necrotic lesions, and Labyrinthula cells were identified with histology. Disease prevalence among sites varied from 6 to 79%. The probability of a shoot being diseased was higher in longer shoots, in patches of higher shoot density, and in shoots with higher levels of biofouling from epiphytes. Phenolic concentration was higher in diseased leaves. We hypothesize that this results from the induction of phenols during infection. Additional research is needed to evaluate whether phenols are an adaptive defense against Labyrinthula infection. The high site-level variation in disease prevalence emphasizes the potential for wasting disease to be causing some of the observed decline in eelgrass beds.

Host demography influences the prevalence and severity of eelgrass wasting disease.

Many marine pathogens are opportunists, present in the environment, but causing disease only under certain conditions such as immunosuppression due to environmental stress or host factors such as age. In the temperate eelgrass Zostera marina, the opportunistic labyrinthulomycete pathogen Labyrinthula zosterae is present in many populations and occasionally causes severe epidemics of wasting disease; however, risk factors associated with these epidemics are unknown. We conducted both field surveys and experimental manipulations to examine the effect of leaf age (inferred from leaf size) on wasting disease prevalence and severity in Z. marina across sites in the San Juan Archipelago, Washington, USA. We confirmed that lesions observed in the field were caused by active Labyrinthula infections both by identifying the etiologic agent through histology and by performing inoculations with cultures of Labyrinthula spp. isolated from observed lesions. We found that disease prevalence increased at shallower depths and with greater leaf size at all sites, and this effect was more pronounced at declining sites. Experimental inoculations with 2 strains of L. zosterae confirmed an increased susceptibility of older leaves to infection. Overall, this pattern suggests that mature beds and shallow beds of eelgrass may be especially susceptible to outbreaks of wasting disease. The study highlights the importance of considering host and environmental factors when evaluating risk of disease from opportunistic pathogens.

Special issue Oceans and Humans Health: the ecology of marine opportunists.

Opportunistic marine pathogens, like opportunistic terrestrial pathogens, are ubiquitous in the environment (waters, sediments, and organisms) and only cause disease in immune-compromised or stressed hosts. In this review, we discuss four host-pathogen interactions within the marine environment that are typically considered opportunistic: sea fan coral-fungus, eelgrass-Labyrinthula zosterae, sea fan-Labyrinthulomycetes, and hard clam-Quahog Parasite Unknown with particular focus on disease ecology, parasite pathology, host response, and known associated environmental conditions. Disease is a natural part of all ecosystems; however, in some cases, a shift in the balance between the host, pathogen, and the environment may lead to epizootics in natural or cultured populations. In marine systems, host-microbe interactions are less understood than their terrestrial counterparts. The biological and physical changes to the world's oceans, coupled with other anthropogenic influences, will likely lead to more opportunistic diseases in the marine environment.

Friend or foe: the association of Labyrinthulomycetes with the Caribbean sea fan Gorgonia ventalina.

A new syndrome in sea fans Gorgonia ventalina consisting of multifocal purple spots (MFPS) has been observed in the Caribbean Sea. Surveys of MFPS on sea fans were conducted from 2006 to 2010 at a shallow and deep site in La Parguera, Puerto Rico (PR). At the shallow site, MFPS increased between 2006 and 2010 (site average ranged from 8 to 23%), with differences found at depths over time using an analysis of covariance (ANCOVA, p < 0.0001). As a potential causative agent we examined a Labyrinthulomycota-like ovoid parasite that was observed to be abundant in MFPS lesions in light micrographs. Labyrinhylomycetes were successfully isolated, cultured and characterized in sea fans from Florida and PR. Sequence information obtained from the small subunit (SSU) rRNA gene indicated that Labyrinthulomycetes in most sea fans (healthy and MFPS sea fans from Florida; MFPS from PR) and the cultured microorganism are in the genus Aplanochytrium, although some healthy sea fans from PR contained members of the genus Thraustochytrium. Both genera fall within the family Thraustochytriidae. Histology confirmed observations of thraustochytrids within apparently healthy and MFPS sea fans from PR, and specific staining indicated a host melanization response only in colonies containing Labyrinthulomycetes or fungal infections. Growth trials indicate that the temperature-growth optima for the cultured microorganism is ~30°C. In inoculation experiments, the cultured Aplanochytrium did not induce purple spots, and histology revealed that many of the apparently healthy recipients contained Labyrinthulomycetes prior to inoculation. Taken together, these results indicate that the Labyrinthulomycetes associated with sea fans is likely an opportunistic pathogen. Further studies are needed to understand the pathogenesis of this microorganism in sea fans and its relationship with MFPS.

Global coral disease prevalence associated with sea temperature anomalies and local factors.

Coral diseases are taking an increasing toll on coral reef structure and biodiversity and are important indicators of declining health in the oceans. We implemented standardized coral disease surveys to pinpoint hotspots of coral disease, reveal vulnerable coral families and test hypotheses about climate drivers from 39 locations worldwide. We analyzed a 3 yr study of coral disease prevalence to identify links between disease and a range of covariates, including thermal anomalies (from satellite data), location and coral cover, using a Generalized Linear Mixed Model. Prevalence of unhealthy corals, i.e. those with signs of known diseases or with other signs of compromised health, exceeded 10% on many reefs and ranged to over 50% on some. Disease prevalence exceeded 10% on 20% of Caribbean reefs and 2.7% of Pacific reefs surveyed. Within the same coral families across oceans, prevalence of unhealthy colonies was higher and some diseases were more common at sites in the Caribbean than those in the Pacific. The effects of high disease prevalence are potentially extensive given that the most affected coral families, the acroporids, faviids and siderastreids, are among the major reef-builders at these sites. The poritids and agaricids stood out in the Caribbean as being the most resistant to disease, even though these families were abundant in our surveys. Regional warm temperature anomalies were strongly correlated with high disease prevalence. The levels of disease reported here will provide a much-needed local reference point against which to compare future change.

Predictable Changes in Eelgrass Microbiomes with Increasing Wasting Disease Prevalence across 23° Latitude in the Northeastern Pacific.

Predicting outcomes of marine disease outbreaks presents a challenge in the face of both global and local stressors. Host-associated microbiomes may play important roles in disease dynamics but remain understudied in marine ecosystems. Host-pathogen-microbiome interactions can vary across host ranges, gradients of disease, and temperature; studying these relationships may aid our ability to forecast disease dynamics. Eelgrass, Zostera marina, is impacted by outbreaks of wasting disease caused by the opportunistic pathogen Labyrinthula zosterae. We investigated how Z. marina phyllosphere microbial communities vary with rising wasting disease lesion prevalence and severity relative to plant and meadow characteristics like shoot density, longest leaf length, and temperature across 23° latitude in the Northeastern Pacific. We detected effects of geography (11%) and smaller, but distinct, effects of temperature (30-day max sea surface temperature, 4%) and disease (lesion prevalence, 3%) on microbiome composition. Declines in alpha diversity on asymptomatic tissue occurred with rising wasting disease prevalence within meadows. However, no change in microbiome variability (dispersion) was detected between asymptomatic and symptomatic tissues. Further, we identified members of Cellvibrionaceae, Colwelliaceae, and Granulosicoccaceae on asymptomatic tissue that are predictive of wasting disease prevalence across the geographic range (3,100 kilometers). Functional roles of Colwelliaceae and Granulosicoccaceae are not known. Cellvibrionaceae, degraders of plant cellulose, were also enriched in lesions and adjacent green tissue relative to nonlesioned leaves. Cellvibrionaceae may play important roles in disease progression by degrading host tissues or overwhelming plant immune responses. Thus, inclusion of microbiomes in wasting disease studies may improve our ability to understand variable rates of infection, disease progression, and plant survival. IMPORTANCE The roles of marine microbiomes in disease remain poorly understood due, in part, to the challenging nature of sampling at appropriate spatiotemporal scales and across natural gradients of disease throughout host ranges. This is especially true for marine vascular plants like eelgrass (Zostera marina) that are vital for ecosystem function and biodiversity but are susceptible to rapid decline and die-off from pathogens like eukaryotic slime-mold Labyrinthula zosterae (wasting disease). We link bacterial members of phyllosphere tissues to the prevalence of wasting disease across the broadest geographic range to date for a marine plant microbiome-disease study (3,100 km). We identify Cellvibrionaceae, plant cell wall degraders, enriched (up to 61% relative abundance) within lesion tissue, which suggests this group may be playing important roles in disease progression. These findings suggest inclusion of microbiomes in marine disease studies will improve our ability to predict ecological outcomes of infection across variable landscapes spanning thousands of kilometers.

Thermal stress and coral cover as drivers of coral disease outbreaks.

Very little is known about how environmental changes such as increasing temperature affect disease dynamics in the ocean, especially at large spatial scales. We asked whether the frequency of warm temperature anomalies is positively related to the frequency of coral disease across 1,500 km of Australia's Great Barrier Reef. We used a new high-resolution satellite dataset of ocean temperature and 6 y of coral disease and coral cover data from annual surveys of 48 reefs to answer this question. We found a highly significant relationship between the frequencies of warm temperature anomalies and of white syndrome, an emergent disease, or potentially, a group of diseases, of Pacific reef-building corals. The effect of temperature was highly dependent on coral cover because white syndrome outbreaks followed warm years, but only on high (>50%) cover reefs, suggesting an important role of host density as a threshold for outbreaks. Our results indicate that the frequency of temperature anomalies, which is predicted to increase in most tropical oceans, can increase the susceptibility of corals to disease, leading to outbreaks where corals are abundant.

What are the physiological and immunological responses of coral to climate warming and disease?

Coral mortality due to climate-associated stress is likely to increase as the oceans get warmer and more acidic. Coral bleaching and an increase in infectious disease are linked to above average sea surface temperatures. Despite the uncertain future for corals, recent studies have revealed physiological mechanisms that improve coral resilience to the effects of climate change. Some taxa of bleached corals can increase heterotrophic food intake and exchange symbionts for more thermally tolerant clades; this plasticity can increase the probability of surviving lethal thermal stress. Corals can fight invading pathogens with a suite of innate immune responses that slow and even arrest pathogen growth and reduce further tissue damage. Several of these responses, such as the melanin cascade, circulating amoebocytes and antioxidants, are induced in coral hosts during pathogen invasion or disease. Some components of immunity show thermal resilience and are enhanced during temperature stress and even in bleached corals. These examples suggest some plasticity and resilience to cope with environmental change and even the potential for evolution of resistance to disease. However, there is huge variability in responses among coral species, and the rate of climate change is projected to be so rapid that only extremely hardy taxa are likely to survive the projected changes in climate stressors.

Coastal urbanization influences human pathogens and microdebris contamination in seafood.

Seafood is one of the leading imported products implicated in foodborne outbreaks worldwide. Coastal marine environments are being increasingly subjected to reduced water quality from urbanization and leading to contamination of important fishery species. Given the importance of seafood exchanged as a global protein source, it is imperative to maintain seafood safety worldwide. To illustrate the potential health risks associated with urbanization in a coastal environment, we use next-generation high-throughput amplicon sequencing of the 16S ribosomal RNA gene combined with infrared spectroscopy to characterize and quantify a vast range of potential human bacterial pathogens and microdebris contaminants in seawater, sediment and an important oyster fishery along the Mergui Archipelago in Myanmar. Through the quantification of >1.25 million high-quality bacterial operational taxonomic unit (OTU) reads, we detected 5459 potential human bacterial pathogens belonging to 87 species that are commonly associated with gut microbiota and an indication of terrestrial runoff of human and agricultural waste. Oyster tissues contained 51% of all sequenced bacterial pathogens that are considered to be both detrimental and of emerging concern to human health. Using infrared spectroscopy, we examined a total of 1225 individual microdebris particles, from which we detected 78 different types of contaminant materials. The predominant microdebris contaminants recovered from oyster tissues included polymers (48%), followed by non-native minerals (20%), oils (14%) and milk supplement powders (14%). Emerging technologies provide novel insights into the impacts of coastal development on food security and risks to human and environmental health.

The role of environment and microorganisms in diseases of corals: overview of DAO Special 5.

Coral reefs are in decline worldwide. In the last several decades, bleaching and disease in a warming ocean have emerged as dominant drivers of ecological change on coral reefs. This special issue of DAO presents papers based on presentations from the 11th International Coral Reef Symposium (2008, Fort Lauderdale, Florida, USA). The articles herein document disease outbreaks involving novel hosts, pathogens and/or locations, experimental studies investigating processes and mechanisms underlying pathogen dynamics, and the application of increasingly sophisticated laboratory and modeling approaches to understanding disease epizootiology.

Immune defenses of healthy, bleached and diseased Montastraea faveolata during a natural bleaching event.

One prominent hypothesis regarding climate change and scleractinian corals is that thermal stress compromises immune competence. To test this hypothesis we tracked how the immune defenses of bleached, apparently healthy and yellow band disease (YBD) diseased Montastraea faveolata colonies varied with natural thermal stress in southwestern Puerto Rico. Colonies were monitored for 21 mo from the peak of the bleaching event in October 2005 to August 2007. Since sea surface temperature was significantly higher in summer and fall 2005 than 2006, year of collection was used as a proxy for temperature stress, and colony fragments collected in 2005 were compared with those collected in 2006. Mortality rate was high (43% overall) and all colonies (except one) either died or became infected with YBD by August 2007. YBD-infected tissue did not bleach (i.e. expel zooxanthellae) during the 2005 bleaching event, even when healthy tissue of these colonies bleached. Immune activity was assayed by measuring prophenoloxidase (PPO), peroxidase (POX), lysozyme-like (LYS) and antibacterial (AB) activity. Immune activity was variable between all coral samples, but there was a significant elevation of PPO activity in bleached colonies collected in 2005 relative to apparently healthy and YBD-diseased corals in 2006. In YBD-diseased colonies, LYS and AB activity were elevated in both healthy and infected tissue, indicating a systemic response; activity levels in these colonies were higher compared to those that appeared healthy. In both these immune parameters, there was a trend for suppression of activity in corals that were bleached in 2005. These data, while complicated by between-genet variability, illustrate the complex interaction between disease and temperature stress on immune function.

Influence of marine reserves on coral disease prevalence.

Predicted increases in disease with climate warming highlight the need for effective management strategies to mitigate disease effects in coral communities. We examined the role of marine protected areas (MPAs) in reducing disease in corals and the hypothesis that the composition of fish communities can influence coral health, by comparing disease prevalence between MPA and non-protected (control) reefs in Palau. Overall, the prevalence of diseases pooled, as well as the prevalence of skeletal eroding band (SEB), brown band disease (BrB) and growth anomalies (GAs) individually in major disease hosts (families Acroporidae and Poritidae), were not significantly reduced within MPAs. In fact, the prevalence of SEB was 2-fold higher within MPAs overall; however, the 4 studied MPAs were ineffective in enhancing coral assemblage or fish stock health. A negative association between the prevalence of SEB and richness of a fish species targeted by fishers in Palau highlights the potential role that well-managed MPAs could play in reducing SEB. The composition of coral communities and their susceptibility to bleaching also influenced the prevalence of disease on the studied reefs. The prevalence of diseases pooled and SEB were positively associated with the cover of major disease hosts (families Acroporidae and Poritidae), and the prevalence of BrB and bleaching were also positively associated. Although our study did not show positive effects of MPAs on coral heath, we did identify the potential for increased fish diversity within MPAs to reduce coral disease. Our study also highlights the complexity of relationships between fish assemblages, coral community composition and coral health on Indo-Pacific reefs.

Plastic waste associated with disease on coral reefs.

Plastic waste can promote microbial colonization by pathogens implicated in outbreaks of disease in the ocean. We assessed the influence of plastic waste on disease risk in 124,000 reef-building corals from 159 reefs in the Asia-Pacific region. The likelihood of disease increases from 4% to 89% when corals are in contact with plastic. Structurally complex corals are eight times more likely to be affected by plastic, suggesting that microhabitats for reef-associated organisms and valuable fisheries will be disproportionately affected. Plastic levels on coral reefs correspond to estimates of terrestrial mismanaged plastic waste entering the ocean. We estimate that 11.1 billion plastic items are entangled on coral reefs across the Asia-Pacific and project this number to increase 40% by 2025. Plastic waste management is critical for reducing diseases that threaten ecosystem health and human livelihoods.