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465
Z. Dubinsky and N. Stambler (eds.), Coral Reefs: An Ecosystem in Transition,
DOI 10.1007/978-94-007-0114-4_27, © Springer Science+Business Media B.V. 2011
1 Introduction
Coral reefs are the jewels of the tropical oceans. They boast
the highest diversity of all marine ecosystems, aid in the
development and protection of other important, productive
coastal marine communities, and have provided millions of
people with food, building materials, protection from storms,
recreation and social stability over thousands of years, and
more recently, income, active pharmacological compounds
and other benefits. These communities have been deteriorat-
ing rapidly in recent times. The continuous emergence of
coral reef diseases and increase in bleaching events caused in
part by high water temperatures among other factors under-
score the need for intensive assessments of their ecological
status and causes and their impact on coral reefs.
In the last few decades, coral reefs around the world
have experienced significant declines with changes in com-
position, structure, and function attributable to one or more
natural and anthropogenic interacting factors (Harvell et al.
1999, 2005, 2007; Hoegh-Guldberg 1999; Ostrander
et al. 2000; Hayes et al. 2001; Jackson et al. 2001; Gardner
et al. 2003; Hughes et al. 2003; Pandolfi et al. 2003; Weil
et al. 2003; Willis et al. 2004; Weil 2004; Sutherland et al.
2004; Wilkinson 2006; Rogers and Miller 2006; Hoegh-
Guldberg et al. 2007; Lesser et al. 2007; Rogers et al.
2008a, b; Miller et al. 2009; Cróquer and Weil 2009b). The
effect of each factor, or combination of factors, varies
within regions and across time. A recent report indicated
that 32% of zooxanthellate scleractinian corals face an
elevated risk of extinction due mainly to bleaching and
disease that seem positively and significantly correlated
with elevated sea water temperature and further exacerbated
by local anthropogenic stressors (Carpenter et al. 2008).
A significant die-off of acroporids and other corals in the
Florida Keys and the Dry Tortugas occurred during severe
cold weather in the winter of 1977–1978 (Roberts et al.
1982). Some presumably minor restricted disease outbreaks
that occurred in the 1970s in the Florida Keys and the Virgin
Islands were followed by two apparently concurrent biotic,
wide-geographic epizootic events during the late 1970s and
early 1980s. [An epizootic or disease outbreak is defined as
“an unexpected increase in disease or mortality in a time or
place where it does not normally occur or at a frequency
greater than previously observed” (Wobeser 1994; Work
et al. 2008a, b; Woodley et al. 2008)]. The white band dis-
ease (WBD) outbreak affected Acropora palmata and
A. cervicornis, two of the most abundant and important reef-
building corals in the region (Gladfelter 1982), and an
unknown pathogen produced the mass-mortality of the black
sea urchin Diadema antillarum, an important and abundant
species in all tropical and subtropical shallow marine habi-
tats of the western Atlantic and Caribbean (Lessios et al.
1984a, b). Coral and sea urchin populations experienced over
90% mortalities over their geographic range, resulting in sig-
nificant losses in genetic diversity, coral cover, and spatial
heterogeneity of coral reefs across the Caribbean.
Almost 30 years after these events, the affected coral and
urchin species have not recovered to their former densities
and populations structures in reefs off Puerto Rico (Weil
et al. 2003, 2005). Furthermore, hurricanes, storms, and two
major widespread bleaching events in 1998 and 2005 led to
further localized mortalities of surviving acroporids and
other major reef-building species (Miller et al. 2006, 2009;
Wilkinson and Souter 2008; McClanahan et al. 2009; Cróquer
and Weil 2009a).
Disease is considered here as “any impairment to health
resulting in physiological dysfunction,” involving an interac-
tion between a host, an agent i.e., pathogen, environment,
genetics, and the environment (Martin et al. 1987; Wobeser
1994). These three components must interact in a precise
way for disease to occur. This definition includes both non-
infectious (produced by genetic mutations, malnutrition,
and/or environmental factors), and infectious diseases (pro-
duced by pathogens). The host is the organism affected by
E. Weil (*)
Department of Marine Sciences, University of Puerto Rico,
P.O. Box 9000, Mayagüez, PR 00680, USA
e-mail: eweil@caribe.net
C.S. Rogers
USGS Caribbean Field Station, 1300 Cruz Bay Creek, St. John,
VI, 00830, USA
Coral Reef Diseases in the Atlantic-Caribbean
Ernesto Weil and Caroline S. Rogers
466 E. Weil and C.S. Rogers
the disease (e.g., coral, octocoral), the agent(s) is/are the
factor(s) that directly or indirectly cause(s) disease. Infectious
agents are capable of causing infection and may be transmis-
sible between hosts (Stedman 1976; Wobeser 2006). The
environment is considered to be the third factor of the dis-
ease triad and provides the stage where host–agent interac-
tions occur (Wobeser 2006; Work et al. 2008a, b).
In a recent controversial report, Lesser et al. (2007) empha-
sized the importance of the environmental drivers causing
disease outbreaks and questioned the generalized conclusion
that diseases of corals are caused by a primary pathogen and
are infectious in nature. They suggested that coral diseases
are most often a secondary phenomenon caused by opportu-
nistic pathogens after physiological stress produced by chang-
ing environmental conditions. Although it is important to
understand the role of environmental co-factors, which in
some cases could render corals more susceptible to disease, it
is important to exercise a balanced approach that would
increase our understanding of the interactions among host,
agent, and environment (Work et al. 2008b). By definition, “if
an organism develops an infectious disease, then there has to
have been some breakdown in host defenses to allow patho-
gens to establish. By this logic, all diseases (e.g., common
cold, TB, AIDS) are opportunist. The distinction that needs to
be made (and that we can make in other animals but not corals
yet) is whether we can measure or quantify the decrease in
host response prior to development of disease, and thus make
the case that this animal had a quantifiable suppression in
immune status before development of disease” (T. Work, per-
sonal communication 2010; Work et al. 2008a).
Studying diseases in the marine environment has proven to
be challenging. For example, it is difficult to collect samples
without contamination and variability in sample collection
methods may confound comparative results. Additionally,
most marine bacteria, possibly including pathogens, are diffi-
cult to culture or are unable to be cultured today, making their
identification, laboratory manipulation, and testing of Koch’s
postulates difficult. Even if a putative pathogen is identified,
testing which environmental variable or driver is responsible
for its emergence is extremely difficult. Furthermore, recent
evidence indicates that bacterial and fungal communities liv-
ing in association with coral tissues are highly dynamic and
different bacteria and fungi may produce similar physiological
responses (i.e., disease signs) (Ritchie 2006; Voss et al. 2007;
Toledo-Hernandez et al. 2008; Sunagawa et al. 2009).
Corals are “ecological communities” (holobionts), har-
boring high diversities and abundances of bacteria, zooxan-
thellae, endolithic algae, fungi, and other boring invertebrates
interacting in complex ways (Knowlton and Rohwer 2003;
Ritchie 2006; Kimes et al. 2010). Changes in environmental
conditions would presumably affect this physiological equi-
librium by changing the resident microbial community,
which could enhance susceptibility to infectious agents and/
or weakening of the host immune system, which could render
corals more susceptible to infection, or loss of zooxanthellae
(Harvell et al. 1999, 2002, 2007; Ritchie 2006; Mydlarz et al.
2009; Thurber et al. 2009). The compromised-host hypothe-
sis suggests that rising ocean temperatures may increase the
number and prevalence of coral diseases by making corals
more susceptible to ubiquitous pathogens or by causing shifts
in microbial communities making some of them pathogenic
(Rosenberg and Ben-Haim 2002).
Few quantitative studies have attempted to relate the
emergence, prevalence, and incidence of coral reef dis-
eases with deterioration/change in environmental quality.
This requires either large spatial and/or long temporal
scales to produce reliable results. Short-term studies, how-
ever, have established significant correlations between
increasing sea water temperatures and increases in preva-
lence of white syndrome (WS) and black band disease
(BBD) in the Great Barrier Reef (GBR), and prevalence
and virulence of Caribbean yellow band disease (YBD)
and white patches (Boyett et al. 2007; Bruno et al. 2007;
Weil 2008; Harvell et al. 2009; Muller et al. 2008; Weil
et al., in press).
Very little is known about the composition and dynamics
of the natural microbial communities living in association
with most reef organisms (but see Rohwer et al. 2001, 2002;
Rosenberg 2004; Ritchie 2006; Rosenberg et al. 2007; Lesser
et al. 2007; Sunagawa et al. 2009; Thurber et al. 2009). A
clear determination of causality, therefore, is difficult to
accomplish. This would require controlled experiments,
which is a problem when moving holobiont colonies or frag-
ments from the field into laboratory conditions. Natural
changes in composition of bacterial populations may follow
the initial infection by a disease-causing agent. Other bacteria
could become dominant and pathogenic producing similar
signs (Bourne et al. 2007; Voss et al. 2007; Toledo-Hernandez
et al. 2008; Sunagawa et al. 2009). The fact that some coral
epizootic events occurred over large geographic scales within
short periods of time, or simultaneously, suggests a response
of already present bacteria (or other pathogens) to similar
changes in environmental conditions favoring the infectious
disease outbreak. We are currently unable to fully explain the
source(s) and sudden emergence of the majority of diseases
and/or the outbreaks in coral reef organisms.
Fig. 1 (continued) aspergillosis and red band disease in G. ventalina (j, k), other compromised health conditions in E. caribbaeorum (i) and P.
nutans (l), and purple spots produced by an unknown protozoan (Labyrinthulomycote) in G. ventalina (m). Disease conditions in the hydrocoral M.
complanata (n), the vase sponge X. muta (o), the tubular sponge C. vaginalis (p) and the zoanthid P. caribbaeorum (q). Caribbean coralline lethal
orange disease (r) and crustose coralline white band disease in N. accretum (s) (Photos E. Weil)
467Coral Reef Diseases in the Atlantic-Caribbean
Fig. 1 Photographs of other conditions affecting Caribbean corals and other reef organisms. Growth anomalies in D. strigosa (a, b) (hyperplasia)
and A. palmata (c) (neoplasia) (photo courtesy of E. Peters), pigmentation responses from unknown conditions producing tissue mortality in M.
faveolata (d), S. siderea (e) and D. labyrinthiformis (f), white syndromes in S. siderea (g) and M. faveolata (h). Diseases in other Cnidarians include
468 E. Weil and C.S. Rogers
The goal of this chapter is to present a historical perspective
of diseases in coral reefs and a summary of the current distri-
bution and status of coral diseases in the Atlantic-Caribbean
along with recommendations for future research. There are
several other important biological members of the coral reef
community such as hydrocorals, sponges, zoanthids, sea
urchins, and crustose coralline algae (CCA) that are affected
by diseases (see Fig. 1) that will not be discussed in this chap-
ter for lack of space. They will be discussed in a future publi-
cation. We have adopted the coral reef disease nomenclature
recently updated in Work et al. (2008a), Raymundo et al.
(2008), Beeden et al. (2008), and Weil and Hooten (2008b).
2 Historical Perspective
Diseases of coral reef organisms have likely been around
for millions of years and may have produced significant
population mortalities in the past, but this cannot be con-
firmed in the fossil record. The emergence of coral reef
diseases in the Caribbean in the past few decades appears
to be unprecedented in the geological record. Limited
paleontological evidence suggests that the white band
disease (WBD) outbreak in the late 1970s, which killed
acroporid corals throughout their geographic distribution,
was unparalleled on a timescale of at least three millennia
(Aronson and Precht 2001a, b). Moreover, in recent years,
large colonies (many over 500 years old) of the other
main reef-building species in the region have succumbed
to single virulent diseases such as white plague disease
(WPD) and Caribbean yellow band disease (YBD), or the
combination of these and bleaching in short periods of
time, further indicating that this seems to be a recent and
expanding problem (Weil et al. 2006; Bruckner and Hill
2009; Weil et al. in press). However, a hiatus in A. pal-
mata accretion occurred 3,000 years ago and again 800
years ago over a wide geographic area. “Understanding
the causes of such large-scale community shifts provides
both opportunities and challenges with respect to unrav-
eling both natural and anthropogenic change” (Hubbard
et al. 2008).
2.1 Black Band Disease
The first scleractinian infectious disease reported in the
Caribbean was black band disease (BBD). It was first
observed in Belize, Bermuda, and Florida in the early 1970s
(Antonius 1973; Garrett and Ducklow 1975), but has since
been found throughout the wider Caribbean and the Indo-Pacific
(Antonius 1985; Willis et al. 2004; Galloway et al. 2007).
It is characterized by a dark bacterial mat of varying com-
position forming a band separating healthy-looking tissue
from the clean skeletal matrix (Table 1, Fig. 2a, b). Little
etiological work was done in the early days but information
on host range, mortality rates, and depth distribution was
provided. It is the better-known coral disease with a signifi-
cant number of studies expanding pathogeneses, etiology,
and epizootiology (Rützler and Santavy 1983; Rützler et al.
1983; Richardson 1997; Aeby and Santavy 2006; Richardson
et al. 2007), and including recent debates concerning the
variability of the microbial community composition (Voss
et al. 2007).
2.2 White Plague Diseases
The first report of a disease outbreak producing significant
coral mortalities occurred in Florida in 1975 and was referred
to as white plague type I. (WPD-I). It mainly affected the
plating coral Mycetophyllia ferox (Dustan 1977) leading to
fears of its disappearing from some areas in the Florida Keys.
During a second WPD-I epizootic event, colonies of M. ferox
were unaffected whereas massive Montastraea were affected
(Dustan 1999), suggesting resistant Mycetophyllia colonies
or a different causative agent. A third and more virulent out-
break of WPD occurred in the Florida Keys in 1995 mainly
affecting Dichocoenia stokesi and 16 additional species over
the next 2 years (Richardson 1998; Richardson et al. 1998a)
(Table 1, Fig. 2e, f). In this case, Aurantimonas coralicida
was isolated from WPD lesions and the disease termed white
plague disease type-II (WPD-II) (Richardson et al. 1998b;
Miller et al. 2001; Denner et al. 2003). In the late 1990s and
early 2000s, a fourth more virulent epizootic was termed
WPD-III and affected mostly Montastraea spp in Florida,
the Virgin Islands, Puerto Rico, and Venezuela (Richardson
and Aronson 2002; Weil 2002; Croquer et al. 2005). However,
the disease agent was not identified (Richardson and Aronson
2002) and the term WPD-III was discarded.
Another condition called shut down reaction (SDR) in
which tissue sloughed off quickly from coral colonies was
described in the mid 1970s (Antonius 1977), but was never
further studied and there have been no reports of this condi-
tion in the region in the last 2 decades.
2.3 White Band Disease and Diadema
Two years after the initial white plague epizootic, an outbreak
of a disease with similar signs but affecting only acroporids
called white band disease type I (WBD-I) devastated high
proportions of A. palmata and A. cervicornis (Fig. 2c, d) pop-
469
Coral Reef Diseases in the Atlantic-Caribbean
Table 1 Common coral reef diseases in the western Atlantic and acronym (ACR), year reported/observed (year), pathogen/agent (P/A) identified = Y, No = N, number of taxa showing disease
signs in corals (CO), octocorals (OC), hydrocorals (HY), sponges (SP), zoanthids (ZO) and crustose coralline algae (CCA) (number in parenthesis are Brasilian spp), depth distribution (DE),
average community prevalence (PR), tissue mortality rate (TM), and their geographic distribution (GD) (WA = western Atlantic, WC = wider Caribbean, VI = Virgin Islands, FL = Florida, BE =
Bermuda, CA = Caribbean, BA = Bahamas. ME = Mexico, PR = Puerto Rico), Updated from Weil et al. (2006) and other sources
Disease ACR Year P/A CO OC HY ZO SP CCA DE
PR (%)
TM GD
(m) (mm/day)
Bleaching BL 1911 N 62 29 5 2 8 0–100 .2–85 ? WA
Growth anomalies GA 1965 N 10 8 1 0–25 – – WC
Black band disease BBD* 1973 Y 19(4) 6 0–25 .3–6 3–10 WA
White band disease-I WBD-I 1977 N 2 0–10 0.1 ? VI,WC?
White plague disease-I WPD-I 1977 N 12 10–21 3.6 3.1 FL
Shut Down reaction SDR 1977 N 6 5–12 – – FL
White band disease-II WBD* 1982 Y 3 1–25 .1–25 3–30 WC not BE
Red band disease RBD 1984 Y 13(1) 5 2–20 – 1 WA
White patch disease1WPA* 1992 Y 1 0–5 .002 15 CA,FL,BA
Caribbean yellow band aYBD * 1994 Y 11 3–20 1–24 0.1–0.4 WC
White plague disease-II WPD* 1995 Y 41(5) 3–30 .9–18 3–30 WA
Aspergillosis ASP* 1996 Y 9(1) 1–25 1.9 .1–2.5 WA
Dark spots disease DSD 2001 N 11(1) 1–25 1.1 – WA
Crustose-Coralline white b. CCWB 2004 N 3 1–20 1–6 .1–2 WCa
Caribbean white syndromes2CWS 2004 N 15 2 1 3 2–25 – – WCa
Caribbean ciliate infection CCI 2006 Y 21 2–25 – WCa
Sea fan purple spots3SFPS 2008 Y 1 2–18 – – ME,FL,PR
Coralline lethal orange disea. CCLOD 2008 N 1 20 – – PR,CY,ME
Other coral health conditions4CCH – 15 8 1–25 – – WA
Other octocoral health condi.4OCH – 8 3–20 – – WA
* = Koch’s postulates fulfilled. 1 = White patch disease is also termed white pox and patchy necrosis, 2 = White syndromes include several patterns of tissue loss exposing bands, stripes, blotches, or
irregular shapes of clean skeleton (different from the other “white” diseases) with very low prevalence. 3 = PS produced by an unknown protozoan (Labyrinthulomycote). 4 = Other coral and octocorals
health conditions include unhealthy-looking tissues with some degree of mortality, low prevalence, and limited geographic distribution with no pathological or etiological information. a = Including
Flower Gardens, north Gulf of Mexico. Western Atlantic distribution includes the wider Caribbean and Brazil. Bleaching-affected species from Brazil have not being included in this list
470 E. Weil and C.S. Rogers
Fig. 2 Photographs of the most common diseases in Caribbean corals. Active black band disease in M. faveolata (a) and D. strigosa (b), white
band disease in A. palmata (c) and A. cervicornis (d), fast moving white plague disease in D strigosa (e) and D. labyrinthiformis (f), two different
471
Coral Reef Diseases in the Atlantic-Caribbean
ulations throughout their geographic range (Aronson and
Precht 2001b). A different pattern or phase of this disease in
A. cervicornis was described in the late 1990s and was named
white band disease type II (WBD-II) (Ritchie and Smith 1998).
It differed from WBD-I in having a bleaching band leading
the necrotic edge of living tissue. These signs have only been
observed in A. cervicornis, and it is not clear if these two pat-
terns were caused by different pathogens, if the disease is
expressed differently in the different species, or if the two
etiologies represent different phases of the same syndrome
(Weil 2004; Bythell et al. 2004).
Mortality of the surviving colonies/populations of acrop-
orids have continued over the years due to recurrent WBD
events, hurricanes and storms, bleaching, predation, and
local environmental deterioration (sedimentation, turbidity,
untreated sewer outflow, etc.) (Bruckner 2003; Weil et al.
2002, 2003; Wilkinson and Souter 2008; McClanahan et al.
2009), which together with the slow recovery of populations,
led to these two corals being listed as threatened under the
US Endangered Species Act (Hogarth 2006).
Almost concurrently with the WBD outbreak, although
occurring over a shorter time span, a widespread and
highly virulent infectious disease wiped out up to 99% of
the populations of the black sea urchin D. antillarum
throughout the wider Caribbean, including Bermuda
(Lessios et al. 1984b; Lessios 1988). This urchin was at the
time a keystone species regulating algae and coral com-
munity structure (Carpenter 1981, 1985, 1990a; Hughes
et al. 1987). The causes of these events were never deter-
mined (but see Peters et al. (1983) and Rosenberg and
Kushmaro, in this book). The consequence of these two
epizootics was a significant change in the structure and
morphology of most shallow-water coral reef communities
throughout the wider Caribbean. These two outbreaks fol-
lowed increasing water temperatures during an intense El
Niño event, which produced limited bleaching in 1983.
2.4 White Patches and Octocoral Mortalities
Other localized invertebrate mass mortalities and disease
outbreaks reported during the 1980s included: a die-off of
the sea-fan Gorgonia flabellum in Panamá (Guzmán and
Cortés 1984), and an outbreak of a thin red cyanobacteria
mat in corals and octocorals termed red band disease (RBD)
in Florida reefs (Rützler et al. 1983), later redescribed by
Santavy and Peters (1997) and Richardson (1998) (Fig. 1k).
The putative pathogens were not identified.
Several new coral and octocoral diseases were reported
during the 1990s with more frequent and virulent epizootic
events. White patches of clean skeletal tissue were observed
in A. palmata (Porter and Meier 1992) which were clearly
different from WBD signs, and were termed patchy necrosis
(Bruckner and Bruckner 1997) and later, white pox
(Rodriguez-Martinez et al. 2001; Patterson et al. 2002)
(Fig. 2m). An early photograph from the USVI suggests this
disease or a similar one could have been affecting A. palmata
in the 1970s (Rogers et al. 2005). Several outbreaks of dis-
eases with similar signs were observed in Florida, Puerto
Rico, USVI, Mexico, and elsewhere in the late 1990s and
early 2000s (Rodriguez-Martinez et al. 2001; Weil and Ruiz
2003; Rogers et al. 2008a) (Fig. 1h). All these terms and dis-
ease signs have now been pooled as white patch disease
(Raymundo et al. 2008)
2.5 Dark Spots Disease
Dark spots disease (DSD) was first documented in the early
1990s in the Islas del Rosario archipelago, Colombia, as a type
of bleaching 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 in other islands off Colombia mainly affecting M.
annularis, Siderastrea siderea, and Stephanocoenia intersepta,
and it was called “enfermedad de los lunares oscuros” (Diaz
et al. 1995) or dark spots disease (DSD) (Figs. 2g, h). Dark spot
lesions were characterized as “small, round, dark areas that
apparently grow in size over time, some of which can be asso-
ciated with a depression of the coral surface and others expand
into a dark ring surrounding dead coral” (Garzón-Ferreira and
Gil 1998). Other names characterizing different manifestations
of the disease include “Dark Spots type II” in S. intersepta,
Colpophyllia natans, and Montastraea cavernosa, and “Dark
Bands” in M. annularis, M. faveolata, S. siderea, and C. natans
(Weil 2004; Weil et al. 2006) (Fig. 2h). These conditions were
all pooled as DSD (Raymundo et al. 2008; Weil and Hooten
2008); however, they could represent different diseases since
their etiologies have not been resolved. Dark spots disease has
now been found throughout the Caribbean basin (Cervino et al.
2001; Weil et al. 2002; Weil and Croquer 2009; Cróquer and
Weil 2009a).
Fig. 2 (continued) etiologies of dark spots disease in S. siderea (g) and S. intersepta (h), bleached colonies of M. faveolata and C. natans (i),
Caribbean yellow band disease in M. franksi (j) and M. faveolata (k), white patches in A. palmata (l, m), and Caribbean ciliate infections in A.
tenuifolia (n) and D. labyrinthiformis (o) (Photos E. Weil)
472 E. Weil and C.S. Rogers
Sixteen important scleractinian species have been reported
to show signs corresponding to those characteristic of the
disease (Table 1), and the disease appears less prevalent in
the more northern portions of the Caribbean (Weil et al.
2002; Gil-Agudelo et al. 2004; Cróquer and Weil 2009a).
Recently, a disease with lesions resembling DSD was
described for Brazil where it was affecting Siderastrea sp.
(Francini-Filho et al. 2008). In the Indo-Pacific, DSD has
been documented in Pavona varians and P. maldivensis from
Kahoolawe, Hawaii and in P. varians, Psammocora nier-
strazi and Montipora sp. from Tutuila, American Samoa
(Work et al. 2008c).
2.6 Caribbean Yellow Band Disease
Caribbean yellow band disease (YBD) (Fig. 1k) was first
reported in the Florida Keys in 1997 by C. Quirolo in
Montastraea colonies (Santavy and Peters 1997); however,
Brown and Ogden (1993) published a photo of a large colony
of M. faveolata from the Florida Keys with clear signs of
YBD in a National Geographic article about bleaching, indi-
cating that the disease could have been around in the 1980s.
As with other diseases, different terms have been used for
this disease (i.e., yellow blotch disease [Santavy et al. 1999],
yellow band disease [Green and Bruckner 2000], and yellow
blotch syndrome [Weil 2004]). Here we use Caribbean yel-
low band disease (YBD) following the original name and the
geographic location to differentiate it from a similar syn-
drome described in the Red Sea with the same name (Korrubel
and Riegl 1998). Signs of YBD were observed throughout
the Caribbean and north to Bermuda in 1999 (Weil et al.
2002), and the disease is now widely distributed. Outbreaks
of YBD were observed in Panamá in 1996 (Santavy et al.
1999), in the Netherland Antilles and Puerto Rico in 1997
(Cervino and Smith 1997; Bruckner and Bruckner 2006) and
in Grenada, Mexico, Bermuda, and Puerto Rico between
2005 and 2009 (Cróquer and Weil 2009a, Weil et al., in press;
Weil, unpublished data). This disease has become one of the
major causes of tissue and colony mortality in three species
of Montastraea (Fig. 2j, k), the most important reef-building
genus in the region (Weil et al. 2006; Bruckner and Hill
2009; Weil et al., in press).
2.7 Caribbean Ciliate Infection
In 2004, ten coral species were observed with dead areas pre-
ceded by a dark band different from BBD in reefs off
Venezuela. This band was formed by dense populations of a
ciliate protozoan (Halofoliculina sp.) (Cróquer et al. 2006a)
(Fig. 2n, o). Further surveys found the same ciliate infecting up
to 22 coral species throughout the Caribbean, and the condi-
tion was termed Caribbean ciliate infection (Cróquer et al.
2006b; Weil et al. 2006; Weil and Hooten 2008; Weil and
Croquer 2009; Cróquer and Weil 2009a; Weil et al., in
press).
2.8 Aspergillosis and Purple Spots
A widespread epizootic of a fungal infection producing wide
areas of tissue mortality surrounded by purple pigmentation
(an immune response by the host) in the early 1990s, affected
thousands of colonies of the sea fan Gorgonia ventalina
(Fig. 1j) in many reef localities (Nagelkerken et al. 2007a, b).
It was suggested that this was the same problem responsible
for widespread Gorgonia mortalities in 1984 in Central
America (Guzmán and Cortés 1984; Garzón-Ferreira and Zea
1992). The putative pathogen was later identified as the com-
mon terrestrial fungus Aspergillus sydowii and the disease
was called aspergillosis (ASP) (Smith et al. 1996). At least
eight other abundant octocoral species throughout the wider
Caribbean have been reported to be affected by ASP (Weil
2001, 2002; Harvell et al. 2001; Smith and Weil 2004; Weil
et al. 2006). Two independent reports have confirmed the
impact of aspergillosis on the reproductive output of G. ven-
talina colonies, essentially reducing fitness and potential
population recovery (Petes et al. 2003; Flynn 2008; Flynn and
Weil 2008). Other disease signs have been observed in other
octocoral species such as the common and abundant encrust-
ing Briareum asbestinum and Erythropodium caribaeorum,
which have been affected throughout their geographic range
by “necrotic-like” lesions, which progress rapidly, sometimes
killing large areas in a short time (Harvell et al. 1999; Weil
2004; Weil et al. 2006) (Fig. 1i).
In the last 4–5 years, colonies of the sea fan G. ventalina
have been observed with small purple spots in Mexico and
Florida (Harvell et al., 2008), and more recently, in Puerto
Rico (Weil and Hooten 2008) (Fig. 1m). These purple spots
are caused by a protozoan (Labyrinthulomycote) that infects
colonies mostly during the summer (C.D. Harvell, personal
communication). Prevalence has been increasing in several
reefs off the southwest coast of Puerto Rico in the last few
years (Weil, unpublished data 2009).
2.9 Other Diseases
Several other signs of presumed diseases such as white
spots, white bands, white stripes and rings, pigmentation
responses, dark bands, tissue loss and tissue “necrosis,”
473
Coral Reef Diseases in the Atlantic-Caribbean
that are usually found in a few colonies of a wide range of
coral and octocoral species have been observed throughout
the region in recent years (Fig. 1d, e, f, g and h). Furthermore,
many other important members of the coral reef commu-
nity such as hydrocorals, sponges, zoanthids, and other
important calcifying organisms have been affected by dis-
eases in the Caribbean for some time (Fig. 1n–s). In the late
1990s and early 2000s, the common crustose coralline alga
(CCA) Neogoniolithon accretum and at least two other spe-
cies were observed with an advancing, thin, white band
separating healthy-looking tissues from dead areas (Weil
2004; Weil and Hooten 2008). The condition was termed
crustose coralline white syndrome (CCWB) (Fig. 1s) and
was found in high prevalence in deep reef habitats (18–23
m) of Puerto Rico and Grenada (Ballantine et al. 2005; Weil
et al. in press; Weil, unpublished data 2007). Since then,
signs of the condition have been observed throughout the
Caribbean and in many locations in the Indo-Pacific and
Indian Ocean (Weil, unpublished data 2008). More recently,
signs similar to coralline orange lethal disease (CLOD)
described for the Pacific (Littler and Littler 1995) have
been observed on deep (20 m) CCA in Puerto Rico, the
Cayman Islands, and Mexico and the condition termed
Caribbean CLOD (CCLOD) (Weil et al., in press)
(Fig. 1r).
3 Current Status of Coral Diseases
The Caribbean has been dubbed a “disease hot spot” due to
the fast emergence and high virulence of coral reef diseases,
their widespread geographic distribution, wide host ranges,
and frequent epizootic events with significant coral mortali-
ties. The Wider Caribbean includes the Gulf of Mexico,
Florida, the Bahamas, and Bermuda and only about 8% of
the coral reef area worldwide (Spalding and Greenfeld 1997),
yet over 60% of all disease reports up to 2000 came from this
region (Green and Bruckner 2000).
Local environmental and anthropogenic stresses in com-
bination with global warming trends have been proposed as
factors that could affect species susceptibility/resistance to
pathogens, as well as enhance bacterial growth and virulence
favoring local disease outbreaks, which can then be dispersed
by the rapid currents in the basin (Peters 1997; Epstein et al.
1998; Goreau et al. 1998; Richardson 1998; Richardson and
Aronson 2002; Weil 2004; Weil et al. 2006; Harvell et al.
2007).
Besides the Caribbean, the south coast of Brazil is the
only other area with significant coral reef formations in the
Western Atlantic, and until recently, no coral diseases had
been reported for this region. Besides distance, two major
dispersion barriers, the outflows of the Amazon and Orinoco
Rivers, separate Caribbean and Brazilian coral reefs, which
could also be effective barriers to dispersing pathogens.
Nevertheless, several diseases with similar signs to those in
the Caribbean were recently described for this region (Acosta
2001; Francini-Filho et al. 2008).
At least eighteen disease conditions affecting corals and
other important reef organisms have been described for the
Wider Caribbean (Table 1, Figs. 1 and 2). Most do not have
defined pathologies nor have they been well characterized
(Bythell et al. 2004; Weil et al. 2006). Of these, ten diseases
affecting corals show consistent signs that allow their recur-
rent identification, black band disease (BBD), white plague
disease (WPD), Caribbean yellow band disease (YBD),
white band disease (WBD), white patches (WPA) (formerly
called patchy necrosis, Acropora serriatosis, and white pox),
dark spots disease (DSD), red band disease (RBD), Caribbean
ciliate infection (CCI), growth anomalies (GA), and bleach-
ing (BL). Other “white” diffuse/inconsistent signs (bands,
spots, stripes, etc.) producing minor tissue loss affect several
corals and have been grouped as Caribbean white syndromes
(CWS). Unhealthy-looking conditions such as dark areas,
bands, pigmentation responses, etc. have been pooled into
“Other compromised health” conditions (OCH) until their
etiologies and pathologies are clarified to avoid further con-
fusion (Table 1, Fig. 1). Most “white” diseases are character-
ized by the recently exposed white skeleton after the tissue
died, so identification is based on the appearance of the skel-
eton in contrast with the edge of live tissue and not on any
pathology of the tissues (Bythell et al. 2004; Lesser et al.
2007; Work et al. 2008a).
Four diseases with consistent signs [aspergillosis (ASP),
red band disease (RBD), growth anomalies (GA), and sea fan
purple spots (PS)], and several other conditions affect com-
mon and abundant octocoral species (Table 1, Fig. 1). Little
histopathological work has been done other than in corals
and a few octocorals (Weil et al. 2006), a significant gap in
our current approaches to the study of cnidarians diseases.
Descriptions of the common Caribbean and Indo-Pacific
coral-octocoral diseases can be found in Richardson (1998),
Rosenberg and Loya (2004), Raymundo et al. (2008), Beeden
et al. 2008; and Weil and Hooten (2008).
Compared to the Caribbean, only a few coral diseases
and diseases in other organisms have been reported for the
Indo-Pacific (Littler and Littler 1995; Korrubel and Riegl
1998; Willis et al. 2004; Galloway et al. 2007) and the Red
Sea (Loya 2004). The first reported coral disease for the
Indo-Pacific was black band disease affecting two massive
faviid species in the Philippines and later, seven other spe-
cies in the Red Sea (Antonius 1985). The disease showed
similar signs to the Caribbean BBD, but the bacterial mat
seemed to have a different species composition (see later).
Besides BBD, brown band disease (BrB), skeletal eroding
band (SEB), ulcerative white spots (UWS), atramentous
474 E. Weil and C.S. Rogers
necrosis (AtN), growth anomalies (GA), and white syndromes
(WS) are the most commonly found diseases with low and
variable prevalence and limited geographic distribution
(Willis et al. 2004; Raymundo et al. 2008; Galloway et al.
2007). The number, distribution, and prevalence of diseases
has been increasing across the Indo-Pacific and the Red Sea
as more research is being done, with several reports of epi-
zootic events across the region (Green and Bruckner 2000;
Willis et al. 2004; Rosenberg and Loya 2004; Weil and
Jordán-Dahlgren 2005; Page and Willis 2006; Raymundo
et al. 2003, 2008; Work and Aeby 2006; Aeby 2006a, b;
Galloway et al. 2007; McClanahan et al. 2009).
3.1 Pathogenesis
Descriptions of many coral diseases are limited and often
confounded by the lack of clear diagnostic criteria and the
absence of pathological observations, so that similar disease
signs may reflect multiple conditions in one or more coral
species (Bythell et al. 2004; Weil 2004; Work and Aeby
2006; Raymundo et al. 2008; Work et al. 2008a). There is
evidence that different pathogenic bacteria and fungi can
produce similar signs in the same and/or in different species
(Toledo-Hernandez et al. 2008; Sunagawa et al. 2009).
Because the BBD microbial mat consistently contained
dominant populations of the same microorganisms, Carlton
and Richardson (1995) proposed that it was caused by a
microbial consortium instead of a single pathogen. The three
mayor players were a cyanobacterium (Phormidium coral-
lyticum), a sulfide-oxidizing bacterium (Beggiatoa sp.), and
a sulfate-reducing bacterium (Desulfovibrio sp.). The dark
coloration during the day is provided by the red cyanobacte-
rial pigment phycoerythrin. Richardson (1997) demonstrated
that BBD sulfate-reducing bacteria are functionally specific
to BBD pathogenicity, and suggested that they may be spe-
cies-specific. Recent molecular studies, however, suggest
that the primary pathogen may be a nonphotosynthetic,
eubacterial heterotroph (Cooney et al. 2002; Frias-Lopez
et al. 2002). Furthermore, these results also showed that
P. corallyticum, originally identified as the cyanobacterial
component of BBD (Rützler and Santavy 1983; Taylor 1983)
may not be the cyanobacterium associated with BBD. Recent
studies indicated that the BBD mat is dominated by an
unidentified cyanobacterium most closely related to the
genus Oscillatoria (Cooney et al. 2002; Frias-Lopez et al.
2003). At least three different taxa of cyanobacteria associ-
ated with BBD were identified by Frias-Lopez et al. (2003),
who showed that they vary between the Caribbean and
Indo-Pacific.
Furthermore, differences in composition of the bacterial
community have been reported for BBD affecting corals in
Florida, the Bahamas, and the US Virgin Islands (Voss et al.
2007). The mat composition seems to be variable spatially
and/or temporally, or the components may have been mis-
identified originally (Voss et al. 2007; Sekar et al. 2008).
Most recently, a single cyanobacteria ribotype was found to
be associated with both red band disease (RBD) and BBD in
corals from Palau, having a 99% sequence identity with a
Caribbean strain (Sussman et al. 2006). Further research is
needed to clarify whether RBD and BBD are the same.
Denner et al. (2003) identified the bacterium A. corali-
cida as the putative pathogen of WPD-II in the coral
D. stokesi in the Florida Keys. Another 40 coral species
have been reported to be susceptible to WPD (Weil 2004;
Sutherland et al. 2004) because they showed signs similar to
those described for D. stokesi colonies infected with A. cor-
alicida (Richardson et al. 1998a). However, A. coralicida
has not been consistently found in corals with signs of WPD,
and probes developed and used to identify the pathogen are
insufficiently specific to consistently incriminate this bacte-
rium (Bythell et al. 2004; Polson et al. 2009). Even though
A. coralicida has been found in a few other coral species,
Koch’s postulates have only been verified for D. stokesi
(Richardson et al. 1998b; Denner et al. 2003; Pantos et al.
2003). Recent analyses of several diseased tissue samples
from Montastraea faveolata colonies with typical WPD-II
signs failed to find A. coralicida (Sunagawa et al. 2009), and
no other experimental data show that any of the other spe-
cies reported with WPD signs have been actually infected
by A. coralicida. Therefore, WPD signs in these colonies
and other species of corals might be caused by a different
agent.
More than 20 years after the WBD epizootic, most popula-
tions of acroporids have not recovered and the disease agent
associated with this epizootic has not been identified. A
potential pathogen named Vibrio charchariae was identified
but Koch’s postulates were never fulfilled until recently.
Results from controlled isolation/inoculation experiments in
Puerto Rico showed that the potential cause of WBD type II
is possibly a Vibrio species very close to Vibrio harveyi, a
synonym of V. charchariae (Gil-Agudelo et al. 2006). This
study also reported that other Vibrio species tested produced
similar WBD signs, but their virulence was lower than
V. harveyi.
The putative pathogen associated with white pox (WPX)
signs on A. palmata in the Florida Keys was identified as the
bacterium Serratia marcescens, a common gut bacterium in
sheep, other mammals, and fish (Patterson et al. 2002). The
disease was then called Acropora serratiosis; however, all
conditions with similar signs (white patches, patchy “necro-
sis”) in A. palmata have been recently pooled as “white
patches” (WPA) (Raymundo et al. 2008; Weil and Hooten
2008). The disease agent in WPA-infected colonies outside
the Florida Keys has never been identified, and preliminary
475
Coral Reef Diseases in the Atlantic-Caribbean
results from a few samples from St. John did not show any
correlation between signs of “white pox” and presence of
S. marcescens (Polson et al. 2009).
The cause of dark spots disease is still unknown. Gil-
Agudelo et al. (2004) examined bacterial flora of mucus in
corals affected with DSD and found that the corals were
infected with Vibrio charchariae whereas this bacterium was
absent in normal corals. Experimental infections of corals in
the field using this bacterium failed to replicate DSD signs.
Corals maintained in aquaria incidentally developed DSD,
and treatment with antibiotics led to further tissue loss,
thereby arguing against a bacterial etiology for DSD (Gil-
Agudelo et al. 2004). In Florida, fungi have been associated
with S. siderea affected with DSD (Galloway et al. 2007).
Chemical analyses of colonies of S. siderea resistant and sus-
ceptible to DSD in Puerto Rico suggested that phenotypic
plasticity in antimicrobial activity may affect microbial
infection and survival in the host colonies (Gotchfeld et al.
2006).
Recent experimental evidence suggests that a particular
combination of four Vibrio species infects and kills zooxan-
thellae in the coral endoderm producing the characteristic
signs of yellow band disease in both Caribbean and Indo-
Pacific corals (Cervino et al. 2004a, b, 2008). However, the
mechanisms by which the zooxanthellae and the coral tissue
are killed are unclear. The onset of infection seemed to be
temperature-dependent (Weil et al. 2009b), and prevalence
increased under high-nutrient conditions (Bruno et al. 2003)
and high water temperatures (Harvell et al. 2009; Weil et al.,
in press).
Further evidence indicates that the dynamics of bacterial
communities in corals are more complicated and more
responsive to changes in environmental conditions than pre-
viously thought (Ritchie 2006; Gil-Agudelo et al. 2006,
2007; Voss et al. 2007; Toledo-Hernandez et al. 2008).
Similar to other coral diseases, recent findings have revealed
that A. sydowii, the pathogen causing aspergillosis in sea
fans and other octocorals (Smith et al. 1996; Smith and Weil
2004) has been found in sea fans without disease signs.
Furthermore, ASP signs could be produced by other
Aspergillus species and fungi in other groups (Toledo-
Hernandez et al. 2008).
Changes in the composition and dynamics of the bacterial
community after environmental or biological changes in the
coral host could be related to different bacteria producing
similar disease signs over time, sometimes indicating
(although not conclusively proving) a potential development
of resistance to the initial pathogenic agent (Reshef et al.
2006). In a recent study of Montastraea corals showing typi-
cal white plague signs in Puerto Rico, the primary WPD
pathogen A. coralicida was not found after screening mucus
and tissue samples (Sunagawa et al. 2009). Similar results
were reported for the fungal disease ASP (Toledo-Hernandez
et al. 2008) and for bacterial bleaching in O. patagonica in
the Mediterranean (Ainsworth et al. 2008). A suite of other
fungal species can produce similar aspergillosis signs in sea
fans (Smith and Weil 2004; Toledo-Hernandez et al. 2008).
These results emphasize the need to examine tissue micro-
scopically in attempts to identify potential causative agents,
to follow up with appropriate laboratory confirmation, and to
be cautious about naming and describing diseases without a
clear pathogenesis.
Many cnidarian diseases have yet to be characterized.
Their etiologies have not been properly described and their
putative pathogens have not been identified (Ritchie et al.
2001; Weil et al. 2006; Work et al. 2008a). As researchers
become more familiar with disease signs and more patho-
logical studies are carried out, the number of described dis-
eases affecting corals and other reef organisms could grow.
Koch’s postulates have only been verified for five diseases
and in most cases, for only one species in each condition
(Table 1); so there is ample room for new pathologies and
changes in our understanding of these diseases.
3.2 Geographic Distribution
Most coral diseases in the Caribbean have spread throughout
the region (Table 1; Fig. 3). White plague, YBD, DSD, ASP,
BBD, CCI, GA, and bleaching show the widest geographic
distribution, from Bermuda to Trinidad and Tobago, the
northern coast of Venezuela and Colombia, Central America,
and the southern region of the Gulf of Mexico (Weil 2004;
Weil and Croquer 2009). With the exception of the white
band disease outbreak and the mass mortality of D. antil-
larum, no correlations between dispersion patterns of most
of the recent epizootic events (ASP, WPD, YBD, etc.) with
current patterns in the region have been reported. There is
some evidence, however, that WBD spread against the pre-
dominant current in St. Croix in the early 1980s (Gladfelter
1982). A dispersion pattern following local and/or regional
water currents is expected for new putative, infectious agents
introduced or “activated” in one particular location, as was
the case of the agent killing the sea urchins in the early
1980s (Lessios et al. 1984a,b Lessios 1988; Carpenter
1990a, b).
Most reefs in the northern Gulf of Mexico are far from the
US mainland and deeper than 22 m where water tempera-
tures are cooler and light conditions are reduced, conditions
that might limit the development of diseases. A short-lived
outbreak of a white syndrome was observed in 2005 in the
deep coral reef areas of the Flower Garden Banks (Hickerson
and Schmahl 2006). Other conditions such as growth anoma-
lies, “mottling syndrome” and “pale ring syndrome” were
reported by Borneman and Wellington (2005), and more
476 E. Weil and C.S. Rogers
recently, Caribbean ciliate infections and GA were observed
during disease surveys in the two major banks (Zimmer et al.
2009). Caribbean ciliate infection (CCI) was first observed
in Venezuela in 2005 (Cróquer et al. 2006a, b), but recent
surveys have reported this condition in corals in at least six
other countries in the region (Bermuda, Puerto Rico, Grenada,
Caymans, Mexico, and Panamá) (Cróquer and Weil 2009a;
Weil and Croquer, unpublished data 2009), but this is the
deepest report so far.
Until recently, only one disease, affecting zoanthids, was
reported from Brazil (Acosta 2001). The first signs of scler-
actinian coral and octocoral diseases were observed in 2005
in the Abrolhos Bank, the largest reef system in Brazil.
Conditions with signs similar to WPD, BBD, RBD, ASP,
GA, and octocoral compromised health conditions (“tissue
necrosis”) were recently reported from this area (Francini-
Filho et al. 2008). From 2005 to 2007, the distribution of
these diseases has widened and their prevalence and viru-
lence have increased producing significant coral and octoc-
oral mortalities in the Abrolhos Bank. Based on estimates of
disease prevalence and progression rates, as well as on the
growth rates of a major reef-building coral species (the
Brazilian-endemic Mussismilia braziliensis), it is predicted
that eastern Brazilian reefs will suffer a massive coral cover
decline in the next 50 years, and that M. braziliensis will be
nearly extinct in less than a century if the current rate of
disease mortality continues (Francini-Filho et al. 2008).
Limited connectivity between the Caribbean and the
Brazilian reefs suggests that either these diseases are produced
by different agents, possibly triggered by similar environ-
mental changes (increase in water temperatures), or they have
similar etiologies to their Caribbean counterparts. If patho-
gens are different, this shows the limited responses (signs)
cnidarians can develop when affected by infectious diseases
and other agents, and the importance of identifying putative
pathogens.
3.3 Depth Distribution
Caribbean wide surveys indicate that WPD, YBD, DSD, and
ASP have the widest depth distribution, from 1 to 25 m (Weil
2004; Cróquer and Weil 2009a, b; Weil et al., in press). If the
pathogens are species-specific, disease infections would be
limited to the depth distribution of the host species. Most of
Fig. 3 Geographic distribution of the most common coral and
octocoral diseases in the wider Caribbean: BBD, WPD, YBD, DSD,
GAN, CCI, ASP, white syndromes and other compromise health
conditions. Crustose coralline white band is also distributed
throughout the wider Caribbean. A virulent white syndrome was
observed in 2005 in the Flower Gardens in the north area of the
Gulf of Mexico and bleaching has affected all reefs across the
region
477
Coral Reef Diseases in the Atlantic-Caribbean
the species affected by the major diseases (M. faveolata, M.
franksi, M. cavernosa, M. ferox, Agaricia lamarcki, etc.)
have a wide depth distribution, some down to 90 m. However,
some diseases affecting these species have limited depth dis-
tribution. White plague disease has been more prevalent in
deeper habitats (10–25 m) in Puerto Rico (Weil et al., in
press); however, recently, a colony of M. ferox was observed
with signs of WPD at 50 m off the southwest coast of Puerto
Rico, the deepest record so far (H. Ruiz, personal communi-
cation). YBD has only recently been observed below 20 m in
the Caymans and Puerto Rico (Weil, unpublished), which
could be related to different zooxanthellae composition in
deeper corals. Bleaching has the deepest distribution of all
diseases with pale or white corals (of a few different
species) observed down to 100 m in some reefs in the
Caymans in 2009 (McCoy C, personal communication 2009).
Aspergillosis has the widest depth distribution among octo-
coral diseases, with sea fan colonies showing signs of this
condition from 1 to 25 m (Jolles et al. 2002; Kim and Harvell
2002; Flynn and Weil 2008; Flynn and Weil, in press).
3.4 Prevalence, Incidence, and Virulence
Prevalence is the proportion of infected colonies in a popula-
tion or a community. It is expressed by absence/presence per
individual and usually does not give any indication of the
severity (virulence) of the disease, which could include the
number (and size) of the lesions that are present, the rate of
tissue mortality, the proportion of the colony that is affected,
or the rate of spread of the disease in the population (Work
et al. 2008a, b; Weil et al. 2008). Most surveys are done
yearly or only during “outbreaks” and, prevalence can vary
greatly even over short periods of time. Prevalence of white
pox disease (= white patches) on A. palmata colonies off St.
John ranged from 0% to 52% (Rogers et al. 2008b). Disease
incidence is a rate expressing the number of newly infected
colonies over time. It requires temporal monitoring of the
same reef area with mapping, tagging, and photographing of
colonies along the sampled area (Weil et al. 2008; Work et al.
2008b).
Average disease prevalence at the coral community level
for major coral diseases in the Caribbean remains low (<6%)
and has not changed significantly in the last 10 years (Weil
et al. 2002; Weil and Croquer 2009). However, in some
localities, prevalence of some chronic diseases within popu-
lations could be much higher and, even low levels of disease
over long periods of time can produce significant mortalities
in reef communities. Frequent monitoring is needed to
address the spatial and temporal variability in prevalence and
virulence (number of lesions and rate of disease advance)
and to assess disease incidence (new cases of infected colo-
nies over time) at population and/or community levels and
their cumulative effects.
One-time surveys are limited in that they only reflect the
disease status at a particular time. Data for different reefs
generated with different methods could be difficult to com-
pare, especially if the areal extent of the surveys are not the
same and the data are collected by different people without
standardization of the disease identification. Similarly, data
generated with the same methods but taken in different sea-
sons and/or different years could also generate problems of
interpretation. Prevalence will go down when the disease has
run its course, and most susceptible colonies have died, so
their proportion relative to the resistant survivors drops. A
recent disease manual with two sets of underwater disease
identification cards, one for the Caribbean and one for the
Indo-Pacific, were published with the goal of standardizing
the disease identifications, nomenclature used to describe
and characterize them, and methodology to estimate preva-
lence, incidence, virulence, and their variability (Raymundo
et al. 2008; Beeden et al. 2008; Weil and Hooten 2008).
Prevalence of WPD, YBD, WBD, BBD, and DSD showed
high seasonal variability in Caribbean localities with usually
higher prevalence and frequent outbreaks during summer’s
high water temperatures (Borger 2003; Gil-Agudelo et al.
2004; Borger and Steiner 2005; Bruckner and Bruckner
2006; Weil et al., in press; Weil, unpublished). In the late
1990s and early 2000s, YBD was a seasonal disease in La
Parguera, Puerto Rico, active and highly visible during
Summer--Fall, nearly disappearing from some colonies and
completely from others during the Winter--Spring. In the last
6 years however, this seasonality disappeared. Prevalence of
YBD increased every year with corresponding increase in
severity (number of lesions and rate of disease advance) to
epizootic levels in many reefs in Puerto Rico and other
Caribbean localities (Bruckner and Bruckner 2006; Weil and
Croquer 2009, Cróquer and Weil 2009a, b; Weil et al., in
press). Moreover, increase in prevalence and severity over
time covaried significantly with increasing average winter
and yearly water temperatures (Fig. 4a, see below) (Weil
2008; Harvell et al. 2009; Weil et al., in press), thus warmer
winters seem to have affected disease dynamics. However,
co-variation does not mean causality, so the increase in prev-
alence could also result from increased incidence (number of
new infected colonies per unit time) until most susceptible
colonies were infected in the population. Prevalence could
stay high due to the warmer temperatures until all susceptible
colonies die from the disease and the relative proportion of
diseased colonies is reduced over time (Bruckner and Hill
2009).
Rates of tissue loss are also highly variable and depend on
the virulence of the pathogen, the susceptibility/resistance of
the host, synergistic environmental conditions, and the dura-
tion of the infection (Bruckner 2002; Bruckner and Bruckner
478 E. Weil and C.S. Rogers
2006; Harvell et al. 2007). For example, rates of tissue loss
were significantly higher during the fourth WPD outbreak
even though the same pathogen seemed to have been the
cause (Richardson and Aronson 2002). In Puerto Rico, the
number of YBD disease lesions in M. faveolata colonies
increased significantly over time with some very large colo-
nies showing over 32 lesions at once. This led to a significant
increase in rate of tissue loss, killing the colonies faster (Weil
et al., in press).
The average rate of tissue loss (advance of the disease
edge) estimated from M. faveolata colonies over the years in
Mona and Desecheo islands was generally low (0.5–1.0 cm/
month) and variable across colonies, months, and localities
(Bruckner and Bruckner 2006). Similar results from over
200 tagged colonies of the same species that were checked
bi-annually were obtained in La Parguera. However, the
rates of tissue loss increased with time, from 0.2 to 3.6 cm
month−1 (Fig. 4b) and the seasonality observed in prevalence
and virulence tended to decline over the years. Both preva-
lence and rates of tissue loss significantly increased from
2003 to 2008 and were correlated with increasing water
temperatures (Weil et al., in press; Weil, unpublished)
(Fig. 4). In Colombia, M. annularis and S. siderea had the
highest prevalence of dark spot disease (10% and 5%,
respectively) whereas the disease was much less common in
M. faveolata, M. franksi, S. intersepta, and M. cavernosa
(Gil-Agudelo 1998). Recent wide geographic surveys in the
Caribbean showed lower prevalence values of DSD than
those reported for Colombia and in general, lower preva-
lence in northern compared to southern localities (Weil and
Croquer 2009).
3.5 Host Ranges
Overall, host ranges for most Caribbean coral reef diseases
have remained stable or have increased over the years with
many other reef organisms observed with similar disease
signs in the region (Table 1) (Weil 2004; Bruckner 2009).
Corals and other reef invertebrates are relatively simple
organisms with a limited range of signs or visible “responses”
to infections. Unless we do histology, most of what we can
see (or characterize) are the external manifestation of
responses of the diseased tissues or, just the pattern of tissue
mortality. These include, but are not limited to, different pat-
terns of tissue loss, pigmentation changes, general tissue
conditions, mucus release, and growth anomalies. There has
been no consistent histopathological research that could pro-
vide reliable descriptors for the different pathologies (Work
and Aeby 2006; Work et al. 2008a).
Bleaching (presumably due to elevated temperature) has
the widest host range affecting at least 62 corals, 29 octocor-
als, eight sponges, five hydrocorals, and two zoanthids in the
Caribbean (McClanahan et al. 2009; Prada et al. 2009)
(Table 1, Fig. 5). Bleached corals are still alive, and if condi-
tions return to normal quickly enough, most colonies can
fully recover. Four coral diseases, WPD, CCI, BBD, and
RBD had the widest host ranges in the Caribbean with 41,
21, 19, and 13 susceptible scleractinian coral species, respec-
tively (Table 1). Caribbean yellow band has been reported in
11 species of important reef-building corals. The total num-
ber of coral species affected by DSD has increased over time
possibly due to the expansion of surveys. Sixteen important
scleractinian species have been reported to show signs cor-
responding to those characteristic of the disease (Table 1)
YBD Prevalence (%)
0
10
20
30
40
50
60
70
Year
Average temperature (°C)
0
10
20
30
40
50
r2=0.787; P < 0.01
r2=0.78 (P< 0.05)
a
b
Rate of tissue loss (cm.month-1
)
0
1
2
3
4
Summer
Winter
Average temperature
0.0
0.5
1.0
1.5
2.0
2.5
3.0
1999
27.6
25.8 26.0 26.2 26.4 26.6 26.8 27.0 27.2 27.4
27.8 28.0 28.2 28.4 28.6 28.8 29.0
2000
2001
2002
2003
2004
2005
2006
2007
19971998 19992000 20012002 20032004 200520062007 20082009
Fig. 4 Temporal changes in the dynamics of Caribbean yellow band
disease. (a) Increase in YBD prevalence in the coral genus Montastraea
in reefs off the south-west coast of Puerto Rico from 1999 to 2007 and
the positive and significant (r² = 0.787, P £ 0.01) correlation with aver-
age yearly surface water temperature (inset). (b) Seasonal variability in
YBD lesion growth rates (virulence) measured in over 100 tagged colo-
nies of M. faveolata in La Parguera, Puerto Rico from 1999 to 2008,
and the significant positive co-variation (r² = 0.54, P £ 0.05) between
linear YBD lesion growth rates and the average seasonal surface seawa-
ter temperature for the same period (inset). (Modified from Weil et al.,
in press)
479
Coral Reef Diseases in the Atlantic-Caribbean
Fig. 5 Bleached colonies of important reef-building species during the 2005 event. In many reefs of Puerto Rico and the US Virgin Islands, up to
90% of all colonies of important reef-building species were fully or significantly bleached [Montastraea faveolata (a, b), A. palmata (c), D. cylin-
drus (d), C. natans and S. intersepta (e), and D. strigosa and S. siderea (j)]. Bleached colonies of species that never been observed bleached in
these reefs included Scolymia cubensis (f) and Mycetophyllia ferox (g) among others. The event produced significant mortalities in the agaricids
and acroporids (h, i). Adjacent colonies of the same species showed significant differences in bleaching intensity in some localities (i.e., M. faveo-
lata and C. natans (k, l), and some species did not bleach in certain areas (i.e., Meandrina meandrites) (m). Several species of octocorals bleached
in many localities (n) (Photos E. Weil)
480 E. Weil and C.S. Rogers
Fig. 6 Potential invertebrate vectors (reservoirs?) of coral diseases in the
western Atlantic include the snails Coralliophila abbreviata and C. carib-
aea, here seen preying on D. labyrinthiformis (a), M. faveolata (b) and A.
palmata (c); the flamingo tongue Cyphoma gibossum, a common predator
of sea fans (d) and other octocorals (e); sea urchins which are “omnivorous”
and can pick up pathogens from sediments or turf algae and move them to
corals (f); and the fireworm Hermodice carunculata which preys on both
octocorals (g) and corals. This fireworm has been frequently observed eat-
ing at the edges of diseased and healthy areas of corals with BBD (h, i),
WPD (j) (Photo by C. Rogers), and white band disease (Photos E. Weil)
481
Coral Reef Diseases in the Atlantic-Caribbean
(Gil-Agudelo et al. 2004; Weil et al. 2002; Cróquer and Weil
2009a).
White plague disease, BBD, RBD, and DSD have been
reported to affect five, four, one, and one coral species,
respectively, in Brazil. Nine of the most common and abun-
dant octocorals in the Caribbean seem to be susceptible to
ASP, six to BBD, at least five to RDB, and several to other
compromised health conditions and growth anomalies.
Overall, at least six different diseases affect five of the most
important and most common reef-building genera (including
Montastraea, Diploria, Colpophyllia, Acropora, and
Agaricia), and four different diseases affect 11 of the main
reef-building genera (Fig. 7).
Most of the information used to compile lists of suscep-
tible species came from single observations in space and
time. A new host was added to the list if a single, or just a
few colonies of a species was (were) observed with the dis-
ease signs without any verification of the pathology and/or
etiology. As mentioned above, Koch’s postulates have only
been verified for a few pathogens in a few species, usually
one for each condition [i.e. Diploria strigosa (BBD) (Rützler
and Santavy 1983, A. palmata (white patches) (Patterson
et al. 2002), D. stokesi (WPD) (Denner et al. 2003); A. cervi-
cornis (WBD) (Gil-Agudelo et al. 2006); G. ventalina, and
G. flabellum (ASP) (Smith et al. 1996; Geiser et al. 1998)].
Confirmation of the pathology of all the potentially suscep-
tible species for each disease has never been done. The tem-
poral dynamics of these infections (species could become
resistant after the first infection, or susceptible colonies could
be quickly eliminated from the population) has never been
properly investigated.
Overall, only a fraction of the listed host species for each
disease is usually observed with the disease signs when con-
ducting typically annual field surveys, and the actual number
of susceptible species (host range) for each disease will only
be determined when the same pathogen is not only found in
each species, but is shown to be the cause of the disease
signs.
3.6 Vectors and Reservoirs
There are only two reports with experimental evidence of
invertebrates acting as reservoirs (organism, substrate, or
other media where the pathogen spends some time and
completes part of its life cycle) and vectors (organisms or
other media that act as a carrier and delivery medium for a
pathogen) of a coral disease. The fireworm Hermodice car-
unculata in the Mediterranean is a vector for Vibrio shiloi,
the pathogen that causes bacterial bleaching in the coral
Oculina patagonica (Sussman et al. 2003), and the predatory
Caribbean snail Coralliophila abbreviata, harbors S. marcescens,
the pathogen responsible for WPA in A. palmata in the
Florida Keys (Williams and Miller 2005) (Fig. 6c).
Hermodice carunculata is a coral predator, ingesting
Vibrio shiloi and keeping it alive in its gut (Sussman et al.
2003). This worm (or a similar species) is very common in
coral reef communities across the Caribbean and is one of
the main predators of acroporid and massive corals, hydroc-
orals, and octocorals. It is frequently observed feeding on the
edges of WPD, YBD, and BBD active lesions in colonies of
M. faveolata, D. strigosa, and C. natans, and ASP-infected
sea fans (Fig. 6g – j). It is then possible that this fireworm
could act as a vector and a reservoir for one or several of
these Caribbean diseases as well. To date, disease reservoirs
have only been identified for BBD (biofilms in reef sedi-
ments, which contain nonpathogenic versions of the BBD
consortium) (Richardson 1997), and WPD (Halimeda opun-
tia mats, which seem to harbor the WPD pathogen) (Nugues
et al. 2004).
Other potential disease vectors and possible reservoirs
include parrotfishes (i.e., Sparisoma viride), damsel fishes
(Stegastes planifrons and Microspathodon chrysurus), and
the butterfly fish Chaetodon capistratus, a common coral
predator capable of moving the BBD pathogen from diseased
to healthy corals in experimental settings (Aeby and Santavy
2006), and the snail Cyphoma gibossum, a predator of sea
fans and other octocorals (Fig. 6d, e). Fishes tend to directly
bite diseased and healthy colonies of important reef-building
species in the Caribbean potentially moving pathogens
around. Vectors may be involved in disease transmission and
spread at both local and regional scales. This is an important
aspect of the dynamics of coral reef diseases, particularly as
populations of many of these potential vectors have been sig-
nificantly increasing (mostly as a consequence of overfishing
*
*
= Important reef-building genus
Number of different diseases/conditions
0
2
4
6
8
10
**
**
**
Montastraea
Colpophyllia
Diploria
Acropora
Agaricia
Siderastrea
Stephanocoenia
Porites
Meandrina
Mycetophyllia
Dichocoenia
Isophyllastrea
Madracis
Fig. 7 The number of different diseases affecting the most important
Caribbean reef-building scleractinian coral genera (*). Eleven genera of
the 26 reported for the Caribbean are affected by at least four or more
different diseases/conditions
482 E. Weil and C.S. Rogers
of their main predators or recent successful reproduction) for
which there is little information.
4 Environmental Drivers
The multiple and complex biological associations within the
coral holobiont and the currently changing environmental
conditions complicate attempts to isolate individual drivers/
causes and to make predictions and/or extrapolations based
on short-term and single-locality studies. Of many potential
factors, increasing sea water temperature seems to be one
that may have favored the emergence of coral diseases
(Harvell et al. 1999, 2002, 2007, 2009). Evidence of this
includes the following:
1. Bleaching events and most of the early disease outbreaks
affecting coral reef organisms and other marine animals
occurred during the warm Summer and early Fall seasons
(Harvell et al. 1999; Weil et al. 2006; Van Oppen and
Lough 2009).
2. The first Caribbean-wide surveys of coral diseases con-
ducted during the Summer--Fall season in 1999 showed
an increase in disease prevalence at the community level
from Bermuda in the north-west Atlantic to the more
tropical southern Caribbean (Venezuela and Colombia),
suggesting a potential relationship with warmer tempera-
tures (Weil et al. 2002).
3. The infection of Pocillopora damicornis by V. coralliilyti-
cus (bacteria producing bleaching in this species) showed
no signs of infection below 22°C, tissue bleaching from
infection between 24°C and 26°C, and rapid tissue lyses
from 27°C to 29°C (Ben-Haim et al. 2003a, b).
4. Recent evidence indicates that high water temperatures
compromise host susceptibility and increase virulence
(Harvell et al. 2002; Ritchie 2006; Bruno et al. 2007; Weil
et al. in press, which would presumably increase preva-
lence and incidence over time.
5. Functional gene analysis of samples from experimental
Porites compressa colonies subjected to environmental
stressors (increased temperature, elevated nutrients and
CO2, and lower pH) showed increased abundance of
microbial genes involved in virulence, stress resistance,
sulfur and nitrogen metabolism, and coral-associated
microbiota (Archaea, Bacteria, protists) shifted from a
healthy community (e.g., Cyanobacteria, Proteobacteria,
and zooxanthellae) to a community of microbes often
found on diseased corals (Thurber et al. 2009)
6. Water temperature and disease prevalence in A. palmata
colonies in St. John, USVI, were positively correlated, but
bleached colonies exhibited a stronger relationship than
unbleached colonies. In addition, a positive relationship
between the severity of disease, as estimated by the area
of the disease lesions, was apparent only for bleached cor-
als (Muller et al. 2008).
7. Bacteria populations in corals change in composition,
abundance, and possibly virulence when temperature
increases (Ritchie 2006; Bourne et al. 2007; Weil et al.
2009b; Harvell et al. 2009; Sunagawa et al. 2009). Similar
correlations of increased prevalence with increasing water
temperatures have been found in a long-term study in the
Great Barrier Reef (Selig et al. 2006; Bruno et al. 2007).
The WPD and YBD outbreaks in the eastern Caribbean have
been associated with higher than normal water temperatures over
the years, which have also produced widespread bleaching in the
area (Bruckner and Bruckner 2006; Miller et al. 2006, 2009;
Rogers et al. 2008a, b; McClanahan et al. 2009). Furthermore, in
contrast to previous WPD outbreaks in La Parguera, Puerto Rico,
the WPD outbreak after the 2005 bleaching event peaked during
the unusually warmer winter season (February–March) (Cróquer
and Weil 2009b, Weil et al., in press).
A positive correlation between increasing water tempera-
tures and increasing prevalence of YBD in Montastraea
colonies was found over a 9-year study in Puerto Rico
(Fig. 4a, b) (Weil 2008; Weil et al., in press.). Furthermore,
the seasonal rates of YBD-induced tissue loss in M. faveo-
lata were significantly different between 1999 and 2004,
with higher rates of tissue loss during the Summer--Fall
compared to the Winter--Spring. These differences, however,
disappeared as winter water temperatures became warmer
after 2004 (Fig. 4b), and YBD has remained active all year
long with similar rates of tissue loss throughout the year
(Weil 2008; Bruckner and Hill 2009; Harvell et al. 2009;
CO HD TR YBD
Mean fecundity (eggs/ polyp)
0
5
10
15
20
25
30
35
a
ab
b
c
Treatment
Fig. 8 Significant decline in reproductive output within diseased and
healthy-looking areas of YBD-infected and control colonies of the
important reef-building coral Montastraea faveolata in La Parguera,
Puerto Rico. CO = control colonies with no signs of disease, HD healthy
looking areas of diseased colonies, TR = transition areas (area between
the YBD pale tissue and the healthy looking tissue), and YBD = disease
area in colony (Modified from Weil et al. 2009a)
483
Coral Reef Diseases in the Atlantic-Caribbean
Weil et al., in press). Warmer winters favor the higher annual
advance rates of lesions, significantly increasing the overall
tissue and colony mortality, reducing fecundity (Fig. 8) and
potentially affecting the short- and long-term recovery of
populations (Weil et al. 2009a, b, in press).
High prevalence of dark spots disease seemed to be related
to high water temperatures and specific depths in some locali-
ties but not in others (Gil-Agudelo and Garzón-Ferreira 2001;
Borger 2003; Gotchfeld et al. 2006). Cróquer and Weil (2009a)
found that populations of S. siderea exhibited a higher preva-
lence of DSD at intermediate (10 m) depths (25–40%),
whereas Stephanocoenia populations were significantly more
affected by DSD in deeper (>15 m) habitats (21–26%). In
South Florida, prevalence of DSD increased during April--
July but decreased during winter months (Borger and Steiner
2005). After 2 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 tempera-
ture, thereby illustrating geographic differences in environ-
mental conditions conducive to development of DSD.
Other factors such as nutrient concentration might also
affect the dynamics of some coral diseases. High nutrient expo-
sure doubled rates of tissue loss in YBD diseased colonies of
M. faveolata in Mexico (Bruno et al. 2003), showing response
of the disease to changing nutrient conditions in surrounding
waters (dissolved nutrients were artificially added). However,
in similar nutrient experiments to those in Mexico, results from
Puerto Rico showed no significant increase in number of lesions
or rates of advance in YBD-infected colonies of M. faveolata
when compared with controls (Bruno and Weil, unpublished).
Another study showed higher prevalence of BBD in reefs closer
to sewage effluents (Kaczmarsky et al. 2005).
Recent studies have shown that A. palmata colonies that
were physically damaged by heavy swells had higher disease
prevalence than undamaged colonies, with statistically greater
prevalence when average monthly water temperature exceeded
28°C (Bright, personal communication 2010). Fragmentation
of A. palmata and A. cervicornis, as well as other branching or
columnar species during storms, leads to increases in number
of colonies in the populations. However, during this process,
open wounds and damaged tissues are presumably more sus-
ceptible to infection by opportunistic bacteria; thus, more
intense storms predicted to occur with climate change could
lead to more disease and higher mortality of these fragments.
5 Consequences and Management
Implications
The potential of disease outbreaks to significantly change
coral reefs was first shown by the massive mortalities of the
acroporids and the black sea urchin D. antillarum in the
Caribbean in the early 1980s. In a relatively short time and
over a wide geographic region, populations of these species
suffered up to 95% mortality (Gladfelter 1982; Lessios et al.
1984a, b; Carpenter 1990a, b) producing a cascade of signifi-
cant ecological changes in the dynamics, function, and struc-
ture of coral reefs at local and geographic scales (Hughes
1994; Harvell et al. 1999; Aronson and Precht 2001a, b; Weil
et al. 2003).
Disease etiology and dynamics seem to be highly vari-
able across different spatial (populations, depth gradients,
and reefs) and temporal scales (Weil et al. 2002; Bruckner
and Bruckner 2006; Weil and Croquer 2009; Cróquer and
Weil 2009a, b). Several infectious diseases have been per-
sistent over the years throughout the Caribbean. Six of
these have wide geographic distributions (BBD, WPD,
YBD, DSD, ASP, and CCI) and could be considered chronic
in many localities (Table 1) (Weil and Croquer 2009;
Cróquer and Weil 2009a). Several more epizootics have
occurred since the widespread WBD outbreak of the early
1980s, three of which have had wide geographic distribu-
tions and significant impact on the host species, WPD,
ASP, and YBD (Bruckner and Bruckner 2006; Bruckner
and Hill 2009; Weil and Croquer 2009; Cróquer and Weil
2009a; Weil et al. 2009a; Flynn and Weil, in press; Weil
et al., in press).
Some of the most important reef-building coral genera
(i.e., Montastraea, Diploria, Siderastrea, Colpophyllia) in
the Caribbean are susceptible to at least five of the most prev-
alent and virulent diseases and several other compromised
health problems (Fig. 7). Local populations of the three spe-
cies of Montastraea and other important reef-building spe-
cies in reefs off the Virgin Islands and Puerto Rico have been
devastated by WPD epizootics, pervasive YBD, two inten-
sive bleaching events, and their synergistic impact. For
example, WPD from 2005 to 2007 caused more coral loss
(over 60% loss in live tissue cover) than any other factor up
until 2005/2006 in the USVI (Miller et al. 2009), some reefs
off the east coast of Puerto Rico (García-Sais et al. 2008),
and Curacao and Grenada (Weil and Cróquer 2009).
Similarly, reefs off La Parguera, on the southwest coast of
Puerto Rico, showed an average loss of coral cover of 53.7%
over 4 years (2004–2007), but as a consequence of two WPD
epizootics, a persistent YBD outbreak and the bleaching
event of 2005 (Weil et al., in press) (Fig. 9). Similar coral
tissue losses have been reported for Mona and Desecheo
islands west of Puerto Rico where YBD and bleaching have
been the major problems (Bruckner and Bruckner 2006;
Bruckner and Hill 2009).
As average water temperatures increase, bleaching events
have become more frequent and intense over wider geo-
graphic scales, affecting most zooxanthellae-bearing reef
organisms to increasing depths. Before 2005, bleaching in
the Caribbean caused variable, but generally low coral
484 E. Weil and C.S. Rogers
mortality, nothing like the mass mortalities of the scale
observed in the Indo-Pacific. Only the recent extensive
bleaching of 2005, the worst ever recorded for the region,
produced widespread mortality in several reefs of the eastern
Caribbean, which was compounded with disease outbreaks
in several localities (Miller et al. 2009; Rogers et al. 2008a,
b; McClanahan et al. 2009; Cróquer and Weil 2009a, b).
Significant coral mortality due to bleaching was
observed for the first time in Puerto Rico during this event;
however, this mortality was not widespread across all spe-
cies, suggesting differential susceptibility and specific
resistance to bleaching. Most agaricids, M. ferox, and A.
palmata showed the highest mortality due to bleaching. A
high proportion of other reef organisms (octocorals, hydro-
corals, and zoanthids, and a few sponges) bleached in
many localities (Fig. 5), with some of these showing sig-
nificant population mortalities (i.e. Millepora spp.
Erythropodium caribbaeorum, and Palythoa caribbaeo-
rum) (McClanahan et al. 2009; Prada et al. 2009; Weil
et al., in press).
At the peak of the bleaching, outbreaks of WPD started
to be observed in Puerto Rico, the Virgin Islands, and
Grenada (Hernández-Delgado et al. 2006; Cróquer and Weil
2009b; Miller et al. 2009; Rogers et al. 2008a, b; Weil
et al., in press). Increasing water temperature trends in the
region, possibly associated with global climate change, and
the frequency and intensity of bleaching events could have
affected and will probably affect the emergence, disper-
sion, and virulence of coral reef diseases and their conse-
quences in the recent past and the near future. An increasing
number of colonies and species are being infected by more
than one disease at the same time. Some colonies of
M. faveolata, for example, have been observed with four
different pathologies simultaneously (Cróquer and Weil
2009a, b; Weil and Croquer, unpublished data), which sig-
nificantly increases rates of tissue and colony mortality
over time.
Furthermore, recent studies showed that in addition to the
general tissue loss, some diseases could significantly reduce
the fitness (reproductive output) in important reef species,
similar to what was reported for bleaching almost 20 years
ago (Szmant and Gassman 1990). Sexual reproduction is
critical to coral population dynamics and the long-term
regeneration of coral reefs. Recurrent recruitment failure and
low reproductive output in corals have been highlighted as
explanations as to why reefs are not recovering from major
coral losses (Hughes and Connell 1999; Hughes and Tanner
2000). Recent data showed that ASP significantly reduced
fecundity (fitness) in G. ventalina (Flynn and Weil 2008)
and YBD significantly affected the reproductive output of
M. faveolata (Weil et al. 2009). Furthermore, Cervino et al.
(2001, 2004a, 2008) indicated that all the pale, yellowish
areas in the yellow band lesions are depleted of zooxanthel-
lae, which would reduce local energy supply and potential
energy available for the rest of the colony.
Thirty two percent of reef-building scleractinian corals
around the world face an elevated risk of extinction due
mainly to bleaching and disease driven presumably by ele-
vated sea water temperature and further exacerbated by local
anthropogenic stressors (Carpenter et al. 2008). The propor-
tion of threatened (not including Near Threatened coral spe-
cies) recognized by IUCN exceeds that of most terrestrial
animal groups apart from amphibians, particularly because
of corals’ apparent susceptibility to climate change (particu-
larly high sea water temperatures) and local anthropogenic
factors (Carpenter et al. 2008). This plus all the recent reports
of high mortality rates due to local and/or extensive disease
outbreaks affecting coral reefs worldwide is a major cause of
concern for the future of these important tropical marine
communities.
Progress in coral disease research requires collaboration
among experts across many different disciplines, including
genetics, physiology, cell biology, ecology, pathology,
microbiology, and epidemiology. We need innovative, pref-
erably nondestructive techniques to diagnose diseases. One
promising new approach involves the use of custom-de-
signed microarrays to characterize microbial patterns
(Kellogg and Zawada 2009). Sequential, frequent sampling
of coral colonies with and without disease will reveal
changes in microbial communities over time. Additional
histological analysis of healthy and diseased corals should
provide further clues. Further understanding will come
from laboratory experiments that test the effects of tem-
perature, irradiance, sediments, nutrients, and other pollut-
ants on the development and progression of disease in
corals. Currently, the tools for genotyping coral colonies
Fig. 9 Average loss in live coral cover in nine reefs off La Parguera
between 2003 and 2004, and 2007. The average loss in live coral tissue
for the area was 53.7% (±7.2%) (Modified from Weil et al., in press)
485
Coral Reef Diseases in the Atlantic-Caribbean
are available for only a few species, and developing these
tools for other major reef-building species would help us to
evaluate whether or not certain genotypes are more resis-
tant to diseases.
Even after more than 35 years since the first report of a
coral disease in the Caribbean, researchers keep finding new
diseases affecting corals and other important invertebrates
and CCA groups responsible for building and maintaining
these important tropical communities. Diseases of coral reef
organisms have become one of the most, if not the most,
important factors accelerating the decline of coral reefs and
the potential loss of biodiversity (when the food and energy
sources and the three-dimensional limestone framework in
these communities disappear), compromising the future
integrity of many coral reefs in the western Atlantic. However,
to date there is no report of any coral species that has been
extirpated from disease, even locally.
Reefs in the Caribbean have gone through significant
changes in community structure with decreases in coral
cover and increases in macroalgal cover (Edmunds 1991;
Carpenter 1990a, b; Hughes 1994; Bellwood et al. 2004;
Rogers and Miller 2006; Weil et al., in press). The impact
of diseases on the reproductive output of corals and octoc-
orals further hinder their potential future recovery. Ongoing
monitoring programs and yearly surveys in many localities
have failed to show any significant recovery following the
recent outbreaks (Weil, unpublished data; C.S. Rogers,
personal communication). Even after 25 years, the acropo-
rids and sea urchin populations have not been able to
recover from the epizootic events of the early 1980s.
Collapsed coral populations would produce significantly
fewer larvae, so recruitment and juvenile survivorship
would be potentially very low making it difficult, or slow,
for populations to recover, even if environmental condi-
tions and other factors are favorable. In Puerto Rico, sur-
viving populations and new recruits and juveniles of A.
palmata were frequently affected by storms, hurricanes,
sedimentation, and anthropogenic impacts after the mass
mortalities of the 1980s (Weil et al. 2003).
Even though some positive results indicating lower num-
bers and prevalence of coral diseases inside marine pro-
tected areas (MPAs) and/or marine reserves have been
reported (Raymundo et al. 2008), more information is
needed to generalize the potential “protection” these areas
provide to coral populations. Coral reefs within and outside
of MPAs in the US Virgin Islands had losses of over 60% of
the coral cover following the disease outbreak associated
with the 2005 bleaching episode (Miller et al. 2009; Rogers
et al. 2008a, b). In other localities, disease prevalence inside
MPAs was not lower than outside MPAs (Coelho and
Manfrino 2007: Page et al. 2009). It is challenging to test
the hypothesis that coral reefs within MPAs will be less sus-
ceptible to diseases than those outside protected areas. A
variety of complex factors has to be controlled for, for
example:
The actual level of protection that the area receives •
(reflecting compliance with regulations and effectiveness
of enforcement)
The length of time that protective measures have been in •
place
The type of protection (prohibition of fishing, anchoring, •
etc.)
The history of fishing and any other extractive uses before •
the area was effectively protected [some areas might have
had very little fishing to begin with, for example]
Other stressors like runoff, pollution that could affect the •
condition of the marine resources
Prevalence of diseases before the MPA was established•
The validity of the control (“reference”) areas used for •
comparison with protected areas
Our current limited knowledge of the pathogenesis and
other important aspects of most coral reef diseases (Lesser
et al. 2007) undermines our ability to develop strategies to
solve the problem in the near future. MPA boundaries will
not prevent disease outbreaks or bleaching events, but, pro-
tecting large, genetically variable fecund populations of the
most important reef-building groups could increase the
species survivorship by protecting potentially resistant gen-
otypes that could then reseed other degraded populations
outside the reserves (Vollmer and Kline 2008).
6 Summary
Coral reefs are declining around the world due to natural and/
or human-produced stressors, including global climate
change. Recently, diseases of coral reef organisms have
become increasingly important in the deterioration of these
important marine communities. The Caribbean has been
dubbed a “disease hot spot” due to the fast emergence of dis-
eases and frequent epizootic events with significant coral
mortalities in the last 30 years. Fifteen disease conditions
affecting corals and other important reef organisms have been
described, but most do not have defined pathologies nor have
they been well characterized. Of these, ten conditions with
consistent signs are affecting most of the important reef-
building coral species, five are affecting at least 12 species of
octocorals, two at least three species of crustose coralline
algae (CCA), and two a single zoanthid species, while several
uncharacterized conditions affect sponges and other reef
organisms. Variability in disease manifestation and distribution
complicates their characterization and identification. Most of
these diseases have a Wider Caribbean distribution with a
few, like black band disease, showing worldwide distributions.
486 E. Weil and C.S. Rogers
Three widespread and several local outbreaks produced sig-
nificant mortalities over a wide geographic range, with a cas-
cade of significant changes in community structure, decreases
in coral cover, and increases in macroalgal cover. The impact
of diseases on the reproductive output of corals and octocor-
als further hinders their potential for recovery. Our limited
understanding of the pathogenesis of most coral reef diseases
undermines our ability to develop strategies to reduce their
effects in the near future. Further advances in coral disease
research require collaboration among experts across many
different disciplines, development and use of new techniques,
and controlled laboratory experiments. Caribbean coral reefs
will benefit from protection of resistant coral genotypes along
with greater efforts to reduce the manageable stresses caused
by humans. Protecting large, genetically variable fecund pop-
ulations of the most important reef-building species could
increase the survivorship of resistant genotypes that could
then reseed degraded populations. However, this has to come
together with greater efforts to manage human activities that
stress coral reefs, and the reestablishment of former environ-
mental quality for the survival of coral reefs in the region.
Acknowledgments We thank Zvy and Maya Dubinsky for their kind
invitation to be part of this book. Thierry Work, Kim Ritchie, Ken Sulak,
Noga Stambler, and an anonymous reviewer made important comments
and suggestions that helped improve this contribution. Some results
presented here come from research funded by the GEF-World Bank
CRTR program through the disease working group and NOAA-CRES
Grant (NA170P2919) to E. Weil.
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