MONOGENETIC TREMATODES. Monogenetic tre- matodes, including Gyrodactylus, Dactylogyrus (known as Cichlidogyrus in cichlid fishes; M.K. Soliman, Alexandria, 2005, personal communication) and
Cleidodiscus, have been reported to parasitize tilapia,
especially on gills and skin, in both farmed and wild fish (Ramadan, 1991; Omoregie et al., 1995; Plumb, 1997; Shoemaker et al., 2000). Roberts and Sommerville (1982) reviewed the occurrence of monogenetic and digenetic trematodes in cultured tilapia. Three species of monogenetic trematodes (Cichlidogyrus sclerosus, Cichlidogyrus tilapiae and
Gyrodactylus niloticus) have been recorded in cultured
tilapia in Vietnam (Te et al., 1999). The infection of tilapia by monogenetic trematodes is affected by fish species, sex and size and environmental condi- tions. Ramadan (1991) found that T. zillii in Lake Manzala, Egypt, were more infected with
Dactylogyrus than O. niloticus, and larger fish were also
more infected than smaller fish. Furthermore, females were more susceptible to the disease than males, and the infection rate was higher in winter than in summer.
Gyrodactylus infection of pond-reared tilapia
was recorded in Uganda, causing corneal damage
(Fryer and Iles, 1972b) and Kenya (C. Sommerville and R.D. Haller, unpublished results). Infection is usually associated with poor handling and high stocking density. Nguenga (1988) reported an infection of Nile tilapia with Dactylogyrus (Cichlido-
gyrus) sp. in Cameroon. Infested fish showed rapid
opercular movements and the opercula held open, thickened edges of the gills and destruction of branchial epithelium. Cichlidogyrus and Gyro-
dactylus have also been reported to infect tilapia in
a number of fish farms in the eastern region of Saudi Arabia (FRRC, 2001). Infected fish suffered from difficulties in respiration, due to the damage of gills, haemorrhage, fin rot and increased mucus secretion.
Dactylogyrus was successfully treated with a
single dose of formalin (250 ppm for 35–40 min) or two repeated applications of potassium permanga- nate at a dose of 5 ppm in static water with a 2-day interval (Nguenga, 1988). Table salt (sodium chlo- ride) is also commonly used in tanks for preventive measures at a rate of 25 g/l of water (Nguenga, 1988). A number of other chemicals have been reported to control these parasites effectively in other fish species. The list includes a KMnO4bath,
acriflavine, sodium hydroxide, methylene blue, formalin, magnesium sulphate, sodium perborate and many other chemicals (see Hoffman and Meyer, 1974, for details). The doses and methods of application depend on fish species and size and duration of treatment.
DIGENETIC TREMATODES. Digenetic parasitic trematodes can be very problematic to tilapia culture, and can cause heavy loss among fingerling and juvenile fish (Roberts and Sommerville, 1982). The life cycle of these parasites involves three hosts: a snail, a fish and a fish-eating vertebrate. Therefore, they may not cause any problems in closed systems, since one or more of the hosts may not be available. In open systems, they can infest the fish when the cercariae migrate to the target organ to develop into metacercariae (Shoemaker
et al., 2000).
A number of digenetic trematodes have been associated with disease infection in cultured and wild tilapia. Clinostomum sp., which is generally known as ‘yellow grub’ or ‘white grub’, is one of the most important digenetic trematodes that infect tilapia. The metacercariae cause bulging and distortion of the fish body profile, spoiling their appearance and make them more susceptible
Stress and Diseases 147
to handling (Roberts and Sommerville, 1982).
Clinostomum sp. has been recovered from wild
tilapia (Oreochromis leucostictus) in Lake Naivasha, Kenya (Aloo et al., 1995) and O. niloticus, S. galilaeus and T. zillii in Lake Kompienga (Burkina Faso) (Coulibaly and Salembere, 1998). The prevalence of the parasite was highest in O. niloticus (56.2%), fol- lowed by S. galilaeus (45.79%) and T. zillii (18.21%). Omoregie et al. (1995) recorded C. tilapiae in Nile tilapia from a fish farm and petroleum-polluted water in Nigeria.
Another digenetic trematode, Diplostimum (eye fluke), was recorded in the same fish farm in Nigeria (Omoregie et al., 1995). Okaeme and Okojie (1989) also found that feral tilapia, O. niloticus and S. galilaeus, in Nigeria were infected with
Diplostimim tregenna. This parasite can cause com- plete blindness and loss of reflex and pigmentation control when the number of metacercariae infect- ing the eye is high (Roberts and Sommerville, 1982).
Black-spot disease, which is caused by Neascus metacercariae, has also been reported in Nile tilapia and S. galilaeus in Lake Kainji, Nigeria (Okaeme and Okojie, 1989). Neascus metacercariae stimulate the accumulation of the host capsule in the skin, resulting in obvious black spots, which can be easily observed (Roberts and Sommerville, 1982). The real effect of this parasite is that it makes the fish unmarketable if the infection is heavy.
Haplorchis sp. is another digenetic trematode that is
found in a wide range of freshwater fishes, includ- ing tilapia, in many countries, such as Egypt, Kenya, Israel, the Philippines, China and Japan (Roberts and Sommerville, 1982). Mass penetra- tion of fish skin by large numbers of cercariae and the migration of metacercariae to accumulate at fin bases may lead to the loss of skin function and cause fish mortality (Roberts and Sommerville, 1982).
As far as I know, no specific drugs have been suggested for controlling digenetic trematodes in tilapia. However, di-N-butyl tin oxide has been effective in salmonids. Sand-gravel filtration of culture water has also been effective (Hoffman and Meyer, 1974). Above all, snail control remains the best method of controlling digenetic trematodes. In this regard, fish ponds should be dried and limed prior to stocking, to eliminate any trematodes that might have been present in pond water and/or mud. This practice is widely applied in the Philippines (Fig. 8.2).
PARASI TI C NEMATODES, CESTODES AND ACANTHOCEPHALANS. Several nematode species have been reported in wild and cultured tilapia, but little information is available on their parasitic significance (Fryer and Iles, 1972b; Scott, 1977). The nematode Contacaecum sp. has been reported to cause pathological effects and growth
Fig. 8.2. Drying and liming earthen ponds in the Philippines to eliminate trematodes and other parasites that might have been present in the pond water and mud.
retardation in Sarotherodon grahami in Kenya (Scott, 1977). They have also been recorded in
O. leucostictus in Lake Naivasha in Kenya (Aloo et al., 1995), where males were more parasitized
than females. This parasite can also be a problem to the consumer, since it occurs as large encysted worms throughout fish muscles.
Limited information is also available on the parasitic effects of cestodes and acanthocephalans on tilapia, despite the fact that they have been reported in wild and farmed tilapia (Fryer and Iles, 1972b; Ramadan, 1991; Aloo et al., 1995; Omoregie et al., 1995). Omoregie et al. (1995) isolated two cestodes, Eubothrium tragenna and
Polyonchobothrium sp. from farmed Nile tilapia and
oil-polluted water. The infection was concentrated in the intestines, stomach, liver and brain, while the muscles and gonads were significantly infected in adult and subadult fish. The acanthocephalan
Polycanthorhynchus kenyensis was also recorded in O. leucostictus in Lake Naivasha, Kenya (Aloo et al.,
1995) and T. zillii and S. galilaeus in Lake Manzala in Egypt (Ramadan, 1991).