Disease outbreaks have been involved in the deterioration of coral reefs worldwide and have been par- ticularly striking among crustose coralline algae (CCA). Although CCA represent important cues for coral settle- ment, the impact of CCA diseases on the survival and settlement of coral planulae is unknown. Exposing coral larvae to healthy, diseased, and recently dead crusts from three important CCA species, we show a negative effect of disease in the inductive CCA species Hydrolithon boergesenii on larval survivorship of Orbicella faveolata and settlement of O. faveolata and Diploria labyrinthi- formis on the CCA surface. No effect was found with the less inductive CCA species Neogoniolithon mamillare and Paragoniolithon accretum. Additionally, a majority of planulae that settled on top of diseased H. boergesenii crusts were on healthy rather than diseased/dying tissue. Our experiments suggest that CCA diseases have the po- tential to reduce the survivorship and settlement of coral planulae on coral reefs.
Crustose coralline algae (CCA) are major benthic calci ers that play crucial roles in marine ecosystems, particularly coral reefs. Over the past two decades, epizootics have been reported for several CCA species on coral reefs worldwide. However, their causes remain often unknown in part because few studies have investigated CCA pathologies at a microscopic scale. We studied the cellular changes associated with two syndromes: Coralline White Band Syndrome (CWBS) and Coralline White Patch Disease (CWPD) from samples collected in Curac ̧ao, southern Caribbean. Healthy-looking tissue of diseased CCA did not di er from healthy tissue of healthy CCA. In diseased tissues of both pathologies, the three characteristic cell layers of CCA revealed cells completely depleted of protoplasmic content, but presenting an intact cell wall. In addition, CWBS showed a transition area between healthy and diseased tissues consisting of cells partially deprived of protoplasmic material, most likely corresponding to the white band characterizing the disease at the macroscopic level. This transition area was absent in CWPD. Regrowth at the lesion boundary were sometimes observed in both syndromes. Tissues of both healthy and diseased CCA were colonised by diverse boring organisms. Fungal infections associated with the diseased cells were not seen. However, other bioeroders were more abundant in diseased vs healthy CCA and in diseased vs healthy-looking tissues of diseased CCA. Although their role in the pathogenesis is unclear, this suggests that disease increases CCA susceptibility to bioerosion. Further investigations using an integrated approach are needed to carry out the complete diagnosis of these diseases.