Perkinsosis here refers only to the diseases caused by Perkinsus marinus and P. olseni/atlanticus. Other described species of Perkinsus include P. chesapeaki from Mya arenaria ( 26 ) , P. andrewsi in Macoma balthica ( 14 ), both from the east coast of the United States of America ( USA ) , and P. qugwadi from Patinopecten yessoensis from western Canada ( 5 ) . These species are not considered at this time to cause diseases notifiable to the OIE. Other unidentified Perkinsus spp. infect many species of bivalves in tropical and subtropical waters ( 22 ). Until more is known about the identity, biology and pathology of these other Perkinsus spp., their presence in any bivalve should be regarded as potentially serious and the OIE Reference Laboratory should be consulted.
Perkinsosis is an infection of marine molluscs caused by protistan parasites of the genus Perkinsus. Recent investigations using molecular sequence data ( 21, 39, 42 ) indicate that Perkinsus is not in the phylum Apicomplexa as suggested by ultrastructural data ( 25 ) , but is closely related to the Dinoflagellida. Some authors have placed Perkinsus in the phylum Perkinsozoa ( 33 ) , or the phylum Dinozoa subphylum Protalveolata ( 12 ), but more molecular data are necessary on Perkinsus and genera related to Perkinsus before phylogenetic relationships will be clear.
Perkinsus marinus causes disease of economic importance in Crassostrea virginica( 2, 7 ) . Although infection of C. gigas and C. ariakensis is possible, these species seem to be more resistant to the disease ( 4, 9, 10 ) . Perkinsus marinus was formerly named Dermocystidium marinum ( 29 ) , and then Labyrinthomyxa marina ( 30 ) . Infection by P. marinus is commonly known as 'Dermo disease' ( 19 ) . Perkinsus marinus is found on the east coast of the USA ( 2, 7 ) from Maine to Florida, and along the Gulf of Mexico coast to the Yucutan Peninsula ( 6 ) . The recent northward range extension of P. marinus into Delaware Bay, New Jersey, Cape Cod and Maine, USA, is attributed to repeated introductions over several years in conjunction with recent increases in winter sea-surface temperatures ( 13, 18 ) . The effects of P. marinus infection in C. virginica range from a pale appearance of the digestive gland and reduction in condition index, to severe emaciation, gaping, retraction of the mantle, inhibition of gonadal development, retarded growth, and death ( 27, 28 ) .
Perkinsus olseni was originally described from Haliotis ruber in Australia ( 24 ) and P. atlanticus was originally described from Ruditapes decussatus in Portugal ( 3 ) . Similarities in the nucleotide sequences of the internal transcribed spacers ( ITS ) of the ribosomal RNA gene cluster ( 20 ) have long suggested that P. olseni is conspecific with P. atlanticus. Recently, the synonymy of the two species has been formally established based also on sequence similarities in the rRNA nontranscribed spacer ( NTS ) region ( 32 ) ; Perkinsus olseni has taxonomic priority. Other susceptible hosts for P. olseni/atlanticus include Haliotis cyclobates, H. scalaris , H. laevigata, Anadara trapezia, Austrovenus stutchburyi and Ruditapes philippinarum( 22, 23, 32, 34 ) . The geographical distribution of P. olseni/atlanticus is eastern and southern Australia, New Zealand, Korea, Japan, Portugal, France, Italy and Spain ( 1, 3, 11, 22, 23, 34, 40 ).
Proliferation of P. olseni/atlanticus results in the disruption of connective tissue and epithelial cells leading to weakening. Cysts are visible macroscopically on the gills of infected R. decussatus( 3 ) . Abscesses occasionally can be noted in abalone (Haliotis spp.)( 24 ). Pustules up to 8 mm in diameter in the foot and mantle of infected Haliotis spp. reduce market value. Perkinsus olseni/atlanticus was directly associated with high losses of the abalone H. laevigata in Australia ( 22 ) and mortality in the clam R. decussatus in Portugal ( 3 ) and in the clam R. philippinarum in Korea ( 34 ) .
Morphology of life history stages is similar for all Perkinsus species. Trophozoites, characterised by a large vacuole and a displaced nucleus, occur intercellularly in connective and epithelial tissue. Mature trophozoites divide by successive binary fission resulting in the release of 8-32 immature trophozoites ( 36, 44 ) . The developmental cycle of P. marinus often occurs within phagocytes. Proliferation of all Perkinsus species is correlated with warm summer water temperatures ( higher than 20°C ) when pathogenicity and associated mortalities are highest. All life history stages appear to be infective ( 45 ) . Under certain, poorly understood, conditions mature trophozoites enlarge and undergo zoosporulation. Although biflagellate zoospores are infective, the role of the zoospore in transmission in nature is unclear.
Reference methods for the detection of Perkinsus spp. are histological sections and culture in fluid thioglycollate medium ( 8, 17, 37, 38 ) . For diagnosis, the recommended guidelines for sampling are those stated in Chapter 1.1.4 and Chapter I.2. of this Aquatic Manual .