Diseases of the Australian Freshwater Fish Silver Perch (Bidyanus bidyanus) - Part 3

DISEASES AND PATHOGENS

Ecto‑parasitic protozoans

Protozoans are usually single celled organisms that reproduce by binary fission and have specialised organelles such as cilia or flagella for locomotion. When present in large numbers, they greatly impair the epithelium, particularly of gill tissue. Some protozoans feed on the cells and mucus, while others cause physical injury, and some may produce toxins. Protozoans cause more diseases in silver perch culture than any other group of organisms. 

Chilodonellosis

Infestations of the protozoan 

Chilodonella hexasticha cause the disease chilodonellosis in silver perch in ponds, cages and tanks. The disease usually progresses rapidly; however, the parasite may exist in low numbers (e.g. 1–2 organisms on 5 fish) over a period of months before predisposing conditions cause a rapid increase in parasite numbers. The parasite can cause serious losses of silver perch, especially fingerlings. Outbreaks in all seasons, particularly autumn, winter and early spring, and over the temperature range of 10–30°C. Needs to be diagnosed and treated quickly to avoid large losses. May have a cyst stage. 

Pathogen

Chilodonella hexasticha is a ciliate protozoan; ovoid to kidney shaped; dorso‑ventrally flattened; 50–70 µm in length, 20–40 µm wide. 

Signs

• Chronic to acute morbidity and/or mortality rates

• Loss of appetite

• Flashing

• Lethargy, swimming slowly, head‑up position, often near surface and edges

• Ragged fins

• Emaciation

• Skin may have mottled and/or grey appearance

Diagnosis

Microscopic examination at 100× magnification. Found mainly on gills but also skin (Figs. 23 and 24). Infested fish may have heavy or light parasitic loads (Fig. 25); large variation between individual fish can sometimes make diagnosis difficult in the early stages of an outbreak; important to examine at least 4 fish from pond. The organism can quickly become immotile or detach rendering detection more difficult; prompt examination required following slide preparation. Cytoplasm often appears granular; cilia noticeable at higher magnification. Characteristic gliding motion; often slow or little movement at low temperatures; groups of individuals often clumped on gill tips.

Treatment

Tanks: 

•  10 g/L salt (NaCl) for 60 min, flush and repeat following day. 

• 5 g/L salt continuous (including purging) and/or formalin 25 mg/L continuous bath for at least 8 h, flush and repeat the following day; aerate well; no feeding.

• formalin 150 mg/L for 60 minutes (not larvae or fry); observe during treatment; aerate well (oxygen, if needed); flush well on completion. 

Ponds/cages: 

• formalin 25–30 mg/L, maintain 24 h aeration for 4–5 days; one treatment usually sufficient; re‑examine pond fish to gauge treatment effectiveness; may need to re‑treat ponds after 3–4 weeks.

• prophylactic for broodfish: formalin 25–30 mg/L winter/early spring (e.g. June then again in August)

Prevention

Quarantine and treat all fish prophylactically (2–5 g/L salt), including fingerlings prior to stocking, new arrivals to the farm, and fish being moved between ponds. Maintain good water quality and nutrition. Do not overstock. If possible, use source water having no trash fish and prevent bird activity on ponds.

Ichthyophthiriosis

(white spot, ich) One of the most common and serious diseases of silver perch. Infestations of the ciliate protozoan, Ichthyophthirius multifiliis, cause the disease known as white spot or ich. Occurs in silver perch in ponds, tanks and cages. Disease can progress rapidly and cause 100% mortality. Affects fish of all sizes. There is some evidence in other species of freshwater fish that survivors of white spot develop immunity against future infestation. Occurs year round; decrease in water temperatures to/below 15°C in autumn associated with outbreaks. Needs to be quickly diagnosed and treated. Has a complex life cycle (Fig. 26) involving attached, encysted and free‑swimming stages; stages of life‑cycle temperature‑dependent, less than 4 days, >24°C; more than 5 weeks, <7°C; some evidence of parasite reproducing underneath epithelium without a free‑swimming stage; only free‑swimming stages susceptible to chemicals. 

Pathogen

Ichthyophthirius multifiliis is a ciliate protozoan; trophonts, 50–1,000 µm (1,000 µm = 1 mm) attach to fish (Figs. 27 and 28); mature trophonts leave fish and encyst on substrate and equipment (such as nets) as tomonts; division into numerous tomites; then released as free‑swimming, infestive theronts that are oval or round shaped, granular appearance, 20–50 µm; attach to fish using a penetrating gland.

Signs 

• Chronic to acute morbidity and/or mortality

• White nodules on skin (advanced cases)

• Opaque to white eyes (advanced cases)

• Positioned in water currents and/or at sides of ponds

• Lethargy and loss of appetite

• Flashing (often strong and repeated on pond bottom, standpipes, ropes) (Figs. 29 and 30)

• Ragged fins, skin raised and broken

• Mild skin haemorrhaging; striated skin markings or mottling

• Skin lesions and secondary bacterial and fungal infections

Diagnosis

Microscopic examination of skin and gill tissue. Parasites readily seen at 40 –100× magnification. Trophonts usually embedded under gill and skin epithelium (Figs. 31 and 32); can be present only on gills; cytoplasm usually dark granular with slow ‘swirling’ motion; horseshoe‑shaped macronucleus sometimes visible in mature trophonts, spherical nucleus in immature individuals; body with uniform cilia; theronts ciliated, usually clearer cytoplasm than trophonts. 

Treatment

Tanks: 

• salt (NaCl) 2–5 g/L salt continuous until disease controlled, may be for up to 20 days; aerate well; no feeding; 

• temperature manipulation to decrease length of life cycle–raise to 30°C for 10 days.

Ponds/cages: 

• formalin 30 mg/L initially (when water temperature <25°C), then maintain levels between 25–30 mg/L until disease controlled (see chapter Calculations, Treatments and Dose Rates); aeration continuous, monitor DO daily and provide additional aeration if necessary; or

• copper (as copper sulfate, CuSO4) 0.1–0.2 mg/L, recommend 0.2 mg/L initially, then monitor and adjust free Cu+ ion levels daily to maintain concentration between 0.1 and 0.2 mg/L; continuous aeration during treatment until disease controlled; for copper treatment, alkalinity must be >50 mg/L (see chapter Calculations, Treatments and Dose Rates). Caution: copper sulfate is an algacide, the decay of algae can cause dan gerously low DO.

Prevention 

Quarantine and treat all fish prophylactically (2–5 g/L salt), especially fingerlings and new fish on farm prior to stocking. Maintain good water quality. Quarantine infected ponds including equipment, vehicles, water; prevent aquatic birds spreading disease. Nil water exchange when source water known to hold diseased fish. Closely observe/monitor fish in all ponds and tanks when white spot is diagnosed in any pond or tank. It is common for more than one pond or tank to be affected simultaneously by this parasite. Dry and de‑silt ponds between crops.

Ichthyobodosis

(originally called Costiosis)

Ichthyobodo necator (previously known as Costia necatrix) is a flagellate protozoan that causes the disease ichthyobodosis. It is one of the smallest parasites and is often overlooked during monitoring. Ichthyobodo necator is particularly dangerous for fingerlings and larger fish held at high stocking densities in tanks and cages. Outbreaks have been common in recirculating aquaculture systems (Fig. 33). Ichthyobodo necator exists in a detached, mobile form or an attached form; the latter usually feeding on gill tissue (Fig. 34). Ichthyobodo necator causes disease over a wide temperature range. Epizootics have been uncommon during grow‑out of silver perch in ponds.

Pathogen

Ichthyobodo necator free‑swimming form, kidney‑shaped, dorso‑ventrally flattened, 10–20 µm in size. Two flagella attached to ventral part of body; attached form, pear‑shaped (Fig. 35). Some evidence in other fishes of salt resistance in I. necator. 

Signs 

• Chronic morbidity and/or mortality

• Mucus secretion and epidermal sloughing

• Fish may have a ‘bluish’ sheen to the skin

• Flashing

• Ragged fins

• Hyper‑ventilation

• Lethargy and loss of appetite

Diagnosis 

Microscopic examination of gill and skin; parasites often detach from host – prompt examination of fresh tissue. Freeswimming form may exhibit a flicking motion; often rapid swimming around tissue sample; flagella difficult to see; attached pearshaped parasites seen at 100–400× magnification on gill epithelium (Figs. 34 and 36); gill hyperplasia, particularly between secondary lamellae. 

Treatment 

Tanks: 

• salt (NaCl) 10–13 g/L for 60 min, flush and repeat following day; and/or 

• formalin 25 mg/L, continuous bath, flush and repeat after 1 or 2 days; aerate water well; no feeding. 

• formalin 150 mg/L for 60 minutes (not larvae or fry); observe during treatment; aerate well (oxygen if needed); flush well on completion Ponds/cages: 

• formalin 25–30 mg/L, may need to repeat after 1 or 2 days; maintain 24 h aeration for 4–5 days; one treatment usually sufficient in ponds; repeated treatments may be required in RAS. 

Prevention 

Quarantine and treat all fish prophylatically, especially fingerlings prior to stocking. Maintain good water quality and nutrition in cages and tanks. Reduce stress and overcrowding. Regularly sample, examine and monitor stock. 

Trichodinosis 

Trichodinosis is a relatively innocuous disease caused by infestations of the ciliated protozoans, Trichodina spp. 

Trichodina spp. are widely distributed, but seldom cause mortalities in large (>100 g) silver perch. Trichodina can infect silver perch larvae and fingerlings in large numbers, but rarely cause high level mortality in the shortterm. Trichodinosis is often associated with poor water quality and high organic loadings, and is commonly found on juvenile fish that are overcrowded, debilitated with other diseases or in poor condition. Common on postlarvae and fry in larval rearing ponds.

Pathogen 

Trichodina spp. are circular, saucershaped, 25–100 µm in diameter with a fringe of cilia around the perimeter; circular arrangement of toothlike structures within the body; browses over skin and gill surface often with a spinning motion (Figs. 37 and 38). 

Signs 

• Chronic morbidity and/or mortality 

• Emaciation 

• Excess mucus production 

• Frayed fins, skin erosion, dark skin 

• Flashing and flaring of opercula 

• Lethargy 

• Headup, swimming near surface 

Diagnosis 

Microscopic examination of skin and gill; easily recognised at 100× magnification and common on skin and fin tissue (Fig. 39); observation of low numbers (e.g. 1–3 parasite/field of view) is inconsequential. Increasing levels of infestations to above 20 parasites/field of view may require treatment. 

Treatment 

Tanks: 

• salt (NaCl) 10 g/L for 60 min; 

• formalin 25 mg/L, continuous bath for at least 8 h; aerate water; no feeding. 

Ponds/cages: 

• formalin 15–20 mg/L, maintain 24 h aeration for 4–5 days, one treatment usually sufficient for ponds; or • copper (as copper sulfate, CuSO4) 0.2 mg/L, alkalinity must be >50 mg/L, continuous aeration during treatment, one treatment should be sufficient; monitor water quality for 4–5 days after treatment. 

Prevention 

Quarantine and treat all fish prophylactically (2–5 g/L salt), especially fingerlings prior to stocking. Eliminate poor water quality by reducing feeding, maintaining or increasing aeration, and  implementing water exchange. Maintain  wellfed larvae and fry, and reduce overcrowding

Tetrahymenosis 

Tetrahymena spp. are freeliving saprophytic ciliates that cause the disease tetrahymenosis in silver perch; however, it is rarely a problem on farms. Tetrahymena spp. are similar in appearance to Chilodonella hexasticha but are usually more pearshaped and often larger (up 100 µm in length)  (Fig. 40). Severe losses have occurred  in silver perch fry associated with  a high organic load in the water. In  advanced cases in other fish species such as carp, catfish, and salmon, the parasite can penetrate muscle tissue and organs causing swelling, necrosis and ulceration.

Pathogen

Tetrahymena is pyriform or radially symmetrical, ovoid body 30–60 µm wide, 50–100 µm long; evenlydistributed cilia; movement is often ‘spiralling’ compared to the ‘gliding’ of C. hexasticha. Granular appearance of cytoplasm (Fig. 41). May be confused with nonpathogenic ciliates.

Signs

• Chronic morbidity and/or mortality

• Excess mucus production

• Epithelial damage, e.g. localised swelling, ulceration, and necrosis

• Loss of appetite and lethargy

• White patches or spots on skin

• Emaciation

Diagnosis

Microscopic examination of skin and gill tissue; parasite recognisable at 100× magnification; relatively fast ‘gliding’ movement; penetration of Tetrahymena into muscle or organ tissues possible; however, few cases reported for silver perch.

Treatment

Tanks:

• formalin 25 mg/L, continuous bath for at least 8 h; aerate water; no feeding.

Ponds/cages:

• formalin 15–20 mg/L; maintain 24 h aeration for 4–5 days; one treatment usually sufficient for ponds; systemic infections may be difficult to treat.

Prevention

Improve water quality; reduce stress and overcrowding

Myxozoan infections 

Many species of myxosporidians are found worldwide in a variety of fish hosts. They are obligate parasites with different life stages and intermediate hosts. There have been few records of myxosporidians causing disease in silver perch and light infections usually do not cause mortalities or affect growth. 

However in one epizootic, a high infection rate (>90% of fish affected) of Henneguya sp. on silver perch (300–450 g) resulted in chronic mortality (40/day) over two weeks before the disease was controlled. Gill function was severely compromised; most secondary lamellae were invaded by multiple sporeproducing, histozoic plasmodia. There is evidence Henneguya spp. utilise annelids (worms) as an intermediate host in their lifecycle. The lifecycle of the species infecting silver perch it not known. Most infestations have occurred at temperatures >20°C. 

Pathogen 

Myxosporidian (Henneguya spp.), spore size can vary, 8 to15 µm × 4 to10 µm, tail 40 to 50 µm; two polar capsules and two caudal appendages (Figs. 42, 43 and 44). 

Signs 

• Chronic fish mortality 

• Fish listless at pond surface; individual or small groups 

• Loss of appetite 

• Gills grossly thickened with nodules 

• Poor growth and emaciation 

Diagnosis 

Grossly thickened gill lamellar tissue with mildly nodular appearance (Fig. 45). 

Microscopic examination of gills, 100× magnification; dark brown/tan encysted plasmodium (Fig. 46); intralamellar, ~ 80–150 µm in diameter, ovoid to round in shape, inflammatory response marked in resolving plasmodia; squashed preparation of plasmodium, spores as per description above (Fig. 47); plasmodium could be confused with ‘Ich’. No motility of spores or encysted plasmodia.

 

Treatment 

Ponds/cages: 

Treatments not well defined; 

• formalin, 25 mg/L may control outbreaks by targeting freeswimming spore stages; retreat after 2–3 days; aerate 24 h for several days. 

Prevention 

Quarantine fish before stocking, examine a subsample microscopically. Maintain good water quality and appropriate stocking densities; dry and desilt ponds regularly (every 1 to 2 years); control intermediate hosts. Disinfect tank systems and equipment on a regular base.