Characterization of the Coral Disease 'Porites Bleaching with Tissue Loss' (PBTL) From Hawaii
Authors:   , Sudek Mareike 
Published: November 2021

<p>Coral reefs around the world are facing many threats and have sustained severe losses in coral cover over the past few decades. Coral bleaching and disease outbreaks have contributed substantially to this reef decline, however our understanding of factors contributing to the increase in coral disease prevalence are poorly understood. Information on the disease dynamics of different diseases affecting a reef system is essential for the development of effective management strategies.  The aim of this research was to characterise and build a case study of a bleaching response affecting Porites compressa in Kaneohoe Bay, Oahu, Hawaii. It manifests as a localised, discrete area on the coral colony with a bleached coenenchyme and pigmented polyps, giving the affected area a “speckled” appearance. A disease by definition is any interruption, cessation or disorder of body functions, systems or organs. Results of this study showed that this localised bleaching causes tissue loss and a reduction in the number of gametes, and hence harm to the host. It was therefore classified as a disease and named Porites bleaching with tissue loss (PBTL). In addition, PBTL does not appear to represent a common thermal bleaching response as it was present throughout the year during times when seawater temperature was well within the coral’s thermal threshold.  Symbiodinium cell density in PBTL-affected areas of the coral colony was reduced by 65%, and examination of affected host tissue using light microscopy showed fragmentation and necrosis. However, no potential pathogen was observed. Transmission electron microscopy (TEM) revealed a high occurrence of potential apoptotic Symbiodinium cells and a potential increase in the abundance of virus-like particles (VLPs) in PBTL-affected tissue. However a causal relationship remains to be established. Long-term monitoring showed spatio-temporal variations in PBTL prevalence. Temporal variations in prevalence reflected a seasonal trend with a peak during the summer months, linked to increasing seawater temperature. Spatial variations in disease prevalence were correlated with parrotfish density, turbidity and water motion. Of these, a negative correlation with variability (SD) in turbidity explained most of the variability in PBTL prevalence (12.8%). A positive correlation with water motion explained 9% and a positive correlation with the variability in parrotfish density explained 4.4%. Overall, only a relatively small proportion of variability in PBTL prevalence could be explained by these three factors (26.2%), suggesting that other factors, not investigated in this study, play a more important role in explaining PBTL patterns or that temporal variation in temperature is the overall major driving force.  Monitoring of individually tagged P. compressa colonies showed that >80% of affected colonies sustained partial colony mortality (tissue loss) within two months; on average, one third of the colony is lost. The amount of tissue loss sustained was correlated to lesion size but not colony size. Case fatality (total mortality) was low (2.6%), however this disease can affect the same colonies repeatedly, suggesting a potential for progressive damage which could cause increased tissue loss over time. PBTL was not transmissible through direct contact or the water column in controlled aquaria experiments, suggesting that this disease might not be caused by a pathogen, is not highly infectious, or perhaps requires a vector for transmission. At present, PBTL has only been observed within Kaneohe Bay. An investigation of the potential role of host and Symbiodinium genetics in disease susceptibility revealed the same Symbiodinium sub-clade (C15) in healthy and PBTL-affected colonies, suggesting no involvement of Symbiodinium type in disease etiology. Results regarding host genetics remained inconclusive; however a difference in allele frequency at one microsatellite locus was observed between healthy and diseased samples. This difference could, however, be due to a lower amplification of PBTL-affected samples at this locus and needs to be regarded with some caution.  The results of this study provide a case definition of PBTL which can be used as a baseline in further studies. P. compressa is the main framework building species in Kaneohe Bay, and the information gathered here on disease dynamics and virulence suggests that PBTL has the potential to negatively impact the resilience of reefs within the bay. Further research into the etiology of PBTL is necessary to fully understand the impact that this disease could have on coral reefs in Hawaii.</p>