The mass mortality of a herbivorous sea urchin is not unprecedented, nor is the subsequent increase in macroalgal cover, although the range and proportion of affected individuals were higher in D. antillarum than in any previously recorded mass mortality (Lessios 1995). Previous urchin mass mortalities include the red sea urchin off the California coast and green sea urchins in Nova Scotia, Canada.
In 1976, an unidentified biological pathogen swept through a localized population of the red sea urchin Strongylocentrotus franciscanus on the seaward side of a kelp forest off the coast of central California (Pearse & Hines 1979). The mortality reduced population density in this area by over 50%, with nearly complete die-out in certain study areas. The result, as predicted from previous exclusion experiments, was the seaward expansion of the kelp forest. The newly expanded area was eventually taken over by a dense stand consisting almost exclusively of one macroalgal species (Pearse & Hines 1979). The central California kelp forest ecosystem has yet another parallel to the Caribbean coral reefs, in that the urchins' primary predators (in this case, sea otters) have been hunted or otherwise killed by humans to near extinction. This had allowed the urchins to grow to abnormal densities, with abnormally high rates of herbivory (Duggins 1980). As in the case of D. antillarum, this state made S. franciscanus more susceptible to contagious pathogens, and made the resultant decline in herbivory more profound (Pearse & Hines 1979; Hughes 1994).
Another documented case of sea urchin mass mortality involves the green sea urchin Strongylocentrotus droebachiensis, which lives on the southern coast of Nova Scotia (Miller & Colodey 1983). As D. antillarum formerly was, S. droebachiensis is considered the most important benthic herbivore in its ecosystem. During the autumns of 1980 and 1981, populations of this species in various rocky shore habitats of Nova Scotia were afflicted with a contagious biological pathogen. Total urchin biomass was reduced by as much as 99% in some areas, while other areas just 15 km away showed no observable mortality (Miller & Colodey 1983). Miller & Colodey performed laboratory experiments to confirm that the cause of mortality was a waterborne pathogen. By placing diseased urchins upstream of healthy individuals in laboratory tanks, and observing the effects on the downstream individuals (compared with appropriate control groups in separate tanks), Miller & Colodey demonstrated that the cause of mass mortality in their urchins was a contagious pathogen, transferred in water currents (Miller & Colodey 1983). Although data on algal response to the urchin mortality were not available when their article went to press, Miller & Colodey predicted that algal cover and primary production would increase sharply, as has been observed in other mass mortalities of herbivorous sea urchins (e.g., Pearse & Hines 1979).
Given these and other examples in different types of animals and plants, it seems that significant mortalities can be a part of a regular cycle of increase and decline in population density. An intriguing case is the feral sheep population of Hirta, an island off Scotland. Every third or fourth year, as many as 70% of these sheep may starve to death, but the population continues to thrive (Clutton-Brock 1994). Several other land mammals are known to experience regular mortalities claiming up to 90% of the population, but these mortalities are generally limited to isolated local populations, often limited by geographical boundaries (Clutton-Brock 1994). The waterborne nature of the urchin-killing pathogen made it capable of spreading through every known habitat of D. antillarum, as water connects all of these habitats. The fact that the New England and California mortalities did not spread as quickly or as widely as the Caribbean one suggests that D. antillarum was struck by a relatively virulent pathogen. This hypothesis is further supported by the observation that all of the above named mortalities saw recovery within a few years, whereas D. antillarum has gone 13 years without any substantial recovery. Thus it seems clear that the mass mortality of D. antillarum has greatly exceeded the bounds of what can be considered a normal fluctuation.