, Volume 32, Issue 3, pp 879-889

Direct and indirect effects of a new disease of alcyonacean soft corals

Rent the article at a discount

Rent now

* Final gross prices may vary according to local VAT.

Get Access

Abstract

Alcyonacean soft corals form major components of the biomass and biodiversity on many shallow Indo-Pacific reefs. In spite of the observed increase in marine diseases worldwide, disease has rarely been reported from this taxonomic group. Here, we describe a chronic tissue loss disease affecting soft corals of the genus Sinularia on reefs in Guam. The disease presents as a diffuse wrinkling of the otherwise smooth fingers, followed by tissue sloughing, necrosis, and disintegration. Until a cause has been confirmed, we propose the name Sinularia Tissue Loss Disease. This disease was first observed at low prevalence (<1 %) in 2001 affecting Sinularia polydactyla and it was later found in Sinularia maxima and the hybrid S. maxima x polydactyla. Disease prevalence is now significantly greater in the hybrid (11–12 %) than in either parent species (2–3 %). Histological examination of healthy and affected tissues of hybrid soft corals demonstrates a loss of structural integrity, increased densities of amoebocytes and inclusion of unidentified foreign eukaryotic cells that resemble oocysts, in the diseased tissues. The presence of disease is associated with reduced concentrations of cellular protein levels, although lipids and carbohydrates were unaffected. Results from a common garden transplant experiment indicate that disease also has an indirect effect on hybrid soft corals by increasing rates of butterflyfish predation over the levels found on healthy hybrids or on healthy and diseased parent species. Our results indicate that interactions between the parent and hybrid soft coral populations are more dynamic than previously reported. Loss of hybrid soft corals on already degraded back-reefs of Guam could have significant repercussions for these reef communities.

Communicated by Biology Editor Dr. Mark Vermeij