daveman
Diamond Member
- Thread starter
- #21
Why do you keep ignoring Post #10, where global warming is declared responsible, and Post #11, WHERE YOU YOURSELF posted links declaring global warming responsible?Yes..it's some unidentified disease...
That just makes so much sense!
What do you think would make more sense?
From:
Mass Mortality in Diadema antillarum (Echinodermata:Echinoidea): A Large-Scale Natura
THE EPIDEMIC
The occurrence of unusual mortality of Diadema was first observed in mid-January, 1983, on the Caribbean coast of Panama, close to the mouth of the Panama Canal (Lessios et al. 1984). Death appeared to occur rapidly, soon after symptoms appeared, and virtually all individuals died. Affected organisms initially developed an accumulation of sediment, and lost pigment and some spines. As the disease progressed, the animals were unable to remain attached to their substrates. Eventually, they literally seemed to fall apart. Behavioral changes were also noted, as the animals did not typically seek shelter during daylight, and were observed being preyed on by fish not normally seen feeding on healthy Diadema. Within days of the first observation of the disease, most individuals in this population were dead, reduced to bleached tests.
After a lag of several months, the disease was noted in other locations. First affected were Diadema in the San Blas Islands of Panama. Populations across the Caribbean were eventually affected by this spreading disease, which traveled in a pattern consistent with major surface currents. The disease moved from Panama in both a westward and an eastward direction on these currents. The disease spread at a rate of roughly 2000 km/ yr to the east, and nearly 3000 km/yr to the west (Lessios 1988a). Eventually, the entire Caribbean was involved, as the disease spread to Florida and north to Bermuda. 3.5 million square kilometers of ocean habitat were affected, and it does not appear that any population of D. antillarum in this area escaped massive mortality. Populations of this species in the eastern Atlantic, and a sibling species in the Eastern Pacific were apparently not affected. The Pacific species might be assumed to be at risk due to potential transmission of the pathogen through the canal. In practice, such movement of organisms appears to be very rare, probably due to the fresh-water nature of the canal, and the fact that water flows from the continental divide at the high point of the canal out into both oceans.
The disease was not only widespread, but highly virulent. The actual intensity of the disease across the 3.5 million square kilometers affected is difficult to compare, due to variations in sampling protocol, but Lessios (1988a) reports that mortality averaged 98%, exceeding 93% at all locations examined, and ranging to over 99.9%. The disease seemed to stop affecting urchins in February, 1984, roughly one year after it appeared. It did re-appear, however, in October-December of 1985. At this time, the disease seemed much less virulent, with less than 1% of the surviving populations in affected Panama and St. Croix developing symptoms.
No causative agent for the disease has been conclusively identified. Lessios (1988a) cites strong circumstantial evidence that a waterborne, host-specific pathogen was responsible. This evidence includes the tendency of the outbreaks to follow the direction and speed of water currents, the involvement of captive Diadema populations in aquaria fed by seawater, lack of decrease in the mortality with distance, development of symptoms when healthy individuals were experimentally exposed to affected animals, and the apparent limitation of the disease to a single species. Two species of spore-forming Clostridium were cultured from an affected population of urchins (Bauer and Agerter 1987). Healthy individuals died when injected with these bacteria, but the connection between the epidemic and these bacteria was not considered conclusive. Mortality appeared to be density independent. Overall, there does not seem to have been a significant relationship between initial population density and the intensity of the die-off at individual locations (Lessios 1988a).