Idiopathic lesions and visual deficits in the american lobster (Homarus americanus) from Long Island Sound, NY.

Abstract

In 1999, a mass mortality of the American lobster (Homarus americanus) occurred in western Long Island Sound (WLIS). Although the etiology of this event remains unknown, bottom water temperature, hypoxia, heavy metal poisoning, and pesticides are potential causal factors. Lobsters from WLIS continue to display signs of morbidity, including lethargy and cloudy grey eyes that contain idiopathic lesions. As the effect of these lesions on lobster vision is unknown, we used electroretinography (ERG) to document changes in visual function in lobsters from WLIS, while using histology to quantify the extent of physical damage. Seventy-three percent of lobsters from WLIS showed damage to photoreceptors and optic nerve fibers, including necrosis, cellular breakdown, and hemocyte infiltration in the optic nerves, rhabdoms, and ommatidia. Animals with more than 15% of their photoreceptors exhibiting damage also displayed markedly reduced responses to 10-ms flashes of a broad-spectrum white light. Specifically, maximum voltage (Vmax) responses were significantly lower and occurred at a lower light intensity compared to responses from lobsters lacking idiopathic lesions. Nearly a decade after the 1999 mortality event, lobsters from WLIS still appear to be subjected to a stressor of unknown etiology that causes significant functional damage to the eyes.