Kidney Coccidia of Abalone
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Category
Category 1 (Not Reported in Canada)
Common, generally accepted names of the organism or disease agent
Abalone kidney coccidia.
Scientific name or taxonomic affiliation
Margolisiella (=Pseudoklossia) haliotis (see Desser and Bower (1997) for an explanation of the systematics). Other species of coccidia have been described from the kidneys of oysters, mussels, scallops and clams from various locations around the world.
Geographic distribution
California, USA and Baja California, Mexico. In 1991, the vegetative stages of the parasite were observed in 2 of 40 Haliotis rufescens illegally imported from California into barrel culture in Bamfield, British Columbia. In January 2005, one broodstock Haliotis kamtschatkana collected from the vicinity of Bamfield and held in captivity for about 1.5 years had a heavy infection. The distribution of this parasite in British Columbia is not known. Renal coccidia have also been reported from Haliotis midae cultured in South Africa (Mouton 2000, Sales and Britz 2000). Meronts and merozoites morphologically similar to those described by Friedman et al. (1995) were reported from the epithelium of the esophageal pouch of Haliotis iris from an abalone culture facility in New Zealand (Diggles and Oliver 2005).
Host species
Haliotis cracherodii, Haliotis rufescens, Haliotis corrugata, Haliotis fulgens, Haliotis walallensis, Haliotis kamtschatkana, and this or another species in Haliotis midae. In experimental trials in California, the coccidian was directly transmitted from H. rufescens to H. kamtschatkana after 10.5 months of cohabitation and all H. kamtschatkana were infected within 17 months.
Impact on the host
Infected kidney epithelial cells become extremely hypertrophied and heavy infections appear to cause serious kidney damage. However, M. haliotis elicits no haemocytic response suggesting that it is not recognised as an invader by the abalone host (Friedman et al. 1995). The life cycle appears to be homoxenous (complete life cycle in one host; infection developed following exposure to water occupied previously by infected abalone). The parasite was implicated in black abalone mass mortalities (withering syndrome) in the late 1980s and early 1990s but is no longer considered to be the cause of this disease and is now thought to be benign in nature (Friedman 1991, Kuris et al. 1994, Friedman et al. 1997). Despite the heavy natural and experimental infections that have been observed in the field and as a result of laboratory experiments, no change in the condition of the abalone nor mortalities have been observed (Friedman et al. 1993).
Diagnostic techniques
Squash Preparations
A preliminary diagnosis can be made on the presence of large mature macrogamonts in squashes of kidney tissues.
Histology
All stages in the life cycle of M. haliotis, including vegetative multiplication (merogony with development of meronts containing merozoites) and sexual reproduction (gametogony with development of microgametes, macrogametes and oocysts containing sporocysts with sporozoites), occur within the epithelial cells of the abalone kidney (Friedman et al. 1995). Infection is initiated when an elongate sporozoite (about 7 µm by 2.5 µm) penetrates a kidney epithelial cell and develops by ectomerogony to form a meront (about 13 µm in diameter) containing about 28 merozoites and a single residuum. After an unknown number of generations of merogony (vegetative multiplication), elongate meozoites (about 10 µm by 3 µm) that infect a kidney epithelial cell will develop into either a microgamont (about 20 µm in diameter) containing about 40 microgametocytes or into a single macrogametocyte (about 25 µm in diameter). Following fertilisation by a microgametocyte, the macrogametocyte develops into an oocyst (about 31 µm in diameter) containing 6 to 12 sporocysts and a residuum. Each sporocyst contains two sporozoites (about 7µm long and 2.5 µm wide) and a sporocyst residuum. The oocysts rupture the host cell and are believed to exit the abalone via the nephridial ducts to initiate the infection in another abalone making this parasite homoxenous (complete life cycle in one host).
Methods of control
No known methods of prevention or control.
References
Bower, S.M. 2000. Infectious diseases of abalone (Haliotis spp.) and risks associated with transplantation. In: Campbell, A. (Editor), Workshop on Rebuilding Abalone Stocks in British Columbia. Canadian Special Publication of Fisheries and Aquatic Sciences 130: 111-122.
Caceres-Martinez, J. and G.D. Tinoco-Orta. 2001. Symbionts of cultured red abalone, Haliotis rufescens from Baja California, Mexico. Journal of Shellfish Research 20: 875-881.
Desser, S.S. and S.M. Bower. 1997. Margolisiella kabatai gen. et sp. n. (Apicomplexa: Eimeriidae), a parasite of native littleneck clams, Protothaca staminea, from British Columbia, Canada, with a taxonomic revision of the coccidian parasites of bivalves (Mollusca: Bivalvia). Folia Parasitologica 44: 241-247.
Diggles, B.K. and M. Oliver. 2005. Diseases of cultured paua (Haliotis iris) in New Zealand. In: Walker, P.J., R.G. Lester, M.G. Bondad-Reantaso (eds.) Diseases in Asian Aquaculture V. Proceedings of the 5th Symposium on Diseases in Asian Aquaculture. Fish Health Section, Asian Fisheries Society, Manila. pp. 275-287.
Friedman, C.S. 1991. Coccidiosis of California abalone, Haliotis spp. (Abstract) Journal of Shellfish Research 10: 236.
Friedman, C.S., W. Roberts, G. Kismohandaka and R.P. Hedrick. 1993. Transmissibility of a coccidian parasite of abalone, Haliotis spp. Journal of Shellfish Research 12: 201-205.
Friedman, C.S., G.R. Gardner, R.P. Hedrick, M. Stephenson, R.J. Cawthorn and S.J. Upton. 1995. Pseudoklossia haliotis sp.n. (Apicomplexa) from the kidney of California abalone, Haliotis spp. (Mollusca). Journal of Invertebrate Pathology 66: 33-38.
Friedman, C.S., M. Thomson, C. Chun, P. Haaker, and R.P. Hedrick. 1997. Withering syndrome of the black abalone, Haliotis cracherodii (Leach): water temperature, food availability, and parasites as possible causes. Journal of Shellfish Research 16: 403-411.
Haaker, P.L., D.O. Parker, H. Togstad, D. Richards V, G.E. Davis and C.S. Friedman. 1992. Mass mortality and withering foot syndrome in black abalone, Haliotis cracherodii, in California. In: S.A. Shepard, M.J. Tegner and S.A. Guzman del Proo (eds.), Abalone of the World: Biology, Fisheries and Culture. Proceedings of the 1st International Symposium on Abalone. Fishing News Books, Cambridge, p. 214-224.
Kuris, A.M., R.J. Schmitt and R. Hedrick. 1994. Abalone wasting disease: role of coccidian parasites and environmental factors. In: none (eds), California Sea Grant Biennial Report of Completed Projects 1990-92. California Sea Grant College, La Jolla, CA, pp. 120-123.
Martínez, J.C. and G.D.T. Orta. 2000. Symbionts of red abalone Haliotis rufescens from Baja California, Mexico. (Abstract) Journal of Shellfish Research 19: 503.
Mouton, A. 2000. Health management and disease surveillance in abalone, Haliotis midae, in South Africa. (Abstract) Journal of Shellfish Research 19: 526.
Sales, J. and P.J. Britz. 2000. South African abalone culture succeeds through collaboration. World Aquaculture 31: 44,45,49,50,61.
Steinbeck, J. R. S., Groft, J. M., Friedman, C. S., McDowelly, T. and R.P. Hedrick, R. P. 1989. A coccidian-like protozoan from the California black abalone Haliotis cracherodii. In: Abstracts, First International Symposium on Abalone Biology, Fisheries, and Culture, 21-25 Nov. 1989, La Paz, Mexico, p. 23.
Steinbeck, J.R., J.M. Groff, C.S. Friedman, T. McDowell and R.P. Hedrick. 1992. Investigations into a mortality among populations of the California black abalone, Haliotis cracherodii, on the central coast of California, USA. In: S.A. Shepard, M.J. Tegner and S.A. Guzman del Proo (eds.), Abalone of the World: Biology, Fisheries and Culture. Proceedings of the 1st International Symposium on Abalone. Fishing News Books, Cambridge, p. 203-213.
Citation Information
Bower, S.M. (2006): Synopsis of Infectious Diseases and Parasites of Commercially Exploited Shellfish: Kidney Coccidia of Abalone.
Date last revised: December 2006
Comments to Susan Bower
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