Deformation of the notochord by pressure from the swim bladder may cause malformation of the -vertebral -column in cultured Atlantic cod Gadus morhua -larvae: a case study

Abstract

This study describes a malformation that frequently occurs in Atlantic cod Gadus morhua in intensive culture systems. The malformation is characterised by a slight upward tilt of the head and an indented dorsal body contour at the transition between the head and the trunk, and is first evident to the fish farmer when the cod reach the juvenile stage. These abnormalities are associated with malformations of the neurocranium, the cranial region of the vertebral column and the cranial part of the epaxial lateral muscles. The pathogenesis involves deformation of the notochord, which can be observed in larvae about 7 d post-hatch (dph) and onwards. The deformation consists of an increase in dorsal curvature of the notochord in the region above the swim bladder. In the same region, the notochord has an abnormal cross-sectional outline, characterised by a groove-shaped, longitudinal impression along the ventral surface of the sheath. In most cases, the swim bladder fills the impression, and in severely affected larvae it forms a hernia-like lesion in the notochord. The deformation of the notochord seems to be conveyed to the vertebral body anlagen (chordacentra), which in teleosts are formed by mineralisation within the notochordal sheath. The vertebral bodies adopt an abnormal wedge shape, with a ventral concavity, and the neural arches are most often S-shaped. A continuous range of degrees of the malformation can be observed. All these pathomorphological characteristics are compatible with the notion that the notochord has been subjected to an upward mechanical force, probably generated by a persistent increase in pressure between the swim bladder and the notochord during the period of development of the vertebral anlagen. Our results thus indicate that the critical time window with regard to development of the malformation is from 18 to 36 dph, when the initial formation of the vertebrae takes place. Chronic overinflation of the swim bladder or pathological dilatation of the digestive tract may cause the lesions, and aetiology may be related to factors that influence the function of these organs.