Stained prawn disease (SPD) with clinical signs of black discolouration of the cuticula, especially around the edges of body segments, and black stippling on the surface of the hepatopancreas was caused by a rickettsia-like microorganism with a n affinity for fixed phagocytes and haemocytes. This disease was found in prawns from various localities throughout Howe Sound and at one location in the S t r a~t of Georgia, British Columb~a, Canada. The distribution of SPD wlthin Howe Sound has not changed since it was first detected In 1989. However, the prevalence has declined to about 4 % from a record high of about 15% In July 1990 and March 1991 In areas with these high prevalences, an above-average level of mortality, equated to a decline in survival rates from 57 to 15'X,, was detected. These mortalities were not attributable to fishing pressure because the affected area has been closed to fish~ng since November 1988 due to unacceptable levels of dioxin and furan compounds In shellfish tissue samples. Laboratory studies indicated that the SPD agent can be transm~tted horizontally by cannibalism and via the water [exposure to screened (1 mm pore size) effluent from lnfected prawns] and remained infectious for 10 d or more of storage at -lO°C. About 50% of the prawns that fed on infected prawns (both fresh and after being frozen) and 25 % of the prawns exposed to contaminated water became infected. Most mortalities attributable to SPD occurred between 2 and 4 mo after exposure to the etiological agent in the laboratory.
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