We investigated interactions between the corallivorous gastropod Coralliophila violacea and its preferred hosts Porites spp. Our objectives were to experimentally determine whether tissue loss could progress in Porites during or after Coralliophila predation on corals with and without tissue loss and to histologically document snail predation. In 64% of feeding scars, tissue regenerated within 3 wk, leaving no trace of predation. However, in roughly 28% of scars, lesions progressed to subacute tissue loss resembling white syndrome. In feeding experiments, scars from snails previously fed diseased tissue developed progressive tissue loss twice as frequently as scars from snails previously fed healthy tissue. Scars from previously healthy-fed snails were 3 times as likely to heal as those from previously diseased-fed snails. Histology revealed marked differences in host responses to snails; P. cylindrica manifested a robust inflammatory response with fewer secondary colonizing organisms such as algae, sponges, and helminths, whereas P. rus showed no evident inflammation and more secondary colonization. We conclude that lesion progression associated with Coralliophila may be associated with secondary colonization of coral tissues damaged by predator-induced trauma and necrosis. Importantly, variation at the cellular level should be considered when explaining interspecific differences in host responses in corals impacted by phenomena such as predation.

White syndrome (WS) is currently the most prevalent disease of scleractinian corals in the Indo-Pacific region, with an ability to exist in both epizootic and enzootic states. Here, we present results of an examination of WS lesion dynamics and show that potentially associated traits of host morphology (i.e., branching vs. massive), lesion size, and tissue deposition rate influence disease severity and recovery. Lesion healing rate was positively correlated with initial lesion size in both morphologies, but the rate at which lesions healed differed between morphologies. New lesions in branching Porites cylindrica appeared less frequently, were smaller and healed more quickly, but were more abundant than in closely-related massive Porites sp(p). The positive association between lesion size and healing rate was partly explained by geometry; branching limited lesion maximum size, and larger lesion margins contained more polyps producing new tissue, resulting in faster healing. However, massive colonies deposited tissue more slowly than branching colonies, resulting in slower recovery and more persistent lesions. Corallite size and density did not differ between species and did not, therefore, influence healing rate. We demonstrated multiple modes of pathogen transmission, which may be influenced by the greater potential for pathogen entrainment in branching vs. massive morphologies. We suggest that attributes such as colony morphology and species-specific growth rates require consideration as we expand our understanding of disease dynamics in colonial organisms such as coral.

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