The prevention of fish diseases is essential for the betterment of the fisheries industry, the improvement of farming production, and the increase in fish resources. Because of the complexity of their environment, fish are susceptible to viral, bacterial, fungal, and parasitic infections. These infections will adversely affect growth and development and a serious infection can be fatal. An outbreak of disease jeopardizes regular aquaculture and threatens fish yields. Therefore, controlling disease is one of the most vital tasks in fish culture.
The principle of fish disease control in China is all-round prophylaxis: “prevention is better than treatment”. In the event of an outbreak of disease, fish should be treated in the early stages. However, because of the difficulty in observing the activities of the fish, it is difficult to correctly diagnose and treat an infection in its early stages. In addition, because many diseases severely interfere with the feeding process, orally administered drugs may be ineffective. Parenteral drug administration is an alternative; however, dip treatments are confined to small containers or spread measures to fish ponds. This type of treatment is impractical for large lakes, rivers, and reservoirs. Therefore, prevention is the key to disease control.
Infectious diseases are mainly caused by viruses, bacteria, fungi, or unicellular algae (“ichthyomicrobial diseases”); e.g. bacterial enteritis, bacterial gill rot, and bacterial erythema. Infectious diseases account for 60 per cent of the production lost as result of disease. For this reason, the study of infectious disease is of primary significance to the development of aquaculture.
Infectious diseases can be divided into acute, subacute, and chronic forms based on the clinical picture. For example, if enteritis of grass carp or black carp occurs in an acute form, it develops rapidly and soon results in a high rate of mortality; it can also quickly disappear. Chronic enteritis, however, kills only a few fish per day but lasts a long time.
Bacterial pathogens of infectious diseases are not strictly parasitic micro-organisms. If the conditions for parasitism are unsuitable, saprophytic relationship will develop. Bacterial pathogens have a high adaptability to environmental changes. For example, the enteritis pathogen of grass carp and black carp will be ineffective if the water temperature is below 20°C; however, a water temperature between 20 and 25°C will enhance its virulence. The main epidemic season runs from late spring to early summer. Zoospores of Saprolegnia become attached to the fish skin and, if the host has been previously injured, the zoospores will grow and multiply, and the fish will become infected.
Most pathogens of infectious diseases show a preference for certain species and certain organs (organotropism). For example, bacteria of enteritis only affect grass carp and black carp. Likewise, branchiomyces parasitize only the gills.
There are three stages in the course of an infectious diseases: a latent period, a symptomatic period, and an attacking period. There are two types of infection: pure (one causative agent) and mixed (two or more pathogens on a single fish). Examples of a mixed infection are grass carp suffering from both saprolegniasis and gill rot and a black carp with enteritis and red skin disease.
Mode of infection
There are two sources of infection: primary and secondary. A primary infection originates within the pond. The pathogen may infect the fish directly or through the discharge of pathogenic agents into the water occasionally, “healthy” fish act as disease carriers and an outbreak of disease will occur under certain conditions. A secondary infection originates outside the pond. For example, a disease-free pond could be polluted with pond water from a diseased pond, diseased or contaminated silt, feeds and equipment. Pathogens are commonly spread through these vehicles.
Infectious diseases normally attack the fish through tissues and organs (skin, gills, intestines or excretory organs). Fish, however, do possess resistance mechanisms against pathogenic microbes. For example, skin texture and mucous membranes of the fish function as barriers to infectious microorganisms. Pathogenic microbes entering via the digestive tract will be attacked by various disinfecting secretions. White blood cells, lymphoid tissue cells, and reticuloendothelial cells of the spleen, liver, and blood vessels can eliminate foreign bodies, including pathogenic microorganisms. In addition, fish blood contains bactericidin, which is toxic to pathogenic bacteria.
Invasive diseases are caused by animal parasites such as trichodinasis, ichthyphthiriasis, lernaesis, argulusis, etc. Fish carrying parasites or the carcasses of diseased fish is a primary source of invasive diseases. Contaminated feeds, gears, pond water, silt, etc., are secondary sources. For example, mature oocytes of Eimeria or mature myxosporidia may enter the water with the fish and precipitate to the bottom of the pond. The pond silt is contaminated as a secondary source of invasive disease.
Like infectious diseases, invasive diseases often appear in different seasons. This is because the pathogens and the fish are influenced by external factors (location, climate, physico-chemical properties of the water, farming skills, etc.) and internal factors (growth and physiological status). Invasive pathogens may also be species specific or organotropic.
Physical and chemical factors or the influence of other organisms within the pond may retard growth or even kill the fish. For example, gasping and suffocation may upset the physiological balance of the fish and if serious, cause mass mortality.
Prevention of Disease
The concept that “prevention is better than treatment” is fundamental to the maintenance of a healthy stock of fish. Because fish are schooling animals, they are hard to observe individually, making the diagnosis and treatment of disease difficult. In addition, some fish diseases are still essentially incurable, e.g., diplostomulumsis. Therefore, preventive measures are essential to the control of disease.
Pond regulation is effective in improving environmental conditions, preventing disease and raising fish yields. There are two main aspects (see chapter 4) to pond regulation: pond trimming and pond disinfection.
A reliable person should be responsible for the daily management of the pond (stocking, feeding, manuring, disease prevention, etc.). The “four fix” feeding procedure, which benefits fish yield and disease prevention, should be used (see chapters 4 and 5). Variations in water quality must be observed carefully. According to these observations, fertilizers or fresh water should be added. Pond inspection is essential in the morning, particularly in dismal weather or after a torrential rainfall during the epidemic season (May to September). Besides, it is necessary to remove the weeds along the pond sides and clear the feeding platforms to prevent the occurrence of disease. Netting, transferring, and transporting should be performed with great care.
Fingerling disinfection — Fingerling disinfection can be performed during their transfer to a larger body of water. The procedure can be done in a boat, cabin, jar, pail, cage, etc., depending on local conditions.
Feeding disinfection — Hang small bamboo baskets containing bleaching powder or cloth bags containing a mixture of copper sulphate and ferrous sulphate (5:2) around the feeding platform. When the fish come to feed, their skin will be disinfected.
Hanging basket method — This method prevents bacterial diseases in fish such as grass carp that mainly feed on buoyant food. Place a triangular or square bamboo frame at a shallow corner of the pond. Along the frame, hang three to six small bamboo baskets with their tops 3 cm out of the water and put a small stone inside each basket to make them stand vertically in the water. As soon as feeding begins in the spring, add 100–150 g of bleaching powder to each container daily. After hanging the containers, duck weed or tender grass can be used to attract fish (Fig. 6.1). Clean the container after feeding. To prevent bacterial diseases in black carp, the containers are placed in a line, attached to a bamboo rod, and sunk to 15–18 cm above the bottom (Fig. 6.2). Each container is covered with a lid to keep the bleaching powder in.
Fig. 6.1. Hanging bag, bleaching powder method for the control of bacterial red skin and gill rot diseases of grass carp.
Fig. 6.2. Hanging basket, bleaching powder method for the control of bacterial red skin disease of black carp.
Hanging bag — This method is similar to the hanging basket method except that the bleaching powder is substituted with a mixture of copper sulphate and ferrous sulphate. The chemicals ooze out of the fine-cloth bag slowly (the shortest duration for this process is 3–4 h). The number of bags hung daily and the chemical dose depend on water depth and size of feeding place. With a 3×3 ×3 m triangular frame, Table 6.1 gives appropriate dosages at various water depths. Six bags are used (two per side) (Fig. 6.3).
Table 6.1. Dosage of chemicals in each fine-cloth bag.
Fig. 6.3. Hanging bag method with copper sulphate and ferrous sulphate to control parasitic gill disease of grass carp.
There are many other chemical treatments used in the disinfection of finger-lings (Table 6.2).
Feed, feeding platform and equipment disinfection
Contaminated or spoiled feeds may introduce pathogenic bacteria to the pond. Leftover feeds, which decompose in the water, facilitate the rapid multiplication of pathogenic bacteria. For this reason, feeds and manures must be disinfected before application. Animal feeds such as snails must be washed and supplied to the fish when they are fresh and alive. As for plant feeds, aquatic grasses are disinfected by immersing them in a 6 ppm bleaching powder solution for 20–30 min. Before organic manure application, 120 g bleaching powder is mixed into 500 kg manure.
In addition to the hanging basket and hanging bag methods of feeding area disinfection, during the epidemic season (May-September), a solution of 250 g bleaching powder in 12 L water should be spread over the area once or twice monthly.
Table 6.2 Some solutions for fingerling disinfection.
|Bleaching powder||10||10–15||20–30||Bacterial skin and gill diseases.||Immersion duration depends on the health of fish and water temperature; the chlorine concentration must be above 10%; the solution should prepared on the spot.|
|Copper sulphate||8||10–15||20–30||Cryptobiosis, costiasis, trichodinosis & chilodonelliosis.|
|Copper sulphate & bleaching powder||8a, 10b||10–15||20–30||Bacterial gill rot, red-skin, cryptobiosis, costiasis, trichodinasis, chilodonellasis, trichophryiosis, etc.||Dissolve the two chemicals in separate tanks before mixing.|
|Potassium permanganate||20||10–20||20–30||Gyrodactyliosis, dactylogriosis, trichodinosis, chilodonelliosis, lernaesis.||Immersion duration depends on the health of fish; prepare solution on the spot; avoid immersing in direct sunlight.|
|Sodium chloride||30,000–50,000||5||Dermatomycosis||Dosage depends on the health of fish and water temperature.|
|Dipterex (90% of crystal)||2,000–2,500||3–15||Gillrot, red skin, enteritis||Add fish (and solution) to pond when they begin to become irritated and start moving their head in the immersing tank.|
a Dosage of copper sulphate;
b Dosage of bleaching powder.
The equipment used during the epidemic season (nets, pails, dip nets, etc.) must be disinfected after each use. Large nets can be exposed to sunlight for 1 or 2 days and wooden pails can be sterilized by immersing them in a quicklime solution or in a 10 ppm copper sulphate solution for 5 min.
Spreading chemicals over the entire pond is a common method of disease prevention. Before or shortly after stocking fry, 1 g of 2.5 per cent dipterex should be sprayed over the pond. This treatment is particularly needed for weedy ponds. Three months later, the pond should be treated with a 0.7 ppm solution of copper sulphate and ferrous sulphate (5:2). After June, bleaching powder (1 ppm) should be sprayed over the pond once or twice monthly.
To improve deteriorated pond water, for each metre of depth, 20–25 kg/mu quicklime should be added. This will improve water quality and prevent disease. The quicklime chunks should be dissolved in a little water, and the solution diluted, stirred, and sprayed evenly over the pond.
During the epidemic season of grass carp enteritis, medicated feeds are an effective preventive measure. Use 1–2 kg garlic per 100 kg of fish once a day for 6 consecutive days. Pulp and blend the garlic with the feed; disease prevention is enhanced if 40 g of table salt is added to every 5 kg of food. For adult fish, mix the pulped garlic with some binder and spread the mixture onto fresh grass feed. Apply the feed after it is dry. Medicated feed may also be given in a pellet form.
Chinese medicine for disease control
Controlling disease with Chinese herbal medicines has many advantages. These include the vast supply of materials, the proven effectiveness, the low cost, and the relative ease of teaching the techniques involved. In production, farmers have been using various Chinese herbal medicines to control diseases and getting good results. For example, in Zhejiang Province, Euphorbia humifusa and Acalypha australis are used for enteritis and, in Guangdong Province, Thysanospermum diffusum is used to cure bacterial skin disease, gill rot, and enteritis. The Institute of Hydrobiology, Academia Sinica, has recently reported promising results with the application of Chinese tallow tree (Sapium sebiferum) with Chinese rhubarb (Rheum officinale) for “white-head-and-white-mouth” disease and bacterial gill rot.
Establishing a quarantine system
Geographic and climatic conditions can produce epidemic diseases in certain regions. The disease of grass carp yearlings caused by Bothriocephalus gowkongensis and branchiomycosis of mud carp used to occur only in Guangdong and Guangxi provinces. Likewise, oodiniosis was localized to Jiangxi Province and Liang County, Guangdong Province while ichthyophthiriasis was unique to Human and Hubei provinces. However, as the freshwater farming industry develops rapidly and the transportation of fry and fingerlings among provinces becomes more frequent, local diseases are tending to spread. Quarantine work should now be emphasized. The transportation of diseased fish should be strictly prohibited.
Disease diagnosis is the first step toward effective treatment, and care must be taken in making a diagnosis. The fish must be alive or recently dead and the body must be kept damp. Try to keep the dissected organs as complete as possible. Keep the autopsy instruments clean to avoid intercontamination of pathogens among organs. Use distilled water for microscopic observation of the skin and use 0.85 per cent normal saline for microscopic observation of the internal organs. Preserve the samples for further identification if there is any doubt about the pathogens or the clinical signs. If complications are discovered during the diagnosis, diagnose the primary and secondary disease and implement the appropriate treatments separately or simultaneously.
Methods of diagnosis include surveying the pond and examining the fish with the naked eye and microscopically.
Survey the diseased pond — Determine if the water source is seriously polluted. If it is, find the source of the pollution. Observe the behaviour of the diseased fish and take an inventory of the rearing status (pond clearing, stocking density, feeding, preventive methods, and mortality, etc.).
Body — Put the diseased fish on an enamel ware plate and examine the head, eyes, gill cover, scales, and fins for visible pathogens such as nematodes, Argulus, Glochidium, and Saprolegnia. It is also possible to see the pathogens of bacterial erythrodermatitis, albinoderm, stigmatosis, and furunculosis with the naked eye.
Gills — Inspect the gills, with an emphasis on the gill filaments. Observe the colour of the gill lamella, the quantity of mucus, and the congestion and putridity of filament tips after an opercular incision is performed.
Internal organs — Mainly check the intestines. Begin to observe abdominal hydrops and visible parasites, (e.g., Ichthyoxenus, Nematodes, cysts of Myxosporidia, Ligulos, then observe other internal organs. Extract the internal organs with a knife and scissors and separate the liver, gall bladder, air bladder, etc. Finally, open the intestine to search for any signs of pathological change.
Normally, only the skin, gills, intestines, eyes, and brain need be observed microscopically.
Skin — Scrape a little tissue and mucus from the skin, put them on a slide with a drop of distilled water, and observe the combination under a microscope after pressing with a coverslip. One should always start with the low power objectives. Samples from at least three different points on the skin should be inspected. Common parasites on the skin are Trichodina, Ichthyophthirius, Chilodonella, Costia, Glochidium, and Myxosporidia.
Gill — Place some gill filaments and mucus onto a slide. The following parasites may be identified through microscopic observation: Dactylogyrus, Gyrodactylus, Cryptobia, and Myxosporidia.
Intestines — Transfer a little mucus from the anterior intestinal wall to the slide. Nematodes, Eimeria, and Myxosporidia may be seen.
Eyes — Press the entire ocular bulb or crystaline body on the slide. Cysts of Diplostomulums are an indicator of diplostumulumsis.
Brain — Open the central cavity of a fish with whirling disease. White cysts of myxosporidia in the lymphatic fluid beside the brain should be observed. Remove the cysts and place them on a slide; after crushing with a coverslip, the spores can be seen.
Hemorrhagic speticemia (Fig. 6.4)
Pathogen — Reovirus is spherical or hexagonal in shape, with an average diameter of 69 mm. The electron-dense area in the middle of the particle has an average diameter of 32 mm. This “nucleus” is surrounded by a membrane that is about 20 mm wide. Another variety of the virus shows an even electron distribution throughout and has no “nuclear membrane”. This particle has an average diameter of 52 mm and is found in the includion bodies of the nucleus or cytoplasm. The viral particles always appear in sanguifying (blood-making) tissues of the kidney and are not found in red cells or granular white cells. The virus is sensitive to ether, acid, and alkali, and insensitive to drugs of the tetracycline family. It shows a high resistance to heat (Table 6.3).
Table 6.3. Heat resistance of reovirus.
|Fish mortality after infection (%)|
Fig. 6.4. Grass carp with hemorrhagic septicaemia symptoms. This disease can be easily diagnosed observing the muscle congestion (1) and the congested operculum, fin base, intestine and air bladder etc. (2).
Fig. 6.5. Black carp infected with erythroderma.
Symptoms and pathological changes — The main symptom of this disease is congestion. The fish usually becomes dark and slightly red. If you observe diseased juvenile fingerlings against the light, hypodermic hyperemia can be seen. Some fish show congestion around the mouth, lower jaw, skull or orbit, and exophthalmos (abnormal protrusion of the eyeball). Congestion of the operculum and fin base are visible after peeling away the skin of the diseased fish. The musculature of the fish shows punctiform or lump congestion. In serious cases, the entire musculature becomes bright red with “white gill” (i.e., bright red patch congestion appears on the operculum); some diseased fish show no gill discolouration. As for the internal organs, intestinal congestion is common. All or part of the intestine becomes red owing to congestion. The mesentery and its peripheral fat often shows punctiform congestion. In a few cases, the liver, spleen, and kidney are pale or locally congested. The walls of air bladder and gall bladder are often bloodshot.
The disease can be classified into three types based on symptoms and pathological changes. Each type is distinct; however, they occur together in the fish and are difficult to separate.
Red-muscle type: The skin shows little or no hemorrhagic symptoms, but the muscles are heavily congested. Usually all muscles are red and gill lamellae are white because of loss of blood. This type of hemorrhagic septicemia is common among grass carp fingerlings at 7–10 cm in body length.
Red-fin, red-operculum type: Congestion on the operculum, the base of the fins, the skull, orbit, and mouth cavity are obvious. There is some congestion beneath the scales and, possibly, some spotted congestion in the muscles. This type is common among grass carp fingerlings over 13 cm in body length.
Enteritis types: Instead of the skin and muscles, the intestine is seriously congested. All or part of the intestine is bright red. Occasionally, there is punctiform congestion in the mesentery, fat, and wall of the air bladder. This type is ubiquitous among grass carp fingerlings.
Epidemic situation — Hemorrhagic septicemia is one of the most common and harmful viral diseases encountered during the fingerling-nurturing period. The epidemic season is long (June-September), incidence is high, and mass mortality of grass carp fingerlings is common. Grass carp and black carp are both susceptible to this disease, with the former as the main victim. The disease is widespread in China and reaches its peak incidence in August when the water temperature is above 27°C. It gradually diminishes after mid-September when the water temperature drops below 25°C.
Control measures — There are three strategies of control.
First, vaccinate the fingerlings with deactivated virus. This will produce a resistance that may last up to 14 months.
Second, decoct 250–550 g of pulverized Chinese rhubarb or Chinese sweet gum leaves (Liguidambar taiwaniana) overnight and, after blending it with the feed, give it to the fish for 5 consecutive days. Next, spray the pond with enough Dyrene such that the pond water has a copper sulphate or copper acetate concentration of 0.6 or 0.7 ppm or a copper chloride concentration of 0.7 ppm. If copper sulphate is used, 2 days treatment is required per course, and two courses are needed to achieve good results.
Third, use improved farming techniques and ensure proper pond management.
Pathogen—Pseudomonas fluorescens is a short, rodlike bacteria with round ends. It measures 0.7–0.75 × 0.4–0.45 μm and exists either singly or in pairs. It is motile with a single polar flagellum, has no gemma, and is gram negative. Agar colonies of P. fluorescens are circular in shape, semiopaque, and greyish white. The colonies produce a yellowish green pigment after a 24-h incubation.
Symptoms and pathological changes — Symptoms include inflammation, bleeding from the skin, and a loss of scales, particularly on the sides of the abdomen. Blood shot on the fin base, necrosis of the terminal of fins, and red blotches around the upper and lower jaws are also symptomatic of erythroderma. Occasionally, congestion and inflammation along the intestines also occurs (Fig. 6.5).
Epidemic situation — Erythroderma is a common disease of grass carp and black carp and is widespread on all farming sites. Mechanical lesions obtained during stocking or netting allow the bacteria to invade the fish. Frostbite also facilitates infection. In addition, wounds may result from fish rubbing against solid objects in the water. Because of these factors, erythroderma is a year-round disease.
Prevention — Thorough pond clearing and disinfection and gentle netting, carrying, and stocking are effective preventive measures. A promising method of prevention involves dipping fingerlings in a 5–10 ppm bleaching powder solution for 30 min before stocking. The fingerlings may also be vaccinated.
Treatment — Because the pathogenic bacteria not only infect the skin and the muscle but also invade the blood, medicine should, therefore, be administered both internally and externally.
Internally, sulphathiazole should be given orally once a day for 6 consecutive days. The 1st-day dose should be 10 g/100 kg fish; the dose for the remaining 5 days is 5 g/100 kg fish. The medicine is mixed with the feed using a binder. Externally, bleaching powder (containing 30 per cent available chlorine) should be spread over the pond to a concentration of 1 ppm. Alternatively, Chinese gall (Galla chinesis) could be applied at a concentration of 2–4 ppm.
Pathogen — Although still under debate, some people believe the pathogen to be Aeromonas punctata f. intestinalis, which is a short rod-shaped bacteria with two round ends. It measures 0.4–0.5 × 1–1.3 μm and exists mostly in pairs. It has a single polar flagellum, no gemma, and is gram negative. Agar colonies of this pathogen are round and a semiopaque, brownish pigment is produced around the colony after 1 or 2 days of incubation. The bacterium is pathogenic under certain conditions. Pathogenicity increases at a suitable water temperature (around 25°C) as water quality deteriorates, as air pressure decreases, and when fish are overfed.
Symptoms and pathological changes — The diseased fish has an expanded abdomen with red blotches; the fins are congested and decayed, the anus is red and swollen, and, when slight pressure is applied to the abdomen, a yellow mucus is released from the anus. Ascites can be seen if the abdomen is dissected. The intestinal walls show hyperaemia and inflammation. Cells of mucous membrane ulcerate and drop off, becoming bloody mucus and blocking the intestine. The diseased fish shows a loss of appetite, swims slowly and alone, and soon dies.
Epidemic situation — Enteritis is common among grass carp and black carp, with a few cases in bighead and common carp. Underyearlings of grass carp and yearlings of grass carp and black carp are more likely to contract the disease and show a high mortality, commonly ranging from 50 to 90 per cent. Therefore, enteritis is one of the most harmful diseases to cultivated fish in China. The disease is commonly found everywhere in farming sites, but the season of prevalence and degree of incidence differ slightly with respect to climate and rearing management. Generally, there are two distinct epidemic seasons: May to June for 1–2 year old grass carp and black carp, and August to September for underyearlings of grass carp. The disease is often complicated with bacterial gill rot.
Prevention — Maintaining water quality strictly following the “four disinfection” and “four fix” techniques is vital to the prevention of enteritis. During the epidemic season, feeding should be limited and prophylaxis performed regularly.
Treatment — Integrate oral administration with external administration. Externally, bleaching powder should be sprayed into the pond to a concentration of 1 ppm or quicklime should be scattered over the pond at a dose of 15–25 kg/mu per metre water depth. The following medicines can be mixed into feeds.
Sulphaguanidine: for the first day, use the medicine in a dose of 1 g for every 10 kg of fish; the dose for the next 5 days is 1 g for every 20 kg of fish.
Chinese gall: when enteritis and gill rot appear simultaneously, spray a decoction of the Chinese gall over the pond to a concentration of 2–3 ppm. Meanwhile, feed the fish with furazolidone for 6 days at a dose of 1 g/100 kg fish; for a serious case, double this dosage in the first treatment.
Garlic: add 1–2 kg garlic/100 kg fish daily for 6 consecutive days.
Euphorbia humifusa: add 500 g dry herb or 2500 g fresh herb for every 100 kg of fish daily for 3 consecutive days.
Acalypha australis: add 500 g dry herb or 2000 g fresh herb for every 100 kg of fish daily for 3 consecutive days.
Water knotweed (Polygonum hydropiper): add 500 g dry herb or 2000 g fresh herb for every 100 kg of fish once daily for 3 consecutive days.
Andrographis paniculata: add 2 kg dry herb or 3 kg fresh herb for every 100 kg of fish daily for 5–7 consecutive days.
Euphorbia humifusa, A. australis, and P. hydropiper can be used separately or in combinations of two or all three. Disease resistance can be fortified through vaccination.
Bacterial gill rot
Pathogen — Myxococcus piscicolus is a slender, soft, and easy to coil bacterium. Its length varies greatly (2–37 μm, it is gram-negative, and a colony on peptone agar diffused to pseudomycorrhiza is about 3 mm in diameter. Growth stops after 5 days of culture.
Fig. 6.6. Grass carp infected with enteritis.
Fig. 6.7. Grass carp infected with gill rot disease shows the dark discolouration at the gill filaments.
Symptoms and pathological changes - Diseased fish are black in appearance, especially the head. The gill filaments, which are often covered with mud and mucus, are putrid and pale. In a serious case, hyperemia and inflammation are found on the inside and outside of the opercula. The epidermis of the opercula often rots away leaving a transparent area. Histological studies of bacterial gill rot in grass carp found that it can be divided into chronic and acute types. The chronic disease lasts longer, with prevalent cellular hyperplasia. The acute disease is short with inflammatory dropsy or cell necrosis as the main symptoms (Fig. 6.7).
Epidemic situation — Bacterial gill rot affects grass carp, black carp, bighead, common carp and other fishes; grass carp is the main victim. It is one of the most serious diseases of grass carp, occurring year-round on all fish farms. It seldom appears when the water temperature is below 15°C and begins to occur when the water temperature is above 20°C. Its optimum temperature range is 28–35°C. Therefore, it is more prevalent in the spring, summer, and autumn than in the winter. The disease is often accompanied by enteritis.
Control — There are eight methods of controlling bacterial gill rot. When the disease is prevalent, disinfect the pond water and the pond sides weekly with dissolved bleaching powder at a rate of 0.25 kg/mu. For prevention purposes, bleaching powder baskets should be hung around the feeding platforms or bleaching powder should be spread into the pond water to a concentration of 1 ppm.
Add a dry powder of Chinese tallow tree (Sapium sebiferum) leaves to the pond water to a concentration of 6.25 ppm. If fresh leaves are used, the dosage should be increased four times. The solution is prepared by immersing the leaf powder in 2 per cent quicklime solution for 6–12 h, (powder:quicklime, 1:2). Boil this solution for 10 min or until the pH reaches 12 before spraying.
Add Chinese rhubarb (Rheum officinable) to the pond to a concentration of 2.5–3.7 ppm. Immerse the rhubarb in 0.3 per cent ammonia water (rhubarb:water, 1:20) for 12 h before spraying.
Spray the pond with erythromycin to a concentration of 0.3 ppm. Then mix erythromycin with the fish feeds and apply this mixture for 6 consecutive days. Use 4 g erythromycin for every 100 kg of fish for the 1st day; and reduce this dosage in half for the remaining 5 days.
Add pulverized Chinese gall to the pond water to a concentration of 2–4 ppm.
Spread a solution of maple leaves over the pond. For each mu of pond, and 10 kg water to 20 kg of pulped Chinese sweet gum leaves before application.
Spray the pond water with quicklime to a concentration of 20 ppm.
Enhance immunity by vaccinating grass carp before transferring or stocking.
Vertical scale disease
Pathogen — Pseudomonas punctata seems to be responsible for vertical scale disease; however, Japanese data indicate that the pathogen is Aeromonas sp.
Symptoms and pathological changes — The skin of the diseased fish appears rather rough, and some scales (especially on the posterior part of the body) are stretched out, resembling pinecones. Thus, this disease is also called the “pinecone disease.” The scale capsule contains a semiopaque or sanguineous liquid that makes the scale vertical. If slight pressure is applied to the scale, the liquid will exude from the scale base and the scales will immediately drop off. Other symptoms include congestion on the fin bases, mild bleeding and inflammation on the skin, reddish ulceration on the desquamated area, exophthalmos (protruding eyeballs), and abdominal distension. As the disease develops, fish swim slowly, show dyspnea, and the abdomen turns upward. The fish will die 2 or 3 days later.
Fig. 6.8. Common carp infected with vertical scale disease.
Epidemic situation — This disease mainly infects common carp, crucian carp, grass carp, silver carp, and, occasionally, goldfish (Cyprinus auratus). It usually occurs in northeastern, central, and eastern China. The disease is prevalent during spawning and overwintering of common carp. Normally, the disease first appears between late April and early July. The average mortality of parent fish as a result of vertical scale disease is 45 per cent. The maximum recorded mortality was 85 per cent and the mortality of yearling common carp may be over 50 per cent. The outbreak of the disease is related to injured skin, contaminated pond water, and poor disease resistance.
Control — There are four main methods of controlling vertical scale disease.
Avoid injuries during netting, transferring, and stocking.
Drain the spawning pond of parent common carp in the winter and disinfect the pond with quicklime or bleaching powder.
Mix impure aureomycin or terramycin with the feed in a dose of 5 per cent of the feeding amount to make a pelleted feed.
Inject 3–6 mg chloromycetin into the abdominal cavity.
Pathogen — The pathogen is a mould belonging to family Saprolegniaceae class Phycomycetes. The most common pathogenic genera are Saprolegnia and Achlya. The mould is a coenocytic mycelium without a cell wall. One end of the mould, resembling a root, attaches to the wounded part of the fish. Many branches (mycelia) then penetrate the skin and muscle and extract nutrients from the host. The external portion of the mould is flocculent and consists of hyphae (Fig. 6.9). These hyphae may be up to 3 cm long. On a dead fish, the mould can spread and cover the entire body in 12–24 hours.
Fig. 6.9. Bighead infected with saprolegniasis.
Symptoms and pathological changes — There are no abnormal signs in the initial stages of infection. When the disease becomes visible, the mould has already penetrated the skin. The mycelia penetrate deep into the muscles, permeating tissue cells and branching heavily. Hyphae develop into a grey, flocculent mass (Fig. 6.9). The mould secretes a substance that decomposes tissues and because of the irritation, the fish secretes a great deal of mucus. The diseased fish behaves abnormally, fidgeting and rubbing against solid materials. As the mould continues to grow, morbid muscle rots and the fish loses its appetite, moves slowly, and eventually dies.
Epidemic situation — This disease is common in all farming areas year-round. It can affect any developmental stage of all the cultured species. The mould invades wounds inflicted during netting, transporting, and stocking. Saprolegniasis is particularly prevalent in overwintering ponds with a high stocking density.
Control — There are eight methods of controlling saprolegniasis.
Disinfect the pond with quicklime.
Avoid lesions caused by catching, transporting, or stocking.
Select healthy parent fish and smear them with 1 per cent malachite green ontment or sulfa ointment.
If the disease occurs in an eel-culturing pond, sprinkle the infected pond with malachite green solution or methylene blue solution to concentrations of 0.15–0.2 and 2–3 ppm, respectively. If there is no apparent effect, repeat the same dosage 3–4 days after the first application.
To prevent saprolegniasis of eggs, raise the rate of fertilization. Choose fine days for artificial spawning and hatch the eggs indoors under showering water.
Disinfect viscid eggs by immersing them with a 7 ppm malachite green solution for 10–15 min for 2 consecutive days. Afterwards, sprinkle the hatching shelf in the morning and evening with 10–15 kg of a 10–100 ppm malachite green solution until the fry are hatched.
Apply malachite green solution every 6–8 h to the circular incubation tank to make the water light green. Repeat this procedure until hatching. This method diminishes mould infection and improves hatchability.
Immerse the eggs nests in 3–5 per cent formalin for 2–3 min or in a 1–3 per cent table salt solution for 20 min.
Pathogen — Cryptobia branchialis is a flattened creature with a wide anterior end and a narrow posterior end (like a willow leaf). The body length measures 5–12 μm. There are two flagella, both originating at the anterior end. One stretches forward and is called the anterior flagellum. The other forms an undulating membrane along the surface of the body and stretches posteriorly; it is called the posterior flagellum. In the middle of the body there is a round nucleus; in front of this nucleus there is an ovoid kinetonucleus (Fig. 6.10). Around the nucleus there are chromatin granules. The endosoma is in the centre of the nucleus. The posterior flagellum of the live parasite penetrates into the epidermal tissue of the gill of a fish (Fig. 6.10). When leaving the host, the anterior flagellum and undulating membrane move the body forward.
Symptoms and pathological changes — The parasite generally fixes itself to the gill of the host destroying the epithelia on the gill lamella and producing thrombi (blood clots) in the blood vessels of the gill lamella. This inflammation of the branchial organs retards normal blood circulation. Meanwhile, the mucus secreted in response to the irritation will cover the intact part of gill; thus, respiration is impeded. If the disease is allowed to continue, the fish will experience dyspnea and eventually die of suffocation.
Fig. 6.10. Cryptobia branchialis: (A) attached to the gill of a fish; (B) basic morphology.
Epidemic situation — Cryptobia branchialis is not host-specific. It can invade any freshwater fish (especially pond fish), cause disease, and result in mass mortality. Grass carp summer fingerlings are especially susceptible. The disease has been reported from fish farms throughout China. The epidemic season runs from May to October, with a peak from July to September often in the acute form.
Control — There are four methods of controlling Cryptobia branchialis.
Bathe the fingerlings in a 8 ppm copper sulphate solution for 20–30 min before stocking.
Disinfect the feeding area with a mixture of copper sulphate and ferrous sulphate by the hanging bag method during disease prevalence.
Treat the infected pond with a mixture of copper sulphate and ferrous sulphate to a concentration of 0.7 ppm.
Bathe the fish with a 2–3 per cent table salt solution for 5 min.
Pathogen — The many parasitic species of the order Myxosporidia, class Sporozoa, have the ability to parasitize any organ or tissue of all varities of fish. Over 100 species that are parasitic to freshwater fish have been found in China. Some species can become epidemic. A spore of Myxosporidia consists of two identical chitinous shells surrounding plasmodium (Fig. 6.11). The line where the two shells join is called the sutural line. There is a ridge along the sutural line called the sutural ridge. The side with the sutural ridge is called the sutural side or lateral side. The side without the sutural ridge is called the shell side or front side. The plasmodium consists of a polar capsule(s) and the sporolasm. The number of polar capsules varies with species but is usually, from one to four. Each polar capsule contains a spiral polar filament. The number of nuclei inside the sporoplasm varies depending on the developmental stage of the spore. Some species contain an iodinephilous vacuole that can be stained brown with Lugol's solution.
Fig. 6.11. Principal structures of a spore of Myxosporidia. (a) shell view; (b) sutural view; (c) top view.
Myxosporidia parasitize the host generally in the form of a cytocyst. The most dangerous Myxosporidia that parasitize fish skin are seen in Fig. 6.12. Myxosporidia that commonly parasitize fish gills are seen in Fig. 6.13. Myxosporidia that commonly attack the intestines are seen in Fig. 6.14. Myxobolus lieni (Fig. 6.15) parasitizes the central nervous system and sensory organs of silver carp and bighead, causing whirling disease.
Control — There are three methods of controlling myxosporidiasis.
Eradicate the spore by sterilizing the pond with 100 kg/mu of nitrolime (CaN2) or 125 kg/mu of quicklime. In the fry and fingerling stages of silver carp (June-September), sprinkle dipterex powder into the pond to a concentration of 5 ppm twice monthly to prevent whirling disease of silver carp.
Bathe mud carp with 1 per cent crystal dipterex (90 per cent effective element) for 3–10 min and, at the same time, sprinkle crystal dipterex into the pond to a concentration of 0.2–0.3 ppm. This effectively controls myxosporidiasis of mud carp.
To control Myxobolus artus, feed 2 g paludrine to every 10,000 fry 5 days after fry nursing for 6 consecutive days.
Fig. 6.12. Myxosporidia commonly found on the skin of cultivated fish.
|1–2. Myxobolus abitus||6–7. Myxobolus ellipsoides|
|3. Thelohanellus rohitae||8–9. Myxobolus cyprinicola|
|4–5. Myxobolus koi||10–11. Hennerguya sinensis|
Fig. 6.13. Myxosporidia commonly found on the gills of cultivated fish.
1–3. Sphaerospora amurensis
4–5. Myxosoma varius
6–7. Myxobolus musculi
8–9. Myxobolus dipar
Fig. 6.14. Myxosporidia easily found in the intestines of cultured fish.
|A. Myxosoma sinensis||F. M. symetricus, sutural view|
|B. M. sinensis sutural view||G. Myxobolus lomi, side view|
|C. Myxosoma lieni, side view||H. M. lomi, sutural view|
|D. M. lieni, sutural view||I. Myxobolus artus, side view|
|E. Myxobolus symetricus, side view||J-K. M. artus, sutural views|
Fig. 6.15. Myxobolus lieni parasitising the brain of silver carp.
|A-D. Shell views of the spore||E. Sutural view of the spore|
Pathogen — The pathogen, Ichthyophthirius multifilis, varies considerably with developmental stage (Fig. 6.16).
Symptoms and pathological changes — The skin, fin rays and operculum become covered with many white protuberant pustules; for this reason, ichthyophythiriasis is also called “white dot disease.” These white dots are a proliferation of epidermal cells with mucus secreted because of the irritation caused by the drilling of parasites on the epidermis. In a serious case, the skin is covered with a white membrane. The diseased fish swims and responds to stimulus slowly, spending much of its time near the surface. It also continually rubs itself against other objects or jumps out of the water. The damage caused by the parasites and secondary bacterial infection results in epidermal inflammation, local necrosis and desquamation, and the rotting and splitting of fin-rays. Parasites on the branchial tissues destroy the gill lamella and stimulate the secretion of mucus. The branchial epithelia around the parasites proliferate. Infection also results in the congestion of gill veins or histological anemia of the gills. The parasite may invade the cornea and cause inflammation and blindness. Ichthyophythiriasis results in mass mortality because of dyspnea and a loss of appetite (starvation).
Fig. 6.16. Ichthyophirius multifiliis
A,D, mature stage
C,B, Larval stage
Epidemic situation — This disease occurs throughout China, and is one of the major protozoan diseases. Freshwater fishes of all developmental stages are vulnerable to infection with fingerlings as the main victim. Ornamental fish in aquaria or petty cement tanks may also become infected. The optimum water temperature for the proliferation of the parasite is 15–25°C. Therefore, early winter and late spring are its prevalent seasons. Fish in high-density, overwintering ponds are more susceptible to the disease.
Control — There are four methods of controlling ichthyophythiriasis.
To prevent transmission of the disease, disinfect the pond with quicklime, rear fry at a reasonable density, quarantine and disinfect fingerlings before stocking.
Bathe the fingerlings with a solution of 0.05 ppm malachite green and 25 ppm formalin twice daily. This should not be done in grow-out fish ponds.
Immerse fingerlings in 0.2–0.4 ppm malachite green for 2 h. This method was developed by the Beijing Fishery Research Institute.
Methylene blue can be used to combat the disease or infected fish can be treated with sea water (salinity over 1 per cent). These methods are commonly used in Europe.
Trichodinasis and trichodinelliasis
Pathogen - Many species of the genera Trichodina and Trichodinelia are responsible for these — diseases. Viewed laterally, the parasite resembles a hat; in aboral view, the parasite resembles a round plate. The convex part of the parasite is called the adoral end. Opposite of the adoral end is the aboral end. At the aboral end there is a counterclockwise adoral groove stretching to the cytostome (Fig. 6.17). On each side of the adoral groove there is a line of cilia, forming an oral zone that extends to the vestibule. The cytostome is linked with the cytopharynx and, near the cytopharynx, there is a contractile vacuole. The shape of macronucleus varies with species (horseshoe shaped, sausage shaped, etc.). The micronucleus is rod shaped or sphere shaped and generally close to the outer margin of the macro-nucleus end. At the aboral end there is a posterior girdle of cilia. There are two rows of rather short cilia: upper marginal and lower marginal cilia. Some species have a thin, transparent membrane called the border membrane, behind the lower marginal cilia (Fig. 6.17). The aboral end is concave and its most conspicuous structure are a circular denticulating ring and a chitinuous striated ring. The denticulating ring is formed by many denticles joined together. The number and shape of the denticules and the number of radiant rays on each denticle differ with species. The parasite attaches itself to the skin or gill of the host with its adhesive disc. Some times the parasite contracts its border membrane, moves its posterior girdle of cilia, and slides over the skin and gill. When swimming freely, the parasite spins like a wheel with its aboral end forward. Reproduction involves a sexual longitudinal division and sexual conjugation. The optimum temperature for the reproduction of Trichodina is 20–28°C.
Fig.6.17. Structure of Trichodina showing lateral view (A), partial cross section (B) and two segments of the dentivulating ring (C).
Symptoms and pathological changes - Trichodina can infect fish at any developmental stage, but the main victims are juvenile fish, especially those under 5 cm in body length. Generally, the parasites do not infect adult fish. Trichodina mainly invades the skin of juvenile fish, feeding on the tissue, and destroying the skin. Trichodinelia mainly parasitizes the gills, concentrating on the branchial periphery or between the gill filaments. With a serious infection, the gill tissue rots and the cartilage becomes exposed. As a result, respiration is seriously impaired and the fish dies.
Epidemic situation - Trichodinasis is a dangerous disease during the fry and fingerling stages. It is prevalent throughout China and especially on farms along the Yangtze River valley and the West River valley. Every year from May to August, when fry are nurtured to summer fingerlings, there is a serious outbreak of trichodinasis and a high mortality of fry and fingerlings. The disease is more likely to occur in small, shallow ponds with poor water quality and high fish density and trichodinelliasis under conditions of continuous rain.
Control — There are four methods of controlling trichodinasis and trichodinelliasis.
Disinfect the fingerlings with 8 ppm copper sulphate solution for 20–30 min or with a 1–2 per cent aqueous solution of table salt for 2–10 min.
The reproduction of Trichodina can be inhibited by adding 15–20 kg/mu of chinaberry (Melia azedarach) leaves once a week. Sprinkling 25–30 kg/mu of a decoction of fresh chinaberry branches and leaves is also effective.
Treat the pond with a mixture of copper sulphate and ferrous sulphate (5:2) to a concentration of 0.7 ppm.
Formalin at a concentration of 30 ppm can kill Trichodina on juvenile eel gill; however, this treatment also adversely affects water quality and appetite.
Pathogen — Many species of the genus Dactylogyrus are responsible for this disease. The following four pathogenic species parasitize cultured fish in China.
Dactylogyrus lamellatus parasitizes the gills, skin, and fins of grass carp. It is flat, 0.192–0.529 mm long, and 0.072–0.136 mm wide, (Fig. 6.18).
Dactylogyrus aristichthys parasitizes the gills of bighead.
Dactylogyrus hypopthalmichthys parasitizes the gill filaments of silver carp.
Dactylogyrus vastator parasitizes the gill filaments of common carp, crucian carp, and pet fish.
Fig. 6.18. The ventral view of a Dactylogyrus lamellatus Achmerov.
Symptoms and pathological changes — An infestation of one of the above species of Dactylogyrus causes the fish to secrete more mucus; in addition, gills become pale, the operculum opens, dyspnea occurs, and there is evident dropsy of the gills (more distinct in bighead). The infected fish swims slowly and is anemic. The number of monocytes and coenocytic leukocytes increases.
Epidemic situation — Dactylogyrosis is a common disease, prevalent in late spring and early summer. The optimum temperature for the parasite is 20–25°C. The disease is mainly found on silver carp, bighead, and grass carp.
Control — There are four methods of treating dactylogyrosis.
Before stocking, bathe fingerlings in 20 ppm potassium permanganate for 15–30 min.
When the water temperature is 20–30°C, spread 90 per cent crystal dipterex into the pond to a concentration of 0.2–0.3 ppm.
Treat the pond water with 2.5 per cent dipterex powder to a concentration of 1–2 ppm.
Sprinkle a mixture of dipterex and sodium carbonate (1:0.6) into the pond water to a concentration of 0.1–0.24 ppm.
Pathogen — Females of some species of the genus Sinergasilus parasitize fish gills. The following three species of Sinergasilus parasitize cultivated fish.
Sinergasilus polycolpus (Fig. 6.19) parasitizes the interior side of the gill filament tips of silver carp and bighead and the gill rakers of silver carp.
Sinergasilus undulatus parasitizes the interior side of gill filament tips of common carp and crucian carp.
Sinergasilus major (Fig. 6.19) parasitizes the interior side of the gill filament tips of grass carp, black carp, catfish, trout, and freshwater salmon.
The body of the adult female is slim and cylindrical, with three distinct sections: head, thorax, and abdomen.
The head is triangle shaped and has five pairs of appendages. The second pair of antenna has developed into a hook capable of attaching to gill filament tissues. The width of the first four thoracic segments equals their length. The fourth segment may be somewhat wider than it is long. The fifth thoracic segment is comparatively small. The sixth segment is a narrow genital segment on which a pair of ovisacs can be seen hanging down during the breeding season. There are five pairs of biramous swimmerets on the thorax. The abdomen has three segments, with short pseudosegments between the first and second and between the second and third segments. There is a pair of caudal furca at the tail end. The male is many times smaller than the female and has a pair of maxillipeds on its head to embrace the female during mating.
Fig. 6.19. Female Sinergasilus major (A) and Sinergasilus polycolpus (B).
Symptoms and pathological changes - Sinergasilus major is more harmful than S. polycolpus and S. undulatus. It usually invades grass carp that are over 2 years old and occasionally parasitizes gill filaments of large underyearling grass carp. The female parasite clutches the gill with its second antennae, wounding the gill tissue and causing local inflammation of the gill filaments and curving and deformation of the gill filament tips (Fig. 6.20). As S. major feeds, it secretes an enzyme that dissolves the tissues of the host, breaking down the branchial epidermis, damaging nearby capillaries, and causing anemia in some parts of the gills. The diseased fish displays an uneasy behaviour, often jumping out of the water.
Fig.6.20. Gill of a 2-year-old grass carp infected with Singergasilus major.
Epidemic situation This disease is widespread throughout China. The reproductive period lasts from April to November along the Yangtze River valley. The epidemic season is from May to September. Sinergasilus major mainly attacks grass carp over 2 years of age; S. polycolpus is usually found on silver carp and bighead over 2 years of age. A serious infection can be lethal.
Control — There are four methods of controlling sinergasilusis.
Because of the strict selectivity of the pathogen, rotary farming effectively prevents infection.
Before stocking, bathe the fingerlings with a 7 ppm solution of copper sulphate and ferrous sulphate (5:2) for 30 min.
Spray the pond with a solution of copper sulphate and ferrous sulphate (5:2) to a concentration of 0.7 ppm.
Treat the pond with mixture of 2.5 per cent dipterex powder and ferrous sulphate (1.2:0.2) to a concentration of 1.4 ppm.
Lernaesis (anchor worm)
Pathogen — some species of the genus Lernaea are pathogenic to Chinese carp. The following three species are the most prevalent.
Lernaea polymorpha parasitizes silver carp, bighead, and wuchang fish.
Lernaea cyprinacea parasitizes common carp, crucian carp, silver carp, and bighead.
Lernaea ctenopharyngodontis parasitizes grass carp.
The female parasite is needle shaped. The body is 6–12.4 mm long and consists of a head, thorax, and abdomen. There is no distinctive demarkation between the three sections. On the head, there is a pair of dorsal horns and a pair of abdominal horns. They function as anchors, enabling the parasite to fix itself to the host's musculature; this parasite is also known as the “anchor worm”. The shape of the cephalic horns differs from species to species; the thoracic region is long and cylindrical. The anterior portion is narrow, becoming broader toward the posterior end. There is a pair of genital pores at the end of the abdomen. In the reproductive season, a pair of long (2–3 mm) ovisacs can be seen hanging down from the genital pores. The thoracic region of the female parasite has five pairs of swimming legs (Fig. 6.21). After feeding, the thorax expands and extends. This causes the five pairs of swimmerets to degenerate and split apart. The male is small and only occasionally parasitic.
|1. Ventral horn|
|2. Head lobe|
|3. Dorsal horn|
|4. First swimming leg|
|5. Second swimming leg|
|6. Third swimming leg|
|7. Fourth swimming leg|
|8. Fifth swimming leg|
|9. The front part of genital segment is protuberant.|
|10. Ovulation pore|
|11. Caudal furca|
|12. Egg sac|
Fig. 6.21. Structure of a female Lernaea.
After parasitizing a fish, the female develops into three phases: “baby parasite”, “mature parasite”, and “old parasite”. The baby parasite resembles a fine white hair and has no ovisacs. The mature parasite is transparent, making its intestines visible, and there is a pair of green ovisacs near the genital pore. When touched, the parasite becomes erect. The old parasite is rather turbid and soft and carries many protozoans (e.g. Epistylis). Such parasites quickly die and fall off the fish.
Symptoms and pathological changes — Initially, the diseased fish behaves uneasily, has a poor appetite, is thin, and moves slowly. The areas that Lernaea has penetrated are inflammed and swollen, and tissues are necrotic. The wounds are often invaded by Saprolegnia. On a juvenile fish, four or five Lernaea 6–9 cm long can be lethal. On a young fish, just one or two parasites can retard growth or cause deformation.
Epidemic situation — Lernaeasis is widespread in Guangdong, Guangsi, and Fujian provinces. In these areas, incidence is high and intensity is great. The season of prevalence is long. The epidemic season along the Yangtze River valley lasts from April to October (when the water temperature is 15–33°C) and coincides with Lernaeas, reproductive season.
Control — There are five major methods of controlling Lernaea.
Bathe the fingerlings attacked by Lernaea with a 10–20 potassium permanganate solution for 1.5–2 h before stocking.
Spray the pond three or four times with 90 per cent crystal dipterex to a concentration of 0.3–0.5 ppm every 3 or 4 days.
Bathe diseased grass carp for 1.5–2 h with a 20 ppm solution of potassium permanganate at a water temperature of 15–20°C, or with a 10 ppm solution at 21–30°C. For diseased silver carp and bighead, immerse the fish in a potassium permanganate solution of the following concentration at the following water temperature: 33 ppm, below 10°C; 20 ppm, 10– 20°C; 12.5 ppm, 20–30°C; 10 ppm, over 30°C.
Because of the strict selectivity of Lernaea, rotation culturing and immunization are effective preventive measures. Immunized finger-lings are resistant to Lernaea for 1 year. Stocking fish into a large culture pond reduces the incidence of lernaeasis.
Change the water quality suddenly, e.g. add 400 kg/mu of fermented cow dung or pig manure or 100–150 kg/mu of distiller's dregs for every metre of water depth.
Other diseases and fish enemies
Inappropriate water temperature and water quality, mechnical lesions, insufficient feeding, and foreign chemical substances may all cause diseases, which may be fatal. These diseases include gas bubble disease, horse-running disease, and deformity (Fig. 6.22).
In the fry-nurturing stage, diseases caused by lower plants are common: e.g., silkweed and filamentous green algae (Fig. 6.23). Diseases caused by animals are also frequently observed: e.g., water centipede and fish killer (Kirkaldyia deyrollei) (Fig. 6.24). Frogs are also serious predators of fry and fingerlings.
Fig. 6.22. Grass carp fingerling suffering from deformity.
Fig. 6.23. Filamentous green algae which are often dangerous to larvae and young fish.
1. Spyrogyra sp;
2. Zygnema sp;
3-4. Mougeotia sp;
5. Hydrodictyon recticulatum, a fry is shown to be trapped in this dangerous, web-like filamentous alga.
Fig. 6.24. Harmful aquatic insects.