Trends in Ecology and Evolution, Volume 13, Number 11, 1 November 1998 , pp. 438-443(6) 

Laurie L. Richardson
Department of Biological Sciences, Florida International University, Miami, FL 33199, USA
(ricardl@fiu.edu)

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 other multiple disease names have been applied to symptoms that may have been caused by a single disease. Despite the current confusion, rapid progress is being made.

Coral disease emergence in the 1990s
There have been many reports of new coral diseases in the 1990s. These include red band disease, yellow band disease, yellow blotch disease, dark spot disease, white pox, sea fan disease and rapid wasting disease. The emergence of theses dideases was broadcast in the popular literature, on coral reef websites and on coral-reef related internet servers as anecdotal observations. For most of these diseases, supporting data were limited to photographs of afflicted coral colonies. In many cases, it is not clear that what is being shown is actually a disease. The status of these new diseases is extremely confusing.

Only one of the recently emerging new coral diseases has been systematically characterized. Asperillogosis of sea fans (gorgonian corals) rapidly swept through the reefs of the Caribbean and the Florida Keys in 1995 and 1996, resulting in mass mortalities as result of tissue-degrading lesions. A team of investigators, using both laboratory and field techniques, showed that the lesions were caused by the terrestrial fungus Apergillus sydowii (proven in laboratory experiments that fulfilled Koch’s postulates, see Koch’s postulates for demonstrating the identity of a pathogenic microorganism), and that disease incidence was correlated with water depth and protection from wave exposure. The disease still persists throughouht the western Atlantic. These investigators have postulated that an unexplained, but well documented, mass mortality of sea fans that occured throughout the Caribbean during the 1980s was an earlier epizootic of the same disease. This conjecture is based on photographs of diseased sea fans from the 1980s event that reveal the same lesions now known to be caused by A. sydowii. The effect of this extensive sea-fan mortality on the reef ecosystem is not known.

Results of Studies of individual coral diseases
A summary of what is currently known about coral diseases (including only peer-reviewed literature that contains original data) is presented in Koch’s postulates (see Koch’s postulates for demonstrating the identity of a pathogenic microorganism). The main conclusions are as follows:

• There are currently only four diseases for which both coral tissue destruction leading to mortality, and the presence of a consistent, characteristic microorganism (or microbila consortium) associated with the disease are known. These are aspergillosis, black band disease, white band disease type II and plague type II. This is in contrast to the 13 individual coral diseases put forth by various investigators.
• Only 3 diseases (aspergillosis, black band disease and plague type II) have an associated microorganism (or microbial consortium) that has been demonstrated to be the disease pathogen.
• The mechanism of coral tissue death is known only for black band disease.
• Only white band disease has been shown to restructure a reef on a regional scale.

Most coral diseases, including new ones and some new ones that were first described in the 1970s and 1980s, have been only partially characterized. These include white band type I, plague type I, shut down reaction, red band disease, yellow blotch, rapid wasting disease, dark spot disease and white pox. No pathogens have been identified for nay of these diseases, and confusion is prevalent. Despite this, many of these syndromes are currently included in monitoring programs designed to evaluate coral reef health.

Current research by many of the investigators cited in this review is focusing on new areas, such as discerning mechanisms of aspergillosis resistance in sea fans, applying molecular probes to confirm identities of pathogens in outbreaks in different regions, and experimental manipulations to trigger disease activity from reservoir populations. Moreover, much current research is aimed at determining the relationship, if any between increased nutrients and coral disease.

The continuation of rigorous research efforts of recent years, specifically those that go beyond descriptive studies, is of critical importance for a complete understanding of coral diseases. A word of caution, however: until a pathogern has been identified for each of the uncharacterized coral diseases (including fulfillment of Koch’s postulates), these syndromes should be clearly identified as potential disease states and not coral diseases.

Koch’s Postulates

Disease related research in other areas of scientific endeavor always includes strict attention to fulfillment of Koch’s postulates ( a procedure set forth by Robert Koch in the 1870s) by which a presumed disease pathogen is demonstrated to be the cause of a disease. To demonstrate unequivocally the identity of a pathogenic microorganism, the following must be carried out:

• The microorganism must be documented as always being found associated with a particular disease.
• The microorganism must be isolated from the disease state and grown in pure culture under laboratory conditions.
• The pure culture of the microorganism must produce the disease when inoculated into a healthy animal.
• The microorganism must be re-isolated from the newly diseased animal and identified as the same microorganism as the presumptive pathogen.

Satifaction of Koch’s postulates when the host is a coral is challenging for several reasons. First, duplication of the normal reef environment in library aquaria is difficult, especially in terms of water movement (currents vs. Aeration) and microorganisms present in the water column. Second, the natural mode of infection is not known as a coral disease. Consequently, inoculation by syringe or after wounding the host tissue could be as unnatural as exposure to concentrated suspensions of pathogen in aquarium water of placement of colonies on pathogen-inoculated plates. Finally, it is difficult to prove the re-isolation of the pathogen by sampling the newly diseased experimental coral. Because some diseases are present on the surface of coral tissue, and experimental inoculation usually involves inoculation of the aquarium environment, recovery of the test microorganism could be compromised by the presence of contaminated aquarium water.

Microbial Pests–Coral Disease in the Western Atlantic

Proc. 8th Int. Coral Reef Symp. 1:607-612.  1997

D.L. Santavy and E.C. Peters
U.S. Environmental Protection Agency, Gulf Ecology Division, 1 Sabine Dr., Gulf Breeze, Florida 32561, U.S.A
Tetra Tech., Inc. 10306 Eaton Place, Suite 340, Fairfax, Virginia 22030, U.S.A

ABSTRACT

Diseases of sceleractinian corals have increased significantly over the last decade, affecting greater number of species around the world. Gross signs of coral disease are often observed in tissue loss on the skeleton, making differential diagnosis difficult. Using the histopathological and infrastructural techniques, coupled with microbiological analyses, the importance of microorganisms as pathogens in coral diseases is becoming more apparent.

This paper addresses the ecology of pathogens on reefs, specifically bacreria and cynobacteria that produce disease in scleractinian and acyonarian corals.

We review the nature of the disease and the influence of adverse environmental conditions. An update is presented on research concerning the bacteria associated with black- and white- band diseases; observations are presented concerning other coral diseases in the western Atlantic that appear to be caused by bacteria. We conclude with suggestions for improving the recognition that include research to identify bacterial pathogens and the role of environmental factors in the development of coral disease.

0003-0147/2004/1640S5-40257$15.00DOI: 10.1086/424609

Kiho Kim^1,* and  C. Drew Harvell^2,†

1. Department of Biology, American University, Washington, D.C. 20016‐8007;

2. Department of Ecology and Evolutionary Biology, Cornell University, Ithaca, New York 14853

http://www.everglades.org/articles/special-report-pg1.html

The dominant hypothesis for explaining many of the changes, however, is that reduced water flow into Florida Bay from the Everglades led to hypersaline conditions, which then led to massive seagrass dieoff. This hypothesis further proposes that the seagrass dieoff and subsequent organic decomposition and sediment resuspension released nutrients which then generated the algal blooms. This hypothesis has been used as a rationale for pumping more fresh water into Florida Bay as part of a large scale alteration of water management in South Florida. The hypothesis is a reasonable one to begin with, but an examination of the data available leads to serious doubts about the validity of the hypothesis and the predicted ecological consequences of pumping more freshwater into Florida Bay.

CONCLUSIONS:

The dominant hypothesis for explaining many of the ecological changes that have occurred in Florida Bay in the past 2 decades is that reduced flow into Florida Bay from the Everglades led to hypersaline conditions, which then led to massive seagrass die-off. This hypothesis further proposes that the seagrass dieoff and subsequent organic decomposition and sediment resuspension released nutrients which then generated algal blooms. The data, however, show that hypersaline conditions cannot explain either the spatial or temporal distribution of seagrass dieoff in Florida Bay. Furthermore, seagrass dieoff cannot explain the spatial or temporal distribution of nutrients and algal blooms in Florida Bay.

It is hypothesized that the large algal blooms in Florida Bay are the result of nitrogen-rich waters in eastern Florida Bay meeting phosphorus-rich waters in western Florida Bay. Nutrient bioassays confirm that phosphorus is the limiting nutrient in the east and nitrogen is the limiting nutrient in the west, as predicted by the spatial distribution of N:P ratios.

It is hypothesized that much of the P comes from Miocene phosphorite deposits by way of Peace River erosion and subsequent coastal current transport along the southwest coast, and by way of groundwater through phosphorite-rich quartz sand deposits underneath certain areas of the coastal waters. It is argued that this P source has not changed significantly over the past few decades. It appears that much of the N comes from freshwater runoff from agricultural lands through the Everglades. It is argued that changes in water management practices in the past two decades have led to an increase in N inputs to eastern Florida Bay. Mixing of this water from the east with the P-rich water from the west has led to the large algal blooms that have developed in northcentral Florida Bay, altering the entire ecosystem. Some of this enriched water is transported to the middle and lower Florida Keys, where it may be adversely affecting the coral reefs and other oligotrophic ecosystems there.

In conclusion, it is hypothesized that if more freshwater from the Everglades-agricultural system is pumped into Florida Bay, as proposed (United States Army Corps of Engineers and South Florida Water Management District, 1999), the algal blooms will increase and the ecological problems of Florida Bay will get worse, not better. It is also hypothesized that if more passages along the Florida Keys between Florida Bay and the coral reefs are opened up, as proposed, the coral reefs will experience lower water quality.