Natural and experimentally induced lesions of the body wall of the sea urchin Strongy-locentrotus droebachiensis

Abstract

Lesions of the body wall occurred in about 7 % of sea urchins Strongylocentrotus droebachiensis in a healthy population off Nova Scotia, Canada. Lesions occurred predominantly in the oral hemisphere in both ambulacral and interambulacral areas. On average, lesions covered 8 to 12 % of the total test surface of individuals, although lesion size was quite variable. Lesioned areas of test generally were darkly pigmented, covered with a mucoid layer, and devoid of spines, pedicellariae and tube feet. Three morphological types of lesions were identified, which appeared as progressive stages: Stage 1 w ~ t h a thln mucoid layer, nearly transparent to pinlush in coloration; Stage 2 with a thick more darkly p~gmented mucoid layer, ranging from reddish to purplish-black; and Stage 3 with spine regeneration through a pigmented mucoid layer. The test in lesioned areas was often friable, but rarely perforated. Scannlng electron microscopy ind~cated extensive degeneration of the epidermis and stereom. Gonads of lesioned Individuals were frequently discoloured, but gonad slzes were not significantly different between healthy and lesioned ~ndividuals. Microflora normally found on healthy body surfaces of the sea urchin proliferated in lesioned areas. Of 85 isolates identified from swab samples of lesioned and healthy test surfaces, 93 8 0 were Gram-negative bacteria belonging mainly to the taxa Acinetobacter, Alcaligenes, Flavobacterium, Pseudomonas and Enterobacteriaceae. The total number of microorganisms and the numbers of Acinetobacter and Alcaligenes were significantly higher on lesioned surfaces (Stage 1 or Stage 2) than on healthy surfaces of the same individuals. Most bacterial types increased in abundance from Stage 1 to Stage 2 lesions, although this increase was statistically significantly only for Acinetobacter. Vibrionaceae, Cram-positive bacteria and fungi occurred sporadically and in low abundance on lesioned and healthy test surfaces. Mechanical abrasion of the test surface of the sea urchin produced lesions s~rnilar in gross morphology to naturally occurring ones. In laboratory experiments, lesions developed in all abraded individuals, Irrespective of exposure to iesioned or healthy conspecifics either by a waterborne route or by direct contact. Lesion development was accelerated, and recovery retarded, by directly contacting the abraded test surface with material from a natural lesion. Unabraded sea urchins did not develop lesions ~ n d i c a t ~ n g that removal of the epidermis provides a route of infection. Rate of recovery of experimentally abraded individuals (as measured by spine regeneration and reduction in lesion size) was significantly higher at 16OC than at 3°C. Provision of food (kelp) had a significant positive effect on recovery after 12 wk. Body wall lesions of S. droebachiensis appear to be symptoms of chronic, superficial infections from which sea urchins generally recover. The increased incidence of lesions in this species (and others) during or after outbreaks of acute disease may reflect secondary bacterial and/or fungal infections.