bubble_chart Overview

Schistosomiasis is a disease caused by blood flukes. Currently, five species of schistosomes are known to infect humans: Schistosoma japonicum, S. haematobium, S. mansoni, S. intercalatum, and S. mekongi. Additionally, human cases of infection by S. bovis, S. matteei, and S. spindalis have also been reported.

bubble_chart Epidemiology

This disease is prevalent in China, as well as in Japan, the Philippines, and other regions. Initial investigations indicate that the disease is widespread in the Yangtze River basin and 13 provinces, municipalities, and autonomous regions south of the Yangtze River, including Shanghai, Jiangsu, Anhui, Jiangxi, Hunan, Hubei, Sichuan, Zhejiang, Fujian, Taiwan, Guangdong, Guangxi, and Yunnan. Its distribution is so extensive that it affects most of the grain-producing areas in southern China. It is estimated that there are about 10 million patients, with over 100 million people at risk. Schistosomiasis is one of the five major parasitic diseases in China. The government has mobilized and organized large numbers of professionals to conduct widespread surveys and treatments in endemic areas. According to a 1989 report, out of the 373 counties previously affected by schistosomiasis, 263 have now met the standards for elimination or basic elimination set by the Ministry of Health. A total of 94% of patients have been cured, and the original area inhabited by Oncomelania snails (the intermediate host) has been reduced by 80%. Shanghai, Guangdong, and Fujian have already met the ministry's standards for the elimination of schistosomiasis. Currently, there are still 1.5 million schistosomiasis patients in China, including 55,000 advanced-stage patients.

The prevalence of schistosomiasis requires three key components:

(1) Source of infection: Japanese schistosomiasis is a zoonotic disease. Schistosomiasis patients and reservoir hosts such as cattle (both yellow and water buffalo), pigs, dogs, cats, sheep, rabbits, deer, rodents, monkeys, etc., can become sources of infection by excreting eggs in their feces. Among reservoir hosts, water buffalo and yellow cattle are the most commonly infected with schistosomiasis.

(2) Transmission route: The source of infection deposits egg-containing feces into water bodies, where Oncomelania snails thrive, and people have the opportunity to come into contact with contaminated water. These three factors constitute the transmission route of schistosomiasis.

(3) Susceptible population: Regardless of age, gender, or ethnicity, people are susceptible to Japanese schistosomiasis. However, the highest infection rates occur among those aged 15–44. Individuals already infected with schistosomiasis may develop partial acquired immunity to reinfection, known as concomitant immunity.

bubble_chart Pathogen

(1) Adult worm: The worm body is cylindrical in shape, resembling a nematode in appearance. It is dioecious. The male worm is grayish-white, relatively thick and short, measuring 12-20mm in length and 0.5-0.55mm in width, with one oral sucker and one ventral sucker each. There is a gynecophoric groove on the ventral side for clasping the female worm, and seven testes are located on the dorsal side behind the ventral sucker. The female worm is more slender than the male, cylindrical in shape, dark brown in color, with oral and ventral suckers that are less prominent compared to the male. The worm body measures 12-26mm in length and 0.3mm in width, possessing a well-developed reproductive system, including ovaries, yolk glands, etc.

(2) Eggs: Pale yellow, elliptical in shape, without an operculum. The eggshell is uniform, with a small spine on one side located between the mid-transverse line and the apex of the egg. The outer shell is often coated with mucus and fecal debris, containing a miracidium inside. The egg size ranges from (70-100)×(50-65)μm.

bubble_chart Pathological Changes

The cercariae, juvenile worms, adult worms, and eggs of schistosomes can all cause certain damage to the human body, but the eggs are the most harmful. They primarily cause lesions in the large intestine and liver. The eggs become embedded in the intestinal wall tissues, where cellular infiltration occurs around them, forming egg granulomas. This is the fundamental cause of chronic schistosomal liver and intestinal lesions. The pathological process of granuloma formation and development is closely related to the developmental stage of the eggs. When the eggs have not yet formed miracidia, the surrounding tissues show no reaction or only a mild reaction. As the miracidia develop inside the eggs, inflammatory reactions begin to appear in the tissues. Once the miracidia mature, the enzymes, proteins, and sugars secreted by them (soluble egg antigens) cause tissue necrosis and acute inflammatory reactions. The sites where eggs accumulate often exhibit endovasculitis and form eosinophilic abscesses; in severe infections, neutrophilic abscesses may also form. The granulomas of Schistosoma japonicum eggs often contain clusters of eggs, making the damage they cause more severe than that of other schistosomes.

The granulomatous reaction can destroy normal host tissues, and the continuously forming egg granulomas create interconnected scars, leading to a series of lesions such as pipestem cirrhosis and intestinal wall fibrosis. On the other hand, the granulomatous reaction helps destroy and clear the eggs, confining the antigens secreted by the eggs to the surrounding area to reduce or avoid systemic damage caused by antigen-antibody complexes. As the infection progresses, the host's granulomatous reaction may exhibit modulation, manifested by a gradual weakening of the reaction intensity. This phenomenon is induced by soluble egg antigens rather than adult worm antigens. After the host develops immune modulation, the ability to destroy eggs continues to strengthen, which is of great significance in protecting the host.

Damage caused by immune complexes: Schistosome cercariae, juvenile worms, adult worms, and eggs have both stage-specific antigens and some common antigens, and the host produces corresponding antibodies. Antigens and their corresponding antibodies can form complexes in the host. When there is an excess of antigen, the soluble complexes formed may cause immune complex-mediated hypersensitivity, leading to vascular damage. It is currently believed that acute schistosomiasis and schistosomal kidney damage belong to this category of lesions.

Schistosomal lesions are mostly confined to the distribution range of the superior hemorrhoidal vein and the inferior mesenteric vein, with the colon, especially the rectum, descending colon, and sigmoid colon, being the most affected. Small intestine lesions are rare and only seen in grade III infections. Early changes include many yellow or brown granular deposits in the rectal mucosa, caused by egg deposition and the resulting inflammatory reactions, local congestion, edema, and further necrosis leading to eosinophilic abscesses. After the overlying intestinal mucosa necroses and sloughs off, superficial ulcers form with congested edges, allowing large numbers of eggs to enter the intestinal lumen. Clinically, symptoms such as abdominal pain, diarrhea, and hematochezia may appear, and large numbers of eggs can be detected in the stool. After the acute inflammatory changes subside, connective tissue proliferation follows. Advanced-stage changes mainly involve thickening of the intestinal wall due to fibrous tissue proliferation, with some mucosal damage, sloughing, or atrophy due to malnutrition, reducing the chances of positive stool tests at this stage. Some mucosal proliferation forms polyps. Due to repeated infections and continuous egg production by adult worms, eggs are deposited in batches in the intestinal wall, causing lesions of varying ages, so the intestinal mucosa may show a mix of yellow-brown granular deposits, ulcers, and polyps. Polyps formed by schistosomiasis lesions have the potential to transform into cancer. Severe intestinal lesions may lead to intestinal stenosis after healing. Additionally, eggs can cause lesions in the spleen, brain, lungs, and other organs.

bubble_chart Clinical Manifestations

Within a few hours to 2–3 days after exposure to infested water, red punctate rashes resembling flea bites appear at the sites where cercariae have penetrated, known as cercarial dermatitis, accompanied by cutaneous pruritus, which resolves spontaneously within a few days. When cercariae migrate through the lungs, they may cause cough and expectoration of blood. The clinical manifestations of schistosomiasis are highly complex and diverse, varying depending on the location of egg deposition, the severity of infection, and the host's immune response. Based on the disease course and primary clinical features, it can be classified into acute, chronic, and advanced schistosomiasis.

(1) Acute Schistosomiasis: Acute schistosomiasis is a seasonal pestilence, predominantly occurring in summer and autumn, with a higher incidence among young adult males. Most cases involve individuals with no prior immunity who have recently been heavily infected with cercariae, primarily due to frequent contact with infested water. Patients typically have a clear history of infection, and many report a history of cercarial dermatitis. Systemic symptoms include fever and allergic reactions, both caused by toxins from the eggs and metabolic byproducts of tissue damage. Due to the massive deposition of eggs in the intestines, acute colitis develops, with over half of patients experiencing abdominal pain and diarrhea. Diarrhea occurs 2–3 times daily, with loose stools that may contain blood and mucus. Sigmoidoscopy reveals congested and edematous mucous membranes, along with small yellow granules (egg nodules), which are pathognomonic pathological changes in the acute phase. In the initial stage, some cases may present only with constipation. In grade III infections, extensive egg deposition in the serosal layer of the colon and mesentery can lead to peritoneal irritation symptoms, abdominal distension, doughy sensation, and tenderness, often misdiagnosed as tuberculous peritonitis. A few patients may develop ascites due to inflammatory exudates from acute egg nodules and extensive liver lesions caused by the eggs, leading to impaired hepatic blood flow, increased lymph production, and fistula formation into the abdominal cavity. Other findings may include hepatosplenomegaly.

(2) Chronic Schistosomiasis: Not all patients with schistosomiasis have a history of acute episodes. In endemic areas, farmers repeatedly exposed to contaminated water with low-level infections often present with chronic schistosomiasis. Depending on the severity of infection, chronic schistosomiasis can be asymptomatic or symptomatic.

1. Asymptomatic Patients: In grade I endemic areas, the majority of cases are asymptomatic, with no impact on health or work capacity. These cases are often detected incidentally during mass screenings or evaluations for other illnesses. Most urban cases of schistosomiasis also fall into this category, with patients showing no symptoms or positive signs, though a minority may exhibit grade I hepatomegaly or splenomegaly.

2. Symptomatic Patients: The sigmoid colon and rectum are the primary sites of schistosomiasis lesions, making diarrhea and dysentery-like stools common. Severity varies with the degree of infection, with mild cases predominating. Patients may experience occasional diarrhea, 2–3 times daily, sometimes with blood in the stool. Severe cases may present with colicky abdominal pain, tenesmus, and dysentery-like stools. The sigmoid colon thickens due to egg deposition and fibrosis, accompanied by tenderness. Schistosome eggs are easily detected in the stool. Additionally, the thickened greater omentum, mesentery, and enlarged mesenteric or retroperitoneal lymph nodes often form irregular, firm, and fixed masses due to egg deposition, granuloma formation, and fibrosis, predominantly in the lower abdomen. Most patients exhibit varying degrees of anemia, emaciation, malnutrition, and reduced work capacity. Hepatosplenomegaly is common, with the liver initially larger than the spleen, smooth, and slightly firm. In mild infections, the disease may stabilize at this stage without progression. In severe, prolonged cases, it may progress to cirrhosis, with the liver gradually shrinking but remaining palpable, particularly the left lobe, which becomes hard and nodular. Subsequently, the spleen becomes congested and enlarges.

(3) Advanced schistosomiasis: Due to repeated infections, the condition gradually worsens, leading to liver cirrhosis. Increased portal vein pressure causes ascites, significant splenomegaly, and varices in the lower esophagus or gastric fundus. Some patients often experience fever, abdominal pain, diarrhea, dysentery, loss of appetite, and weight loss, along with frequent anemia and nutritional edema. Severe infections in children can affect growth, potentially resulting in dwarfism. Some patients frequently have fever, usually not exceeding 38°C, which may be related to the destruction of liver tissue by toxins from the parasite eggs. Additionally, sexual function often declines, with males experiencing decreased libido and impotence, while females may suffer from amenorrhea and infertility. This is caused by severe liver damage leading to systemic malnutrition and weakened hormone inactivation, which suppresses pituitary function and causes varying degrees of atrophy in the gonads and other endocrine glands. Patients appear prematurely aged and emaciated, looking older than their actual age, often with brown pigmentation on the face. In the advanced stage, the liver shrinks further, with an uneven surface and hardened texture, while the spleen gradually becomes congestively enlarged.

bubble_chart Diagnosis

(1) Medical History: A history of contact with epidemic water in endemic areas should raise suspicion of schistosomiasis. Therefore, the patient's place of origin, occupation, and history of exposure to epidemic water are crucial diagnostic references, especially for asymptomatic patients without signs.

(2) Clinical Manifestations:

1. Acute Schistosomiasis: In endemic areas, patients with a clear history of exposure to epidemic water about one month before onset, presenting with prolonged fever along with the following characteristics, should be considered for acute schistosomiasis: ① History of cercarial dermatitis, hepatomegaly with tenderness, diarrhea, etc. ② Significant increase in total white blood cell count and eosinophils in the blood. ③ Sigmoidoscopy reveals rectal mucosal congestion, edema, and yellow granular egg nodules.

2. Chronic and Advanced Schistosomiasis: Most chronic patients have no obvious symptoms, or past symptoms may have been forgotten, making it difficult to associate these symptoms with the disease for diagnostic purposes. In endemic areas, patients with long-term unexplained abdominal pain or hematochezia, hepatosplenomegaly, significant eosinophilia, recent epilepsy in young adults, acute or chronic appendicitis episodes, manifestations of liver cirrhosis with portal hypertension (such as massive splenomegaly, ascites, hematemesis), or dwarfism should be suspected of having schistosomiasis and undergo pathogen examination for confirmation.

(3) Pathogen Examination

1. Stool Examination: Detection of eggs or hatched miracidia in stool can aid in diagnosis and treatment evaluation. However, for Grade I infections, advanced-stage patients, or those with incomplete treatment, the egg count in stool is low, resulting in a low detection rate. Thus, a negative stool test does not rule out schistosomiasis.

⑴ Direct Smear Method: The detection rate is very low and can only identify heavily infected early-stage patients. Selecting pus, blood, or mucus for smears may increase detection chances.

⑵ Sedimentation and Hatching Method:

① Natural Sedimentation Method: This method is superior to direct smears but remains ineffective for patients with low egg counts. Take about 30g (egg-sized) of stool with a bamboo stick, place it in a beaker, add a small amount of water, and mix into a paste. Dilute further with more water. Place a wire sieve over a conical measuring cup, pour the stool mixture through the sieve, and rinse the residue with water 1–2 times. Fill the conical cup with water to the brim, let it stand for 20 minutes, then decant the supernatant. Repeat until the supernatant is clear. After the final decantation, use a pipette to take a small amount of sediment for three smear slides to examine for eggs.

② Miracidium Hatching Method: If the natural sedimentation method yields negative results, this method can be used. Transfer all sediment into a 250 or 125ml Erlenmeyer flask, add water to about 1cm below the rim (optimal pH 7.2–7.6). Place the flask in an illuminated incubator at 20–30°C. If room temperature exceeds 20°C, incubate under light indoors. Observe with the naked eye or a magnifying glass after 4 hours. Miracidia appear as grayish-white dots moving linearly near the water surface. If no miracidia are seen after 24 hours, the result is negative.

2. Intestinal Mucosal Biopsy: Insert a sigmoidoscope or proctoscope per routine and visually inspect the mucosal changes. Acute stages show mainly congestion and edema, while chronic stages exhibit pale, thickened mucosa with scarring. Typical nodules or patches may be seen in all stages. Suspected egg-containing nodules are biopsied and pressed between slides for microscopy. For untreated patients, finding eggs (live or dead) confirms diagnosis. For treated patients, only live or recently degenerated eggs are diagnostically significant.

(4) Immunodiagnosis:

1. Circumoval Precipitin Test (COPT): This is a specific immunoserological test using intact schistosome eggs as antigens. Antigenic substances secreted or excreted by miracidia or embryos within the eggs diffuse through micropores in the eggshell and bind to specific antibodies in the test serum, forming distinctive precipitate complexes around the eggs. The reaction intensity is assessed under a microscope, and the percentage of reactive eggs is calculated as the circumoval precipitation rate. The conventional method is performed on glass slides or concave slides. After adding the serum sample, an appropriate number of fresh or preserved eggs (100–150, isolated from infected animal livers) are placed and covered with a 24×24 mm coverslip, sealed with paraffin wax around the edges. The slides are incubated at 37°C for 48 hours before observation under low magnification. If necessary, results may be read after 72 hours. A typical positive reaction shows refractile precipitates in bubble-like, finger-like, flaky, or elongated coiled shapes, with neat edges firmly adhering to the eggshell. For negative reactions, the entire slide must be examined. For positive reactions, 100 mature eggs are observed to calculate the circumoval rate and the proportion of reaction intensities. Grading criteria for reaction intensity: - **+**: Bubble-like or finger-like precipitates cover less than 1/4 of the egg circumference; flaky precipitates cover less than 1/2; elongated coiled precipitates are shorter than the egg’s long axis. - **++**: Bubble-like or finger-like precipitates cover more than 1/4 of the egg circumference; flaky precipitates cover more than 1/2; coiled precipitates equal or exceed the egg’s long axis. - **+++**: Bubble-like or finger-like precipitates cover more than 1/2 of the egg circumference; flaky precipitates match or exceed the egg’s size; coiled precipitates extend several times the egg’s long axis.

The schistosome dried egg antigen slide (or membrane slide) circumoval precipitation test is an improved method developed in recent years. Utilizing the heat-resistant properties of the circumoval antigenic active substances, the isolated pure eggs are ultrasonicated and heat-treated, then quantitatively dripped and baked onto fixed glass slides or pre-made polyethylene thin membrane slides. This type of dried egg membrane slide has a longer storage time (6 months at 4°C) and is commercially available. During the test, only serum samples need to be added, incubated in a wet chamber, and the results are interpreted the same as the conventional method. The dried egg membrane slide method also offers advantages such as simplified procedures, standardized egg antigen requirements, and long-term storage.

2. Cercarial membrane reaction: Mix 2 drops of the subject's serum with about 10 cercariae on a glass slide, cover with a coverslip sealed with paraffin, and incubate at a constant 25°C for 24 hours. Observe under low magnification; a positive reaction is indicated by the formation of a gelatinous membrane around the cercariae. The reaction weakens after serum inactivation, and serum stored for more than 3 days requires complement addition. Currently, this reaction is considered a partially complement-dependent antigen-antibody reaction. This test has significant diagnostic value for early-stage new infection cases, with a positive rate of over 95%. In the absence of reinfection opportunities, cercarial membrane reaction antibodies may naturally decline, leading to more false negatives. Therefore, this test is not suitable for diagnosing chronic infections in areas where the disease has been largely eradicated. Cross-reactions may occur in patients with paddy-field dermatitis infected with avian cercariae, so testing should be avoided during the dermatitis season. The time to seroconversion is later than that of the circumoval precipitation reaction, so its value as a reference for evaluating treatment efficacy is limited.

3. Indirect hemagglutination test with egg antigen: The indirect hemagglutination test yields positive results earlier than stool examinations and is highly sensitive. Human "O" type or sheep red blood cells are fixed with glutaraldehyde, treated with tannic acid, and then sensitized with freeze-dried schistosome egg cold-extracted antigen solution before being freeze-dried. The freeze-dried antigen can be stored at 4°C for over 1 year. For the test, collect 6 drops of blood from the earlobe or finger, and use only one drop of serum at different dilutions. Mix with one drop of 2.5% red blood cell suspension on a hemagglutination plate, and let stand at room temperature for 15–30 minutes before observing the results. If the tested serum contains corresponding egg antibodies, agglutination will occur. A dilution of 1:10 is diagnostically significant, with a positive rate of over 95%. The stronger the reaction, the easier it is to detect eggs in stool examinations. Low-titer positives may yield false positives at a rate of 1%–3.5%. Cross-reactions with Paragonimus are relatively high, ranging from 14% to 84.2%. Since serum from schistosomiasis patients does not cross-react with Paragonimus antigen in complement fixation tests, this can be used for differentiation. The indirect hemagglutination test is simple to perform and provides rapid results, making it one of the sensitive methods for large-scale field screenings.

4. Schistosome circulating antigen (CAg): It was initially one of the sensitive methods for screening Schistosoma japonicum infections.

Circulating antigens were detected in the serum of infected mice. Over the past decade, domestic and international researchers have conducted extensive studies on circulating antigens and have achieved some reference-worthy results. Detecting circulating antigens provides a new approach for evaluating the efficacy of schistosomiasis treatments. Currently, this method is still in the exploratory stage.

bubble_chart Treatment Measures

The drugs used to treat schistosomiasis include praziquantel, furapromide, nithiocyanamine, and others, but currently, praziquantel is the preferred drug.

(1) Praziquantel: This is a new broad-spectrum antihelminthic drug with killing worms effects against the three major types of schistosomes and filariae in humans. Results from animal experimental treatments suggest that praziquantel is a low-toxicity, short-course, and highly effective anti-schistosomal drug. The treatment dose for adults is 10mg/kg per dose, three times a day at 4-hour intervals, for a 2-day course. Alternatively, a single-day treatment can be used with 20mg/kg per dose, three times a day. The total dose is 60mg/kg, while for children, the total dose is 70mg/kg per day, divided into three doses, with a 1-day course. For acute schistosomiasis, the dose and course are increased: 10mg/kg per dose, three times a day for 4 consecutive days, with a total dose of 120mg/kg. The side effects of praziquantel are mild and short-lived, appearing about 1 hour after administration, mainly including dizziness, headache, lack of strength, grade I abdominal pain, etc. These do not require treatment and disappear within a few hours after discontinuation. In some patients, liver function tests may show elevated alanine aminotransferase. A few patients may experience premature beats, but no regular changes are observed in electrocardiograms or electroencephalograms before and after treatment. Praziquantel is highly effective in treating Japanese schistosomiasis. Fecal incubation tests turn negative within 18–20 days, with a short-term efficacy rate of 100%.

(2) Furapromide: This Yaodui has certain killing effects against both juvenile and adult schistosomes. Practical experience from various regions indicates that the 20-day furapromide treatment regimen has high efficacy. Currently, a slow-release enteric-coated tablet form is used, with a daily dose of 60mg/kg (not exceeding 3g per day for adults) for 10 days, totaling 600mg/kg. The side effects of this drug include gastrointestinal reactions, mainly loss of appetite, nausea, vomiting, abdominal pain, and diarrhea, with occasional hematochezia. Muscle spasms are a unique side effect of furapromide. Neuropsychiatric symptoms primarily occur in patients with advanced schistosomiasis and liver decompensation, manifesting as memory loss, reticence, depression, apathy, confusion, or erratic crying and laughing, auditory and visual hallucinations, etc. A few patients may experience grade I liver or kidney function impairment during treatment, which resolves quickly after discontinuation.

(3) Nithiocyanamine: This is a broad-spectrum vermifugal medicinal, currently mainly used in micro-powder capsule form with particle diameters of 3–6μm. The total dose is 6–7mg/kg, divided into three equal doses, taken once nightly for a 3-day course. The long-term fecal examination negative conversion rate can reach around 80%. For acute schistosomiasis, a total dose of 10mg/kg is used over a 6-day course. Generally, body temperature returns to normal 8–24 days after starting treatment, with symptom improvement, and the long-term fecal examination negative conversion rate can reach 80%. The side effects of this drug are mostly neurological symptoms, such as dizziness, headache, vertigo, lack of strength, drowsiness or insomnia, unsteady gait, ocular tremor, excessive sweating, and muscle tremors. A few may experience psychiatric symptoms and digestive system symptoms. It is contraindicated in patients with advanced schistosomiasis and poor liver function compensation, those with acute hepatitis in the stage of convalescence for less than one year or chronic hepatitis, a history of mental illness, pregnant or breastfeeding women, and those with chronic heart, kidney, or other diseases and weak constitution.

bubble_chart Prevention

(1) Eliminating the source of pestilence: Treat infected patients and livestock, strengthen fecal management, and avoid contamination of water sources by fresh feces. For example, construct harmless septic tanks; or store mixed feces and urine under cover to allow urea to decompose into ammonia, which can kill parasite eggs. Adding quicklime or ammonium bicarbonate to feces can also kill parasite eggs.

(2) Eliminating intermediate host snails: Snail eradication should be based on the ecological characteristics of snails and local geographical conditions, with treatment tailored to local conditions. Methods include altering snail breeding environments and combining physical and chemical snail eradication techniques. Physical methods include grass removal, burning, and soil burial. Chemical snail eradication agents include niclosamide, sodium pentachlorophenate, and nicotinamide, among others.

(3) Personal protection: Avoid contact with infested water as much as possible. If working in infested water is necessary, take protective measures such as applying protective agents like niclosamide or dibutyl phthalate ointment or emulsion to the skin, or wearing waterproof rubber boots and plastic protective pants.

bubble_chart Differentiation

Acute schistosomiasis presents with symptoms such as fever, hepatomegaly with tenderness, abdominal pain, and diarrhea, and needs to be differentiated from cold-damage disease, amoebic liver abscess, sepsis, and subcutaneous nodular peritonitis. When complicated by ectopic pulmonary lesions, it should be distinguished from miliary subcutaneous nodules. A significant increase in eosinophils in the blood count holds important diagnostic value. Chronic and advanced schistosomiasis should be differentiated from non-jaundiced syphilitic hepatitis. The latter is characterized by more pronounced loss of appetite, weakness, liver pain, and impaired liver function, with no increase in eosinophils and a positive hepatitis B surface antigen test. Schistosomiasis patients with diarrhea and hematochezia should be distinguished from amoebic dysentery and chronic bacterial dysentery. The former typically shows positive stool hatching for miracidia. Advanced schistosomiasis with massive splenomegaly and ascites can be difficult to distinguish from portal and necrotic cirrhosis. The former often has a history of chronic diarrhea and dysentery, with jaundice, spider angiomas, and palmar erythema being less common, and liver function impairment being milder.