Species affected and geographical range
Parasitic dinoflagellids, the marine Amyloodinium ocellatum and the freshwater Piscinoodinium pillulare and P. limneticum, are not discriminatory in their choice of piscine hosts and have been implicated in mass mortalities of tropical marine and freshwater aquarium fish (Jacobs, 1946; Schaeperclaus, 1954; Paperna, 1980). A. ocellatum has infected sea water acclimatised Oreochromis mossambicus and Aphanius dispar in inland salt pans; some strains of this parasite survive in salinities as low as 10 ppt. Schaperclaus (1954) reports P. pillulare infection in 14 species of tropical ornamental freshwater fish of diverse families as well as in carp and crucian carp. Epizootic infections and mortalities were recently reported in farmed cyprinid fish in Malaysia, including grass carp (Ctenopharyngodon idella), bighead (Aristichthys nobilis), Leptobarbus hoevenii and Puntius gonionotus (Shaharom-Harrison et al., 1990). The presence of P. pillulare has never been established in Africa, but this ubiquitous parasite may eventually be found. If introduced with culture seed, it is likely to become established.
Diagnosis
Trophonts, when reaching the final stage of growth, are visible to the naked eye (80–100 μm diameter) as white spots (similar to that seen in ichthyophthiriasis) and turn dark blue when exposed to Lugol's-iodine. They are oval with a smooth wall and with inner aggregates of globules. In Malaysian fish, clinical signs of P. pillulare infection comprise both a rust-coloured appearance of the skin, indicating the presence of the parasite trophonts (20–75 × 14–50 μm), and a dense covering of mucus (Shaharom- Harrison et al., 1990).
Life cycle and biology
The life cycle of the dinoflagellid fish parasite is comprised of a parasitic feeding stage (trophont) which attaches to integumentary epithelial cells, and an encysted dividing stage (tomont) which is detached from the host. The trophonts of P. pillulare derive an essential part of their nutrition from photosynthesis. Trophonts dislodged at any time during their trophic stage will transform into a dividing tomont. Divisions yield a motile infective stage (dinospore) which attaches to a new host. There are several detailed studies of A. ocellatum (Paperna, 1984a), but comparable detailed data on the freshwater fish dinoflagellids are lacking. Data on P. limneticum growth and division (Jacobs, 1946), suggests that parasites reach a “maturation” prior to detachment. P. pillulare trophonts on the gills, at 23–25°C, develop from dinospore to detached tomont in three to four days. The tomont then completes division to the dinospore stage within 50–70 hours. At 15–17°C, the process of division is lengthened to 11 days (Schaperclaus, 1954).
Pathology and epizootiology
In larval fish, infections were limited to the skin, whereas in large fish the highest parasite densities occurred on the gill filaments and in the buccal-pharyngeal integument. Fish recovering from the epizootic infestation through a gradual decrease in infection, could not be reinfected (Paperna, 1980).
A. ocellatum is attached to and feeds from the host epithelial cell by means of rhizoids, which penetrate the host cell. The consumed cell gradually degenerates and collapses. Damage to infected cells leads to focal erosion of the epithelium. Prolonged infection exhausts a generation of mucus cells and leads to accelerated desquamation. Proliferation of the epithelium causes obliteration of the gill lamellae, while the inner strata of the epithelium become spongious and in some cases undergo complete lysis (Paperna, 1980). Attachment and penetration organelles of P. pillulare differ from those seen in A. ocellatum, in that the host cell is penetrated by nail-like extensions. However, damage to the host cell is similar (Lom & Schubert, 1983). Significant histopathological changes are only seen in the gills, where most of the infection occurs, namely a massive proliferation of the branchial epithelium which causes fusion of the lamellae by a confluent cellular mass (Shaharom-Harrison et al., 1990).
Piscinoodinium infection in Malaysia initially occurred among ornamental fish, but it spread eventually to pond farmed local and exotic cyprinids, causing mortality in fry of Puntius gonionotus in particular, although clinical signs were also apparent in a wider range of cyprinid fish species (Shaharom-Harrison et al., 1990).
Control
A. ocellatum is controlled by continuous application of copper sulphate, 0.75 ppm into infected tanks. A further option is a mixture of 5-hydrate copper sulphate with citric acid monohydrate, to yield 0.15 ppm copper ion concentration in the water (Hignette, 1981; Kabata, 1985). The same methodology will apparently effectively control Piscinoodinium infection, although concentrations should be adjusted to the freshwater medium and the fish targeted for treatment. In freshwater with a pH below 7.0 (in tropical aquaculture), concentrations above 0.3 ppm may be lethal to fish (e.g. Puntius gonionotus fry).
Parasitic dinoflagellids, the marine Amyloodinium ocellatum and the freshwater Piscinoodinium pillulare and P. limneticum, are not discriminatory in their choice of piscine hosts and have been implicated in mass mortalities of tropical marine and freshwater aquarium fish (Jacobs, 1946; Schaeperclaus, 1954; Paperna, 1980). A. ocellatum has infected sea water acclimatised Oreochromis mossambicus and Aphanius dispar in inland salt pans; some strains of this parasite survive in salinities as low as 10 ppt. Schaperclaus (1954) reports P. pillulare infection in 14 species of tropical ornamental freshwater fish of diverse families as well as in carp and crucian carp. Epizootic infections and mortalities were recently reported in farmed cyprinid fish in Malaysia, including grass carp (Ctenopharyngodon idella), bighead (Aristichthys nobilis), Leptobarbus hoevenii and Puntius gonionotus (Shaharom-Harrison et al., 1990). The presence of P. pillulare has never been established in Africa, but this ubiquitous parasite may eventually be found. If introduced with culture seed, it is likely to become established.
Diagnosis
Trophonts, when reaching the final stage of growth, are visible to the naked eye (80–100 μm diameter) as white spots (similar to that seen in ichthyophthiriasis) and turn dark blue when exposed to Lugol's-iodine. They are oval with a smooth wall and with inner aggregates of globules. In Malaysian fish, clinical signs of P. pillulare infection comprise both a rust-coloured appearance of the skin, indicating the presence of the parasite trophonts (20–75 × 14–50 μm), and a dense covering of mucus (Shaharom- Harrison et al., 1990).
Life cycle and biology
The life cycle of the dinoflagellid fish parasite is comprised of a parasitic feeding stage (trophont) which attaches to integumentary epithelial cells, and an encysted dividing stage (tomont) which is detached from the host. The trophonts of P. pillulare derive an essential part of their nutrition from photosynthesis. Trophonts dislodged at any time during their trophic stage will transform into a dividing tomont. Divisions yield a motile infective stage (dinospore) which attaches to a new host. There are several detailed studies of A. ocellatum (Paperna, 1984a), but comparable detailed data on the freshwater fish dinoflagellids are lacking. Data on P. limneticum growth and division (Jacobs, 1946), suggests that parasites reach a “maturation” prior to detachment. P. pillulare trophonts on the gills, at 23–25°C, develop from dinospore to detached tomont in three to four days. The tomont then completes division to the dinospore stage within 50–70 hours. At 15–17°C, the process of division is lengthened to 11 days (Schaperclaus, 1954).
Pathology and epizootiology
In larval fish, infections were limited to the skin, whereas in large fish the highest parasite densities occurred on the gill filaments and in the buccal-pharyngeal integument. Fish recovering from the epizootic infestation through a gradual decrease in infection, could not be reinfected (Paperna, 1980).
A. ocellatum is attached to and feeds from the host epithelial cell by means of rhizoids, which penetrate the host cell. The consumed cell gradually degenerates and collapses. Damage to infected cells leads to focal erosion of the epithelium. Prolonged infection exhausts a generation of mucus cells and leads to accelerated desquamation. Proliferation of the epithelium causes obliteration of the gill lamellae, while the inner strata of the epithelium become spongious and in some cases undergo complete lysis (Paperna, 1980). Attachment and penetration organelles of P. pillulare differ from those seen in A. ocellatum, in that the host cell is penetrated by nail-like extensions. However, damage to the host cell is similar (Lom & Schubert, 1983). Significant histopathological changes are only seen in the gills, where most of the infection occurs, namely a massive proliferation of the branchial epithelium which causes fusion of the lamellae by a confluent cellular mass (Shaharom-Harrison et al., 1990).
Piscinoodinium infection in Malaysia initially occurred among ornamental fish, but it spread eventually to pond farmed local and exotic cyprinids, causing mortality in fry of Puntius gonionotus in particular, although clinical signs were also apparent in a wider range of cyprinid fish species (Shaharom-Harrison et al., 1990).
Control
A. ocellatum is controlled by continuous application of copper sulphate, 0.75 ppm into infected tanks. A further option is a mixture of 5-hydrate copper sulphate with citric acid monohydrate, to yield 0.15 ppm copper ion concentration in the water (Hignette, 1981; Kabata, 1985). The same methodology will apparently effectively control Piscinoodinium infection, although concentrations should be adjusted to the freshwater medium and the fish targeted for treatment. In freshwater with a pH below 7.0 (in tropical aquaculture), concentrations above 0.3 ppm may be lethal to fish (e.g. Puntius gonionotus fry).
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