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11. MICROSPORA

Plate 19 (p. 100) and Fig. 2 M, N (p. 90)

Species affected
Thus far, only reported in cichlids from Africa and the Near East.

Geographic range
Microsporidian infection has been described from many Holarctic marine and freshwater fish. There are very few reports of infections in fish in the tropics. Microsporidian infections were reported from Lake George, East Africa (Swimbladder of Haplochromis spp.) (Paperna, 1973) and in the Republic of Benin (in gills and viscera of Tilapia and Sarotherodon spp.) (Sakiti & Bouix, 1987). Microsporidian spores were also detected in kidneys of Oreochromis aureus and its hybrids, in Israel. Plistophora (syn. Pleistophora) infection has been reported from glass eels and elvers in the Umtata and Keiskama rivers in Transkei (southern Africa) (Jackson, 1978).

Description, taxonomy and diagnosis
Microsporidia are obligate intracellular parasites. Infected cells usually enlarge to accommodate the proliferating parasite. Such enlarged cells are termed xenomas. Within these xenomas, parasites undergo merogonous and sporogonous development which culminates in the production of spores (Canning & Lom, 1986; Lom & Dykova, 1992). The spores are thick walled and contain a characteristic coiled polar filament and one (Pleistophoridida) or two nuclei (Nosematidida) (Weiser, 1985). Infection is readily detectable by the presence of spores in tissue smears (fresh or Giemsa stained), or in histological section. Hypertrophic infected cells may reach macroscopic sizes and often yield characteristic gross pathological signs; multiple whitish nodules in tissues, or in case of the swimbladder, a significant thickening of the walls. Differentiation from other aetiological agents, inducing cellular hypertrophy (Lymphocystis, Epitheliocystis and Myxosporea), is achieved by demonstration of spores in such tissues.

Generic and specific differentiation is often aided by ultrastructural data (Canning & Lom, 1986). Keys for generic differentiation were prepared by Weiser (1985).

Life history and biology
All active stages of the microsporidians develop in the host cell. Two microsporidia were reported to develop within the host cell nucleus (in Rodlet cells - Modin, 1981 and in haematopoietic cells - Hedrick et al., 1991). The spores are the infective stage transmissible to new hosts. In the invasive stage, the uni- or binucleate sporoplasm of the spore is released through the hollowed polar filament. Development of the parasites often takes place in tissues far removed from the site of hatching, wandering macrophages and other non-differentiated mesenchymal cells probably aid their distribution or serve as hosts. Infected host cells often become grossly hypertrophic (xenoma), with concurrent enlargement of the nuclear mass (remaining single or becoming fragmented) and multiplication of nucleoli. Microsporidia are unusual in lacking mitochondria and their ribosomes are unusually large. In some microsporidia nuclei appear single (‘isolated’), whereas in others nuclei are paired. Development within the xenoma proceeds through a merogonous and a sporogonous process. The sporoblasts formed from sporonts differentiate into spores (Putz & McLaughlin, 1970; Weiser, 1985; Canning & Lom, 1986).

Pathology and epizootiology
The effect of microsporidian infection on the piscine host is variable: fish seem to survive infections, in spite of the presence of huge xenomata often pressing on and displacing important organs, while infection by some microsporidians undoubtedly has a morbid effect on the fish (Putz & McLaughlin, 1970; Morrison & Sprague 1981). Intranuclear infection of haematopoietic cells was associated with acute anaemia (Elston et al., 1987).

In Plistophora infected Haplochromis angustifrons and H. elegans, the swimbladder walls were thick and white. Microscopic examination revealed most wall tissue to be loaded with inclusions (pansporoblasts) containing up to 48 spores. Prevalence of infection in L. George was very low (below 1%, out of 302 fish examined from both species) (Paperna, 1973). Infections by Nosemoides tilapia in Tilapia zillii, T. guinensis and Sarotherodon melanotheron were common (13–30% prevalence in Lake Nakoue and Porto Novo lagoon), with some fish demonstrating numerous xenomata on the gills (some reaching 560 × 800 μm in size) as well as in the mesenteries, the gut wall and in the liver (up to 40–100 μm in size), but without apparent clinical effect on the fish (Sakiti et Bouix, 1987). Prevalences of infection with Plistophora (?) in glass eels and elvers in Transkei rivers were 6.8–9.5% and 2.6% respectively. Microsporidial infection of kidneys in Oreochromis spp. are rare and do not induce any detectable pathological changes.

Control
There is no routine treatment. Fumagilin DCH used to control Nosema infections in bees has been tested for efficacy in treatment of microsporidial infections in fish. The drug administered in food, 0.1 g/kg food at 1.5% body weight daily ratio for four weeks, prevented mortalities and relieved Enterocytozoon-infected chinook salmon from clinical signs (Hedrick et al., 1991). Recurrences of infection occur in treated Plistophora infected eels (Kano & Fukui, 1982). With elevation of doses and prolongation of treatment, toxic side-effects (haematological and stress-linked) occur (Sitja-Bobadilla & Alvares-Pelleteiro, 1992).

Toltrazuril (Beyer product - 2.5% A.I.) administered by a 1h bath of 20 μg/ml (or a 4h bath of 5 μg/ml), repeated six times at two day intervals, damaged developmental stages of the microsporidian Glugea anomala in sticklebacks, but did not affect spores (Schmahl & Mehlhorn, 1989).

REFERENCES

Canning, E. & Lom, J., 1986. The microsporidia of vertebrates. Academic Press.

Elston, R.A., Kent, M.L. & Harrel, L.H., 1987. An intranuclear microsporidium associated with acute anaemia in the chinook salmon. J. Protozool., 34: 247–277.

Hedrick, R.P., Groff, J. M. & Baxa, D.V., 1991. Experimental infection with Enterocytozoon salmonis Chilmonczyk, Cox, Hedrick (Microsporea) : an intranuclear microsporidium from chinook salmon Onchorhynchus tshawytscha. Dis. Aquat. Org., 10: 103–108.

Jackson, P.B.N., 1978. Health and disease in intensive aquaculture. J. S.A. Vet. Ass., 49: 57–59.

Kano, T. & Fukui, H., 1982. Studies on Pleistophora infection in eel, Anguilla japonica -I. Experimental induction of microsporidiosis and fumagilin efficacy. Fish Pathol., 16: 193–200.

Lom, J. & Dykova, I., 1992. Protozoan parasites of fishes. Elsevier, Amsterdam, London, New York, Tokyo.

Modin, J.C., 1981. Microsporidium rhabdophilia n. sp. from the rodlet cells of salmonid fishes. J. Fish Dis., 4: 203–211.

Morrison, C. M. & Sprague, V., 1981. Microsporidian parasites in the gills of salmonid fishes. J. Fish Dis., 4: 203–211.

Paperna, I., 1973. Occurrence of Cnidospora infections in freshwater fishes in Africa. Bull Inst. Fond. Afr. Noir, 35 (A-3): 509–521.

Putz, R.E. & McLaughlin, J.J.A., 1970. Biology of Nosematidae (Microsporidia) from freshwater and euryhaline fishes. In: Snieszko F.S. (ed.) A symposium on diseases of fishes and shellfish. Amer. Fish. Soc. Wash. Special Pub., 5, pp. 124–132.

Sakiti, N.G. & Bouix, G., 1987. Nosemoides tilapiae n. sp., microsporidie parasite de poissons Cichlidae des eaux saumatres du Benin: implantation et caracteres ultrastructuraux. Parasitol. Res., 73: 203–212.

Sitja-Bobadilla, A. & Alvares-Pelleteiro, P., 1992. Effect of Fumagillin treatments on sea bass Dicentrarchus labrax parasitized by Sphaerospora testicularis (Myxosporea: Bivalvulida). Dis. Aquat. Org., 14: 171–178.

Schmahl, G. & Mehlhorn, H., 1989. Treatment of fish parasites 6. Effects of Sym. Triazinone (Tolrazuril) on developmental stages of Glugea anomala, Moniez, 1887 (Microsporidia): A light and electron microscopic study. Europ. J. Protistol., 24: 252–259.

Weiser, J., 1989. Phylum Microspora Sprague, 1969. In: Lee et al., (eds.) Illustrated guide to protozoa. Society of Protozoologists. pp. 375–383.


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