3. Coral Diseases (pathologic syndromes of reef corals)

In order to understand the growing appearance of coral diseases and to stabilize at least the current status quo, coral pathology has to step out of its neglected existence to become a growing side-branch of coral reef science. Reefs are very sensitive to environmental conditions. They are adapted to extreme oligotrophic conditions. Under normal conditions, diseased or even dead corals never exceeds 5% of the total undisturbed reefs. But changes in coral health and vitality (disease, algal overgrowth, bleaching, etc.) may be more sensitive indicators of changing environmental conditions. All the man-made stresses (chemical and thermal pollution, sedimentation, dredging, blasting, boat anchoring, recreational activities, etc.) not only exert considerable pressure on these organisms, but also enforce the frequencies of coral pathogens. Thus, pathologic syndromes of reef corals are commonly grouped into those acting without and those mediated by a pathogen.
3.a Disease working without a pathogen: Although no pathogen is involved in the progress of the disease, the pathogenic reaction is caused by external (i.e. abiotic) influences as in the cases of Tissue Bleaching (TBL), Shut-Down-Reaction (SDR), and White Band Disease (WBD).
  • Tissue Bleaching (TBL): Coral bleaching or tissue bleaching refers to the whitening of coral colonies brought about by a reduction in the number of zooxanthellae from the tissues of polyps, by a loss of photosynthetic pigment, or by a combination of both. This loss exposes the white calcium carbonate skeletons of the coral colony (fig.7). Corals naturally loose less than 0.1% of their zooxanthellae during processes of regulation and replacement. However, adverse changes in a coral's environment can cause an increase in the number of zooxanthellae lost. There are a number of stresses or environmental changes that may cause bleaching including excess shade, increased levels of ultraviolet radiation, sedimentation (necrosis in soft corals), pollution, salinity changes, elevated atmospheric CO2 levels, industrial seawater pollution, or excess freshwater runoffs. But the strongest evidence was found to be an increased surface water temperature that is quite often linked to the phenomenon known as ENSO (El Nino and Southern Oscillation) - see also the NOAA web site about Sea Surface Temperatures. (TBL in deeper water, without perceptible temperature changes, remain largely unexplained).
    TBL is not necessarily lethal, and corals are usually able to recover their symbionts once environmental conditions return to normal. However, for the duration of the bleaching event, tissue biomass, growth rate, and reproduction rate are all negatively affected, and, if stresses last long enough, the condition may eventually lead to the death of the specimen or even to the demise of the entire section of a reef tract (fig.8).
    Corals bleach in response to prolonged temperature change (due to the combined affect of clear skies, calm sea and maximum summer solar irradiation) and not due to rapidly fluctuating temperatures. Lab experiments show that corals bleach when water reaches or exceeds a constant 32C and an increase of UV exposure. The amount of mycosporine-like amino acids in a coral's tissues helps to determine how much UV it can withstand without bleaching.

 


Fig.7 TBL (120kB)


Fig.8 Montastrea faveolata
before and after (190kB)

  • Shut-Down-Reaction (SDR) - often referred to as Rapid Wasting (RW), Rapid- or Stress- Related Tissue Necrosis (RTN/SrTN), White Plague (WP), or White Death (WD) - (fig.9). Observations in laboratory experiment and field observations of corals under sublethal (abiotic) stress such as elevated temperature, sedimentation, chemical pollution, have revealed that specimens can die from a simple scratch. Such sudden disintegration of the coral tissue, that starts at the margins of the injury, is characterized by sloughing off the tissue in thick strands of blobs from the coenosarc, leaving behind a completely denuded coral skeleton. From the initial interface, the phenomenon proceeds in an enlarging circle on massive corals, or moves along the branches in ramose forms, spreading to all side-branches upon reaching a junction. It is still unclear if SDR represents a disease on its own, as the thriggers match those in WBD or WS (see below), although there seem to be significant differences regarding the speed this disease effects a colony. Thus, SDR is especially dangerous as it can spread with an average speed of 10cm/hour - fast enough to be visually observed! Being contagious, SDR can be transmitted by a floating strand of dissolved, contaminated tissue to produce an onset on a neighboring stressed colony. Thus, triggering a catastrophic chain reaction, which may occur several times during the course of a season. It usually affects species of the Caribbean, such as small star corals Dichocoenia stokesii, pillar corals Dendrogyra cylindrus, and boulder corals Montastrea annularis (fig. 10).

 


Fig.9 Mycetophyllia ferox (70kB)

 


Fig.10 Necrosis on Montastrea annularis (70kB)
  • White Band Disease (WBD): As the name suggests, it refers to a band of white coral skeleton that represents a moving front of tissue destruction of scleractinian corals (fig.11, 12). Although less aggressive and not infectious and contagious as SDR (it advances with an average speed of a few mm/day), it nearly irradicated the Caribbean Acropora palmata over large areas during the 1970s and 80s (fig.13). Several attempts at finding a distinct pathogen have been unsuccessful, although smears of WBD regularly yield a considerable variety of bacteria (GramPOS, GramNEG, and cyanophyta).
    WBD is strongly affected by abiotic conditions (e.g. temperature) and can be triggered by the settlement of blue-green algae (which are toxic to corals). The site of settlement is usually outlined at the interface of the coral corpus with the benthic sediment; i.e. the shaded area, at the base of the coral. An algal turf of green color, e.g. Chlorophyta, is considered harmless, whereas a dark pigmented algal overgrowth of Cyanophyta may trigger WDB. Settlement of blue-green algae can also occur on damaged surfaces caused by external influences (wave action or even uncontrolled impacts with snorkelers or divers). These facts indicat that stressed colonies with an already low tolerance to further impacts are easily susceptible (see fig.5 - stress phases). Reef structures affected by WBD can lead to a massive die-off, favoring tumors and is always accompanied by biotic activity of epizoic parasites such as GramNEG rod-shaped bacteria, ciliates, protozoans, acoel turbellarians, nematodes, tiny copepods and/or amphipods. The forming algal overgrowth subsequently results in the death of the coral colony by successively becoming colonized by bioeroding endolithic invertebrates, gastropods, and boring cloinid sponges rendering the remaining "healthy" structure more susceptible to breakage during storms.
    Recent studies tend to further differentiate WBD into the classical form as type I and a somewhat altered form WBD-II;
    WBD-I: GramNEG rod-shaped bacteria were found in the tissues of affected corals. However, as mentioned above, the role of this microorganism in the development of disease has not yet been determined.
    WBD-II: In this disease, a margin of bleached tissue appears before the tissue is lost. Bacteria of the genus Vibrio have been found in the surface mucus of the bleached margin.

    .... please continue with section "Diseases acting with a pathogen"

 


Fig.10 Favia pallida (150kB)

 


Fig.11 Diploria strigosa (left); Agaricia agaricites (right); even interspecific competition may triger WBD (70kB)

 


Fig.12 WBD on Acropora palmata (70kB)