3.b Diseases with pathogens: These involve the presence of a distinct disease causing agent;
this group includes Black Band Disease (BBD), Black Overgrowing Cyanophyta (BOC), Black Aggressive Band (BAB),
Bacterial Infection (BI), Fungal Infection (FI), Lethal Orange Disease on reef building coralline algae (LOD), as well as
recent discoveries like Skeleton Eroding Band (SED) and (PEY).
- Bacterial Infection (BI): Mucus production is the main defense mechanism against outside intruders and is important
to fight diseases. But sometimes the mucal slime (fig.13), consisting mainly of glycopeptides, can lead to an unwanted cultivation
of carbon and nitrogen feeding microorganisms, dominated by Desulvovibrio and Beggiatoa species in its final
stages. In sever cases, when attacked by Phormidium corallyticum it is almost certainly will infect the coral tissue with
Black Band Disease (BBD - see below). Heavy microbial activity along with trapped sediments, quickly lowers the dissolved
oxygen level of the closely surrounding waters, suffocating the delicate coral tissue underneath. Only strong wave action or
currents can save the coral by mechanically ripping off the slimy coverage within days after formation.
Fig.13 Protective mucus on Siderastrea sidera (40kB)
Black Band Disease (BBD): It is probably the best-known pathogenically caused
coral disease. Similarly as in WBD a black band of "grazing" bacterium called Phormidium corallyticum =
Oscillatoria submembranacea (fig.19); a photosynthesizing, gliding, filamentous cyanobacterium that appears in
association with other cyanobacteria; e.g. Spirulina sp.; it proceeds progressively outward, thus
affecting the entire colony. Being contagious, BBD can spread easily to other corals by means of wave action.
P.corallyticum eats its way from the upper surface where it spreads relatively fast, to the edges of the coral
surface (fig.15). Under certain circumstances microscopic densely interwoven algal filaments (trichomes without
significant cell wall constructions) of the pathogen originating from diseased coral colonies, form a blackish mat
(predominantly on scleractinians of the family Faviidae - fig.16).
If enough light is available, to form a tiny algal spot, it gradually turns into a dark ring of tissue-stripped coral skeleton
that proceed onwards with a few cm/week, enlarging the denuded area (fig.17). Small corals can be
deprived entirely of their living tissue, while larger ones can resist, once the black ring reaches the less illuminated
flanks of the colony (fig.18). In many cases the coral can fight BBD by producing an excess of mucus, thus starving the
Although it is suggested that BBD may have a role in maintaining coral diversity because it is most prevalent in coral species
that form large colonies and provide a structural framework for epibenthic organisms, BBD in combination with other diseases
on a stressed reef can have devastating effects. BBD has a higher rate of infection in warmer water.
Thus, not only seasonal temperatures, but anthropogenic disturbances as well (under eutrophic conditions
even coral species immune to it are attacked and even killed) affect the spread of BBD. Similarly, as in WDB,
coral stocks suffering from BBD are likewise susceptible to tumors and parasitic worms.
Fig.17 Montastrea cavernosa (80kB)
Fig.18 Montastrea annularis (110kB)
Red Band Disease (RBD): As the name indicates, the "band" is a soft microbial
mat that is brick red or dark brown, not black, in color and easily dislodged from the surface of the coral tissue.
This disease affects hard star, staghorn, and brain corals (fig.20) of the Caribbean and the Great Barrier Reef.
The band in RBD appears to be composed of different cyanobacteria and microorganisms
than those found in BBD and the microbial mat movement is different; the types of microbes present might be
different depending on the coral host, but little is known about this. Several scientists are studying the composition
of these microbial mats to determine how they differ from the BBD mats.
Fig.20 RBD on Colpophylia natans (90kB)
Black Overgrowing Cyanophyta (BOC): A number of other cyanophytic species
like Calothrix crustacea, C.scopulorum, Hormothamnium solutum, Langbia confervoides, L.semiplena, Phormidium
spongeliae, and Spirulina subtilissima sometimes simply overgrow the coral, starving the polyps (fig.21). But
in other cases they even actively penetrate and erode the coral skeleton, leading to the structural collapse of a
branching coral. In some cases, under eutrophic conditions, BOC is not only more common but may even trigger WBD.
Fig.21 Acropora sp. with BOC (70kB)
Black Aggressive Band (BAB): Although similar in appearance to BBD,
the band material is somewhat thinner and appears gray rather than black allowing the tissue-deprived coral to
shine through. Recent studies revealed another cyanobacterial genus (Spirulina) as one possible cause,
but it is not excluded that even a spirochete Ballesteros sp. could be the main pathogenic agent.
High phosphorous contents in affected tissues suggest that eutrophication may be one way to trigger of BAB,
since its appearance is closely related to shallow and coastal areas.
Lethal Orange Disease (LOD): A yet unknown bacterial pathogen causes
death of the reef-building coralline algae Porolithon onkodes. This coralline alga is the principle cementing
agent that maintains the intertidal wave-resistant reef crest. It helps the coral reef community by cementing together
sand, coral fragments, and other debris into a suitable hard substrate for the establishment of coral colonies.
It absorbs wave energy in the outer reef rim that would otherwise erode the shoreline and destroy many
shallow-water reef communities. LOD leaves the coralline algae skeleton white as it progresses in an orange band,
destroying the algae (fig.22). When spreading, the front reaches the margin of the algal thallus, it forms upright filaments
and globules, similar to those formed by terrestrial slime molds. The globules can be caught by waves and easily spread
to nearby corallines.
Coralline Lethal Disease (CLD): It lacks the characteristic orange color of LOD, but is lethal, nonetheless.
CLD is apparent as concentric white circles surrounding patches of green filamentous algae that have colonized
the dead portion of the coralline algae Halimeda sp. (fig.23).
Fig.22 Coralline algae (70kB)
Fig.23 Coralline algae (100kB)
- Fungal Infection (FI): As the name indicates, fungal infestations on corals are the main agent but have been
observed to occur along with other pathogens. A lower phycomycetous fungus has been associated with BBD in certain
star corals (Montastrea annularis - see also Parrotfish bites in association with fungal infection - further below);
whereas BBD has been found to appear along with an ascomycetous fungus. Other cases which involve a hyphomycetous
fungus (Scolecobasidium sp.) are considered true fungal infections that affect only massive or platy corals. It forms
necrotic patches (thus, termed also FIN) that reveal a zoned pattern. The top layer of the necrotic patch is overgrown with
epilithic algae, sometimes intermingled with fungus. This is followed by a thin zone of fungal growth giving way to a green band
containing shell-boring algae. Beneath this strip lies a dense layer of fungal growth. The fungal zones above and below
the green band (only about 0.5 to 1.5cm in width), appear brown to black and sometimes penetrate deeply into
the coral skeleton. Aspergillus sp. (Eumycota) is a known pathogen commonly found on Gorgonians (fig.24).
Fig.26 Fungal infection on Gorgonia sp. (192kB)
- Yellow Band Disease (YBD also Yellow-Blotch Disease): It manifests itself as
a broad yellow band moving across healthy coral tissue in a manner similar to the BBD. A band of decaying and
sloughing off tissue is observed. However, the entire area denuded by the infection can retain the characteristic
yellow color which can penetrate some millimeters into the skeleton. The YBD appears to be in no way similar to
the aggressive LOD, which attacks coralline algae. Investigations into establishing a pathogen are underway.
Species found to be affected by YBD are sclerectinians such as staghorn (Acropora sp., Porites sp.),
honeycomb corals of the family Faviidae, plate corals (Turbinaria sp.), and even ecrusting species of the
Fig.28 Montastrea faveolata (50kB)
- Dark Spot Disease (DSD): It is based on increases in the occurrence of lesions and
observations of loss of tissue associated with the spots (fig.29). Dark purple to gray or brown patches of discolored
tissue, often circular in shape but also occurring in irregular shapes and patterns, are scattered on the surface of the
colony (bright purple patches have also been seen on bleaching colonies) or appear adjacent to the sediment/algal
margin of a colony. Sediment can accumulate in the centers of these patches, with bare skeleton occasionally
seen when the sediment is brushed off. Investigations to isolate a distinct pathogen have not yet been successful.
It could well be that a combination of pathogens may trigger this disease.
Fig. 29 Siderastrea sidera - (60kB)
- Skeleton Eroding Band (SEB): A novel type of coral disease has been identified on Indo-Oacific reefs. It is caused
by Halofolliculina corallasia, an eukyryotic protozoan, or more specifically, a colonial, heterotrich ciliate that
damages not only the living tissue nut also the skeleton of the coral. The syndrome is found on a wide variety of massive and
branching corals, and progresses similarly as in cases of BBD. The skeleton eroding band (fig.30) consists of masses of black
loricae (black shaped housings) of the ciliate, with bifurcated, beige wings sticking out, resembling a bed of microscopic garden
eels (about 200um - fig.30, bottom right). Upon asexual reproduction, the loricae of the ciliate kill the colonized area by emitting
chemicals that cause lysis of the coral tissue. The dotted appearance of the white zone behind the front distinguishes SEB from
BBD. SEB was found on reefs of the Sinai (Red Sea), Mauritius, (Indian Ocean) and Lizard Island (Pacific, GBR).
Fig.30 Acropora sp. (125kB)
- Epizoism (EZ): Under certain circumstances, various epizoic organism were observed to overgrow
living sclerectinian corals. The phaeophyta Lopophora variegata, the sponge Terpios hoshinota (fig.31),
the zoanthid Palythoa sp., some ascidians (e.g. Didemnidae), or the octocoral Erythropodium sp. Although
epizoism per se does not represent a disease, but is rather associated with interspecific competition, it is of perticular interest, as
current antropogenically induced nutrient shifts and global warming may induce booming reproduction of faster growing epizoic
organisms by upsetting the existing a/biotic balance and ultimately altering a once flourishing coral reef from a "catch-up" reef
to a "give-up" reefs (for a more detailed look about threats to coral reefs, try
Fig.31 Epizoic sponge (170kB)
PEYssonnelia (PEY): Among recently described syndromes of epizoism on reef corals, is one caused by an unusual
species of Rhodophyta, Corallinaceae - Metapeyssonnelia corallepida. It is a new species of a genus known only
from the Mediterranean Sea. This epizoic disease destroys corals on reef crest areas, where it was not recorded at all 25yrs
ago. M.corallepida is capable of overgrowing entire corals - mainly those hydrocorals of the genera Millepora
(M.complanata, M.alcicornis) and the scleractinians of the genus Porites P.porites, P.astreoides. The
affected species shown in fig.32 reveals the pattern of the disease. It starts at the dead base of the colony and proceeds
upwards by overgrowing and destroying living polyps and soenosarc. PEY forms a tightly attached "skin" on the coral surface
without a trace of coral tissue left below the algal cover (fig.32, right).
Fig.32 Millepora complanata (130kB)
- PNEophyllum (PNE): A coralline red algal species Pneophyllum conicum (Corallinacea) that like PEY
overgrows and kills living corals. It predominantly occurs from intertidal reef-crests to depths >30m; and from sun-drenched upper
reef surfaces deep into poorly illuminated caves. The color of the alga tends to correspond to the exposure to light (dark purple
in the dark to gray at bright sites). It usually starts from the dead basal portion of the coral colony (or cracks and crevices) and
expands its way up to the living portions. Usually this corallinacea does not pose a threat to corals, but under certain conditions
(that still await demystification) can be quite lethal to most Pocilloporidae, some Porites sp., and Faviidae ( Favia
stelligera, Favites complanata, F.abdita, F.flexuosa, Goniastrea retiformis - fig.33, Platygyra daedalea, P.lamellina, Leptoria
Fig.33 Goniastrea retiformis overgrown by P. conicum
3.c Diseases involving a combination of various diseases
- White Syndromes (WS): A disease characterized by the combining effects of WBD, TBL, and SDR.
WS seems to be linked to the corallivorous snails Drupella cornus (fig.34) or Coralliophila violacea.
It is suggested that WS-Drupella interaction occurs in three phases:
Phase 1: D.cornus snail, when occurring in low numbers, are attracted by the disintegrating coral
tissue and usually feed on the exact interface of WBD - at that stage, they do not attack healthy coral tissue.
Phase 2: Larger concentrations of D.cornus feed on healthy tissue at a speed far exceeding that of
Phase 3: The impact of excessive feeding by D.cornus triggers SDR, destroying more coral tissue than is
occupied by snails; being stranded on a coral branch without tissue, the horde of D.cornus will move on to new
Fig.34 Drupella sp. (90kB)
3.d Mutations and other Tissue Abnormalities: |
The white calcium carbonate skeleton of a hard coral is deposited by a thin layer of cells known as the
calicoblastic epithelium. Skeletal morphology is primarily controlled by genetics. The shape of the skeleton
which protects the colony of polyps varies with species, resulting in a number of characteristic shapes
that allow even the non-professional observer to distinguish between many coral species.
Skeletal deposition can change as a result of the actions of mussels, barnacles, christmas tree worms,
and commensal crabs, all of which may bore holes in the coral skeleton and cause the coral to change
the pattern of skeletal deposition. Other skeletal anomalies are caused by changes in the coral cells that
deposit the carbonate skeleton. Two such changes are hyperplasia and neoplasia (cancer).
- Hyperplasia (hyperplasm): A biological process that leads to an increase in the number
of cells in a tissue or organ, thereby increasing the bulk of the tissue or the organ (fig.35). A hyperplasm is a mass
formed through the increase in the number of cells. It appears that such growth originate from a single budded
polyp that undergoes localized, rapid growth, while retaining functional fusion of its tissues with those covering
the normal colony skeletonas well as reproductive properties and are found in most coral species. Although, it
originates from somatic cells (non sex cell) mutations, they may well be a source of instant new species development
Fig.35 Diplora clivosa (left) D.strigosa (right)
- Neoplasia (neoplasm): A pathologic process that results in the formation and proliferation of
an undifferentiated mass of cells. These cells grow and multiply more rapidly than normal and lack the structural organization
and function of the normal tissue. These calcified protuberant masses on branching corals have lost their normal
structure and have been shown to consist of undifferentiated calicoblastic epithelial cells. A study of the stable
carbon isotope ratio of the calcium carbonate coral skeleton demonstrated that it was deposited in a very
different manner, being laid down much more rapidly than normal, a finding consistent with the rapid metabolic
rate of the tumor. White, protuberant, irregularly shaped, calcified masses or tumors, covered by a thin layer of
translucent tissue, occur on the surfaces of branches of Acropora spp. and other members of the acroporid
and pocilloporid families of hard corals (fig.36).
Fig.36 Acropora palmata (145kB)
The cells found in the tumor resemble the more metabolically active and rapidly dividing cells of the growing branch
tips, and like the branch tips, also lack the symbiotic algae. The epidermis covering the tumor also loses the mucus
secretory cells that help remove sediments from the coral surface. The result is that sediment accumulations lead to
tissue death and invasion of the skeleton by algae and boring organisms. The presence of the tumors on a branch is
also associated with a decrease in/or halting of branch tip growth, suggesting changes in the transport of nutrients
in the colony. This locally invasive abnormal mass of tissue and unusually porous skeleton grows faster than the
surrounding normal tissue and skeleton. It proceeds to destroy the polyps and cause the death of the coral tissue.
Based on these factors, this condition has been termed a neoplasm (cancer), calicoblastic epithelioma.
4. Other bio-destructive agents acting on reef corals: Because coral tissue is only a few
millimeters thick, any contact (touch, bumped or walked on) can abrade this tissue from the surface. A certain
amount of abrasion is not catastrophic for corals because they are very plastic and can regenerate quickly
(similarly as in human skin); but if the affected area is continually scraped, the healing process is interrupted
and the wound becomes infected by bacteria and fungus. Often tumors can be triggered by an injury in which
the healing process goes awry (see above).
Parrotfish feed on the endosymbiont of the coral tissue, producing extensive scrape marks and destruction of tissue
and skeleton. The scrapes have often mistakenly been diagnosed as White Pox Disease (WPD) or Rapid
Wasting (RW), as it leaves blotches all over the coral, from base to tip. In its advanced stages the living tissue of the coral
is reduced by 50-80%. At certain locations, it has decimated 50-80% of elkhorn corals (Acropora palmata), the major
reef-building coral for shallow Atlantic reefs (fig.6). In stressed colonies these patches are often colonized by filamentous algae,
whereas under normal conditions, the coral tissue and skeleton is showing regrowth (sometimes covering the algal patch by a
translucent white "lip" of tissue and skeleton).
Terminal-phase males of the stoplight parrotfish Sparisoma viride that repeatedly attack corals like M. annularis
(fig.38) leave characteristic nibbling imprints on these corals and are a mediating element in transmitting diseases from one
colony to the next. In several cases a yet unidentified fungus has been found at the scar surface of the corals. The combination
of mechanical abbasion of parrotfish and fungal infection coined the degenerative terminology of rapid wasting. Examination of
samples of tissue and skeleton from affected coral colonies revealed that the fungus is able to penetrate into the exposed coral
skeleton coral tissue.
Fig.37 Sparisoma viride (145kB)
Fig.38 Montastrea annularis (60kB)
Damselfish have far-reaching consequences for maintaining reef diversity. They are highly territorial species and
aggressively defend their algal cultivations and thus, inhibit not only recolonization by coral planulae larva, but by preferentially
consuming macroalgae, remov fouling epibionts from corals, as well as exclud other herbivorous fish (e.g. Scaridae). They can
maintain territories with markedly different algal community compositions, higher productivities, and diversities than in surrounding
unprotected ares (for a more detailed insight about CoT, try this
Some well known outright predators include the polychaete Hermodice carunculata(fig.39), the gastropods of the genera
Turbo sp., Drupella sp., (fig.34), and Cyphoma sp., as well as several seastars, with the most prominent
predator known as the crown of thorn (CoT), Acanthaster planci (fig.40).
Fireworms are quite commonly found beneath boulders and coral heads. Hermodice caranculata (fig.39) feeds at
night on live corals, mainly Porites. The common name results from sharp setae which project in tufts from the parapodia,
and which tend to penetrate the skin and break off inside the flesh of those who handle them. They can cause quite
intense local pain and the wounds sometimes become infected.
An indirect anthropogenic effect is described by the Caribbean-wide mortality in the reef dwelling sea urchin
Diadema antillarum was shown to indirectly affect coral reefs since it functions as both a grazer on
algae that can otherwise smother coral and as a bioeroder of corals as it feeds on them. Quite the opposite is observed by the
CoT (fig.40). This nocturnal predator feeds by everting its gastric pouches. Doing so enables the CoT to dissolve the
living tissue of not only of flat table corals but also unevenly shaped colonies. As the dissolving chemicals attract more CoT to
the feeding ground, they prey even during the day (for a more detailed insight about CoT, try
.... please continue with section "Reef Monitoring"
Fig.39 the fireworm Hermodice carunculata (140kB)
Fig.40 Acanthaster planci (150kB)