Host Susceptibility Hypothesis for Shell Disease in American Lobsters

Abstract

Abstract.-Epizootic shell disease (ESD) in American lobsters Homarus americanus is the bacterial degradation of the carapace resulting in extensive irregular, deep erosions. The disease is having a major impact on the health and mortality of some American lobster populations, and its effects are being transferred to the economics of the fishery. While the onset and progression of ESD in American lobsters is undoubtedly multifactorial, there is little understanding of the direct causality of this disease. The host susceptibility hypothesis developed here states that although numerous environmental and pathological factors may vary around a lobster, it is eventually the lobster's internal state that is permissive to or shields it from the final onset of the diseased state. To support the host susceptibility hypothesis, we conceptualized a model of shell disease onset and severity to allow further research on shell disease to progress from a structured model. The model states that shell disease onset will occur when the net cuticle degradation (bacterial degradation, decrease of host immune response to bacteria, natural wear, and resorption) is greater than the net deposition (growth, maintenance, and inflammatory response) of the shell. Furthermore, lesion severity depends on the extent to which cuticle degradation exceeds deposition. This model is consistent with natural observations of shell disease in American lobster.

Lesion bacterial communities in American lobsters with diet-induced shell disease

“…Koch's postulates have not yet been fulfilled for any single bacterial species as the primary cause of any shell lesion type. Thus, the possibility exists that a complex microbial community might become established in and induce erosions as a result of specific environmental and host factors that compromise lobster health, carapace composition or immune competence , Tlusty et al 2007). One such factor that can induce shell disease and mortality in juvenile Homarus americanus is inadequate diet (Tlusty et al 2008).…”

Altered gene expression associated with epizootic shell disease in the American lobster, Homarus americanus

“…In addition, the disease is not highly contagious, has proven difficult to induce in the laboratory, and has historically occurred at low levels (<2%). Several researchers have suggested that the etiology of epizootic shell disease may involve a combination of environmental stressors leading to increased susceptibility of lobsters to microbial infection [10,12,13]. For example, anomalously warm water temperatures have been correlated with spatiotemporal variation in the incidence of epizootic shell disease [6].…”

“…For example, anomalously warm water temperatures have been correlated with spatiotemporal variation in the incidence of epizootic shell disease [6]. Others have examined the role of diet [12,14,15], environmental chemicals [16][17][18] and hypoxia [19].…”

Shell disease in Crangon crangon (Linnaeus, 1758): The interaction of temperature and stress response

“…temperature increase, chemical pollution) or mechanical damage, they can degrade the cuticle and thereby facilitate the entrance of other pathogens (Baross et al, 1978;Cook and Lofton, 1973;Schlotfeldt, 1972;Shields, 2013;Vogan et al, 2001). Shell disease is therefore interpreted as a maladaptation to changing environmental conditions by decreasing the immunocompetence of the organisms (Chen et al, 1995;Dove et al, 2005) and reducing the defense mechanisms against pathogens (Sindermann, 1979;Tlusty et al, 2007). Due to the altered expression of different genes and hormones crustaceans can be energetically compromised or produce elevated levels of ecdysone, pointing towards changes in the molting behavior (Castro et al, 2006;Laufer et al, 2005;Tarrant et al, 2012).…”

“…In all ectothermic organisms such as C. crangon, temperature determines and interacts with embryogenesis, growth, molting frequencies and also the reproduction and survival (Caudri, 1939;Hufnagl and Temming, 2011a;Lloyd and Yonge, 1947;Siegel et al, 2008;Tiews, 1954). Hence, increasing water temperatures can result in physiological stress and therefore decreased defense mechanisms, which in turn lead to more susceptibility to shell disease as has been shown in the American lobster (Homarus americanus) (Dove et al, 2005;Glenn and Pugh, 2006;Tlusty et al, 2007). Additionally, elevated water temperature enhances the amount of bacteria and thus the risk of an infection (Dove et al, 2005;Glenn and Pugh, 2006).…”