What’s Eating Those Lobsters?: Understanding Shell Disease in American Lobsters
Answers Are In From Sea Grant's Recent Symposium
Antoinette Clemetson, NYSG Marine Fisheries Specialist, firstname.lastname@example.org
Riverhead, NY, September 14, 2010 - Researchers gathered at the 9th Annual Ronald C. Baird Sea Grant Symposium in mid-August to review the results of three years research into the shell disease that has been affecting American lobsters in Southern New England. A federal grant of $2.3 million was used to fund nine studies and enhance American lobster monitoring coordination in two state agencies in New England. This collaboration featured cross-disciplinary approaches that encompass the fields of crustacean endocrinology, genetics, veterinary medicine, behavior, microbiology, chemistry, environmental science, and epidemiology, matched with cutting edge laboratory techniques. Shell disease was first reported in 1989 (Rhode Island) and has since spread south to Long Island Sound and north as far as Massachusetts.
Healthy American lobsters carry complex bacterial communities on their shell; however, lobsters suffering with the disease possess significantly higher abundance in bacteria that are associated with enzymic activity. In the wild, the bacterium Aquimarina homaria has been consistently isolated from lesions in unusually high abundance when compared to bacterial communities that exist on healthy animals in the wild. This bacterium is believed to be responsible for degrading the shell and scientists managed to simulate the same lesions in a laboratory study using white (Albino) lobsters. These laboratory induced infections occurred only after the shell was breached in some way (such as abrasion by sandpaper). In another experiment, the area under rubber bands that were placed on the claws showed no signs of disease. Furthermore, bacteria must be present in critical levels under the right environmental conditions (such as temperature, diet) or even biological conditions (such as molt cycle) before the lobster can develop epizootic shell disease. Nonetheless, critical temperature for this disease occurs at ~15ºC, when there is a significant difference in the inflammatory response in the animal. Researchers also discovered that lobsters in Western Long Island Sound have shells that are significantly thicker when compared to the shells on lobsters from other adjoining areas (such as Eastern Long Island Sound).
Changes in Host Physiology and Immunity
Researchers use the term ‘asymptomatic’ to refer to lobsters that do not show visual disease symptoms at the time of handling, although they may be carriers or can develop the disease at a later time. Epizootic shell disease infections manifest as an “outside-in” progression, meaning the infection begins on the surface and works inwards towards the epidermis. As the disease progresses, it eventually compromise the complex calcite layer that makes up the shell. Diseased lobsters possess a different physiological chemistry indicative of immune system deficiency. Epizootic shell disease is rare in Maine, making these lobsters an excellent subject to use in control experiments. When asymptomatic lobsters taken from areas with high shell disease prevalence were compared to lobsters from Maine, they all show significantly reduced immune response, supporting the theory of a highly stressed Southern New England stock that is susceptible to pathogens and other factors.
Impacts of the Environment
American lobster lives primarily in cold water and animals caught in Southern New England (Rhode Island to New Jersey) live under conditions on the high end of their tolerance limit. There has been an increase in sea temperature and ocean acidification (pH) from 2000-2007, and the region has also been impacted by other noteworthy anthropogenic influences such as oil spills, pollution from naval bases, pesticides, sewage inputs, etc. In a laboratory study using white lobsters, epizootic shell disease incidence was enhanced by both temperature and diet rich in herring. In a survey of common environmental contaminants, lobsters infected with the disease generally possessed 2-3 times higher levels of chromium and mercury in the hepatopancreas.
Alkylphenols are organic compounds most often used in the production of detergents, plastics, and some pesticides, and they tend to persist in the environment. They (alkylphenols) can have a hormonal effect when incorporated in the molt cycle, and are generally toxic to larvae. Approximately 39 percent of the lobsters that were sampled possess these chemicals, and the highest concentrations were isolated from the hepatopancreas.
There is a new insight into lobster behavior and population genetics. Behaviorists were surprised to discover that American lobsters form and maintain tight knit populations at the local level – multiple discrete populations can exists within a few kilometers. Female lobsters also prefer to associate with males from their own population, even if it means choosing a male that was infected with the disease.
Chronic Disease Consequences
Studying a chronic disease that is slow moving creates special challenges. Nonetheless, there is evidence to indicate that epizootic shell disease is more than just an eye sore –there are significant impacts on the entire being of animals with the disease. Infected lobsters are energetically compromised, experience hormonal interference, possess significantly reduced immunity, and slow growth. Physiological conditions in egg bearing females that are infected place them at a higher risk to molt. At this point in the research, it is unknown if the disease is affecting the overall reproductive selection process as the lobster population makes its evolutionary adaptation. Also, there is need to quantify the disease mortality in the lobster population and determine how this factor translates to the fishery and stock assessments.
Although a lot of information and insight has been gained into this chronic emergent disease, several unanswered questions are lurking beneath the surface. What are the factors that trigger A. homaria, which is a new pathogen to the northeast (although it has been reported from the Pacific)? We still don’t know about the full range for this disease and if the difference in genetic make-up of these populations and differences in environmental conditions (i.e., waters in Maine versus Southern New England) have any bearing. Given the increased attention to climate change, managers must have the necessary data collections systems on stream to track possible range expansion for this disease. Since this disease is likely to persist for many years, it will be interesting to observe its evolution over time. Perhaps the greatest uncertain is how best to manage this fishery under these disease conditions.
Sea Grant would like to thank all the researchers, managers, and industry representative who participated in this collaboration. This funding was jointly managed by the National Oceanic and Atmospheric Administration National Marine Fisheries Service, University of Rhode Island, and Rhode Island Sea Grant. Content for this article was summarized from research results presented at the 9th Annual Ronald C. Baird Sea Grant Symposium, held at the University of Rhode Island, Kingston, RI. August 10-11, 2010.
– Antoinette Clemetson, NYSG’s Marine Fisheries Specialist