Control methods for diplostomiasis in the big-head schizothoracin (Aspiorhynchus laticeps)
The big-head schizothoracin (Aspiorhynchus laticeps) is a national first-class protected animal. In recent years, as attention to and emphasis on the conservation of this species has grown, its artificial breeding has been placed on the agenda of the **Autonomous Region for the protection of aquatic wildlife. In 2004, during the course of conducting the research project "Artificial Breeding of the Big-head Schizothoracin," the **Fisheries Science Research Institute found that some of the collected and bred broodstock of the big-head schizothoracin became diseased, showing symptoms such as blindness and cataracts of the eyeball, and drug treatment produced little effect, which affected the artificial breeding work of the big-head schizothoracin. To identify the cause of the disease, the author investigated the collection and rearing of big-head schizothoracin broodstock, took samples for examination and analysis, and confirmed the diagnosis as diplostomiasis, then adopted prevention and control measures and achieved some therapeutic effect and prevention and control experience. The characteristics and control methods of diplostomiasis in the big-head schizothoracin are described below:
I. Morphological characteristics of the pathogen
Diplostomum belongs to the class Trematoda, family Diplostomidae, genus Diplostomum, and its morphological types are mainly divided into miracidium, sporocyst, cercaria, metacercaria and adult. When parasitizing fish, its developmental form is the metacercaria. Diplostomiasis is also called cataract disease or diplostomiasis.
The metacercaria's morphology is divided into anterior and posterior parts; it is transparent, flat and oval, with an oral sucker at the anterior end, one lateral organ on each side, a mouth in the middle of the oral sucker, a pharynx below it, and intestinal branches extending to the posterior end of the body. In the posterior half of the worm body there is a ventral sucker similar in size to the oral sucker, below which is an oval adhesive organ, and at the posterior end there is a diamond-shaped excretory bladder, from the anterior end of which excretory ducts branch off; many granular and glistening calcareous bodies are distributed within the body.
When stationary in water, the cercaria assumes a "T" shape and continuously swims up and down in the upper layer of the water body, with obvious phototaxis. The worm body is divided into a body portion and a tail portion, and the body is covered with fine, dense small spines. At the anterior end of the body portion is a head organ, below which is a muscular pharynx with a prepharynx, connected below to an intestine that splits into two forks; in the middle of the body there is a ventral sucker, behind which are two pairs of penetration cells, with ducts leading into the head organ; at the end of the body portion there is an excretory bladder. The tail portion consists of a tail stem and tail furcae; the tail stem is well developed and has 9 pairs of flame cells, and many tail bodies and several tail hairs are distributed within the tail stem.
II. Life history of the pathogen
The adult Diplostomum parasitizes the intestinal tract of gulls. The eggs are discharged with gull feces and fall into the water, and after 3 weeks hatch into miracidia (when the water temperature varies from 25°C to 35°C, the hatching period shortens as the water temperature rises). The miracidia swim in the water, select Radix snails, Lymnaea snails and the like as the first intermediate host, bore into the liver area and the outer intestinal wall within their bodies and develop into sporocysts; the sporocysts produce cercariae, which move to the mantle cavity of the snail, quickly escape into the water body, and in the water body alternately sink and float, showing regular intermittent movement. Fish are its second intermediate host. When fish pass through the water layer containing cercariae, they are quickly attached by the cercariae; the cercariae shed their tails and bore into the fish muscles, then bore from the muscles into nearby blood vessels, finally move to the heart, travel upward to the head, enter the eyeball from the optic blood vessels, and develop into metacercariae within the lens over 1 month. After gulls eat fish bodies carrying Diplostomum, the metacercariae develop into adults in their intestinal tract.
III. Symptoms and pathological changes of the fish disease
Infection with diplostomiasis is divided into acute and chronic types. In acute infection, a large number of cercariae bore into the fish body within a short period; because the cercariae invade the eyeball from the blood vessels, the optic blood vessels become especially enlarged during the migration process, causing mechanical damage and leading to destruction of the optic blood vessels, which results in congestion of the fish's brain and eyeballs. The diseased fish swim rapidly and struggle in the water, then swim slowly, lie flat on the water surface, and sometimes move uncontrollably, head down and tail up, turning back and forth up and down in the water, and finally swim slowly and die. Chronic infection is manifested as a small number of cercariae invading each time, with no acute symptoms, and the diseased fish do not die; as the fish grows, the pathogen accumulates and increases within the eye, causing clouding of the lens, with part or all of the eye turning white, showing "cataract" symptoms, and some diseased fish have congestion around the orbit, and the lens may even fall out. In addition, cercariae boring in from the gills can block the gill blood vessels; when cercariae migrate in the blood vessels and heart, they can cause circulatory disturbance; when cercariae invade the nervous system, they can cause bending of the fish body, and this is relatively common in acute infection of fry.
IV. Epidemiological situation
Diplostomiasis generally occurs from May to August in spring and summer, and is relatively prevalent in central China, where there are more gulls and Lymnaea snails. Economically important cyprinid fishes such as silver carp, bighead carp, blunt snout bream, common carp and crucian carp can all be parasitized. In acute infection of fingerlings, death is rapid and mortality is high; chronic infection can cause "cataract" symptoms and occurs throughout the year, making it a relatively serious fish disease. Infection and prevalence of this disease in the big-head schizothoracin is the first reported case.
V. Diagnosis
A preliminary diagnosis can be made based on the white turbidity symptoms of the diseased fish's eyes. For further examination, first remove the fish eye, cut it open, then take out the lens and place it in physiological saline or clean water, scrape off the surface layer of the lens, and observe with a microscope; if Diplostomum is found, the disease can be confirmed. In acute infection of fry and fingerlings, the eyes generally do not turn white, and the number of parasite bodies in the eyes is not large, so it is also necessary to use observation results such as whether the head of the diseased fish is congested, whether the fish body is bent, whether the fish body moves frantically or swims rapidly, and whether there are Lymnaea snails in the pond as references for diagnosis.
VI. Prevention and control methods
Because the pathogen invasion, transfer route and parasitic site of diplostomiasis are relatively special, it is not easy to treat. At present, the main measures for preventing and controlling the disease are mainly to cut off the links in the pathogen's life history, such as driving away gulls, eliminating eggs, miracidia and intermediate hosts, etc., while also supplementing with drug treatment. The main methods adopted are:
1. Remove excess sludge from the pond and thoroughly disinfect with quicklime or bleaching powder; when the water depth is 1.0 m, the amount of quicklime used is 100 kg/mu to 150 kg/mu; or use tea seed cake to clear the pond with water, and when the water depth is 1.0 m, the amount used is 50 kg/mu.
2. For diseased ponds, 0.7 mg/L copper sulfate can be splashed over the whole pond, used repeatedly 2 times within 24 hours, which can kill the intermediate host animals.
3. During the season when the fish disease is prevalent, splash crystal trichlorfon over the whole pond so that the concentration of the drug in the pond water is 0.5 mg/L, which can kill cercariae.
4. Feed trichlorfon medicated bait; mix 15 g to 20 g of crystal trichlorfon into the feed for every 10,000 fish, feed once a day, and feed continuously for 5 days.