Coccidian parasites infect marine and freshwater fish worldwide.
Coccidia infect common carp, goldfish, grass carp and silver carp. Other tropical fish found to host coccidia are farmed Gouramies (Trichogaster trichopterus) and, in South America, cichlids and characids (Serrasalmus niger), both with visceral coccidia (Calyptospora spp).
Eimeria vanasi and Goussia cichlidarum occur in cichlid fish in Israel, Uganda and South Africa. E. vanasi has also been recovered from Oreochromis niloticus introduced to Thailand (from Egypt via Japan). Carp and goldfish in Israel, as elsewhere, are infected by Goussia carpelli. A second species found on Eurasian carp, Goussia subepithelialis, and Eimeria sinensis in silvercarp and bighead are absent from Israeli farmed fish. Introduced cyprinids in South Africa have not, thus far, been examined. Visceral tissue coccidioses are as yet unknown in African fish, however, liver and gonadal infections by Calyptospora spp. were reported from South American hosts (as well as from euryhaline killifishes in the southern USA. The only known coccidia from Southeast Asian tropical fish is Goussia trichogasteri from Gourami.
Piscine coccidia are intracellular organisms of the epithelium (of the gut, the gall bladder, the swimbladder and the kidney tubules) and tissues (liver) of epithelial origin. Developing intracellular (endogenous) stages may be detected within their host tissues by microscopic examination of fresh tissue and stained impressions and smears (with buffered [to pH 7.2] Giemsa, after being air dried and fixed in absolute methanol). Oocysts of digestive tract-coccidia may be detected in faeces. The oocyst wall of piscine coccidia, with a few exceptions (of eels), is soft and fragile and is often lost by the end of sporulation. Therefore, if sporulation occurs prior to defecation, only the smaller naked sporocysts may be found in faeces.
Coccidia are identified by the morphometry of their oocysts and sporocysts, the site of endogenous development and their position in the host cell .
The sporocyst's hard wall is either bivalved and cleaves by a longitudinal suture, or opens at the sporocyst's apex, at one pole, through a round pore (genus Epieimeria of eels, and some Eimeria s.l.) or a short apical suture. The sporocyst wall of the latter type may also form tubercules or projections and is further enclosed in a veil (genus Calyptospora).
Piscine coccidia develop either in the cytoplasm of the host cell or inside it's nucleus. Epicytoplasmic coccidia develop at the apex of the epithelial cell, below its brush border, bulging as they grow, together with their host cell wall, into the space about the epithelium (intestinal, swimbladder or excretory lumen). Sometimes the same coccidium species has cytoplasmic, intranuclear and epicytoplasmic generations (E. vanasi infecting cichlid fish).
Extraintestinal coccidia apparently reach their target organ via the blood. G. cichlidarum also underwent endodyogenous division before becoming established in the swim-bladder epithelium of its cichlid host.
In the epithelial cell, parasites undergo successive asexual (merogonous) divisions and a sexual process by which microgametes, differentiated from a microgamont, fuse with a macrogamont (macrogamete). The zygote thus formed becomes liberated from the host cell, while being encased in a wall. Through subsequent divisions the zygote divides into four, hard walled sporocysts, each of which further divides into two motile sporozoites.
The pace of development is fast in intestinal coccidia; in E. vanasi 8 days from infection to sporulation (at 24–27°C). In the swimbladder, coccidium (G. cichlidarum) endogenous development to sporozoite-containing sporocysts lasted at least 58 days at 23–26°C. These differences between intestinal and extraintestinal species are confirmed by studies of non-African species.
Oocysts of digestive tract and gall bladder coccidia are evacuated with the faeces. Sporulation of most gut coccidia is completed before evacuation in the faeces (endogenous sporulation). Some intestinal species, notably G. carpelli infecting carp and goldfish, become trapped in the gut epithelium within degenerate host cells (yellow bodies). Oocysts of another carp coccidium, G. subepithelialis, formed in the epithelium are displaced by the regenerating epithelium into the sub-mucosal layer. Oocysts of the epicytoplasmic coccidium of eels Epieimeria anguillae also infiltrate into the mucosa rather than being evacuated into the lumen. Oocysts of visceral and internal cavity coccidia, accumulate, sporulate in the host and will be liberated only after the death of the host.
Direct transmission by feeding on evacuated, sporulated oocysts has been demonstrated in several intestinal species, including those in carp Goussia carpelli and in cichlids E. vanasi. It has also been experimentally demonstrated that tubificid oligochaetes, of the genera Tubifex and Limnodrilus, serve as paratenic hosts: sporozoites of G. carpelli when ingested by the worms, excysted and invaded their gut epithelial cells. Such sporozoites remained infective, when fed with the worm, to carp 9 weeks later. Some eimerine coccidia (Calyptospora funduli) require an obligate intermediate host (grass shrimp) for transmission.
Transmission via predation and necrophagy seems to be the route of transmission not only for extraintestinal coccidia but for endogenously sporulating intestinal coccidia, while still in their host gut tissue or in the intestinal lumen.
The economic damage done by coccidiosis to warm water pisciculture has apparently been grossly underestimated. Since coccidiosis in fish usually manifests itself as a chronic infection, mortality is gradual and is overlooked in most farms. Losses only become evident when yields are checked at the end of the growth period.
Cyprinids and cichlids contract intestinal coccidioses as soon as they hatch. Infection (of G. carpelli) has been identified in 8-day-old goldfish, with mortality occurring 30–45 days later. G. carpelli seems to be more pathogenic to goldfish than to carp. In cichlids (cultured Oreochromis hybrids), intestinal infection (of E. vanasi) was detected in fry by the end of nursing in their parents' mouth, losses became evident when infection reached maximum levels by two or three weeks after hatching. Heavy infections in carp fingerlings (25–50 mm long) have been found to coincide with severe emaciation. Emaciation also occurred in infected cichlid fry. Surviving fish demonstrated spontaneous recovery, infection was low or absent in carp and goldfish or cichlids older than 2 months. Nonspecific defence response parameters (leucocytosis, eosinophylia, activation of phagocytes and elevation of natural antibody titer and of coeruloplasmin) were detected in carp infected with G. subepithelialis.
Damage caused by intestinal coccidioses occurs principally by the rupture of the epithelium by the escaping merozoites and oocysts (in G. carpelli and E. sinensis). In the intestine of cichlid fry infected with E. vanasi, most damage is caused to the mucosal cells by the developing intracytoplasmic parasites. Epicytoplasmic infections seem to have less effect on the gut epithelial layer and the damage induced through consumption of the nuclei by the intranuclear generations has not yet been evaluated. Inflammatory changes in intestinal coccidioses only occur following disintegration of the mucosal layer and in response to accumulated cellular debris. In nodular coccidiosis, caused in carp by G. subepithelialis, the accumulation of oocysts in the lamina propria induces inflammation with intense leucocyte infiltration (enteritis). The G. cichlidarum epicytoplasmic infection leads to an intense desquamation of the swimbladder epithelial lining in cichlids. Proliferation of the mucosal epithelial cells, observed in intestinal and in swimbladder infections, blocks the release of oocysts from the epithelium, resulting in a condition similar to that observed in nodular coccidiosis.
Swim bladders of cichlids with late infections turn opaque white. The pathogenicity of the swim bladder coccidiosis to juvenile cichlids still needs to be critically evaluated.
Coccidia of Clarias gariepinus have not been studied. They form yellow bodies similar to those of G. carpelli. Data on the pathological effect of Epieimeria anguillae infections are available from cultured New Zealand eels (Anguilla australis and A. diffenbachii). Oocysts which aggregate within or below the gut mucosa (in the lamina propria) induce inflammatory infiltration. In more severe infections, the condition is reminiscent of nodular coccidiosis, the basal membrane breaks and, following the aggregation of oocysts, the sub-mucosal tissue degrades and the loosened epithelial mucosa is sloughed off. Mature oocysts and sporocysts are passed out with necrotic tissue, eels become severely emaciated and die. Infected A. mossambica in South Africa passed free sporulated oocysts, and their intestines seemed to be normal.
Host response to oocyst aggregation in the livers of fish with visceral coccidioses (Calyptospora funduli in American killifish, Fundulus spp.), even when replacing up to 85% of the organ's volume, was limited to formation of a thin fibrotic capsule sometimes with collagen, or melanin .
Epizootiology In Israel it would be difficult to find cichlid fry, less than 25 mm in length, of any species, wild or cultured, from earth ponds or from the hatchery, free from infection with Eimeria vanasi. In all these young fish, irrespective of species, intracytoplasmic, epicytoplasmic and intranuclear forms occur simultaneously. Infection declines only after the surviving fish reach 40–50 mm in length (2–3 months old). Infection in all its three forms also seems to be widespread in South African cichlids, similarly affecting all local species. Heavy, morbid infections occurred in larger fish, up to 50 mm in length (O. mossambicus, and Tilapia sparmanii during winter). Persistence, or recurrences of infection, occurred where defence responses were apparently compromised due to low temperature (<13°C) or other stress conditions. Merogonic stages remaining inactive in on-growing fish are suspected to provide the source for renewal of infection in the new generations of fry in the following reproduction season (Paperna, unpublished).
Swimbladder coccidiosis infections occur only in Oreochromis spp. and Sarotherodon galilaeus. Due to the longer endogenous development, prevalence of infection extends to a wider range of age/size classes, while being absent in very young fish (less than 2 months old, (<40–50 mm long). In ponds, often all fish eventually become infected. Infection is retained in O. mossambicus entering marine habitats in South Africa.
Coccidioses in Israeli carp and goldfish are not as frequent as in cichlids, but quantitative data on infections among fish in warm water habitats are lacking.
Control An established protocol for chemotherapy and preventive management has not yet been formulated.
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