Ecological factors mediate immunity and parasitic co-infection in sea fan octocorals

The interplay among environment, demography, and host-parasite
interactions is a challenging frontier. In the ocean, fundamental changes
are occurring due to anthropogenic pressures, including increased disease
outbreaks on coral reefs. These outbreaks often include multiple
parasites, calling into question how coral immunity functions in this
complex milieu. Corals provide an interesting model to study ecological
immunity during co-infection, being highly sensitive to environmental
change, susceptible to many diseases, and defended by the innate immune
system. Our work investigates the interplay of factors influencing coral
co-infection using metrics of the innate immune response: levels of
cellular immunity and the expression of candidate immune genes. We used
existing copepod infections and live pathogen inoculation with Aspergillus
fungus to test the effect of sequential co-infections in a laboratory
experiment. We profile significant increases in the expression of the
immune recognition gene Tachylectin 5A in response to both of these
naturally occurring parasites of the Caribbean sea fan octocoral, Gorgonia
ventalina. Cellular immunity increased significantly by 8.16% in copepod
infections compared to controls and single Aspergillus infections. We
evaluated immunity in reef populations and again detected activation of
cellular immunity, with a 13.6% increase in copepod infections and no
detectable increase in fungal infections. Thus, cellular immunity measured
in the field and lab were similar, increasing with copepod infections and
not Aspergillus. We found random co-occurrence of copepods and fungus
across 15 reefs in Puerto Rico, suggesting other factors prevail in
structuring parasite infection. Sea fan colony size strongly predicted
infection by the copepod parasite. Moreover, the effect of parasitic
infection on immunity was small relative to the explanatory power of site
differences and coral cover, and roughly equivalent to the effect of
reproductive status. We suggest that host size, reproductive status, live
coral cover, and site-specific factors have large effects on parasitic
infections and host immunity that overwhelm effects of the parasites on
each other. Thus, host size and site-specific features emerge as critical
drivers in this multi-parasite system. Parsing the effects of immunity and
ecological factors in coral co-infection shows how disease depends on more
than one host and one parasite.