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Coral reefs are in severe decline. Infections by the human pathogen Serratia marcescens have contributed to precipitous losses in the common Caribbean elkhorn coral, Acropora palmata, culminating in its listing under the United States Endangered Species Act. During a 2003 outbreak of this coral disease, called acroporid serratiosis (APS), a unique strain of the pathogen, Serratia marcescens strain PDR60, was identified from diseased A. palmata, human wastewater, the non-host coral Siderastrea siderea and the corallivorous snail Coralliophila abbreviata. In order to examine humans as a source and other marine invertebrates as vectors and/or reservoirs of the APS pathogen, challenge experiments were conducted with A. palmata maintained in closed aquaria to determine infectivity of strain PDR60 from reef and wastewater sources. Strain PDR60 from wastewater and diseased A. palmata caused disease signs in elkhorn coral in as little as four and five days, respectively, demonstrating that wastewater is a definitive source of APS and identifying human strain PDR60 as a coral pathogen through fulfillment of Koch's postulates. A. palmata inoculated with strain PDR60 from C. abbreviata showed limited virulence, with one of three inoculated fragments developing APS signs within 13 days. Strain PDR60 from non-host coral S. siderea showed a delayed pathogenic effect, with disease signs developing within an average of 20 days. These results suggest that C. abbreviata and non-host corals may function as reservoirs or vectors of the APS pathogen. Our results provide the first example of a marine ''reverse zoonosis'' involving the transmission of a human pathogen (S. marcescens) to a marine invertebrate (A. palmata). These findings underscore the interaction between public health practices and environmental health indices such as coral reef survival. [ABSTRACT FROM AUTHOR]

Caribbean elkhorn coral, Acropora palmata, has been decimated in recent years, resulting in the listing of this species as threatened under the United States Endangered Species Act. A major contributing factor in the decline of this iconic species is white pox disease. In 2002, we identified the faecal enterobacterium, Serratia marcescens, as an etiological agent for white pox. During outbreaks in 2003 a unique strain of S. marcescens was identified in both human sewage and white pox lesions. This strain (PDR60) was also identified from corallivorious snails ( Coralliophila abbreviata), reef water, and two non-acroporid coral species, Siderastrea siderea and Solenastrea bournoni. Identification of PDR60 in sewage, diseased Acropora palmata and other reef invertebrates within a discrete time frame suggests a causal link between white pox and sewage contamination on reefs and supports the conclusion that humans are a likely source of this disease. [ABSTRACT FROM AUTHOR]

Abstract: Disease affects the growth and survival of reef building corals. Prevalence, severity, lethality, and recovery of dark spots syndrome (DSS) was measured on three common scleractinian corals, Montastraea annularis complex, Siderastrea siderea, and Stephanocoenia michelinii on seven reefs in the Florida Keys. Between 2002 and 2004, DSS was the most common disease, responsible for 71.2%±5.7 S.E. of all disease infections in the total coral population. Prevalence ranged from 26.3%±17.6 S.E. for M. annularis, 7.5%±2.9 for S. siderea to 3.0%±0.1 for S. michelinii. DSS severity (expressed as the percent of diseased colony surface area) ranged from 0.55%±0.12 S.E. for M. annularis, 4.8%±0.63 for S. siderea to 0.83%±0.31 for S. michelinii. DSS rarely caused whole colony mortality (0.0%yr−1 for Montastraea annularis, 0.3%yr−1 for Siderastrea siderea, and 3.8%yr−1 for Stephanocoenia michelinii), but was a significant source of partial mortality. During the 2002–2003 survey period, net tissue loss per annum due to DSS was 0.3%yr−1 for M. annularis, 1.0%yr−1 for S. siderea, and 8.8%yr−1 for S. michelinii. Total net tissue loss for these three species, from all sources of mortality, was 0.45%, 1.0%, and 8.8% respectively, demonstrating that DSS was the only source of mortality for S. michelinii and S. siderea during this period, and accounted for two-thirds of all tissue loss from M. annularis colonies. DSS recovery rates were variable, depending on the target species. DSS signs in 86.8% of M. annularis colonies and 73.3% of S. michelinii colonies identified in 2002 and 2003 persisted through the end of the survey (2004). By contrast, among S. siderea only 33.3% of colonies affected in 2002 and 2003 continued to exhibit disease signs by 2004. Annual recovery rates from DSS were also species-dependent: 32.9% of DSS-affected S. siderea colonies recovered annually, but, by contrast, only 6.6% and 10.0% of DSS-affected M. annularis and S. michelinii colonies had done so. DSS appears to be a significant source of both whole and partial mortality for S. michelinii, but not for the other two species during this survey. [Copyright &y& Elsevier]

In recent years, diseases of corals caused by opportunistic pathogens have become widespread. How opportunistic pathogens establish on coral surfaces, interact with native microbiota, and cause disease is not yet clear. This study compared the utilization of coral mucus by coral-associated commensal bacteria ("Photobacterium mandapamensis" and Halomonas meridiana) and by opportunistic Serratia marcescens pathogens. S. marcescens PDL100 (a pathogen associated with white pox disease of Acroporid corals) grew to higher population densities on components of mucus from the host coral. In an in vitro coculture on mucus from Acropora palmata, S. marcescens PDL100 isolates outgrew coral isolates. The white pox pathogen did not differ from other bacteria in growth on mucus from a nonhost coral, Montastraeafaveolata. The ability of S. marcescens to cause disease in acroporid corals may be due, at least in part, to the ability of strain PDL100 to build to higher population numbers within the mucus surface layer of its acroporid host. During growth on mucus from A. palmata, similar glycosidase activities were present in coral commensal bacteria, in S. marcescens PDL100, and in environmental and human isolates of S. marcescens. The temporal regulation of these activities during growth on mucus, however, was distinct in the isolates. During early stages of growth on mucus, enzymatic activities in S. marcescens PDL100 were most similar to those in coral commensals. After overnight incubation on mucus, enzymatic activities in a white pox pathogen were most similar to those in pathogenic Serratia strains isolated from human mucosal surfaces. [ABSTRACT FROM AUTHOR]