Schistosomiasis is a long-lasting parasitic infection caused by blood flukes, small flatworms—from the genus Schistosoma. It is one of the world’s most widespread neglected tropical diseases. People become infected when their skin comes into contact with freshwater that contains the parasite’s larvae, called cercariae, which are released by infected freshwater snails. This exposure often occurs during everyday activities such as swimming, bathing, farming, fishing, or washing clothes. After entering the skin, the larvae travel through the bloodstream and mature into adult worms that live in blood vessels. These worms produce eggs; some leave the body through urine or stool, but many become trapped in organs and cause inflammation and tissue damage.
An estimated 240–250 million people are infected worldwide, and more than 700 million are at risk. Most cases occur in sub-Saharan Africa, though the disease also affects parts of the Middle East, South America, and Asia. Children are especially vulnerable and may experience poor growth, malnutrition, anemia, and difficulties with learning.
Early infection may cause an itchy rash followed by fever, chills, tiredness, muscle pain, and stomach discomfort. This early phase is sometimes called Katayama fever. Long-term infection depends on the species involved: intestinal schistosomiasis can cause chronic abdominal pain, diarrhea, loss of appetite, and blood in the stool, while urogenital schistosomiasis can lead to painful urination, blood in the urine, and gradual damage to the bladder and kidneys. Severe, long-term complications may include high blood pressure in the veins of the liver (portal hypertension), scarring of the liver (liver fibrosis), enlarged spleen (splenomegaly), and, in rare cases, bladder cancer. Other symptoms, such as headaches or shortness of breath, may occur when eggs spread to different parts of the body or trigger immune reactions.
The main treatment is praziquantel, a medication effective against all major Schistosoma species and safe for both adults and children, including pregnant individuals after the first trimester. Other drugs, such as oxamniquine (mainly for S. mansoni) or artemisinins (being studied for young, developing worms), may be used in specific situations. Because people in affected regions are often exposed to contaminated water repeatedly, treatment may need to be given more than once.
Prevention includes avoiding contaminated freshwater when possible, improving access to clean water and sanitation, reducing snail populations, and carrying out mass drug administration (MDA) programs recommended by the World Health Organization. These programs focus on school-aged children and other high-risk groups in areas where the disease is common.
Etiology
Schistosomiasis is caused by parasitic blood flukes belonging to the genus Schistosoma. Several species infect humans, with the most common being Schistosoma haematobium, Schistosoma mansoni, and Schistosoma japonicum. Each species has a distinct geographic range and tends to affect specific organs within the body.
- S. haematobium is found primarily in Africa and the Middle East and is associated mainly with urogenital schistosomiasis, which affects the bladder, ureters, and kidneys.
- S. mansoni occurs in sub-Saharan Africa, parts of the Arabian Peninsula, and regions of South America such as Brazil and Venezuela. It primarily causes intestinal and hepatic disease.
- S. japonicum is endemic to parts of China, the Philippines, and Indonesia and is considered the most pathogenic species due to its high egg output and ability to infect a wide range of mammalian hosts.
Other human-infecting species include S. mekongi, found along the Mekong River basin in Cambodia and Laos, and S. intercalatum and S. guineensis, found in localized regions of Central and West Africa. Each species relies on specific freshwater snail hosts to complete its life cycle, and the distribution of these snails largely determines where transmission occurs. Environmental factors such as climate, water management practices, irrigation development, and human–water contact patterns play major roles in shaping regional disease burden.
Historical Background
The scientific understanding of schistosomiasis began in the mid-19th century with the work of Theodor Bilharz, a German physician stationed in Cairo. In 1851, Bilharz identified Schistosoma haematobium during autopsies and linked the presence of its eggs to urinary symptoms such as blood in the urine, a common complaint among local populations. His findings led to the early name “bilharzia,” which is still used in some regions today.
Throughout the late 19th and early 20th centuries, researchers gradually recognized that schistosomiasis was not a single disease but a group of infections caused by different Schistosoma species with unique life cycles and clinical effects. The discovery that freshwater snails served as intermediate hosts was a major breakthrough, enabling public health officials to understand how environmental and social factors, including irrigation systems, agricultural work, and poor sanitation, contributed to transmission.
Large-scale control programs emerged in the mid-20th century, initially relying heavily on snail control through chemical molluscicides and environmental modification. Over time, the focus shifted toward improving sanitation, providing safe water supplies, and introducing effective chemotherapy. The introduction of praziquantel in the late 1970s revolutionized control efforts, making mass drug administration (MDA) both feasible and cost-effective.
Transmission and Life Cycle
Schistosomiasis is transmitted through direct contact with contaminated freshwater where specific snail species live. The parasite undergoes several developmental stages, involving both humans and snail hosts, before it becomes infectious.
Transmission Routes
Human infection begins when the skin is exposed to water containing cercariae, the free-swimming larval form capable of penetrating human tissue. These larvae are released in large numbers from infected snails and actively seek human hosts. Entry usually occurs during common activities such as swimming, wading, bathing, farming in flooded fields, or washing clothes in contaminated water.
Transmission is strongly associated with poor sanitation. When infected individuals urinate or defecate in or near freshwater sources, they release parasite eggs into the environment. Inadequately treated sewage systems and open defecation dramatically increase contamination, allowing eggs to reach water bodies and sustain the parasite’s life cycle. Areas with irrigation schemes, water reservoirs, and seasonal flooding also show increased risk, as these environments create habitats that support both snail populations and frequent human–water contact.
Snail Hosts
Freshwater snails serve as the intermediate hosts essential for Schistosoma development. Only specific snail genera can support the parasite, and their distribution largely determines where schistosomiasis occurs.
- Biomphalaria snails transmit S. mansoni in Africa, the Middle East, and the Americas.
- Bulinus snails transmit S. haematobium across Africa and parts of the Arabian Peninsula.
- Oncomelania snails transmit S. japonicum in China, the Philippines, and Indonesia.
Snails become infected when miracidia, larvae that hatch from eggs in freshwater, actively penetrate their tissues. Inside the snail, the parasite undergoes asexual multiplication, greatly increasing its numbers. Environmental factors such as water temperature, pH, vegetation, and snail density influence whether snails can support infection, while climate change, dam construction, and agricultural development continue to alter snail habitats and expand transmission zones.
Life Cycle Stages
The life cycle of Schistosoma begins with infected humans releasing parasite eggs in urine (for S. haematobium) or feces (for intestinal species like S. mansoni and S. japonicum). When eggs reach freshwater, they hatch within minutes to hours, releasing miracidia, which must find a suitable snail host within a short lifespan.
Inside the snail, miracidia transform into sporocysts, which undergo several rounds of multiplication. After approximately 4 to 6 weeks, thousands of cercariae are produced and emerge from the snail into the surrounding water. Cercariae swim freely, propelled by their forked tails, and seek human skin to penetrate.
Once inside the human host, cercariae lose their tails and become schistosomula, which migrate through tissues and enter the bloodstream. They travel to the lungs and liver, where they continue to mature before relocating to their final residence in specific blood vessels, around the bladder for S. haematobium or around the intestines and liver for S. mansoni and S. japonicum.
Adult worms typically live in pairs and can survive for 5 to 10 years, sometimes longer, producing hundreds to thousands of eggs daily. These eggs trigger inflammation and tissue damage when they become trapped in organs, and the cycle continues when eggs reach freshwater sources and hatch again.
Types of Schistosomiasis
Schistosomiasis presents in several distinct forms, each caused by different species of the Schistosoma parasite. These forms vary in symptoms, affected organs, and geographical distribution.
Intestinal Schistosomiasis
Intestinal schistosomiasis is primarily caused by Schistosoma mansoni and Schistosoma japonicum, although S. mekongi and S. intercalatum can also produce intestinal forms of the disease. In these infections, adult worms inhabit the mesenteric veins surrounding the intestines, leading to chronic inflammation in both the intestines and liver.
Common symptoms include abdominal pain, chronic or intermittent diarrhea, and the presence of blood in the stool, reflecting injury caused by parasite eggs passing through the intestinal wall. Over time, repeated egg deposition and immune responses can lead to more serious complications, such as liver enlargement (hepatomegaly), scarring of liver tissue (periportal fibrosis), and increased blood pressure in the portal vein system (portal hypertension). In advanced cases, patients may develop ascites (fluid buildup in the abdomen), esophageal varices, or splenomegaly.
Schistosoma japonicum, found in China, the Philippines, and parts of Indonesia, is often considered the most pathogenic species because of its high egg output and broad range of animal reservoir hosts, including cattle, water buffalo, and dogs. This zoonotic aspect makes control efforts more challenging. S. mansoni, prevalent in Africa, the Middle East, Brazil, and several other South American countries, is responsible for the greatest global burden of intestinal schistosomiasis.
Urogenital Schistosomiasis
Urogenital schistosomiasis is caused almost exclusively by Schistosoma haematobium, a species found across much of Africa and localized parts of the Middle East. In this form, adult worms settle in the venous plexus surrounding the bladder, leading to injury and inflammation throughout the lower urinary tract.
The hallmark symptom is hematuria, or blood in the urine, often described as “red urine”, which is especially common among school-aged children in endemic regions. Additional symptoms include painful urination, increased urinary frequency, and recurrent urinary tract infections. Chronic infections can result in urinary bladder fibrosis, ureteral obstruction, hydronephrosis, and kidney damage. Importantly, long-term S. haematobium infection significantly increases the risk of squamous cell carcinoma of the bladder, one of the most serious complications associated with schistosomiasis.
Reproductive health consequences are also notable. Women may develop female genital schistosomiasis (FGS), characterized by lesions in the cervix, vagina, or vulva, which can contribute to infertility, chronic pelvic pain, and increased susceptibility to sexually transmitted infections, including HIV. Men may experience inflammation of the seminal vesicles, prostate, or epididymis, contributing to infertility.
Other Forms
Less common species, such as Schistosoma intercalatum and Schistosoma mekongi, cause other forms of schistosomiasis. These variants may affect the intestines but are geographically limited.
Schistosoma mekongi is found mainly in the Mekong River region and causes symptoms similar to intestinal schistosomiasis. Schistosoma intercalatum is observed in limited West African areas.
The clinical impact and diagnostic methods are similar to more common schistosomiasis types, with praziquantel remaining the treatment choice.
Symptoms and Clinical Manifestations
Schistosomiasis presents with a range of symptoms that vary based on the stage of infection.
Acute Symptoms
Acute schistosomiasis, also known as Katayama syndrome or Katayama fever, typically arises 2–12 weeks after initial infection, particularly in individuals with no previous exposure to the parasite, such as travelers entering endemic areas. The condition reflects a strong immune reaction to migrating immature worms and newly deposited eggs.
One of the earliest signs may be cercarial dermatitis, often called swimmer’s itch, which occurs when infective larvae penetrate the skin. This presents as an itchy, red, localized rash at the point of entry. While usually mild and self-limiting, it signals the start of the infection process.
As the parasites mature and begin migrating through the bloodstream, systemic symptoms develop. These can include:
- Fever and chills
- Fatigue and generalized weakness
- Cough, often due to migration through the lungs
- Muscle and joint aches
- Headache
- Diarrhea or abdominal discomfort
- Lymphadenopathy (swollen lymph nodes)
The immune reaction can also cause transient respiratory symptoms, such as wheezing or shortness of breath, particularly when inflammatory responses occur in lung tissues. In some individuals, especially travelers, symptoms can be severe and may mimic other febrile illnesses, such as malaria or typhoid.
Chronic Manifestations
Chronic schistosomiasis develops over months to years and results primarily from the body’s reaction to egg deposition within tissues. The immune system forms granulomas, clusters of immune cells, around the eggs, which helps limit parasite spread but causes tissue scarring (fibrosis) over time. The organs affected depend on the species of Schistosoma.
Urogenital Schistosomiasis (S. haematobium)
Schistosoma haematobium preferentially inhabits blood vessels of the bladder and urinary tract. Chronic infection produces characteristic symptoms such as:
- Hematuria (blood in urine), often one of the earliest signs
- Dysuria (painful urination)
- Frequent urination and bladder discomfort
Persistent egg deposition can cause bladder wall thickening, fibrosis, and calcification, impairing urinary flow. Over time, this may lead to:
- Obstructive uropathy, including hydronephrosis (kidney swelling)
- Recurrent urinary tract infections
- Reduced kidney function or chronic kidney disease
In longstanding cases, chronic inflammation significantly increases the risk of squamous cell carcinoma of the bladder, making S. haematobium infection the most common parasitic cause of cancer worldwide.
Intestinal Schistosomiasis (S. mansoni, S. japonicum, S. mekongi)
Intestinal forms of the disease affect the intestines and liver, leading to progressive pathology. Common symptoms include:
- Chronic abdominal pain
- Diarrhea, sometimes alternating with constipation
- Blood in the stool
- Loss of appetite (anorexia)
Egg deposition in the liver causes periportal fibrosis, a pattern of scarring that can obstruct blood flow through the portal vein. This leads to:
- Hepatomegaly (enlarged liver)
- Splenomegaly (enlarged spleen)
- Portal hypertension, which may cause: Esophageal varices (enlarged veins prone to bleeding), Ascites (fluid accumulation in the abdomen)
Children in endemic regions often suffer from malnutrition, stunted growth, anemia, and reduced cognitive development, due to a combination of chronic inflammation, nutrient loss, and decreased physical activity related to illness.
Complications
Beyond the urinary and intestinal systems, chronic schistosomiasis can affect multiple organs depending on where eggs migrate or become trapped. Some individuals may present with:
- Pulmonary hypertension, when eggs reach the lungs
- Cardiac complications, including right-sided heart strain
- Neurological involvement, such as: Seizures, Weakness or paralysis, Spinal cord compression, especially with S. japonicum, which produces large numbers of eggs capable of reaching the central nervous system
Systemic symptoms such as fatigue, headaches, and reduced exercise tolerance may reflect widespread inflammation and immune-mediated effects.
If left untreated, schistosomiasis can cause decades-long morbidity and irreversible organ damage. Key long-term outcomes include:
- Chronic kidney disease from obstructed urinary outflow
- Severe liver disease, including advanced fibrosis
- Life-threatening variceal bleeding due to portal hypertension
- Infertility or reproductive complications, including scarring of the cervix, uterus, or fallopian tubes in females and damage to seminal vesicles or prostate in males
- Increased susceptibility to HIV infection, particularly in women with genital schistosomiasis due to mucosal lesions
Diagnosis of Schistosomiasis
Diagnosis of schistosomiasis involves evaluating symptoms, detecting parasite evidence, and assessing organ involvement. Each method provides essential information to confirm infection and determine the disease stage.
Clinical Evaluation
Clinical evaluation focuses on identifying symptoms and exposure history. Patients often report fever, fatigue, abdominal pain, and diarrhea in early infection stages. A key factor is history of freshwater contact in endemic areas.
Physical examination may reveal hepatosplenomegaly or signs of portal hypertension in chronic cases. Skin manifestations like swimmer’s itch can also be present. Accurate clinical assessment guides the need for further diagnostic tests.
Laboratory Testing
Laboratory testing confirms schistosomiasis by detecting parasite eggs or antibodies. Stool and urine microscopy are standard for identifying eggs. S. haematobium eggs appear in urine, while S. mansoni and S. japonicum eggs are found in stool samples.
Serological tests detect antibodies but cannot differentiate past from active infection. Polymerase chain reaction (PCR) assays offer high sensitivity and specificity but are less widely available.
Blood tests may show eosinophilia, especially in the acute phase, supporting the diagnosis but lacking specificity.
Imaging Studies
Imaging identifies organ damage and assists in assessing disease severity. Ultrasound is commonly used to detect liver fibrosis, bladder wall thickening, and kidney abnormalities caused by schistosomiasis.
Computed tomography (CT) and magnetic resonance imaging (MRI) provide detailed visualization of affected organs, particularly the liver and central nervous system. These modalities help evaluate complications like portal hypertension or spinal cord involvement.
Treatment Methods
Pharmacological Therapy
Pharmacological treatment is the cornerstone of schistosomiasis management, with praziquantel serving as the globally recommended first-line medication. Praziquantel is effective against all major human-infecting Schistosoma species—S. haematobium, S. mansoni, S. japonicum, and others, making it the most versatile therapeutic option. Its mechanism of action involves increasing the permeability of the parasite’s tegument (outer surface) to calcium ions, leading to sustained muscle contraction, paralysis, and eventual dislodgement of the worm from host tissues. The damaged worms are subsequently destroyed by the host’s immune system.
The standard treatment dosage for schistosomiasis is 40 mg/kg, administered either as a single dose or divided into two doses within one day. For certain infections, such as those caused by S. japonicum or S. mekongi, doses of 60 mg/kg may be recommended to ensure optimal efficacy. Although praziquantel targets adult worms effectively, it has minimal effect on immature schistosomula, which may lead to persistent infection if treatment is administered too early. In high-transmission regions, clinicians often recommend re-treatment after several weeks to target maturing worms. Patients with heavy worm burdens may require repeated dosing to fully clear the infection, especially when organ involvement is advanced or symptoms are severe.
While praziquantel remains the primary therapeutic agent, alternative drugs have been used in specific contexts. Oxamniquine is effective against S. mansoni but is limited geographically due to cost, availability, and the need for species specificity. Metrifonate, once used for S. haematobium, is largely outdated because of its side effects, lower efficacy, and the dominance of praziquantel-based treatment programs. Despite praziquantel’s excellent safety profile, side effects such as dizziness, abdominal discomfort, fatigue, and headache may occur, particularly in individuals with heavy infections where rapid worm death triggers an inflammatory response.
Supportive Care
Supportive management plays a critical role, particularly in individuals experiencing chronic disease manifestations or complications resulting from long-term parasite-induced inflammation and fibrosis. Chronic intestinal schistosomiasis may lead to anemia due to chronic blood loss, nutritional deficiencies, and impaired absorption; therefore, iron supplementation, dietary support, and treatment of coexisting malnutrition are essential for recovery, especially in children. In patients with hepatic involvement, including periportal fibrosis and early portal hypertension, supportive care focuses on minimizing further liver damage, monitoring liver function, and managing complications such as ascites or splenomegaly.
Advanced hepatosplenic schistosomiasis may require endoscopic or surgical intervention to manage complications like esophageal varices. Endoscopic band ligation, sclerotherapy, and beta-blockers are common strategies for preventing fatal variceal bleeding. In severe urinary schistosomiasis caused by S. haematobium, supportive measures include addressing hematuria, preventing secondary urinary tract infections, and evaluating bladder function. Chronic inflammation of the bladder may increase the risk of squamous cell carcinoma, making long-term follow-up vital in regions with historically high prevalence.
Treatment Challenges
One of the most significant concerns is the potential development of praziquantel resistance, especially in areas with long-standing mass drug administration programs. Although confirmed resistance is rare, reduced efficacy and treatment failures have been documented in some localized settings, urging researchers to explore new drug combinations, vaccine development, and improved diagnostic tools. Continued reliance on a single medication remains a public health vulnerability.
In many endemic regions, individuals return to contaminated freshwater sources immediately after treatment due to limited alternatives for bathing, swimming, farming, fishing, or collecting water. As a result, even highly effective treatment can provide only temporary relief unless accompanied by long-term improvements in water, sanitation, and hygiene (WASH) conditions. This problem is particularly pronounced among school-aged children, who have the highest exposure rates and frequently require repeated treatment throughout their childhood.
Access to healthcare services and medication remains uneven. Rural communities may experience shortages of praziquantel, lack of trained healthcare workers, or inadequate diagnostic facilities, leading to delayed or incomplete treatment. Financial constraints, poor transportation networks, and weak health infrastructure further limit timely care. A major barrier is the large percentage of asymptomatic individuals, who do not seek medical attention and continue to contribute to transmission
Epidemiology and Global Distribution
Prevalence rates of schistosomiasis differ widely between countries and even within regions of the same country. Some areas maintain prevalence levels below 5% due to effective control programs or ecological characteristics that limit snail populations.
Conversely, high-transmission zones, particularly in sub-Saharan Africa, may show prevalence rates exceeding 50% or even 70% in certain communities, especially those located near rivers, irrigation schemes, and fishing areas. These high-burden regions often experience continuous reinfection cycles because exposure to contaminated water is embedded in daily activities such as bathing, farming, and collecting water.
Sub-Saharan Africa accounts for approximately 90% of all schistosomiasis cases worldwide. Schistosoma mansoni and Schistosoma haematobium dominate this region, with overlapping distribution in many countries.
In East Africa and the Horn of Africa, large freshwater bodies such as Lake Victoria and Lake Malawi serve as major transmission hotspots. West and Central African countries also record high endemicity due to extensive river systems and seasonal flooding patterns that support snail proliferation.
Prevention and Control Strategies
Effective management of schistosomiasis requires addressing the parasite’s lifecycle and transmission environment.
Water Sanitation
Access to clean water and effective sanitation systems plays a central role in interrupting the cycle of schistosomiasis transmission. Humans introduce Schistosoma eggs into freshwater when they urinate or defecate in or near lakes, rivers, streams, and irrigation canals. By improving sanitation facilities and reducing contamination of water bodies, communities help break the reproductive cycle of the parasite.
WASH initiatives focus on the construction and proper maintenance of latrines, septic systems, and sewage infrastructure to ensure safe disposal of human waste. Education programs encourage consistent latrine use, discourage open defecation, and promote hygienic behaviors. Water treatment methods, including chlorination, filtration, and safe water storage,help remove or kill harmful organisms, including infectious larval stages of Schistosoma. In areas where piped water systems are not feasible, protected wells, boreholes, rainwater harvesting, and standpipes offer safer alternatives to potentially contaminated surface waters.
Public health campaigns encourage residents to avoid swimming, washing clothes, bathing, or fishing in unsafe water sources, especially during peak snail activity periods. Schools, community groups, and agricultural workers are often targeted for outreach, as they are among the most exposed populations. In regions where avoidance is difficult due to livelihood dependence on freshwater, protective measures such as using footwear, waterproof gloves, or designated safe washing sites can reduce risk.
Snail Control
Snail populations are essential for the Schistosoma life cycle, making snail control an important strategy for reducing transmission. Historically, snail control has played a major role in some of the most successful national elimination programs, including those in Japan, China, and parts of the Caribbean.
Environmental management is a primary approach. Modifying water bodies by improving drainage, lining irrigation canals with concrete, removing slow-moving water zones, reducing aquatic vegetation, and altering shorelines can disrupt snail habitats and breeding sites. These interventions can be particularly effective in agricultural and irrigation-dependent communities.
Chemical molluscicides, such as niclosamide, are used to directly reduce snail populations. Their application requires careful planning to avoid ecological damage, as molluscicides may impact fish and other aquatic organisms. Regular, targeted application is often combined with drug treatment campaigns to ensure long-term reduction in transmission. Despite being effective, molluscicides are typically part of broader strategies rather than stand-alone solutions due to cost, environmental considerations, and the potential for rapid snail repopulation.
Biological control approaches have also been explored. These include introducing natural snail predators such as certain fish, crayfish, or competitor snail species, to suppress populations. While promising, biological control must be implemented cautiously, as introducing non-native species can disrupt ecosystems and lead to unintended consequences.
Long-Term Effects and Prognosis
Schistosomiasis can cause significant lasting health issues, especially if untreated. The disease often leads to ongoing tissue damage and complications affecting various organs. Risk of reinfection remains high in endemic areas, influencing the long-term outlook.
Chronic Health Impacts
Chronic schistosomiasis results from persistent egg deposition in organs such as the liver, intestines, or bladder. This leads to granuloma formation and fibrosis, causing symptoms like portal hypertension, liver cirrhosis, and bladder wall thickening.
In urinary schistosomiasis, prolonged infection can cause hematuria, bladder calcification, and increase risk of squamous cell carcinoma. Intestinal forms may cause abdominal pain, diarrhea, and malnutrition due to chronic inflammation.
Neurological damage can occur if eggs lodge in the spinal cord or brain, causing seizures or paralysis. Without treatment, these complications often worsen, significantly impairing quality of life and increasing mortality risk.
Reinfection Risks
People living in endemic regions face repeated exposure to contaminated freshwater where snails harbor the parasite. Reinfection is common despite treatment because the parasite lifecycle quickly resumes if water contact continues.
Preventive measures such as avoiding freshwater contact, improved sanitation, and snail control are essential but often difficult to implement fully. Multiple rounds of treatment with praziquantel may be necessary to manage reinfections over time.
Reinfection elevates the risk of severe chronic disease manifestations by compounding tissue damage. Monitoring and ongoing public health efforts are critical to reduce the cycle of infection and improve long-term prognosis.