Co-infection of bay scallops Argopecten irradians with Perkinsus karlssoni (Apicomplexa, Perkinsea) and an unidentified coccidian parasite

• Published in: Diseases of aquatic organisms Vol. 18; no. 1; pp. 53 - 62
• Main Authors: WHYTE, S. K, CAWTHORN, R. J, MCGLADDERY, S. E
• Format: Journal Article
• Language: English
• Published: Oldendorf Inter-Research 1994
• Subjects: Argopecten irradians; Biological and medical sciences; Coccidia; Fundamental and applied biological sciences. Psychology; Invertebrates; Marine; Mollusca; Pathology; Canada; North Atlantic; North America; Atlantic Ocean; America; Protozoa; Mixed infection; Immune response; Argopecten irradians; Parasite; Inflammation; Coastal zone; Marine environment; Histopathology; Transmission electron microscopy; Bivalvia; Ultrastructure; Invertebrata; Mollusca; Sporozoa
• ISSN: 0177-5103; 1616-1580
• DOI: 10.3354/dao018053

A comparison of the coinfection of bay scallops with Perkinsus karlssoni and an as yet unidentified coccidian is described. P. karlssoni occurred in a range of host tissues including mantle, digestive gland, intestine, gill and gonad. Host tissue response elicited against P. karlssoni ranged from focal encapsulation by haemocytes to formation of abscesses filled with ceroid-containing cells. The coccidian was restricted to the kidney in light infections and occurred within the renal cells and the lumen of the renal tubules. In heavy infections the coccidian also occurred in the mantle, digestive gland, intestine, gill and gonad. There was no apparent host response elicited against the coccidian parasite regardless of the tissue in which it occurred or whether the parasite was intra- or intercellular. In dual infections, dense haemocytic encapsulation and infiltration by ceroid-containing cells masked the causative organism. Ultrastructural examination of lesions from concurrent infections revealed the presence of both parasites. Individual P. karlssoni infections were not found without a host response and the coccidian occurred with no apparent host response. It was therefore assumed that the response elicited in dual infections was caused predominantly by P. karlssoni.