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Disease affects New England Lobsters


Article: Castro, K.M.; Cobb, J.S.; Gomaz-Chiarri, M.; Tlusty, M.; Epizootic shell disease (ESD) in American lobsters Homarus americanus in southern New England; past, present, future. 2012. Diseases of Aquatic Organisms, v. 100, pp. 149-158, doi:10.3354/dao0507


Since the mid-1990s the appearance of enzootic shell disease (ESD) throughout inshore southern New England has intensified, corresponding with a decline in lobster abundance (Figure 1).   Today ESD afflicts 10-40% of the remaining population.

Figure 1: Total abundance vs. ESD prevalence in southern New England (by sea sampling survey done by Rhode Island Department of Environmental Management)

Figure 1: Total abundance vs. ESD prevalence in southern New England (by sea sampling survey done by Rhode Island Department of Environmental Management)

ESD is identified by lesions, pitting, and discoloration on the shell (Figure 2). Degrading enzymes found on lobsters with ESD are produced by bacterial pathogens, Aquimarina ‘homaria’ and ‘Thalassobius’ (sp.).  It was initially postulated that ESD caused no life-cycle problems, however investigation via models, sampling surveys, observations and experiments in the past 10 years suggests that ESD has an effect on the settling (transition of larval and post larval lobster from drifting in water column to ‘settling’ on the rocky bottom), growth (molting), and reproductive cycle of lobsters.  Wahle et al., (2009) note a decrease in settling corresponding to an increase in ESD.   Tagging studies by Castro et al., (2006) and laboratory work by Stevens (2009) confirm the effect of ESD on growth, and Stevens (2009) linked increased mortality during molting with ESD.   Fine-scale data records on ESD from Castro and Somers (2012) show trends of early appearance of ESD in large (>80mm body length) lobsters, particularly those carrying eggs (who keep shells longer before shedding).  Most cases were observed in inshore areas of Narragansett Bay, particularly during molting periods in late spring and early fall.   This observation agrees with research by Chistoserdov et al. (2005) that found lobsters with ESD had more molting hormone (ecdysone), suggesting a role of the endocrine system in defending against disease.   Elevated levels of molting hormone may disrupt an egg-bearing female’s reproductive cycle.

The presence of ESD was originally observed in populations that experience stress from over-crowding and/or environmental conditions, for example, temperature, the degree of pollution, or pH.  Tlusty et al., (2007) found that water temperature plays a role in the spread of ESD: lower temperatures limit the spread of bacteria and higher temperatures cause physiological stress to the host, making it more susceptible to disease.   Further aquarium studies found that lobster lesions would form between 10-20˚C and that immune function didn’t change until 22˚C, indicating that temperature is not the only factor contributing to the spatial distribution of ESD.   There is also indication that ESD can develop in polluted or nutrient deficient waters. For example, there is a relationship between the presence of heavy metals and the prevalence of ESD in lobster populations.  It has been suggested that the occurrence of ESD in Narragansett Bay is related to an oil spill off the shore of Rhode Island during a winter storm in 1996.  The 2700 US tons of fuel oil spilled into the water column and sediment is estimated to have killed 9 million lobsters (Cobb et al. 1999), however there is no direct evidence of a relationship between ESD and the spill.

Most recent research suggests that ESD is caused by an ‘opportunistic pathogen’.   Quinn et al., (2012) looked at the change in bacterial community with disease progression.  The study compared the effect of the two bacteria on shells with and without corrosion.   They found that the bacteria cause the development of lesions in already cracked shells suggesting that a compromised shell is needed for the disease to develop.

Future Work and Importance

There is still work needed to fully understand how ESD with affect future lobster populations.   ESD is of growing concern in fishery management policy because changes in fishing could indirectly affect disease dynamics if they alter mortality, disease transmission, pathogen survival, and host availability.

Models of patterns, causes, and effects of disease on lobster populations (Figure 2) used in the design of lobster fishery management plans should include: where the bacteria and lobsters are, how the bacteria infects the lobster, where else the bacteria is, who else carries the bacteria, how lobsters fight ESD, the impact of the disease on reproduction and if it causes the lobster to die, and the influence of the environmental conditions on ESD.   This work is important for the future of sustainable lobster fisheries and the impact fishing has on the health of the lobster population.

Figure 2: Image of lesions, pitting, and discoloration caused by ESD, and a model of epizootic shell disease (ESD) in Rhode Island.

Figure 2: Image of lesions, pitting, and discoloration caused by ESD, and a model of epizootic shell disease (ESD) in Rhode Island.



  1. […] it has contributed to the decline of American lobster fisheries – for more information, see this great oceanbites article. There are two types of shell disease – epizootic, which is the disease harming American […]

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