Schistosomiasis in children

　　1. Etiology

　　The liver fluke has a body size of (2.0～5.0)cm×(0.8～1.3)cm, with a flat dorsal and ventral surface, resembling a leaf shape, and a deep reddish-brown color. The anterior end is cone-shaped and called the rostrum, and the body suddenly becomes wider after the rostrum, known as the shoulder peak. The oral sucker is smaller and located at the top of the body, while the ventral sucker is slightly larger and located at the base of the rostrum. The eggs are very large (130～150)μm×(63～90)μm, elliptical, light yellow-brown, with thin eggshells divided into two layers. One end has a small lid. The eggs are filled with many yolk cells.

　　2. Pathogenesis

　　The damage caused by Schistosoma hepaticum to humans can be roughly divided into two aspects: the early juvenile worms pass through the intestinal wall into the peritoneal cavity, where they can damage tissues and leave hemorrhagic foci on the worm track. During the migration of juvenile worms in the liver parenchyma, they feed on liver cells and damage liver tissue. As the juvenile worms develop, liver damage becomes more extensive, and fibrous peritonitis may occur. Macroscopically, the liver is obviously congested, with milky white patterns (nodules). Microscopically, the damaged liver tissue is filled with liver cell fragments, eosinophils, neutrophils, lymphocytes, and macrophages. Occasionally, there are small abscesses on the surface of the liver tissue, filled with eosinophils and a large amount of Charcot-Leyden crystals. After about 6 weeks of wandering in the liver, the juvenile worms enter the bile ducts to parasitize and develop into adult worms. The adult worms parasitize in the bile ducts, causing the lumen to become significantly larger and protruding on the surface. The mechanical stimulation of the body of the worm, such as the suckers and skin spines, can cause inflammatory changes and is prone to secondary infection, leading to cellular cholangitis or liver abscess. The worms can produce a large amount of proline, which can induce cholangiocyte hyperplasia. Therefore, the main lesions caused by adult worms are cholangitis and epithelial hyperplasia, leading to narrowing of the bile duct lumen and thickening of the wall, with fibrous tissue hyperplasia around the bile ducts. In severe cases, larger bile ducts may also have chronic obstruction and bile stasis, leading to cholestatic liver cirrhosis.

　　1. Liver cirrhosis

　　According to reports, the incidence of liver cirrhosis in schistosomiasis is about 20%, with liver enlargement (mainly in the left lobe) and deterioration of liver function, as well as portal hypertension and other clinical manifestations. The liver cirrhosis associated with schistosomiasis can have a good prognosis if diagnosed and treated early.

　　2. Leukemic reaction

　　Infection can stimulate the host, leading to a large increase in bone marrow granulocytes and the appearance of a leukemic reaction. White blood cells can reach up to 65%, and bone marrow puncture examination is consistent with the bone marrow picture of hypereosinophilic syndrome. After deworming treatment, it can return to normal.

　　3. Ectopic parasitism and ectopic damage

　　Schistosomiasis has increased the possibility of parasitizing in organs other than the host's liver, which has increased the complexity and diagnostic difficulty of the disease.

　　The patient has symptoms such as aversion to cold, fever, with fever fluctuating between 38～40℃, lasting for 1～2 weeks, even up to 8 weeks; there are often symptoms such as pain in the liver area, fatigue, loss of appetite, nausea, aversion to oil, bloating, vomiting, diarrhea, or constipation, with an increase in eosinophils in the blood. Jaundice is rare during this period. The adult worms parasitize in the bile ducts, causing inflammatory changes in the bile ducts and obstruction of the bile ducts. The patient often has recurrent and persistent upper abdominal distension or biliary colic, irregular fever, jaundice, nausea, urticaria, or itching. The liver is slightly tender, and anemia is one of the characteristics of this period, with a progressive worsening trend. In the late stage, patients may develop biliary cirrhosis and cholestatic liver cirrhosis.

　　Strengthen the management of livestock, divide pastures, avoid water pollution, separate drinking water (including livestock) from general water use, and regularly disinfect drinking water. Strengthen health education and do not drink or eat potentially contaminated raw water or aquatic plants to cut off the transmission route.

　　Symptoms and prevention: Symptoms may vary due to the degree of infection, the host's immune resistance, age, and feeding management conditions. If the feeding management conditions are good, the host's resistance is strong, and the degree of infection is not severe, symptoms may not be present. Conversely, even with mild infection, symptoms may appear. The symptoms in young animals are usually more severe than in adult animals. Generally, they are listless, weak, emaciated, anemic, edematous, and hair loses its luster. Symptoms vary depending on the site of parasitism. Schistosomes that parasitize the liver can cause acute or chronic hepatitis, jaundice, and poor digestion; schistosomes that parasitize the rumen and intestines lead to digestive disorders and diarrhea; schistosomes that parasitize the lungs cause coughing or pleurisy, and when they migrate to the subcutaneous tissue, they form cysts. Schistosomes in the oviducts of poultry can produce shell-less eggs and soft-shelled eggs, etc.

　　1. Laboratory examination

　　1. Blood routine

　　White blood cells and eosinophils are significantly increased, especially in the acute stage, with white blood cell counts usually ranging from (10-43)×109/L, and the highest eosinophil count can reach 0.79. Erythrocyte sedimentation rate (ESR) accelerates, reaching up to 164mm/h, and hemoglobin levels are usually between 70-110g/L, but may be lower.

　　2. Liver function examination

　　Liver function is abnormally increased in the acute stage, with elevated ALT and AST, increased serum bilirubin in the chronic stage, decreased albumin, and globulin levels may increase to 51-81g/L. The albumin/globulin (A/G) ratio is inverted, and IgG, IgM, and IgM levels increase, while IgA levels remain normal.

　　3. Etiological examination

　　Positive results of etiological examination are the basis for diagnosis, but worm eggs are often not found in the early stage of acute infection. Generally, they can be found 2 to 3 months after infection. The eggs can be detected from the feces by methods such as water washing sedimentation, modified Kato-Katz method, or mercuric-aldehyde iodine concentration method. The sedimentation of duodenal drainage fluid or examination after centrifugation has a high positive rate.

　　Abdominal exploration can serve as a basis for diagnosis if adult worms or eggs are found in the bile duct, and laparoscopic biopsy or other tissue pathological examination can serve as a basis for diagnosis if worms or eggs are found.

　　4. Immunological examination

　　Soluble protein antigens of the worm body can be used for serological immunological examination. Methods that can be chosen include enzyme-linked immunosorbent assay (ELISA), indirect fluorescent antibody test (IFA), indirect hemagglutination test (IHA), and counterimmunoelectrophoresis (CIE), etc. The serological test results may show cross-reactions with other schistosome infections, but they still have significant auxiliary diagnostic significance in the early stage of infection when worm eggs cannot be detected. For example, detecting the circulating antigen of Fasciola hepatica in the serum is more valuable than detecting antibodies. The detection of Fasciola hepatica eggs in the patient's feces is positive as early as the 6th week after infection, which has significant early diagnostic value.

　　5. Abdominal fluid examination

　　Abdominal fluid is straw yellow, with cell count above 1000×10^6/L, mainly eosinophils.

　　Secondly, imaging examination

　　1. Ultrasonic examination

　　Ultrasonic examination of the liver shows that the liver fluke in the bile duct is a circular shadow of 0.3-0.5cm, resembling an 'Olympic ring'. During abdominal palpation, this shadow can move.

　　2. CT scan

　　Pseudo-liver tumors may occur.

　　3. Cholangiography

　　During cholangiography, the shadow of the worm body can be seen from different angles, which is thin and curly like a rope in the side view, and other angles can see narrow circular shadows or pseudo-layer disappearance and defect.

　　In addition to the toxins in dead crabs, unrefrigerated and undercooked crabs are also killers of food poisoning. This is because crabs grow in rivers, lakes and ponds, and are fond of eating small organisms, aquatic plants, and decayed animals. The surface, gills, and gastrointestinal tract of crabs are covered with pathogenic microorganisms such as bacteria and viruses. If crabs are eaten raw, pickled, or drunk, they may be infected with a chronic parasitic disease called schistosomiasis.

　　The infection rate and degree of infection of schistosomulae in live crabs are very high. Schistosoma mansoni parasitizes in the lungs, stimulates or damages lung tissue, and can cause coughing, even coughing up blood. If it invades the brain, it can cause paralysis.

　　1. Treatment

　　Firstly, symptomatic treatment is carried out, and praziquantel (thiabendazole) is the first choice for deworming treatment, with a dose of 50mg/(kg·d), taken orally in three divided doses, for 10-15 days continuously or once every other day, with 15 treatment days as a course. Caution should be exercised in patients with severe liver and kidney insufficiency. Praziquantel can be used as an alternative drug, with a dose of 25mg/kg, taken three times a day for three consecutive days, with a total dose of 225mg/kg. In severe infections, a course of treatment is repeated every month. Triclabendazole (10mg/kg) can also be taken in a single dose.

　　2. Prognosis

　　Generally good. During the acute stage, extensive liver hemorrhage may occur due to the migration of a large number of larvae, often leading to death due to misdiagnosis and untimely treatment. In the chronic stage, bacterial biliary tract infection may occur, leading to the deterioration of the condition.