Shell disease syndromes of decapod crustaceans

Abstract

The term shell disease subsumes a number of debilitating conditions affecting the outer integument (the carapace) of decapod crustaceans, such as lobsters and crabs. Herein, we seek to find commonality in the aetiology and pathology of such conditions, and those cases that result in the progressive erosion of the cuticle through to the visceral tissues by a cocktail of microbial-derived enzymes including lipases, proteases and chitinases. Aquimarina spp. are involved in shell disease in many different crustaceans across a wide geographical area, but the overall view is that the condition is polymicrobial in nature leading to dysbiosis within the microbial consortium of the damaged cuticle. The role of environment, decapod behaviour and physiology in triggering this disease is also reviewed. Finally, we provide a conceptual model for disease aetiology and suggest several avenues for future research that could improve our understanding of how such factors trigger, or exacerbate, this condition.

FIGURE 1

Shell disease lesions seen on claws of European lobsters, Homarus gammarus (A). (B) Magnified area in boxed region of (A) showing the nature of pin‐point lesions some with or without melanization. Micrographs courtesy of Drs. E. Wootton and C.L. Vogan.

FIGURE 2

(A–C) Shell disease on ventral carapace of an adult edible crab, Cancer pagurus. The boxed areas in (A) show the regions magnified in Figures 2 B and C. Note superficial small (black arrows) and deeper larger (red arrow) lesions. Micrographs courtesy of Dr. Adam Powell.

FIGURE 3

Enzymatic breakdown of chitin associated with shell disease. The orange and blue arrows indicate enzyme‐mediated hydrolysis and oxidation as the catalytic mechanisms, respectively. Endochitinases can act on random glycosidic bonds along the chitin, generating free ends onto which exochitinases can process. Chitin degradation is enhanced by the presence of lytic chitin monooxygenase.

FIGURE 4

Back burrowed edible crab, Cancer pagurus photographed at Langland Bay, Gower, U.K. Note shell disease lesions visible on dorsal surface of the crab (unlabelled arrows). Micrograph courtesy of Dr. C. L. Vogan.

FIGURE 5

Conceptual model of how temperature (and other factors) may promote changes in both host and surface microbes leading to shell disease. Altered physiology of the host includes moulting frequency. Microbial consortia of shell disease lesions usually display lowered diversity and richness indices when compared to non‐diseased areas of carapace (i.e., they are dysbiotic).