Excretory calcinosis: a new fatal disease of wild American lobsters Homarus americanus

Abstract

A significant number of moribund and dead lobsters Homarus americanus were reported to New York state authorities by lobster fishers in Long Island Sound (LIS) during the summer of 2002. Morbid lobsters were characterised by an orange discolouration of the abdomen, lethargy, an excess of epibionts and poor post-capture survival. On necropsy, severe extensive multifocal or diffuse mineralised granulomatous inflammation of the gills and antennal glands was the most striking pathology. In the gills, granulomas often occluded the lumen of filaments, resulting in congestion, ischemia and coagulative necrosis of gill tissues. In the antennal glands, granulomas were concentrated along the border between the coelomosac and labyrinth. No significant pathogens were recovered from diseased individuals. In prechronic individuals, however, it was evident that granulomas were focused around calcium carbonate (aragonite) crystals. This disease may result from anomalously high sea-bottom temperatures in LIS (~23°C) during the summer of 2002 and associated disruptions of the calcium chemistry of lobsters in favour of deposition of minerals in soft tissues. The ultimate cause of death of affected lobsters is probably respiratory failure due to reduced effective surface area of the gills, exacerbated by hypermetabolic temperatures and an abundance of epibionts.KEY WORDS: Lobster · Homarus · Granuloma · Calcium · Aragonite · Calculus · Calcinosis · TemperatureResale or republication not permitted without written consent of the publisher

Internal organ pathology of wild American lobster (Homarus americanus) from eastern Canada affected with shell disease

“…In 2002, similar gill pathologies were observed for moribund and dead lobsters from Long Island Sound (Dove et al 2004). Although these lobsters were not reported specifically to have shell disease, granulomas were frequently seen to be embolisedin the gill filaments, resulting in congestion, ischemia, and coagulative necrosis of gill tissues.…”

“…Although these lobsters were not reported specifically to have shell disease, granulomas were frequently seen to be embolisedin the gill filaments, resulting in congestion, ischemia, and coagulative necrosis of gill tissues. Dove et al (2004) hypothesised that the lobster deaths were a result of hypercapnia (excess CO 2 in the haemolymph) caused by high sea temperatures (c. 23°C) observed that year. They explained that temperature-related respiratory stress could cause disruptions of the calcium chemistry of lobsters in favour of deposition of calcium minerals in soft tissues and, under appropriate conditions, could represent a fatal positive feedback loop, i.e., cause death (Dove et al 2004).…”

“…Dove et al (2004) hypothesised that the lobster deaths were a result of hypercapnia (excess CO 2 in the haemolymph) caused by high sea temperatures (c. 23°C) observed that year. They explained that temperature-related respiratory stress could cause disruptions of the calcium chemistry of lobsters in favour of deposition of calcium minerals in soft tissues and, under appropriate conditions, could represent a fatal positive feedback loop, i.e., cause death (Dove et al 2004). Temperatures at or above 20°C have been reported yearly in the coastal waters of the southern Gulf of St. Lawrence Paulin et al 2005).…”

Subcuticular Urate Accumulation in an American Lobster (Homarus americanus)

“…4,7 Bowser and Rosemark observed globular, calcium-containing mineral deposits on and in the inner surface of the shed exoskeletons of many juvenile lobsters (H. americanus and H. americanus  H. gammarus hybrids) during an artificial diet trial. 4 The lobsters died during or shortly after molting with dietary stress considered a contributing factor.…”

“…Dove et al described ''excretory calcinosis'' as a condition of extracellular calcium carbonate deposits affecting a significant number of lobsters in 2002. 7 The condition involved the antennal glands and gills, which showed marked inflammation and occasionally necrosis in more chronic lesions. 7 Increased bottom water temperature was suggested as a possible cause.…”