bubble_chart Overview

Different stages of schistosome development, including cercariae, schistosomula, adult worms, and eggs, can cause various damages and complex immune responses in the host. Due to the differences in pathogenic factors at each stage, the affected tissues, organs, and host reactivity vary, leading to distinct pathological changes and clinical manifestations with corresponding characteristics and stages. Based on the immunological nature of the pathogenic factors, some propose classifying schistosomiasis within the category of immune-related diseases.

bubble_chart Epidemiology

Japanese schistosomiasis is prevalent in Asian countries such as China, Japan, the Philippines, and Indonesia. Regardless of gender, age, or race, humans are susceptible to Schistosoma japonicum. In most endemic areas, the age-specific infection rate typically peaks between 11 and 20 years old and then declines. Among the various links in the transmission chain, three critical factors are the contamination of water sources with schistosome eggs in feces, the presence of Oncomelania snails, and human contact with infested water.

bubble_chart Pathogenesis

The penetration of cercariae through the skin can cause dermatitis, with local papules and cutaneous pruritus, which is a type of immediate and delayed hypersensitivity reaction.

During the migration of schistosomula in the host, the organs they pass through (especially the lungs) develop vasculitis, capillary embolism, rupture, leading to local cellular infiltration and petechial hemorrhage. When a large number of schistosomula migrate in the human body, patients may experience fever, cough, blood-streaked sputum, and eosinophilia, which may be due to local inflammation and allergic reactions caused by the metabolic products of the parasites.

Adult worms generally do not cause significant pathogenic effects, though a few may cause mild mechanical damage, such as venous membrane inflammation. However, their metabolic products, secretions, excretions, and the shedding of the outer tegumental membrane can form immune complexes in the body, causing harm to the host.

The pathological changes in schistosomiasis are primarily caused by the eggs. The eggs mainly deposit in the host's liver and colon wall tissues, and the resulting granulomas and fibrosis are the main lesions of schistosomiasis.

The formation of egg granulomas is an immune response of the host to the disease-causing agents. On one hand, the granulomatous reaction destroys and clears the eggs, isolates and removes the antigens released by the eggs, and reduces the formation of antigen-antibody complexes in the bloodstream and their damage to the body. On the other hand, the granulomatous reaction damages the host's normal tissues, and continuously formed egg granulomas create interconnected scars, leading to a series of lesions such as pipestem fibrosis in the liver and fibrosis of the intestinal wall.

Schistosome egg granulomas form in the tissue blood vessels, blocking the vessels and destroying their structure, leading to tissue fibrosis. These lesions are mainly seen in organs with heavy egg deposition, such as the liver and colon. In the liver, egg granulomas are located at the terminal branches of the portal vein and presinusoidal veins, so the liver's structure and function are generally unaffected. In grade III infections, extensive fibrosis occurs around the portal vein. On liver sections, long white fibrous bundles surrounding the portal vein extend into the liver at various angles, known as pipestem fibrosis, which is a characteristic lesion of advanced schistosomiasis sexually transmitted disease.

bubble_chart Pathological Changes

1. Damage caused by cercariae and juvenile worms Cercariae penetrating the skin can cause dermatitis, characterized by local papules and cutaneous pruritus, which is a type of immediate and delayed hypersensitivity reaction. The pathological changes include capillary dilation and congestion, accompanied by hemorrhage and edema, with infiltration of neutrophils and monocytes. Experiments have shown that transferring serum and lymphocytes from infected mice to normal mice, followed by cercariae inoculation (first exposure to cercariae), can also induce cercarial dermatitis. This indicates that the immune response is antibody-mediated in the early stage.

When juvenile worms migrate through the host's body, the organs they pass through (especially the lungs) develop vasculitis, capillary thrombosis, and rupture, leading to local cellular infiltration and petechial hemorrhage. When a large number of juvenile worms migrate in humans, patients may experience fever, cough, blood-streaked sputum, and eosinophilia, which may be due to local inflammation and hypersensitivity reactions caused by the metabolic products of the worms.

2. Damage caused by adult worms Adult worms generally do not cause significant pathogenic effects, but a few may induce mild mechanical damage, such as venous membrane inflammation. However, their metabolic products, secretions, excretions, and the shed outer membrane of the tegument can form immune complexes in the body, causing harm to the host.

3. Damage caused by eggs The lesions of schistosomiasis are primarily caused by eggs. The eggs mainly deposit in the host's liver and intestinal wall tissues, and the resulting granulomas and fibrosis are the main pathological changes of schistosomiasis.

As the disease progresses, the miracidia inside the eggs die, their toxic effects gradually diminish, necrotic material is absorbed, and the eggs rupture or calcify. They become surrounded by epithelioid cells, lymphocytes, and foreign-body giant cells. Eventually, the epithelioid cells transform into fibroblasts and produce collagen fibers, leading to gradual fibrosis of the granuloma and the formation of scar tissue.

bubble_chart Clinical Manifestations

The condition varies depending on factors such as the patient's degree of infection, immune status, nutritional state, and timeliness of treatment. Japanese schistosomiasis can be classified into acute, chronic, and advanced (late-stage or third-stage) phases. After cercariae penetrate the skin, some patients may develop local papules or urticaria, known as cercarial dermatitis. When female worms begin mass egg production, a few patients exhibit acute allergic reactions primarily characterized by fever, typically occurring 1–2 months after exposure to contaminated water. Besides fever, symptoms include abdominal pain, diarrhea, hepatosplenomegaly, and eosinophilia. Detection of schistosome eggs or miracidia in stool tests confirms the diagnosis of acute schistosomiasis. The condition then gradually transitions to the chronic phase. In endemic areas, 90% of schistosomiasis cases are chronic, where most patients show no obvious symptoms or discomfort, though they may intermittently experience subclinical states with manifestations such as diarrhea, mucus and blood in stool, hepatosplenomegaly, anemia, and weight loss. Approximately five years after infection, some heavily infected patients begin to develop advanced-stage lesions. Based on primary clinical presentations, advanced schistosomiasis can be categorized into three types: massive splenomegaly, ascites, and dwarfism. A single patient may exhibit two or more of these conditions. Clinically, it often presents as a syndrome dominated by hepatosplenomegaly, ascites, portal hypertension, and varices in the lower esophagus and gastric fundus due to collateral circulation formation. Advanced-stage patients may suffer life-threatening complications such as upper gastrointestinal bleeding and hepatic coma. Severe infections in children and adolescents can impair anterior pituitary function, among other factors, leading to stunted growth and development as well as reproductive issues, resulting in dwarfism. Since liver fibrosis in the advanced stage is often irreversible and responds poorly to treatment, it frequently leads to clinically refractory advanced schistosomiasis.

bubble_chart Auxiliary Examination

1. Pathogen Diagnosis: Examination of eggs or hatched miracidia from feces and rectal mucosal biopsy for eggs. Methods include: (1) Direct smear method: Eggs of schistosoma can often be detected in the feces of patients from highly endemic areas or in the mucus-blood stools of acute schistosomiasis patients. This method is simple but has a low egg detection rate. (2) Miracidium hatching method: This can improve the positive detection rate. (3) Quantitative transparent method: Used for counting schistosoma eggs. (4) Rectal mucosal biopsy: In chronic and advanced schistosomiasis, the intestinal wall thickens, obstructing egg excretion, making it difficult to detect eggs in feces. A rectal examination can be applied.

2. Immunodiagnosis

(1) Intradermal test (IDT): The concordance rate between IDT and fecal egg detection is generally around 90%, but false-positive or false-negative reactions may occur, and cross-reactions with other trematode infections are common. Additionally, cured patients may still test positive for many years. This method is simple and rapid, often used for field screening of suspected cases.

(2) Antibody detection: Specific antibodies, including IgM, IgG, and IgE, are present in the serum of schistosomiasis patients. If the patient has not undergone pathogen treatment and the specific antibody test is positive, it has significant diagnostic value. However, if the patient has already received pathogen treatment, a positive antibody test does not necessarily indicate the presence of adult worms, as specific antibodies may persist for a long time after cure. Currently, there are many serological diagnostic methods for schistosomiasis antibody detection, including: 1) Circumoval precipitin test (COPT): Typically, if 5% or more of 100 examined eggs show a positive reaction (ring precipitation rate), the result is considered positive. The positive rate of COPT among fecal egg-positive patients averages 97.3% (94.1–100%). 2) Indirect haemagglutination test (IHA): The concordance rate between fecal egg-positive patients and IHA-positive results is 92.3–100%. The false-positive rate in healthy individuals is around 2%, and cross-reactions may occur with infections such as paragonimiasis, clonorchiasis, and trichinosis. IHA is simple to perform, requires minimal blood, and provides rapid results, making it widely used in China. 3) Enzyme-linked immunosorbent assay (ELISA): This test has high sensitivity and specificity and can reflect antibody levels. The positive detection rate is 95–100%, with a false-positive rate of 2.6%. Six months to one year after praziquantel treatment, 50–70% of patients test negative. 4) Immunoenzymic staining test (IEST).

It is worth noting that in recent years, with the advancement of technology, certain high-tech methods and new approaches have been gradually introduced into the field of schistosomiasis diagnosis and research. For example, immunoblotting, also known as Western blot, is a novel immunological technique established at the molecular level based on protein gel electrophoresis and solid-phase immunoassay. This has significantly advanced the progress of serological diagnostic methods for schistosomiasis. It not only enables the analysis and identification of specific protein components of schistosome antigens but also serves as a new serological diagnostic method for diagnosing patients and distinguishing between different stages of schistosomiasis. Another example is the application of hybridoma technology to produce monoclonal antibodies (McAbs). Specific McAbs can be used to purify schistosome antigens for serological diagnosis of schistosomiasis, or to detect circulating antigens, providing new pathways for schistosomiasis diagnosis.

(3) Detection of circulating antigens: Since antibodies persist in the host for a long time after treatment, a positive result often cannot distinguish between current infection and past infection, nor is it easy to evaluate therapeutic efficacy. Circulating antigens are macromolecular particles released by living parasites into the host, mainly derived from excretions, secretions, or shed surface materials of the parasites that possess antigenic properties and can be detected by serological immunoassays. Theoretically, the detection of CAg has its own advantages, as it can not only reflect active infection but also evaluate therapeutic efficacy and estimate parasite species.

bubble_chart Diagnosis

The diagnosis of schistosomiasis consists of two main parts: pathogen diagnosis and immunological diagnosis. Confirming a patient's infection requires detecting eggs or hatching miracidia in stool samples. As schistosomiasis control efforts advance, identifying eggs in stool becomes increasingly challenging. Therefore, diagnostic methods are continuously improved, and a series of serological diagnostic techniques have been developed, which are becoming more refined, simple, and effective.

bubble_chart Treatment Measures

Patients and sick animals detected should be treated promptly. In the 1970s, China synthesized praziquantel, a safe, effective, and easy-to-use therapeutic drug. For advanced-stage patients, it is common to first undergo Chinese medicinal conditioning before receiving worm-killing treatment or surgical intervention.

bubble_chart Follow-up Consultation

A complete cure is achieved when no clinical symptoms or signs occur within 2 to 3 months after thorough treatment, and no parasite eggs are found in stool examinations.

bubble_chart Prevention

1. Treat patients and sick cattle to eliminate the source of pestilence

2. Control and eliminate Oncomelania snails

3. Strengthen fecal management and improve personal protection

bubble_chart Complications

Ectopic damage or ectopic schistosomiasis.