RWD vs. Parrot fish predation??

[Dr. Ernesto Weil]

To Coral List readers interested in Rapid wasting disease and parrot fish
predation
From:  Andrew and Robin Bruckner, University of Puerto Rico

Parrotfish again:  remarks on photographs of RWD posted on the Coral List:

We have just returned from Curacao.  While following up on our YBD study,
we collected additional evidence that damage being attributed to RWD may be
caused by stoplight parrotfish.  We were fortunate to overlap with a
researcher from Groningen University who worked extensively on Sparisoma
viride in Bonaire.   This parrotfish expert, together with one of the
coauthors of the RWD theory working out of CARMABI, made for stimulating
conversation.  We were grateful for the opportunity to share our
observations and photographs with both of them.  We thank Reef Care Curacao
for taking us to East Point during their surveys for ReefKeeper
International; several of the staff witnessed firsthand parrotfish
predation on Montastraea annularis colonies they believed to exhibit signs
of  RWD. 

We have examined the photographs posted on the internet.  The damage
depicted is consistent with what we have directly observed Sparisoma viride
to inflict, and we have similar photos from Bonaire, Curacao and Puerto
Rico illustrating this.  Some of our photos capture the fish in action,
with the mouth of one or more fish, usually terminal phase, clearly biting
live tissue from the tops of  M. annularis colonies.   Unlike other
parrotfish which tend to scrape at the substrate, S. viride is an
excavator, preferring concave substrata over flat surfaces.  The
similarities of  rapid tissue and skeletal destruction on Montastraea sp.
and C. natans are striking, and observed for both RWD and S. viride.  We
suggest that much of the damage attributed to RWD may be caused by S.
viride.  

While we have observed parrotfish to take single bites from undamaged
corals, leaving lesions similar to the close-up photograph of  the coral
with new signs of RWD posted , we have not seen the initial stage of RWD
affecting a single polyp, as described by Goreau et al in an earlier
correspondence.   The second photo of  the same M. annularis after 24 hours
DOES exhibit characteristic bite marks, in the horizontal direction (middle
right side of lesion), identical to those made by stoplight parrotfish!
The macro shot clearly shows the sharp interface between irregularly eroded
skeleton and apparently healthy tissue with no signs of necrosis or pigment
loss, which is consistent with lesions created by mechanical damage, be it
parrotfish or anchor damage.  

We have many questions concerning RWD, and are looking forward to the visit
by J. Cervino to Puerto Rico scheduled for December so we can share more
information.  We are interested in the rate of RWD advance between day and
night.  We suspect "RWD" progresses over a coral primarily during daylight
hours, with little, if any damage at night.  We feel it is unlikely that a
microorganism could modify the pH and maintain an acidity capable of
dissolving calcium carbonate in sea water at such a rapid rate as observed
with RWD.  We are curious about the "bucket and aquaria" studies referred
to previously - Do tissue AND skeleton of corals with RWD continue to
dissolve away when placed in buckets of sea water ?, Is this associated
with a change of pH of the sea water in the buckets?  Have corals with the
initial stages of RWD been placed in aquaria or buckets?  

We have observed S. viride biting many species:  Montastraea annularis, M.
faveolata, M. cavernosa, Diploria labyrinthiformis, D. strigosa, Meandrina
meandrites, Porites porites, P. astreroides, Millepora complanata, Eusmilia
fastigiata, Colpophyllia natans, Acropora palmata and Madracis mirabilis.
These fish leave characteristic bite marks on species such as A. palmata
and P. astreoides, while they often remove only the branch tips from
Madracis, P. porites, Millepora and Eusmilia.  On corals with low density
skeletons such as  Montastraea spp. and C. natans, we have observed large
TP and IP fish return to the same coral repeatedly throughout the day,
producing overlapping bites at the interface of tissue and skeleton.  These
fish predominantly bite at the elevated portions of  M. faveolata (and M.
franksi),  or on the edge of the coral.  S. viride characteristically
remove all tissue from the tops of individual lobes of M. annularis; an
uneven, etched band of tissue always remains at the base or within a
depression of the lobe.  In subsequent dives to the same location, we
observed  S. viride biting at live tissue of adjacent, previously undamaged
lobes on the same colony or an adjacent coral. The fish do not always
approach and bite head on, but often turn their bodies and angle their
bites - they open their moth widely, grab onto a protrusion and by sideways
twisting motions of the head they are able to break off pieces. Repeated
bites by several fish in the same area, as well as bites taken from
different angles, do not always leave well defined bite marks, especially
on low density, relatively "soft" skeletons.   Instead, the live coral
interface may have a jagged or etched, and often crumbly appearance.  We
have photographs of similar damage from the early 1990's, and suggest that
this type of tissue destruction and skeletal erosion is not a new
phenomenon; entire corals are rarely killed. 

We urge anyone who thinks they have observed the Montastraea spp. and  C.
natans with patches of recent, white eroded skeleton lacking any algal
colonization and bordering live, apparently healthy coral tissue, to
observe the corals from a respectful distance, close to the reef rather
than up in the water column, for the length of a dive to rule out the
possibility of predation by  S. viride. 

Andrew and Robin Bruckner          arbruckner at hotmail.com