Chapter25
DarkSpots Disease
Thierry M. Work and Ernesto Weil
History
Darkspots disease (DSD) was first documented in the early
1990s in the Islas del Rosario archipelago, Colombia, as a type of
bleaching disease that affected ca. 16% of Montastraea annularis
colonies; it was called Medallones Mostaza (mustard rings)
(Solano et al. 1993). In 1994, similar signs were observed at San
Andrs and Providencia archipelago (Colombian Caribbean)
mainly affecting M. annularis, Siderastrea siderea and
Stephanocoenia intersepta, and it was called enfermedad de los
lunares oscuros (Diaz et al. 1995) or darkspots disease (DSD).
Other names characterizing different manifestations of the dis-
ease include dark spots type I and type II and dark bands
(Weil 2004; Weil et al. 2006). Since the original discoveries in
Colombia, DSD has been found throughout the Caribbean
basin (Cervino et al. 2001; Weil et al. 2002). More recently, a
disease with lesions resembling DSD has been documented in
Brazil affecting Siderastrea (FranciniFilho et al. 2008) and in
the IndoPacific (Tutuila, America Samoa and Kahoolawe,
Hawaii), where Montipora and Pavona are the main coral genera
affected (Work et al. 2008).
The first detailed study of DSD in the Caribbean was car-
ried out in the Parque Nacional Natural Tayrona in Colombia.
Results showed that Montastraea annularis and Siderastrea
spp. had the highest prevalence of DSD (10 and 5%, respec-
tively) whereas the disease was much less common in
M.faveolata, M.franksi, S. intersepta and M. cavernosa (Gil
Agudelo 1998). Original descriptions of the darkspot lesions
were characterized as small, round, dark spots that appar-
ently grow in size over time, some of which can be associated
with a depression of the coral surface and others expand into
a dark ring surrounding dead coral (GarzonFerreira and
Gil 1998).
Distribution, Host Range and Prevalence
Darkspots disease has a widespread distribution around the
wider Caribbean and has been reported from 23 countries in the
region (Weil et al. 2002; Cervino et al. 2001; GilAgudelo et al.
2004; Weil 2004; Crquer and Weil 2009; Weil and Crquer
Diseases of Coral, First Edition. Edited by Cheryl M. Woodley, Craig A. Downs, Andrew W. Bruckner, James W. Porter and Sylvia B. Galloway.
2016 John Wiley & Sons, Inc. Published 2016 by John Wiley & Sons, Inc.
354
2009) (Fig. 25.1). The most recent reports of DSD are from
Brazil, affecting Siderastrea sp. (FranciniFilho et al. 2008) in
the IndoPacific where Pavona sp. and Montipora sp. have
manifested lesions resembling DSD (Fig. 25.1). The total
number of coral species affected has increased over time
mostly due to the expansion of surveys into many localities
in the regions increased observer awareness, or expansion
of host range. In the Caribbean, 16 important scleractinian
species have been reported to show signs corresponding to
those characterizing of the disease (Table25.1), and the dis-
ease appears less prevalent in the more northern portions of
theCaribbean (Cuba, Dominican Republic, Puerto Rico, US
Virgin Islands, Bahamas, and Florida) (GilAgudelo et al.
2004; Crquer and Weil 2009).
The first quantitative assessment of the spatial distribution
and prevalence of DSD was done during two consecutive years
in coral communities in the Tayrona National Park, Colombia
(GilAgudelo and GarzonFerreira 2001). Of 9398 colonies
(ramets) comprising 21 hard coral species examined, 1545
(16.44%) colonies comprising six species showed clear signs
ofDSD. Disease prevalence was high compared tothat of four
southwestern Caribbean atolls of the oceanic archipelago
of San Andrs and Providencia where DSD prevalence was
2.8%of 2110 hard coral colonies examined (GarzonFerreira
and Gil 1998). The two species most affected by DSD were
M.annularis (10.3%) and S. siderea (5.13%), with another four
affected species (M. faveolata, M. franksi, M. cavernosa and
S.intersepta) accounting for less than 1.1%. S. siderea appears
particularly susceptible to DSD in the wider Caribbean
(Fig.25.2).
In some regions, water depth and temperature appear to play
a role in the presence or absence of DSD. GilAgudelo and
GarznFerreira (2001) showed that DSD in Colombia was
more prevalent during periods of warm water (over 28C), and
at shallow depths less than 10m. Similarly in disease surveys
from the Cayman Islands and Curacao Crquer and Weil
(2009) found that populations of Siderastrea exhibited a
higher prevalence of DSD at intermediate (10m) depth habi-
tats (2540%) whereas Stephanocoenia populations were sig-
nificantly more affected by DSD in deeper (>15m) habitats
(2126%). In contrast, prevalence of DSD does not seem to be

Siderastrea siderea
Montastraea annularis
Montastraea faveolata
Stephanocoenia intersepta
Montastraea franksi
Colpophyllia natans
Montastraea cavernosa
10
Fig.25.1 Peak prevalence of DSD reported in literature for different species of corals in the Caribbean. Each dot represents reported peak prevalence
inreported in a journal article. Some points with identical prevalence within a species were randomly jiggered (Cleveland 1993) to enhance clarity.
SeeTable25.1 for references.
affected by depth in the Bahamas (Gochfeld et al. 2006).
Furthermore, this threeyear study showed a higher prevalence
during January to September but a decline in October. Studies of
DSD in Dominica did not reveal any relation between tempera-
ture, wave height, depth, and current patterns. The lack of a
direct correlation between temperature and disease prevalence
indicated that there might be other seasonal factors contribut-
ing to increases recorded during the summer months in
Dominica (Borger 2003). In a threeyear study in Dominica,
prevalence of DSD increased over time in S. siderea and affected
mainly larger size classes, but no seasonality was seen (Borger
and Steiner 2005). After two years of monitoring Borger and
Steiner (2005) suggested that DSD may be a general stress
response of S. siderea that is exacerbated by an increase in
water temperature thereby illustrating geographic differences
in environmental conditions conducive to development of
DSD. Brandt and McManus (2009) showed that DSD predis-
poses S. siderea from Florida to bleaching events.
For S. siderea, sizes of colonies affected by DSD and their dis-
tribution within a reef can vary between regions. In Dominica,
medium to large size class colonies were most often affected by
DSD, and affected colonies showed a clustered distribution sug-
gesting it could be communicable (Borger 2003); a similar clus-
tering phenomenon was observed in the Bahamas (Voss and
Richardson 2006) and Colombia (GilAgudelo et al. 2004).
However, there does not seem to be a relationship between size
of colony and presence of DSD in the Bahamas (Gochfeld et al.
2006). Borger (2003) did not find any correlation between dis-
ease prevalence and abundance of S. siderea, the only species
affected in Dominica.
In the IndoPacific, DSD has been documented in Pavona
varians and P. maldivensis from Hawaii and in P. varians,
Psamocora nierstrazi and Montipora sp. from Tutuila,
American Samoa (Work et al. 2008). Systematic studies to
assess prevalence and impact of this disease in this region have
not been done.
DarkSpots Disease355
20 30 40 50 60
Peak prevalence (%)
Etiology
The cause of darkspots disease remains unknown. GilAgudelo
et al. (2004) examined bacterial flora of mucus in corals affected
with DSD and found that diseased corals were infected with
Vibrio carchariae whereas this bacterium was absent in normal
corals. Experimental infections of corals in the field using this
bacterium failed to replicate DSD. In the same study corals main-
tained in aquaria incidentally developed DSD, and treatment with
fluoroquinolone antibiotics led to progression of lesions and tis-
sue loss thereby arguing against a bacterial etiology for DSD (Gil
Agudelo et al. 2004). Bacterial flora of M. annularis, M. faveolata,
and S. siderea, affected with DSD differed from normal tis-
sues; however, field experiments involving inoculating corals
with bacteria isolated from DSD lesions failed to reproduce
the disease (GilAgudelo et al. 2007). In the IndoPacific, his-
topathology has revealed unidentified endolithic fungi asso-
ciated with DSD lesions in P. varians and P. maldivensis from
Hawaii and in P. varians, P. nierstrazi and Montipora sp. from
American Samoa (Work et al. 2008). In the Caribbean, similar
microscopic findings have been noted in S. siderea from
Florida (Galloway et al. 2007).
Incubation, Morbidity and Mortality
The most complete study on the pathogenesis of darkspots dis-
ease was done by GarcesBaquero (2000) who found that lesions
within colonies of M. annularis and S. siderea spread slowly
(<2cm/month) and that rate of tissue loss was equally slow
(<1cm/month), with very little regeneration of tissues. Other
studies have shown regeneration of tissues in DSDaffected
corals (Borger, 2005; Gochfeld et al. 2006). Lesions could persist
for years, and in some species such as S. intersepta, the disease
appeared to progress faster (GarcesBaquero, 2000; GilAgudelo
et al. 2004). Borger (2003) reported DSD having the highest
356Diseases of Coral

(a) (b) (c)

(d) (e) (f)

(g) (h) (i)

(j) (k) (l)

(m) (n) (o)

Fig.25.2 Gross lesions of darkspots disease in the species mainly affected in the Caribbean. Lesion sign variability in S. siderea showing multiple focal
points (a, b), the depressed areas (c, d), tissue mortality in advanced stages of the disease (e), and purple bands advancing from colony edges to the center
leaving dead tissue behind (f). Small DSD lesions in M. annularis (g) that develop into larger spots (h, i) and then form bands when tissue starts to die (h).
DSD in M.faveolata (j, k) in Puerto Rico and M. franksi (l) in Bermuda, and in S. intersepta in Venezuela (mo). Source: Photographs: Ernesto Weil.

Table25.1 Species reported with gross lesions resembling DSD.
Species References
Agaricia agaricites GilAgudelo 1998; Weil 2004; Ward et al.
2006
Colpophyllia amaranthus Weil 2004
Colpophyllia natans GarzonFerreira and Gil 1998; Weil 2004
Dichocoenia stellaris Weil 2004
Dichocoenia stokesii Weil 2004
Diploria labyrinthiformis Weil 2004; Ward et al. 2006
Diploria strigosa GilAgudelo et al. 2004; Weil 2004
Isophyllastrea rigida GarznFerreira et al. 2001
Meandrina meandrites GarznFerreira et al. 2001; Weil 2004
Meandrina memorialis Weil 2004
Montastraea annularis Solano et al. 1993; GarznFerreira and Gil,
1998; GilAgudelo 1998; GarznFerreira
etal. 2001; GilAgudelo and GarznFerreira,
2001; Weil 2004; Ward et al. 2006
Montastraea cavernosa GarznFerreira et al. 2001; GilAgudelo and
GarznFerreira 2001; GilAgudelo et al.
2004; Weil 2004; Ward et al. 2006
Montastraea faveolata GarznFerreira and Gil, 1998; Garzn
Ferreira et al. 2001; GilAgudelo and
GarznFerreira, 2001; Weil 2004; Ward et al.
2006
Montastraea franksi GarznFerreira and Gil 1998; GilAgudelo
and GarznFerreira 2001; Weil 2004; Ward
et al. 2006
Montipora sp.* Work et al. 2008
Pavona maldivensis* Work et al. 2008
Pavona varians* Work et al. 2008
Psammocora nierstraszi* Work et al. 2008
Siderastrea radians Weil 2004; Kaczmarsky et al. 2005; Ward
etal. 2006
Siderastrea siderea* Solano et al. 1993; Diaz et al. 1995;
GarznFerreira and Gil, 1998; Cervino et al.
2001; GarznFerreira et al. 2001; Gil
Agudelo and GaronFerreira, 2001; Borger
2003; Weil 2004; Borger and Steiner 2005;
Kaczmarsky et al. 2005; Gochfeld et al. 2006;
Voss and Richardson 2006; Ward et al. 2006;
Galloway et al. 2007; FranciniFilho et al.
2008
Stephanocoenia intersepta Solano et al. 1993; Diaz et al. 1995;
GarznFerreira and Gil, 1998; GilAgudelo,
1998; Cervino et al. 2001; GarznFerreira
etal. 2001; Weil 2004; Borger 2005
Note: Asterisks indicate species where endolithic fungi associated with DSD
have been confirmed histologically.
average number of lesions per colony (13.3 1.6, n = 100) but
these affected the smallest amount of tissue per colony (120%,
n = 100). Even though rates of advance have been reported to be
generally low, Cervino et al. (2001) reported rates of up to 4cm/
month. DSD generally does not appear to cause colony mortality
except, perhaps, for A. agaricites (GilAgudelo et al. 2004) when
the disease caused extensive mortalities of this species over a
one year period in Colombia. In Dominica, there was no tissue
mortality associated with six tagged colonies over a period of
two years suggesting that the overall impact of DSD in terms of
causing significant coral tissue and colony loss might be low
DarkSpots Disease357
(Borger 2005). Similar findings have been documented in the
Bahamas (Gochfeld et al. 2006). In contrast, Cervino et al.
(2001) observed that coral tissues affected by DSD did not
recover. Correa et al. (2009) found that S. siderea tissues with
DSD had reduced amounts of clade D zooxanthellae compared
to nondiseased tissues. No information exists on the pathogen-
esis or lethality of this disease in corals from the IndoPacific.
Gross Lesions
Darkspots disease is characterized grossly by focal to multifo-
cal distinct brown to purple, round to amorphous to oblong
areas of discoloration with smooth to gently undulating edges
(Figs.25.225.3). Lesions range in size from 15cm that some-
times coalesce into larger regions. In some cases the center of
these discolored areas may manifest chronic tissue loss with
overgrowth of skeleton by turf algae. In apparently more
advanced cases, there are central indentations of the skeleton
colonized by turf algae and bordered by an irregular distinct
band of dark discoloration ranging from 13cm in width
(Fig.25.3). Cervino et al. (2001) found that skeleton of S. siderea
affected by DSD was pigmented whereas this was not the case in
S. intersepta.
Histopathology
Histopathology of DSD has been done on S. siderea from the
Caribbean and in P. varians, P. maldivensis, P. nierstrazi and
Montipora sp. from the IndoPacific. In corals from the Indo
Pacific, the skeleton is diffusely invested with mats of filamen-
tous irregular walled branching structures that stain positive
with Grocotts methenamine silver confirming them as fungi
(Fig.25.3h). In some cases, fungal mats efface tissue architecture,
and adjacent tissues are fragmented and necrotic. In other cases
diffuse areas of polyps and coenosarcs (coenenchyme) overlying
mats of fungi manifest atrophy of the epidermis and gastroder-
mis with depletion of zooxanthellae from gastrodermis
(Fig.25.3g) (Work et al. 2008). Similar lesions have been noted in
one S. siderea from the Caribbean (Galloway et al. 2007). In the
Caribbean, tissues of S. michelinii affected with DSD had an
increase in zooxanthellae pigments (Cervino et al. 2001).
Immunity
There are no data on immunology of this disease in corals.
Diagnosis
Current criteria to confirm dark spots require both gross and
microscopic observations. Grossly, affected corals manifest focal
to multifocal distinct brown to purple round to amorphous to
 (a) (b)

(c) (d)

(e) (f)

(g) (h)

Fig.25.3 Corals from American Samoa with DSD gross (ad) and microscopy (eh). (a, b) Pavona varians, (c) Psammocora nierstrarzi, (d) Montipora sp.,
(e) Pavona variansnote mats of fungal hyphae (black arrow) effacing normal coral tissues (arrowhead), and nidus of necrosis (white arrow).
Hematoxylin and eosin, Bar = 200m. (f) Psammocora nierstrarzsinote mats of fungal hyphae (arrow) within skeleton. Hematoxylin and eosin,
Bar = 200m. (g) Close up of white rectangle in (d). Note fungal hyphae (arrow) invading skeleton. Hematoxylin and eosin, Bar = 50m. (h) Same as (g).
Note mesenterial filament (mf) and fungal hyphae (arrowhead). Grocotts methenamine silver stain, bar = 50m. Source: Photographs: Thierry Work.

oblong areas of discoloration (Fig.25.3). These range in size from
110cm and sometimes coalesce. In some cases the discolored
areas are depressed (either growing slower than the rest of the
colony or experiencing decalcification), or the center of these
discolored areas may manifest chronic tissue loss with overgrowth
by turf algae and associated central indentation of the skeleton.
On microscopy, there is evidence of endolithic fungi that may
ormay not be associated with tissue necrosis (Work et al. 2008).
The fungus associated with this lesion has not been cultured
in the laboratory; therefore, its role in causing DSD awaits
confirmation.
Prevention and Control
There is insufficient information to prevent or control this
disease at this time.
Research Needs
The current case definition of dark spots hinges on the presence
of characteristic gross lesions with confirmation of fungal over-
growth of skeleton by histopathology. In regards to epizootiol-
ogy, the disease clearly has a widespread distribution and wide
host range, however, its role in causing mortality of colonies is
less clear, and its overall impact at the population and commu-
nity level appears limited. Limited studies on pathogenesis of
disease at the gross level in Colombia (GilAgudelo et al. 2004)
suggest that it progresses slowly and does not appear to kill coral
colonies except for selected species such as A. agaricites. Borger
and Steiner (2005) found no tissue mortality in tagged colonies
of S. siderea over a twoyear period. Similar studies should be
done in other geographic regions and include all affected taxa to
confirm this phenomenon and to determine whether this dis-
ease has significant demographic effects.
The behavior of this disease (slow progression, chronicity)
and the microscopic pathology are suggestive of a fungal patho-
gen as a potential cause; however, this needs to be confirmed
experimentally by culturing the fungus and carrying out experi-
mental infections in controlled settings. Corals have many
endolithic organisms such as algae and fungi that, together with
the bacterial community, make up a normal portion of the skel-
etal flora, and it is currently unclear whether DSD is a result of
overgrowth of existing endolithic flora or whether the fungus is
an invasive organism not normally present. Characterizing the
normal skeletal fungal biota of apparently healthy corals may
help shed light on some of these questions. Nevertheless, in stud-
ies of tagged colonies in Puerto Rico, S. siderea and C. natans,
DSD waxes and wanes with lesions progressing and regressing.
On the other hand, colonies of M. annularis, M. faveolata and
S.intersepta do not show this variability, and in these species,
lesions will persist and progress to tissue loss at low rates (Weil,
unpublished). Clearly, future investigations should take into
DarkSpots Disease359
account not only the putative fungal pathogen but variations in
host response to infection.
The focal to multifocal distribution of lesions is an interesting
phenomenon and bears further inquiry. In some instances, tis-
sues overlying areas of dark spot are atrophied. One possible
mechanism of disease may involve a primary insult that leads to
focal atrophy of tissues and depletion of zooxanthellae from gas-
trodermis, which can slow growth and then allow overgrowth of
endolithic fungi either because of increased available light or
decreased host defenses. Careful observations with sequential
sampling of lesions over time in a controlled setting should help
answer such questions.
If the etiology of dark spots is determined, field investigations
need to be done to determine the drivers of the etiologic agent
in causation of disease in various hosts. If the disease truly has
adverse demographic impacts to corals, then measures would
need to be implemented to mitigate the environmental drivers
that lead to origination and progression of lesions in corals.
Summary
Darkspots disease is a chronic slowly progressing disease
affecting multiple species of corals throughout the Caribbean
basin, some Brazilian reefs, and in selected locations in the
IndoPacific and Red Sea.
Siderestrea sp. appear disproportionately susceptible, and the
disease waxes and wanes but rarely causes complete colony
mortality.
Available evidence suggests a fungus may be associated with
DSD in the Pacific and the Caribbean, however, its role in
causation remains to be confirmed.
References
Borger, J. (2003) Three scleractinian coral diseases in Dominica, West
Indies: Distribution, infection patterns and contribution to coral tis-
sue mortality. Revista de Biologia Tropical 51, 2538.
Borger, J. (2005) Scleractinian coral diseases in south Florida: Incidence,
species susceptibility, and mortality. Diseases of Aquatic Organisms
67, 249258.
Borger, J. and Steiner, S. (2005) The spatial and temporal dynamics of
coral diseases in Dominica, West Indies. Bulletin of Marine Science
77, 137154.
Brandt, M. and McManus, J. (2009) Disease incidence is related to
bleaching extent in reefbuilding corals. Ecology 90, 28592867.
Cervino, J., Goreau, T., Nagelkerken, I., et al. (2001) Yellow band and
dark spot syndromes in Caribbean corals: Distribution, rate of spread,
cytology, and effects on abundance and division rate of zooxanthellae.
Hydrobiologia 460, 5363.
Cleveland, W. (1993) Visualizing Data. Hobart Press, Summit, NJ.
Correa, A., Brandt, M., Smith, T., et al. (2009) Symbiodinium associa-
tions with diseased and healthy scleractinian corals. Coral Reefs 28,
437448.
360Diseases of Coral
Crquer, A. and Weil, E. (2009) Changes in Caribbean coral disease
prevalence after the 2005 bleaching event. Diseases of Aquatic
Organisms 83, 209222.
Diaz, J., GarzonFerreira, J. and Zea, S. (1995) Los arrecifes coralinos de
la isla de San Andres, Colombia: estado actual y perspectivas para su
conservacion, Academia Colombiana de Ciencias Exactas, Fisicas, y
Naturales, Colleccion Jorge Alvarz Lleras, Bogota.
FranciniFilho, R., Moura, R., Thompson, F., et al. (2008) Diseases lead-
ing to accelerated decline of reef corals in the largest South Atlantic
reef complex (Abrolhos Bank, eastern Brazil). Marine Pollution
Bulletin 56, 10081014.
Galloway, S., Work, T., Bochsler, V. et al. (2007) Coral disease and health
workshop: Coral histopathology II. National Oceanic and Atmospheric
Administration, Silver Spring, MD.
GarcesBaquero, A. (2000) Desarollo de la enfermedad de Lunares
Oscuros en los corales petreos Montastrea annularis y Siderastrea
siderea en la Bahia de Gayraca, Caribe colombiano Marine Biology.
Bachelors thesis. Bogota, Fundacion Universidad de Bogota Jorge
Tadeo Lozano.
GarznFerreira, J. and Gil, D. (1998) Another unknown Caribbean
coral phenomenon? Reef Encounters 24, 10.
GarznFerreira, J., GilAgudelo, D., Barrios, L., et al. (2001) Stony
coral diseases observed in southwestern Caribbean reefs.
Hydrobiologia 460, 6569.
GilAgudelo, D. (1998) Caracteristicas, incidencia y distribucion de la
enfermedad de Lunares oscuros: en corales petreos del Parque
Nacional Natural Tayrona, Caribe colombiano. B.Sc. thesis. Marine
Biology, Universidad de Bogota Jorge Tadeo Lozano, Bogota.
GilAgudelo, D. and GarznFerreira, J. (2001) Spatial and seasonal vari-
ation of dark spots disease in coral communities of the Santa Marta
area (Colombia Caribbean). Bulletin of Marine Science 69, 619629.
GilAgudelo, D., Smith, G., GarznFerreira, J., et al. (2004) Dark spots
disease and yellow band disease, two poorly known coral diseases with
high incidence in Caribbean reefs, in Coral Health and Disease (eds
E.Rosenberg and Y. Loya). Springer, Berlin, Germany, pp. 337341.
Gochfeld, D., Olson, J. and Slattery, M. (2006) Colony versus population
variation in susceptibility and resistance to dark spot syndrome in the
Caribbean coral Siderastrea siderea. Diseases of Aquatic Organisms
69, 5365.
Kaczmarsky, L., Draud, M. and Williams, E. (2005) Is there a relation-
ship between proximity to sewage effluent and the prevalence of coral
disease? Caribbean Journal of Science 41, 124137.
Solano, O., Navas, G. and MorenoForero, S. (1993) Blanqueamiento
coralino de 1990 en el Parque Nacional Natural Corales del Rosario
(Caribe colombiano). Anales del Instituto de Investigacion del Mar,
Punta de Betin 22, 97111.
Voss, J. and Richardson, L. (2006) Coral diseases near Lee Stocking
Island, Bahamas: Patterns and potential drivers. Diseases of Aquatic
Organisms 69, 3340.
Ward, J., Rypien, K., Bruno, J., et al. (2006) Coral diversity and disease
in Mexico. Diseases of Aquatic Organisms 69, 2331.
Weil, E. (2004) Coral reef diseases in the wider Caribbean, in Coral
Health and Disease. (eds E. Rosenberg and Y. Loya). Springer, Berlin,
pp. 3568.
Weil, E. and Crquer, A. (2009). Local and geographic variability in dis-
tribution and prevalence of coral and octocoral diseases in the
Caribbean I: Communitylevel analysis. Diseases of Aquatic Organisms
83, 195208.
Weil, E., Smith, G. and GilAgudelo, D. (2006) Status and progress in
coral reef disease research. Diseases of Aquatic Organisms 69, 17.
Weil, E., Urreiztieta, I. and GarznFerreira, J. (2002) Local and
Geographic Variability in the Incidence of Disease in Western Atlantic
Coral Reefs, in Proceedings of the Ninth International Coral Reef
Symposium, Vol. 2 (eds M. Moosa, S. Soemodihardjo, A. Soegiarto,
et al.). International Society for Reef Studies, Bali, Indonesia,
pp.12311238.
Work, T., Aeby, G., Stanton, F., et al. (2008) Overgrowth of fungi
(endolithic hypermycosis) associated with multifocal to diffuse
distinct dark discoloration of corals in the IndoPacific. Coral
Reefs 27, 663.