Inter-Research > DAO > v50 > n3 > p219-231  
Diseases of Aquatic Organisms

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DAO 50:219-231 (2002)  -  doi:10.3354/dao050219

Pathology of cultured paua Haliotis iris infected with a novel haplosporidian parasite, with some observations on the course of disease

B. K. Diggles1,*, J. Nichol2, P. M. Hine1,**, S. Wakefield2, N. Cochennec-Laureau3, R. D. Roberts4, C. S. Friedman5

1National Institute of Water and Atmospheric Research, PO Box 14-901, Kilbirnie, Wellington, New Zealand
2School of Medicine, University of Otago, Private Bag 7902, Wellington South, New Zealand
3Laboratoire de Genetique et Pathologie, IFREMER, BP 133, 17390, La Tremblade, France
4Cawthron Institute, Private Bag 2, Nelson, New Zealand
5School of Aquatic and Fishery Science, University of Washington, PO Box 355020, Seattle, Washington 98195, USA
*E-mail: **Present address: National Centre for Disease Investigation, MAF Operations, PO Box 40742, Upper Hutt, New Zealand

ABSTRACT: Mortalities among juvenile paua Haliotis iris Martyn 1784 in a commercial culture facility were reported in April 2000. Histology of moribund paua showed heavy systemic infections of a uni- to multi-nucleate stage of a novel organism later confirmed by transmission electron microscopy (TEM) and molecular studies to be a haplosporidian. Multinucleate plasmodia up to 25 µm diameter with up to 17 nuclei were detectable in wet preparations of hemolymph from heavily infected paua. The presence of the haplosporidian in the affected facility was associated with mortalities of slow growing Œrunt¹ paua during the summer months. Total mortalities in affected raceways 6 mo after mortalities began were between 82.5 and 90%. Heavily infected paua exhibited behavioural abnormalities including lethargy, loss of righting reflex, and were easily detached from surfaces. Some heavily infected paua exhibited oedema and pale lesions in the foot and mantle, but no reliable gross signs of disease were noted. Light infections of the haplosporidian were also found in apparently healthy paua from the facility. Histology indicated that the early stages of infection were characterised by small numbers of plasmodia in the connective tissue surrounding the gut, amongst glial cells adjacent to nerves in the mantle and foot and within gill lamellae. In heavy infections, large numbers of small plasmodia (mean size 5.5 x 7 µm in histological sections) were present in the hemolymph, gills, heart, kidneys, mantle, foot, epipodium and connective tissue of the digestive gland. Infections were not transferred horizontally at 14 and 19°C after cohabiting heavily infected paua with uninfected paua for 3 mo in aquaria, or 3 mo after injecting healthy paua with hemolymph containing haplosporidian plasmodia. This may indicate that the prepatent period for disease is longer than 3 mo, that disease is not expressed below 20°C, or that an intermediate host is required for transmission. Spore formation was not observed in juvenile paua but sporocyst-like bodies containing putative spores were observed amongst haplosporidian plasmodia in the right kidney of poorly performing adult paua collected from the wild.

KEY WORDS: Haplosporidia · Abalone · Aquaculture · Pathology · Disease · New Zealand

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