|
Coral diseases: what is really known?
Reports of new and emerging coral diseases have proliferated in recent years. Such coral diseases are often cited as contributing to coral reef decline. Many of these diseases, however, have been described solely on the basis of field characteristics, and in some instances there is disagreement as to whether an observed coral condition is actually a disease. A disease pathogen has been identified for only three coral diseases, and for only two of these has the pathogen been shown (in the laboratory) to be the disease agent. In one case, the same disease name has been used for several widely varying coral syndromes, whereas in another multiple disease names have been applied to symptoms that may be caused by a single disease. Despite the current confusion, rapid progress is being made.
|
Infectious diseases of reef corals
The continuing degradation of coral reefs throughout the world is accompanied by increasing observations of
infectious diseases and disease outbreaks of corals and other coral reef benthic organisms. Microbial pathogens of
both stony corals and gorgonians have been isolated and in some cases characterized. Underlying mechanisms of the
pathogenesis of several diseases are being studied at the microbiological, physiological, and molecular levels. The
short- and long-term ecological effects of disease outbreaks on reefs in different geographic regions are being
documented as they occur. In one paleoecological study a coral disease was revealed to have caused an
unprecedented alteration in community structure. Here we review recent progress in the field of coral disea
|
Histopathological methods for the investigation of microbial communities associated with disease lesions in reef corals
Aims: To determine the spatial structure of microbial communities associated with disease lesions of reef corals (Scleractinia).
Methods and Results: Agarose pre‐embedding preserved the structure of the disease lesion and surrounding tissues prior to demineralization of the carbonate exoskeleton and embedding in resin. Fluorescence in situ hybridization (FISH) was used to localize bacteria in the lesions of various diseases.
Conclusions: The techniques successfully preserved the in situ spatial structure of degenerated coral tissues. In one case (white plague disease), significant bacterial populations were found only in fragmented remnants of degenerated coral tissues at the lesion boundary that would not have been detected using conventional histopathological techniques.
Significance and Impact of the Study: Determining the composition, spatial structure and dynamics of microbial communities within the disease lesions is necessary to understand the process of disease progression. The methods described may be applicable to a wide range of diseases involving necrotic lesion formation and requiring extensive tissue processing, such as skeleton demineralization.
|
The etiology of white pox, a lethal disease of the Caribbean elkhorn coral, Acropora palmata
Populations of the shallow-water Caribbean elkhorn coral, Acropora palmata, are being decimated by white pox disease, with losses of living cover in the Florida Keys typically in excess of 70%. The rate of tissue loss is rapid, averaging 2.5 cm2⋅day−1, and is greatest during periods of seasonally elevated temperature. In Florida, the spread of white pox fits the contagion model, with nearest neighbors most susceptible to infection. In this report, we identify a common fecal enterobacterium, Serratia marcescens, as the causal agent of white pox. This is the first time, to our knowledge, that a bacterial species associated with the human gut has been shown to be a marine invertebrate pathogen.
Epizootics have been reported for several coral species (1–6), and evidence is mounting of substantial declines in the biodiversity and abundance of reef-building corals (7). The greatest losses within the Caribbean are among the branching elkhorn and staghorn corals, Acropora palmata and Acropora cervicornis, for which losses have been documented in St. Croix (8), Belize (9), Jamaica (10–12), Florida (13), and the Bahamas (14). Since the mid-1990s, observations of new coral diseases have been on the rise (1, 6). The Florida Keys National Marine Sanctuary has sustained an ecosystem-wide increase in the number of coral species exhibiting disease as well as the number of reef sites with diseased corals (6). The etiologies and mechanisms of tissue death of the majority of coral diseases are not understood (2), and epidemiological data regarding the losses to coral reef communities due to these diseases are scarce. In this paper, we fulfill Koch's postulates and describe the etiology of white pox disease. We also quantify substantial population losses suffered by white pox-affected colonies of A. palmata in the Florida Keys.
White pox disease was first documented in 1996 on Eastern Dry Rocks Reef (24° 27.715′ North, 81° 50.801′ West) off Key West, FL (15). The disease has since been observed on reefs throughout the Caribbean (6, 16–18). White pox exclusively affects the elkhorn coral, A. palmata, an important Caribbean shallow water species that provides elevated rates of calcium carbonate deposition (19) and the highly complex three-dimensional structure of the shallow water fore reef. Coral colonies affected by white pox disease are characterized by the presence of irregularly shaped white lesions where tissue has disappeared from the skeleton (Fig. 1). Lesions range in area from a few square centimeters to greater than 80 cm2 and can develop simultaneously on all surfaces of the coral colony. The distinct white patches and the potential for tissue loss everywhere on the coral colony distinguish this disease from white-band disease (8), which develops at the base of a coral branch and progresses upward toward the branch tip in a concentric ring. Disease signs also clearly differ from coral bleaching and predation scars produced by the corallivorous snail, Coralliophila abbreviata (20, 21). Newly bared calcium carbonate skeleton of white pox-affected A. palmata is rapidly colonized by a variety of turf algae.
|
|
|
|
Vibrio harveyi as a causative agent of the White Syndrome in tropical stony corals
We investigated bacterial assemblages associated with corals displaying symptoms of the ‘White Syndrome’ (WS), a general term used for indicating the appearance of bands, spots or patches of tissue loss, which is devastating wide areas of tropical ecosystems worldwide. We collected WS‐diseased (n = 15) and healthy (n = 15) corals from the natural reef (Indonesia, Indian Ocean) and from four large public aquaria. By using culture‐dependent and culture‐independent techniques, we found that a large fraction (73%) of the investigated WS events was associated with the presence of a high bacterial abundance and, specifically, of Vibrio spp. Vibrio harveyi, a pathogen of many marine organisms and recently involved in coral Yellow Band disease, was the most represented species, being recovered from five out of 15 diseased corals. In experimental infection assays, two V. harveyi strains, isolated from diseased corals, were inoculated on a total of 62 healthy colonies of Pocillopora damicornis. WS signs appeared in 57 corals, confirming the ability of V. harveyi strains to induce the disease. We conclude that V. harveyi is one of the coral pathogens involved in the appearance of WS. However, not all of the investigated WSs were associated to V. harveyi detection, nor to other Vibrio species (such as V. coralliilyticus), which supports the hypothesis that WS is not caused exclusively by Vibrio spp., but rather can have a multifactorial aetiology, or can represent a group of diseases caused by a variety of agents. Further investigations to identify specific virulence traits will contribute to the understanding of the role of V. harveyi in WS pathogenesis.
|
Vibrio owensii Induces the Tissue Loss Disease Montipora White Syndrome in the Hawaiian Reef Coral Montipora capitata
Incidences of coral disease in the Indo-Pacific are increasing at an alarming rate. In particular, Montipora white syndrome, a tissue-loss disease found on corals throughout the Hawaiian archipelago, has the potential to degrade Hawaii’s reefs. To identify the etiologic agent of Montipora white syndrome, bacteria were isolated from a diseased fragment of Montipora capitata and used in a screen for virulent strains. A single isolate, designated strain OCN002, recreated disease signs in 53% of coral fragments in laboratory infection trials when added to a final concentration of 107 cells/ml of seawater. In addition to displaying similar signs of disease, diseased coral fragments from the field and those from infection trials both had a dramatic increase in the abundance of associated culturable bacteria, with those of the genus Vibiro well represented. Bacteria isolated from diseased fragments used in infection trails were shown to be descendants of the original OCN002 inocula based on both the presence of a plasmid introduced to genetically tag the strain and the sequence of a region of the OCN002 genome. In contrast, OCN002 was not re-isolated from fragments that were exposed to the strain but did not develop tissue loss. Sequencing of the rrsH gene, metabolic characterization, as well as multilocus sequence analysis indicated that OCN002 is a strain of the recently described species Vibrio owensii. This investigation of Montipora white syndrome recognizes V. owensii OCN002 as the first bacterial coral pathogen identified from Hawaii’s reefs and expands the range of bacteria known to cause disease in corals.
|
The significance of emerging diseases in the tropical coral reef ecosystem
Novel pathologies of coral reef organisms, especially reef frame building scleractinian corals, have escalated during the decade between 1987 and 1997. These emerging diseases have appeared with progressively greater frequency and over wider distribution, and have revealed more diversified characteristics than ever before. The causes of most of these infections are no! ye! confirmed, but they evidence a gradual decline in the vital status of the coral reef ecosystem. As specific causes are identified for these afflictions, terminology will shift from non-specific descriptions, such as "white band", "white plague", "white pox", "yellow band" and "black band" diseases, to etiological and pathognomonic characterizations (e.g. aspergillosis and cyanobacteriosis). Stony corals are vulnerable to sedimentation, nutrient overloading, and chemical pollution from agricultural, urban, and domestic sources. They are incapable of relocation to other sites or of self-protection from cumulative effects of exposure to nitrates, phosphates, herbicides, pesticides, and raw sewage. In contrast to stresses attributed to warm water seasonal anomalies (e.g. coral reef bleaching), stresses imparted by pathogenic micro-organisms occur throughout !he calendar year, fluctuate with changing temperature, and invariably result in tissue mortality. The coral has several mechanisms for defense. The epidermis, especially in tentacles of !he coral polyp, contains nematocysts which are released in response to predators. The epidermal cells also possess cilia and a flagellary apparatus which are responsible for generating microcurrents in boundary water adjacent to the organism. These currents facilitate !he entry of food into !he coelenteron for digestion. Mesenterial filaments extend through !he epidermis, sweep !he surface of the colony, initiate digestion of food particles, and eventually return to the coelenteron. Bo!h the epidermis and the gastrodermis contain mucocytes (or "immunocytes") which release a mucous secretion. That mucous blanket physically insulates !he tissue from particulates or soluble toxins, and may also be bacteriostatic because of immunoglobulin (IgA). The recent emergence of diseases in corals may be interpreted as the consequence of (1) changing coastal ocean water quality favoring the proliferation, attachment and colonization of microbes, and (2) reduced efficiency of the coral's normal defenses. In order to appreciate these changes, research efforts to evaluate !he microbial content of reef waters and to analyze the respective roles of mucus, cilia and flagella, and nematocysts of !he corals are necessary. In this study, we have begun to detail the structural, physiological, chemical, and immunological attributes of!he coral. Our analysis suggests that at least some of the emerging coral diseases may be explained by a decline in the capacity of coral colonies to mount effective protection against !he increasing prevalence and varied invasive strategies of marine pathogens.
|
|
|
