Abstract
For several decades, white plagues (WPDs: WPD-I, II and III) and more recently, stony coral tissue loss disease (SCTLD) have significantly impacted Caribbean corals. These diseases are often difficult to separate in the field as they produce similar gross signs. Here we aimed to compare what we know about WPD and SCTLD in terms of: (1) pathology, (2) etiology, and (3) epizootiology. We reviewed over 114 peer-reviewed publications from 1973 to 2021. Overall, WPD and SCTLD resemble each other macroscopically, mainly due to the rapid tissue loss they produce in their hosts, however, SCTLD has a more concise case definition. Multiple-coalescent lesions are often observed in colonies with SCTLD and rarely in WPD. A unique diagnostic sign of SCTLD is the presence of bleached circular areas when SCTLD lesions are first appearing in the colony. The paucity of histopathologic archives for WPDs for multiple species across geographies makes it impossible to tell if WPD is the same as SCTLD. Both diseases alter the coral microbiome. WPD is controversially regarded as a bacterial infection and more recently a viral infection, whereas for SCTLD the etiology has not been identified, but the putative pathogen, likely to be a virus, has not been confirmed yet. Most striking differences between WPD and SCTLD have been related to duration and phases of epizootic events and mortality rates. While both diseases may become highly prevalent on reefs, SCTLD seems to be more persistent even throughout years. Both transmit directly (contact) and horizontally (waterborne), but organism-mediated transmission is only proven for WPD-II. Given the differences and similarities between these diseases, more detailed information is needed for a better comparison. Specifically, it is important to focus on: (1) tagging colonies to look at disease progression and tissue mortality rates, (2) tracking the fate of the epizootic event by looking at initial coral species affected, the features of lesions and how they spread over colonies and to a wider range of hosts, (3) persistence across years, and (4) repetitive sampling to look at changes in the microbiome as the disease progresses. Our review shows that WPDs and SCTLD are the major causes of coral tissue loss recorded in the Caribbean.
Highlights
Coral reef ecosystems worldwide are facing natural and humaninduced stressors resulting in significant declines in coral cover and diversity, and elevated coral extinction risks (Carpenter et al, 2008; Jackson et al, 2014)
Reported linear tissue mortality rates for stony coral tissue loss disease (SCTLD) range from 3.6 to 5.3 cm2 day−1 as lesions quickly coalesce (Aeby et al, 2019) or 3–4 cm/day as colonies die within weeks or months (AGRRA2), with fatality varying from 73 to nearly 100% within a few months depending on location and species (Aeby et al, 2019; Thome et al, 2021)
While there is a strong overlapping on host ranges, susceptibility to both diseases is slightly different, with Orbicella spp. being more susceptible to WPD-II (Nugues, 2002; Sutherland et al, 2004; Weil, 2004; Weil and Cróquer, 2009; Richardson, 2016), and Dendrogyra cylindrus, Meandrina ssp., M. cavernosa, S. siderea, and E. fastigiata being prone to get SCTLD in the field (Walton et al, 2018; Aeby et al, 2019; Alvarez-Filip et al, 2019; Kramer et al, 2020; Brandt et al, 2021; Costa et al, 2021; Estrada-Saldívar et al, 2021)
Summary
Coral reef ecosystems worldwide are facing natural and humaninduced stressors resulting in significant declines in coral cover and diversity, and elevated coral extinction risks (Carpenter et al, 2008; Jackson et al, 2014). In the late 1990s and early 2000s, a fourth more virulent epizootic was termed WPDIII and affected mostly Orbicella spp. and Colpophyllia natans in Florida, the United States Virgin Islands, Puerto Rico, and Venezuela during the 10 years, and it is still present even if not as prevalent as before (Richardson and Aronson, 2002; Weil et al, 2002, 2009; Cróquer et al, 2005; Miller et al, 2009; Bastidas et al, 2012) During this period, the names WPD III and WPD II were used without consistent criteria; and they were even exchanged until the pathogen of WPD-II was described by Denner et al (2003). The presumed putative pathogen Aurantimonas coralicida was not found in analyses of diseased tissue samples from different localities over the years, further indicating inconsistency for the pathogen identification (Sunagawa et al, 2009); the term
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