Im not sure which paper you put up - but there seems to be a fair bit of research on it:
https://onlinelibrary.wiley.com/doi/full/10.1111/mec.13097
( all samples of the disease were specifically associated with the histophagous ciliate
Philaster lucinda. From the pattern of disease progression and histopathology in relation to the selective elimination of microbial groups,
we conclude that these ‘white’ diseases are a result of a nonspecific bacterial infection and a ‘secondary’ infection by the P. lucinda ciliate. Although we have not observed the initiation of infection, a nonspecific, multispecies bacterial infection appears to be a corequirement for WS lesion progression and we hypothesize that the bacterial infection occurs initially, weakening the defences of the host to predation by the ciliates.)
(
Philaster lucinda shared 100% sequence similarity of 596 base pairs to the recently described ciliate (Morph 1) associated with WS in both the Great Barrier Reef and the Solomon Islands (Sweet & Bythell
2012).
This species was absent in all four samples treated with metronidazole, even though the lesion continued to progress in those treatments. However, the advance rate of the lesion slowed from an average of 0.16 to 0.08 cm−3 per day. Furthermore, the exposed skeleton on corals treated with metronidazole was discoloured and the lesion boundary did not exhibit the sharp demarcation, as is characteristic of this disease (Sweet & Bythell
2012).
This result suggested a different pathology occurred with the absence of this ciliate species.)
http://www.korallionlab.com/wp-content/uploads/2012/05/Sweet_and_Sere_2015.pdf
(Here we show that a
wide variety of ciliates are associated with all nine coral diseases assessed. Many of these ciliates such as Trochilia petrani and Glauconema trihymene
feed on the bacteria which are likely colonizing the bare skeleton exposed by the advancing disease lesion or the necrotic tissue itself. Others such as Pseudokeronopsis and Licnophora macfarlandi are common predators of other protozoans and will be attracted by the increase in other ciliate species to the lesion interface. However, a few ciliate species (namely Varistrombidium kielum, Philaster lucinda, Philaster guamense, a Euplotes sp., aTrachelotractus sp. and a Condylostoma sp.) appear to harbor symbiotic algae, potentially from the coral them- selves, a result which may indicate that they play some role in the disease pathology at the very least.
Although, from this study alone we are not able to discern what roles any of these ciliates play in disease causation, the con- sistent presence of such communities with disease lesion interfaces warrants further investigation.)
