*4.2. The Health of Coral Reefs along the North Coast of Timor-Leste*

The prevalence of disease and compromised coral health was expected to be greater at urban sites with larger nutrient input and greater δ15N values at the shallow 5 m transects. Contrary to expectations, disease was highest at Rural-N at 5 m, with levels of WS at ~1% in both survey years. The low levels of disease detected in the current study agree with previous surveys [102,112], although no previous studies were specifically quantifying disease and compromised health. WS was the main pathology consistently observed during surveys. The WS documented at Rural-N was likely an infectious disease [26] and in the Indo-Pacific, WS is known to target acroporids [26,29,113]. Signs of WS spreading between acroporid corals were observed in the field. The pathogen causing WS at Rural-N is unknown but was likely *Vibrio* spp. a genus of bacteria that have been associated with diseases of multiple organisms including corals and humans [114–120]. Additionally, there was a positive association between host abundance and disease prevalence. This follows the classic density-dependent host–pathogen relationship [90–92]. In this study, all but one case of WS were found on acroporids. Rural-N had the highest density of Acroporids and 13 of the 17 recorded WS cases in 2015 and all 10 cases in 2017 were documented at this site [24,29,121,122]. The few cases of coral tissue mortality at other sites could have been from other causes such as unidentified predation; however, the pattern of distribution of corals affected by WS at Rural-N indicated that it was caused by an infectious pathogen.

There was likely coral mortality caused by the WS, inferred from the proportion of dead coral on some colonies (Figure 2a) [123,124], but this was likely not responsible for the decrease in coral cover in Rural-N. WS has the capacity to significantly decrease coral cover through mortality, which is associated with a much higher disease prevalence (>30%) [79]. Additionally, prevalence of WS did not differ between depths (Figure 5) and there was an increase in coral cover at Rural-N 10 m; thus, the changes in coral cover could be attributed to spatial heterogeneity recorded on non-permanent transects. WS recorded here is likely typical background levels of disease comparable to other CT locations, not an outbreak. The prevalence of WS, however, should continue to be monitored [122,125–128]. The low prevalence of coral disease in the CT supports the disease-diversity hypothesis which predicts that higher host species diversity will decrease the severity of outbreaks of a specialist pathogen [129–131]. The majority (>50%) of cases of WS were on tabulate acroporids, which are known to be the most susceptible to this syndrome. Four different acroporid morphologies were documented with WS during surveys likely encompassing different acroporid species with variable resistance to WS.

WS is a dynamic disease and can occur in outbreaks devastating acroporid populations [26,132] and thus altering overall coral community structure [132]. WS outbreaks have been linked to sediment plumes from dredging, terrestrial runoff, and elevated ocean temperature [29,30,133,134]. This is especially relevant given the recent global bleaching event and expected increase in the prevalence and severity of marine diseases given continued ocean warming [135]. A significant relationship between WS and coral bleaching co-infection was found on the GBR during the 2016–2017 global bleaching event. *Acropora* colonies that exhibited both WS and bleaching had seven times more tissue loss than solely bleached colonies [79]. Cooler temperatures could have been a protective factor against outbreaks of WS in Timor-Leste given the cooler subsurface temperatures on reefs compared to SST during the wet season. This phenomenon also coincides with the yearly ocean temperature maximum which is when corals would be most prone to bleaching. Increased sedimentation from catchments, however, is a continued threat as watersheds

in Timor-Leste are degraded [20,136]. Future work assessing the downstream impacts of sedimentation on reefs and coral health is warranted.

The number of indicators of compromised health exceeded the prevalence of disease at surveyed sites. Rural-N at 5 m had the highest prevalence of non-coral invertebrate overgrowth (Figure 5); this could be explained by greater coral cover eliciting more coral-invertebrate interactions, as the cover of invertebrates was comparable between all sites. The infestation of flatworms was found at all sites, except Urban-W 10 m, with a prevalence similar to that reported from Indonesia [122] including some severe cases (Figure 2c). Although their role in coral reef environments is not well understood, flatworms consume coral mucus, reduce heterotrophic feeding, and at high densities inhibit photosynthesis [137–139]. There was also a notable absence of turf overgrowth at Rural-N, while the remaining sites had high levels which could be indicative of depauperate herbivore communities or elevated nutrients at these locations [140,141]. Competitive interactions between corals and other organisms such as boring barnacles, CCA overgrowth, and turf overgrowth were more commonly found on genera with massive morphologies such as *Platygyra*, *Montastrea*, and massive *Porites*.
