COS 17-4 - Multiple stressors mediate coral disease and immunity in field studies and experimental manipulations

Tuesday, August 9, 2016: 9:00 AM
Palm B, Ft Lauderdale Convention Center
Allison M. Tracy, Ecology and Evolutionary Biology, Cornell University, Ernesto Weil, Department of Marine Sciences, University of Puerto Rico, Lajas, PR and C. Drew Harvell, Ecology and Evolutionary Biology, Cornell University, Ithaca, NY

Organisms in natural populations experience environments that alter their ability to fight pathogens. The environment can also activate or suppress pathogens, leading to different disease outcomes. In a natural setting, multiple environmental stressors are the reality and may interact to affect host-pathogen dynamics, often in unpredictable ways. Research on corals has produced classic examples of environmental drivers of disease, but there are important gaps in documenting interactions between multiple stressors. The population of sea fans, Gorgonia ventalina, in Puerto Rico is a tractable system for studying multiple stressors. Sea fans are relatively resistant to bleaching, survived a Caribbean-wide epizootic, and are abundant despite widespread coral decline. They will likely be important reef organisms in the Anthropocene. We surveyed sea fans at 15 sites to identify drivers of prevalence and severity of multifocal purple spots (MFPS) and a labyrinthulid pathogen, as well as the host’s cellular immune response. We conducted a clonally replicated experiment to determine the separate and combined effects of thermal stress and copper pollution on host immunity and the pathogen. While temperature plays a role in many coral diseases, we are not aware of previous studies investigating the role of metal pollutants in coral disease.


Multiple stressors and host demography influence disease and immunity in our sea fan population. Of the several factors measured in the field survey, only copper significantly affected cellular immunity. Immune cell density was significantly higher at reef sites with higher copper levels. While copper had no effect on the labyrinthulid, MFPS prevalence was lowest at intermediate copper levels. MFPS prevalence increased significantly with sea fan size. The laboratory experiment revealed interactive effects of thermal stress, copper pollution, and labyrinthulid infection on immune cell density. Sea fan immunity was induced at high copper levels, unless the host tissue was also injected with the labyrinthulid pathogen. This is consistent with the labyrinthulid constraining the sea fan immune response, in support of previous work. The role of copper pollution in coral disease is a novel finding and we highlight the importance of multiple stressors in the interaction between host, pathogen, and environment.