Species affected and geographical range
Most species of freshwater fish are susceptible, although some may be more so than others. The world wide distribution of I. multifiliis (Hoffman, 1970) has apparently been facilitated by the widespread translocation of cultured and ornamental fish. The presence of this parasite in autochthonous fish, in remote areas of the world including, southern Venezuela (Ventura & Paperna, 1985) and Northern Transvaal in South Africa (Paperna, unpublished) may suggest, however, that many populations, particularly those in the tropics, are comprised of a mix of autochthonous and introduced parasites. Data available from Africa are limited to Southern Africa (in cichlids, carp, Barbus spp., trout and eels - Du Plessis, 1952; Lombard, 1968; Jackson, 1968; Van As & Basson, 1984) and Uganda (on native Barbus amphigramma and exotic Lebistes reticulatus from small streams at Kajansi - Paperna 1972). It is very common in Israel, in both farmed (Sarig, 1971; Hines & Spira, 1973a) and wild fish including cichlids (Ventura & Paperna, 1985).
Description and diagnosis
Gross signs - white spots on the skin and the gills, which under microscopic examination reveal (in skin and gill scrapings) uniformly ciliated organisms with a small cytostome, which may reach up to 1 mm in diameter. Staining with either haematoxylins or Giemsa (after adequate fixation, in such as Bouin) reveals a large crescent-shaped macronucleus and small micronucleus. Ichthyophthirius multifiliis is a monotypic genus of hymenostomatid ciliates.
Life history and biology
Trophonts (feeding stages) develop within the integumentary epithelium, always above the basal membrane (Ventura & Paperna, 1985; Ewing & Kocan, 1992). By maturity, which is reached in 2 days at ambient temperatures of 25–28°C (3–4 days at 21–24°C), the parasite evacuates the host tissue and settles within 2–6 hours on a substrate in the water to form a cyst-encapsulated tomont (dividing stage). Parasites evicted from the tissue before the scheduled time for their spontaneous departure, fail to develop into tomonts and eventually die (Ewing & Kocan, 1992; Paperna, unpublished observations). Within the cyst, tomonts undergo successive binary fissions with a resulting yield of 250–2000 tomites (infective, free swimming stages), which after release will seek a suitable host. The division of tomonts into tomites, in ambient temperatures of 25–28°C, is completed within 15–20 hours (Bauer, 1959; Meyer, 1969; Paperna, unpublished observations; 7–8 hours according to Hoffman, 1978).
Invasion of tomites (teronts) (30–45 μm long) into the host integument is facilitated by the excretion of a sticky substance from subpellicular crystalline organelles named mucocysts. Active penetration causes focal necrosis of the epithelial cells. It has been suggested that hyaluronidase and other enzymes may be produced by the penetrating parasite (Ewing et al., 1985). In the absence of a suitable host, tomites will lose their infective potential within 24 hours at 24–28°C (Ewing & Kocan, 1992). Higher temperatures hasten trophont maturation and tomont division, but at lower temperatures, slower development allows the growth of larger trophonts (0.8–1.0 mm in 5–10°C vs 0.5–0.7 mm in 20–24°C), yielding tomonts with higher numbers of tomite progeny (Ewing et al., 1986). In lower ambient temperatures the survival of the tomites is prolonged, thus, allowing more time to locate a host. Low temperatures do not interrupt propagation, a full cycle is completed at 20°C in 3–5 days, at 15°C in 7–14 days and at 10°C in 21–35 days (Bauer, 1959; Meyer, 1969). Data on the effect of other environmental parameters is less conclusive, although it has been suggested that dissolved oxygen levels below 1 mg/l affect parasite reproduction (Bauer, 1959).
Pathology
Ichthyophthiriasis is fatal to fish of all sizes. Chronic infection will cause serious damage to the skin, fin and gills; corneal infection impairs vision (Hines & Spira, 1973a, 1974a). The infective stage invades the integumentary epithelium and becomes established in the basal layer of the epithelium just above the basal membrane. Cellular damage in low to moderate infections remains restricted to the infected site. In addition to the damage caused to epithelial cells by the feeding and expanding parasites, in heavy infections mass exodus of parasites from the epithelial layer, having completed their scheduled growth, causes its erosion and detachment from the basal membrane. In some infections, parasites cause widespread lysis of the inner layer of the epithelium. Prolonged infection also induces epithelial proliferation and haemorrhagic inflammation, causing the integument to become severely disintegrated (Hines & Spira, 1974a; Ventura & Paperna, 1985; Ewing et al., 1986). Hines and Spira's (1973b, 1974a,b) haematological and clinical data from heavily infected fish reveal evident physiological dysfunction resulting apparently from both direct pathological damage induced by the parasite and as a by-product of the stress response.
Epizootiology
Ichthyophthirius multifiliis is one of the most common, troublesome and difficult to control of fish pathogens. Epizootic infections have been reported in cold water salmonid farms (also in Africa, Du Plessis, 1952; Lombard, 1968) and warm water farmed carp, eels, Clarias gariepinus and Ictalurus punctatus (channel catfish) (Meyer, 1970; Sarig, 1971; Hines & Spira, 1973a; Hine, 1975; Jackson, 1978; Khalifa et al. 1983; Paperna, unpublished). Fish may maintain low, subclinical (enzootic) infection (in preimmunity), while encysted tomonts may persist in the habitat. Enzootic infections in native fish have been found in Lebistes reticulatus in Uganda (Paperna, 1972), in cichlids and cyprinids native to the Lake Kinneret system in Israel (Paperna, unpublished), in glass eels, cyprinids and cichlids in native habitats of South Africa (Jackson, 1978; Van As & Basson, 1984), and in a variety of native fish in the southern United States (Allison & Kelly, 1963). Transition from nonclinical enzootic to epizootic clinical infection is usually stress-mediated, prompted by adverse growth conditions such as overcrowding, poor feeding and excess nitrogenous waste. Epizootic infection, however, never occurs in overwintering tilapia or Clarias gariepinus in Israel, or southern Africa, but rather, coincides (also in southern USA - Meyer, 1970) with the warming of the water in early spring when fish are still kept in overcrowded conditions after winter storage. In South Africa, 6.4% of wild glass eels in the Southern Cape are infected. Via these, fish infection has been introduced into eel nurseries where elvers, especially those not completely acclimated, succumbed to severe infestations (Hine, 1975; Jackson, 1978).
Spontaneous recovery has been observed in both natural infections in natural habitats and in holding facilities, and even in experimental infections in aquaria (Paperna, 1972; Lahav & Sarig, 1973). The potential for spontaneous recovery varied with fish species. Infection in scaled fish, notably cichlids, regressed faster than in smooth skinned fish (eels, Clarias spp. and other siluriforms, mirror and leather carp) (Paperna, 1972 and unpublished observations). After recovery, fish were refractory to reinfection or retained a merely subclinical chronic infection (Hines & Spira, 1974c; Wahli & Meier, 1985; Paperna, unpublished observations). The observed interspecific variation in susceptibility to infection could, however, also result from differential compatibility of various fish species to man-made habitats and variable vulnerability to stress.
Spontaneous recovery from infection and resistance to reinfection of recovered fish indicate that fish are capable of developing defence mechanisms against I. multifiliis (Hines & Spira, 1974c). Spontaneous recovery observed in carp at temperatures as low as 10°C (Lahav & Sarig, 1973) implies some protective responses other than via humoral antibody production, which becomes suppressed in carp below 12°C (Avtalion, 1981).
Hines & Spira (1974c) demonstrated immobilisation of free swimming tomites with sera taken from carp after their recovery from infection. The infective stages were also shown to be unable to penetrate the skin of resistant carp. Immobilisation tests with trophonts showed that in infected trout anti-parasitic activity of the mucus increases quickly after infection and decreases soon after the infection has disappeared. The anti-parasitic activity of the serum, in the same fish, increases slowly but remains at a higher level for at least 7 months (Wahli & Meier, 1985). Fish immunised with Tetrahymena spp. developed a resistance to a challenge of lchthyophthirius infection (Goven et al., 1981).
Carp were immunised following controlled exposure to the infective tomite (teront) stage, and survived challenges with high infective doses, but lost protection after being immunosupressed by the administration of corticosteroids. These results could have simulated a stress mediated situation. Levels of humoral antibodies in immunosuppressed fish, however, remained the same as in the immunised group, which further confirms the involvement of other than humoral type immune systems in the protection processes against l. multifiliis infections (Houghton & Matthews, 1990).
Immunisation with killed vaccines gave less satisfactory results, although better protection was obtained through intraperitoneal inoculation of live teronts (Burkart et al., 1990). Oreochromis aureus mothers vaccinated through the latter method, passively transferred a protective immunity to their fry (Subasinghe & Sommerville, 1989). Additionally to immunity passed from mothers via eggs, demonstrable by antibodies in the soluble extracts of fry tissues, a protective immunity was acquired directly from the parent mouth during the brooding period (Sin et al., 1994).
Control
Both trophonts, localised beneath the epithelial layer of the integument, and the encysted tomonts, attached to substrates in the aquatic habitat, are resistant to practically all externally applied usable antiparasitic agents.
Infection can be effectively controlled only by destruction or elimination of the free dividing tomonts or the tomites they release. In warm water systems (24–28°C), three to four daily transfers of fish to clean tanks will effectively reduce infection, while enabling the fish to develop tolerance to reinfections. Tomonts can be effectively removed from large circulating tanks by repeated brushing with vacuum suction. Spontaneous recovery and transition into a refractory state will be further promoted by management techniques which alleviate stressing conditions (improving water flow, accelerating aeration and reducing stocking densities). Chemical parasiticides will be effective only through continuous or repeated daily application. Of the many listed (Meyer, 1969), the only cost-effective remedy for large scale farming systems is Malachite green at a dose of 0.05 ppm for continuous application (3–4 days) or up to 0.15 ppm (depending on the specific fish tolerance which varies with species - siluriforms are particularly susceptible). Formalin will dislodge some of the trophonts and is often applied mixed with Malachite green (50 ppm with 0.05 ppm) (Sarig, 1971).
Systemic therapy seems to be the only means of effective control. Elimination of tissue trophozoites was reported in several species of ornamental aquarium fish fed medicated food (Tetra, MA 100/50) containing Malachite green in a non-water soluble formulation for 4 days (neither drug concentration in the food, nor daily rations are given; Schmahl et al., 1992). For use in commercial food-fish culture for human consumption, the cost efficiency of Malachite medicated feed formulations and their toxicity to humans must be considered.
Most species of freshwater fish are susceptible, although some may be more so than others. The world wide distribution of I. multifiliis (Hoffman, 1970) has apparently been facilitated by the widespread translocation of cultured and ornamental fish. The presence of this parasite in autochthonous fish, in remote areas of the world including, southern Venezuela (Ventura & Paperna, 1985) and Northern Transvaal in South Africa (Paperna, unpublished) may suggest, however, that many populations, particularly those in the tropics, are comprised of a mix of autochthonous and introduced parasites. Data available from Africa are limited to Southern Africa (in cichlids, carp, Barbus spp., trout and eels - Du Plessis, 1952; Lombard, 1968; Jackson, 1968; Van As & Basson, 1984) and Uganda (on native Barbus amphigramma and exotic Lebistes reticulatus from small streams at Kajansi - Paperna 1972). It is very common in Israel, in both farmed (Sarig, 1971; Hines & Spira, 1973a) and wild fish including cichlids (Ventura & Paperna, 1985).
Description and diagnosis
Gross signs - white spots on the skin and the gills, which under microscopic examination reveal (in skin and gill scrapings) uniformly ciliated organisms with a small cytostome, which may reach up to 1 mm in diameter. Staining with either haematoxylins or Giemsa (after adequate fixation, in such as Bouin) reveals a large crescent-shaped macronucleus and small micronucleus. Ichthyophthirius multifiliis is a monotypic genus of hymenostomatid ciliates.
Life history and biology
Trophonts (feeding stages) develop within the integumentary epithelium, always above the basal membrane (Ventura & Paperna, 1985; Ewing & Kocan, 1992). By maturity, which is reached in 2 days at ambient temperatures of 25–28°C (3–4 days at 21–24°C), the parasite evacuates the host tissue and settles within 2–6 hours on a substrate in the water to form a cyst-encapsulated tomont (dividing stage). Parasites evicted from the tissue before the scheduled time for their spontaneous departure, fail to develop into tomonts and eventually die (Ewing & Kocan, 1992; Paperna, unpublished observations). Within the cyst, tomonts undergo successive binary fissions with a resulting yield of 250–2000 tomites (infective, free swimming stages), which after release will seek a suitable host. The division of tomonts into tomites, in ambient temperatures of 25–28°C, is completed within 15–20 hours (Bauer, 1959; Meyer, 1969; Paperna, unpublished observations; 7–8 hours according to Hoffman, 1978).
Invasion of tomites (teronts) (30–45 μm long) into the host integument is facilitated by the excretion of a sticky substance from subpellicular crystalline organelles named mucocysts. Active penetration causes focal necrosis of the epithelial cells. It has been suggested that hyaluronidase and other enzymes may be produced by the penetrating parasite (Ewing et al., 1985). In the absence of a suitable host, tomites will lose their infective potential within 24 hours at 24–28°C (Ewing & Kocan, 1992). Higher temperatures hasten trophont maturation and tomont division, but at lower temperatures, slower development allows the growth of larger trophonts (0.8–1.0 mm in 5–10°C vs 0.5–0.7 mm in 20–24°C), yielding tomonts with higher numbers of tomite progeny (Ewing et al., 1986). In lower ambient temperatures the survival of the tomites is prolonged, thus, allowing more time to locate a host. Low temperatures do not interrupt propagation, a full cycle is completed at 20°C in 3–5 days, at 15°C in 7–14 days and at 10°C in 21–35 days (Bauer, 1959; Meyer, 1969). Data on the effect of other environmental parameters is less conclusive, although it has been suggested that dissolved oxygen levels below 1 mg/l affect parasite reproduction (Bauer, 1959).
Pathology
Ichthyophthiriasis is fatal to fish of all sizes. Chronic infection will cause serious damage to the skin, fin and gills; corneal infection impairs vision (Hines & Spira, 1973a, 1974a). The infective stage invades the integumentary epithelium and becomes established in the basal layer of the epithelium just above the basal membrane. Cellular damage in low to moderate infections remains restricted to the infected site. In addition to the damage caused to epithelial cells by the feeding and expanding parasites, in heavy infections mass exodus of parasites from the epithelial layer, having completed their scheduled growth, causes its erosion and detachment from the basal membrane. In some infections, parasites cause widespread lysis of the inner layer of the epithelium. Prolonged infection also induces epithelial proliferation and haemorrhagic inflammation, causing the integument to become severely disintegrated (Hines & Spira, 1974a; Ventura & Paperna, 1985; Ewing et al., 1986). Hines and Spira's (1973b, 1974a,b) haematological and clinical data from heavily infected fish reveal evident physiological dysfunction resulting apparently from both direct pathological damage induced by the parasite and as a by-product of the stress response.
Epizootiology
Ichthyophthirius multifiliis is one of the most common, troublesome and difficult to control of fish pathogens. Epizootic infections have been reported in cold water salmonid farms (also in Africa, Du Plessis, 1952; Lombard, 1968) and warm water farmed carp, eels, Clarias gariepinus and Ictalurus punctatus (channel catfish) (Meyer, 1970; Sarig, 1971; Hines & Spira, 1973a; Hine, 1975; Jackson, 1978; Khalifa et al. 1983; Paperna, unpublished). Fish may maintain low, subclinical (enzootic) infection (in preimmunity), while encysted tomonts may persist in the habitat. Enzootic infections in native fish have been found in Lebistes reticulatus in Uganda (Paperna, 1972), in cichlids and cyprinids native to the Lake Kinneret system in Israel (Paperna, unpublished), in glass eels, cyprinids and cichlids in native habitats of South Africa (Jackson, 1978; Van As & Basson, 1984), and in a variety of native fish in the southern United States (Allison & Kelly, 1963). Transition from nonclinical enzootic to epizootic clinical infection is usually stress-mediated, prompted by adverse growth conditions such as overcrowding, poor feeding and excess nitrogenous waste. Epizootic infection, however, never occurs in overwintering tilapia or Clarias gariepinus in Israel, or southern Africa, but rather, coincides (also in southern USA - Meyer, 1970) with the warming of the water in early spring when fish are still kept in overcrowded conditions after winter storage. In South Africa, 6.4% of wild glass eels in the Southern Cape are infected. Via these, fish infection has been introduced into eel nurseries where elvers, especially those not completely acclimated, succumbed to severe infestations (Hine, 1975; Jackson, 1978).
Spontaneous recovery has been observed in both natural infections in natural habitats and in holding facilities, and even in experimental infections in aquaria (Paperna, 1972; Lahav & Sarig, 1973). The potential for spontaneous recovery varied with fish species. Infection in scaled fish, notably cichlids, regressed faster than in smooth skinned fish (eels, Clarias spp. and other siluriforms, mirror and leather carp) (Paperna, 1972 and unpublished observations). After recovery, fish were refractory to reinfection or retained a merely subclinical chronic infection (Hines & Spira, 1974c; Wahli & Meier, 1985; Paperna, unpublished observations). The observed interspecific variation in susceptibility to infection could, however, also result from differential compatibility of various fish species to man-made habitats and variable vulnerability to stress.
Spontaneous recovery from infection and resistance to reinfection of recovered fish indicate that fish are capable of developing defence mechanisms against I. multifiliis (Hines & Spira, 1974c). Spontaneous recovery observed in carp at temperatures as low as 10°C (Lahav & Sarig, 1973) implies some protective responses other than via humoral antibody production, which becomes suppressed in carp below 12°C (Avtalion, 1981).
Hines & Spira (1974c) demonstrated immobilisation of free swimming tomites with sera taken from carp after their recovery from infection. The infective stages were also shown to be unable to penetrate the skin of resistant carp. Immobilisation tests with trophonts showed that in infected trout anti-parasitic activity of the mucus increases quickly after infection and decreases soon after the infection has disappeared. The anti-parasitic activity of the serum, in the same fish, increases slowly but remains at a higher level for at least 7 months (Wahli & Meier, 1985). Fish immunised with Tetrahymena spp. developed a resistance to a challenge of lchthyophthirius infection (Goven et al., 1981).
Carp were immunised following controlled exposure to the infective tomite (teront) stage, and survived challenges with high infective doses, but lost protection after being immunosupressed by the administration of corticosteroids. These results could have simulated a stress mediated situation. Levels of humoral antibodies in immunosuppressed fish, however, remained the same as in the immunised group, which further confirms the involvement of other than humoral type immune systems in the protection processes against l. multifiliis infections (Houghton & Matthews, 1990).
Immunisation with killed vaccines gave less satisfactory results, although better protection was obtained through intraperitoneal inoculation of live teronts (Burkart et al., 1990). Oreochromis aureus mothers vaccinated through the latter method, passively transferred a protective immunity to their fry (Subasinghe & Sommerville, 1989). Additionally to immunity passed from mothers via eggs, demonstrable by antibodies in the soluble extracts of fry tissues, a protective immunity was acquired directly from the parent mouth during the brooding period (Sin et al., 1994).
Control
Both trophonts, localised beneath the epithelial layer of the integument, and the encysted tomonts, attached to substrates in the aquatic habitat, are resistant to practically all externally applied usable antiparasitic agents.
Infection can be effectively controlled only by destruction or elimination of the free dividing tomonts or the tomites they release. In warm water systems (24–28°C), three to four daily transfers of fish to clean tanks will effectively reduce infection, while enabling the fish to develop tolerance to reinfections. Tomonts can be effectively removed from large circulating tanks by repeated brushing with vacuum suction. Spontaneous recovery and transition into a refractory state will be further promoted by management techniques which alleviate stressing conditions (improving water flow, accelerating aeration and reducing stocking densities). Chemical parasiticides will be effective only through continuous or repeated daily application. Of the many listed (Meyer, 1969), the only cost-effective remedy for large scale farming systems is Malachite green at a dose of 0.05 ppm for continuous application (3–4 days) or up to 0.15 ppm (depending on the specific fish tolerance which varies with species - siluriforms are particularly susceptible). Formalin will dislodge some of the trophonts and is often applied mixed with Malachite green (50 ppm with 0.05 ppm) (Sarig, 1971).
Systemic therapy seems to be the only means of effective control. Elimination of tissue trophozoites was reported in several species of ornamental aquarium fish fed medicated food (Tetra, MA 100/50) containing Malachite green in a non-water soluble formulation for 4 days (neither drug concentration in the food, nor daily rations are given; Schmahl et al., 1992). For use in commercial food-fish culture for human consumption, the cost efficiency of Malachite medicated feed formulations and their toxicity to humans must be considered.
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