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The direct impacts of coral diseases on coral populations have been assessed by quantifying coral tissue loss and colony mortality, but the determination of the indirect effects of diseases, such as disruptions in life history functions (e.g. reproduction, growth and maintenance), are more difficult to ascertain and have been scant. This study involved a comparison of various measures of reproductive output from histological slides of healthy tissue samples of Montastraea faveolata and tissue samples from colonies with white plague (WP) infections in Dominica (West Indies). Although the variability in the reproductive data was high, WP had significant negative impacts on the percentage of reproductive polyps per cm2, the percentage of reproductive mesenteries within a polyp, oocyte quantity per polyp, mean oocyte volume (mm3), and fecundity (oocyte volume per cm2 of tissue). However, these effects were only observed in the tissue directly impacted by the WP disease "band" and were not observed in tissue samples taken 20 cm away from the lesion. Therefore, the effects of a coral disease (WP) on reproductive output are localized and not expressed colony-wide. Rev. Biol. Trop. 58 (Suppl. 3): 99-110. Epub 2010 October 01.

Shallow leeward reefs off the western end of Curaçao are dominated by extensive populations of M. annularis (complex). These species are larger in size (mean= 66 cm diameter) than all other species, with few small colonies (10 cm observed within transects, and most exhibited low levels of partial mortality (mean= 22.5%). These species were less abundant (38% of all colonies) in 2005. Partial mortality among live colonies of M. annularis and M. faveolata increased by 85% (mean = 42% partial mortality) and numerous dead colonies of M. faveolata and M. annularis were observed; M. franksi colonies were generally in excellent condition (14% partial tissue mortality). A high prevalence of coral diseases (3-30%) was documented among M. annularis and M. faveolata, while all other species were less frequently affected. Yellow band disease (YBD) emerged shortly after the 1995 bleaching event, and rapidly spread throughout all depths, with the highest prevalence between 1997-1999. YBD caused slow rates of mortality (=1 cm/month), but multiple focal lesions appeared on individual colonies, and these progressively radiated outward as they killed the colonies. By 2005, 44% of the tagged corals were dead; the remainder exhibited active YBD infections (21%) or were in remission (31.6%) but were missing on average >90% of their tissue. Although the incidence of YBD has declined since 2000, white plague (WP) prevalence was unusually high (4-12%) in 2001 and 2005, with affected colonies exhibiting recent mortality of up to 70%. Dead Montastraea spp. surfaces are being colonized by other corals, including poritids, agaricids, and other faviids, while recruits of M. annularis (complex) are absent. If diseases and other biotic stressors persist on these reefs, M. annularis and M. faveolata populations may undergo a decline similar to that observed in the 1980s among Caribbean acroporids. Rev. Biol. Trop. 54 (Suppl. 3): 45- 58. Epub 2007 Jan. 15.Los arrecifes someros a sotavento del oeste de Curaçao están dominados por extensas poblaciones de Montastraea annularis (complejo). Estas especies son mayores en tamaño (promedio= 66 cm de diámetro) que las otras especies, con algunas colonias pequeñas (10 cm observadas en transectos y la mayoría exhibió bajos niveles de mortalidad parcial (prom= 22.5%). En el 2005, fueron menos abundantes (38% de las colonias). La mortalidad parcial en colonias vivas de M. annularis y M. faveolata se incrementó en un 85% (promedio= 42% de mortalidad parcial) y se observaron numerosas colonias de M. annularis y M. faveolata muertas; las colonias de M. franski generalmente se encontraron en excelentes condiciones (14% de mortalidad parcial). Se documentó una alta prevalencia de enfermedades de coral (3-30%) en M. annularis y M. faveolata, mientras que las otras especies se vieron afectadas con menor frecuencia. La enfermedad de banda amarilla (BA) emergió poco después del blanqueamiento de 1995 y se dispersó rápidamente en todas las profundidades, alcanzando su mayor prevalencia entre 1997-1999. La BA causó mortalidades lentas (= 1cm/mes), con aparición de múltiples lesiones focales en colonias individuales; estas lesiones fueron creciendo progresivamente al tiempo que mataban las colonias. Para el año 2005, el 44% de los corales que se etiquetaron habían muerto; los restantes exhibían infecciones activas de BA (21%), o estaban en remisión (31.6%) pero habían perdido un promedio de >90% de su tejido. Aunque la incidencia de BA disminuyó a partir del 2000, la prevalencia de la plaga blanca (PB) fue inusualmente alta (4-12%) en el 2001 y 2005, provocando mortalidades recientes de hasta un 70% en las colonias afectadas. Las superficies muertas de Montastraea spp. han sido colonizadas por otros corales, incluyendo porítidos, agarícidos y otros fávidos, mientras que continúa la ausencia de reclutas de M. annularis (complejo). Si las enfermedades y otros estresores bióticos persisten en estos arrecifes, las poblaciones de M. annularis y M. faveolata podrían decaer de forma similar a como lo hicieron los acropóridos del Caribe durante la década de 1980.

One of the current problems in the field of coral disease research is that of tracking coral pathogens in the natural environment.A promising method to do this is by use of pathogen-specific molecular probes. However,this approach has been little used to date.We constructed,and validated in the laboratory,a fluoro-chrome-labeled molecular probe specific to Aurantimonas coralicida ,the bacterial pathogen of the Caribbean coral disease white plague type II (WPII).We then used the probe to test field samples of diseased coral tissue for the presence of this pathogen.Probe design was based on a unique subset (25 nucleotides)of the complete16S rRNA gene sequence derived from a pure culture of the pathogen.The pathogen-specific probe was labeled with the fluorochrome GreenStar*™FITC (fluorescein isothiocyanate,GeneDetect Ltd,New Zealand).As a control, we used the universal eubacterial probe EUB 338,labeled with a different fluorochrome (TRITC,tetra-methyl-rhodamine isothiocyanate).Both probes were applied to laboratory samples of pure cultures of bacteria, and field samples collected from the surface of the disease line of corals exhibiting signs of white plague (types I and II),healthy controls,and corals with an uncharacterized disease ("patchy necrosis ").All samples were analyzed using fluorescence in situ hybridization (FISH).We have determined that the probe is specific to our laboratory culture of the coral pathogen,and does not react with other bacterial species (the eubacterial probe does).The WPII pathogen was detected in association with diseased coral samples collected from coral colonies on reefs of the Bahamas (n=9 samples)exhibiting signs of both WPI and WPII.Diseased (and healthy)tissue samples (n=4)from corals exhibiting signs of "patchy necrosis "were also assayed.In this case the results were negative, indicating that the same pathogen is not involved in the two diseases.Incorporation and use of pathogen-specific probes can significantly expand our knowledge of the etiology of coral diseases.Uno de los problemas actuales en el campo de la investigación sobre las enfermedades de corales es el de poder seguir a los patógenos en el ambiente natural.Un método prometedor para lograrlo es el uso de sondas moleculares específicas para el patógeno.Sin embargo,esta técnica ha sido poco usada hasta la fecha.Construimos y validamos en el laboratorio una sonda molecular de fluorocromo marcado específicamente para Aurantimonas coralicida ,la bacteria responsable de la enfermedad de corales del Caribe,plaga blanca Tipo II (PBII).Después usamos la sonda con muestras de campo de tejidos de corales enfermos para detectar la presencia del patógeno.La sonda se diseñó usando un sub-grupo único de 25 nucleótidos del gen 16S del rARN derivado de cultivos puros del patógeno.La sonda específica para el patógeno se marcó con fluorocromo GreenStar*™ FITC (fluorescein isotiocianato,GeneDetect Ltd,New Zealand).Como testigo usamos la sonda universal de eubacterias EUB 338,marcada con un fluorocromo diferente (TRITC,tetra-metil-rodamina isotiocianato).Ambas sondas fueron usadas con muestras de laboratorio de cultivos puros de bacterias,y muestras de campo recolectadas de la superficie de la línea de la enfermedad en corales con signos de plaga blanca (tipos I y II),de corales sanos y de corales con enfermedades no características (parches de tejido necrótico).Todas las muestras fueron analizadas usando hibridización fluorescente in situ .Determinamos que la sonda es específica para el patógeno cultivado en nuestro laboratorio y no reacciona con otras especies de bacterias (la sonda para eubacterias sí).El patógeno de PBII fue detectado en muestras de corales enfermos (exhibían signos de PBI y PBII)recolectadas en arrecifes de Bahamas (n=9 muestras).Muestras de tejidos enfermos (y sanos)(n=4)de corales con parches necróticos fueron probados.En este caso los resultados fueron negativos,indicando que el mismo patógeno no es responsable de las dos enfermedades.El desarrollo y uso de sondas específicas para cierto patógeno puede ampliar significativamente nuestro conocimiento de la etiología de enfermedades de corales.