Schistosomiasis (Bilharzia)

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Background

Schistosomiasis is a parasitic disease caused by flukes (trematodes) of the genus Schistosoma. After malaria and intestinal helminthiasis, schistosomiasis is the third most devastating tropical disease in the world, being a major source of morbidity and mortality for developing countries in Africa, South America, the Caribbean, the Middle East, and Asia. (See Epidemiology and Prognosis.)[1]

More than 207 million people, 85% of who live in Africa, are infected with schistosomiasis,[1] and an estimated 700 million people are at risk of infection in 76 countries where the disease is considered endemic, as their agricultural work, domestic chores, and recreational activities expose them to infested water.[1, 2] Globally, 200,000 deaths are attributed to schistosomiasis annually.[3] Transmission is interrupted in some countries.[2] (See Etiology and Epidemiology.)

Sometimes referred to as bilharzias, bilharziasis, or snail fever, schistosomiasis was discovered by Theodore Bilharz, a German surgeon working in Cairo, who first identified the etiological agent Schistosoma hematobium in 1851.[4] A Schistosoma egg is seen below.



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Egg of Schistosoma hematobium, with its typical terminal spine.

Most human schistosomiasis is caused by S haematobium, S mansoni, and S japonicum. Less prevalent species, such as S mekongi and S intercalatum, may also cause systemic human disease. Less importantly, other schistosomes with avian or mammalian primary hosts can cause severe dermatitis in humans (eg, swimmer's itch secondary to Trichobilharzia ocellata). (See Etiology.)

Characteristics of schistosomiasis

Schistosomiasis is due to immunologic reactions to Schistosoma eggs trapped in tissues. Antigens released from the egg stimulate a granulomatous reaction involving T cells, macrophages, and eosinophils that results in clinical disease (see the image below). Symptoms and signs depend on the number and location of eggs trapped in the tissues. Initially, the inflammatory reaction is readily reversible. In the latter stages of the disease, the pathology is associated with collagen deposition and fibrosis, resulting in organ damage that may be only partially reversible. (See Pathophysiology, Etiology, and Presentation.)



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Granuloma in the liver due to Schistosoma mansoni. The S mansoni egg is at the center of the granuloma.

Eggs can end up in the skin, brain, muscle, adrenal glands, and eyes. As the eggs penetrate the urinary system, they can find their way to the female genital region and form granulomas in the uterus, fallopian tube, and ovaries. Central nervous system (CNS) involvement occurs because of embolization of eggs from the portal mesenteric system to the brain and spinal cord via the paravertebral venous plexus.[5, 6, 7]

Snail hosts

The different species of Schistosoma have different types of snails serving as their intermediate hosts; these hosts are as follows[8, 9, 10] :

At-risk populations

Today, 120 million people are symptomatic with schistosomiasis, with 20 million having severe clinical disease.[1] More than 200,000 deaths per year are due to schistosomiasis in sub-Saharan Africa.[11] Women washing clothes in infested water are at risk.[12] Hygiene and playing in mud and water make children vulnerable to infection. Forty million women of childbearing age are infected.[13] Approximately 10 million women in Africa have schistosomiasis during pregnancy.[13] In endemic areas, the infection is usually acquired as a child.[2]

In Brazil and Africa, refugee movements and migration to urban areas are introducing the disease to new locations. Increasing population size and corresponding needs for power and water have led to increased transmission. Infections are not uniformly distributed within communities. It has been estimated that 5-10% of an endemic community may be heavily infected, and the remainder has mild to moderate infections. The risk of infection is highest amongst those who lived near lakes or rivers.[14] In Uganda, almost no transmission was found to have occurred at altitudes greater than 1400 m or where the annual rainfall was less than 900 mm.[14]

With the rise of tourism and travel, an increasing number of tourists are contracting it. Tourists often present with severe acute infection and unusual problems including paralysis.

The intensity and prevalence of infection rises with age and peaks usually between ages 15 and 20 years. In older adults, no significant change is found in the prevalence of disease, but the parasite burden or the intensity decreases.[8, 15, 16] The disease is not endemic in United States.

Complications

Complications of schistosomiasis include the following:

Pathophysiology

Acute schistosomiasis

Acute schistosomiasis (Katayama syndrome) is a systemic, serum sickness-like illness that develops after several weeks in some, but not most, individuals with new schistosomal infections. It may correspond to the first cycle of egg deposition and is associated with marked peripheral eosinophilia and circulating immune complexes. It is most common with S japonicum and S mansoni infections and is most likely to occur in heavily infected individuals after primary infection.

Symptoms usually resolve over several weeks, but the syndrome can be fatal. Early treatment with cidal drugs may exacerbate this syndrome and necessitate concomitant glucocorticoid therapy. Tourists and travelers are most likely to present to emergency departments (EDs) in the United States with this syndrome. A history of the patient’s contact with fresh water, such as through swimming, boating, rafting, or water skiing, should be obtained.

Mild, maculopapular skin lesions may develop in acute infection within hours after exposure to cercariae. Significant dermatitis is rare with the major human schistosomal pathogens, probably because the invading and developing cercariae are minimally immunogenic. However, abortive human infection with schistosomal species that rely on other primary hosts may cause marked dermatitis or swimmer's itch. This self-limited process may recur more intensely with subsequent exposures to the same species.

Chronic schistosomiasis

The pathology of chronic schistosomiasis, which is far more common than the acute form of the infection, results from egg-induced immune response, granuloma formation, and associated fibrotic changes. Although cercarial and adult worms are minimally immunogenic, schistosomal eggs are highly immunogenic and induce vigorous circulating and local immune responses. (Eggs may require an intense immune response to aid their migration through the body.) Adult worms can absorb host proteins. If not attacked by the immune system, they can live for years in the blood stream as they are coated with host antigens.

Egg retention and granuloma formation in the bowel wall (usually S mansoni or S japonicum) may cause bloody diarrhea, cramping, and, eventually, inflammatory colonic polyposis. Patients with heavy bowel wall involvement have an increased rate of recurrent Salmonella infection, generally with positive blood cultures and negative stool cultures. Chronic intestinal schistosomiasis can present with acute complications of appendicitis,[17, 18] perforation, and bleeding long after travel-related (or endemic) exposure. Rectal perforation caused by S haematobium has also been described in a case report.[19]

Eggs can penetrate the bowel adjacent to mesenteric vessels where adult worms are residing. Unshed eggs, which are swept back to the portal circulation, lodge there and induce granulomatous reactions in the portal tracts.

Heavy infestations are more likely to produce hepatic disease. Eventually, severe periportal fibrosis in a characteristic pipestem pattern (Symmers pipestem fibrosis) may occur. Although hepatocellular function is spared, periportal fibrosis can lead to portal hypertension with the usual potential sequelae, including splenomegaly, ascites, esophageal variceal bleeding, and development of portosystemic collaterals. Through these collaterals (or directly from the inferior vena cava in the case of bladder wall schistosomiasis), eggs can reach the pulmonary circulation. The resulting pulmonary granulomatosis and fibrosis can lead to pulmonary hypertension and frank cor pulmonale with a high mortality rate.

In one series, pulmonary hypertension was found in 18.5% of patients with known hepatosplenic schistosomiasis.[20] Co-infection with hepatitis B or hepatitis C can accelerate hepatic dysfunction and raise the risk for hepatocellular carcinoma beyond that seen with hepatitis alone. In addition, gallbladder cancer may be associated with schistosomal infection.

Egg retention and granuloma formation in the urinary tract (S haematobium) can lead to hematuria, dysuria, bladder polyps and ulcers, and even obstructive uropathies. S haematobium infection is also associated with an increased rate of bladder cancer, usually squamous cell rather than transitional cell.[21]

Ectopic egg deposition can lead to additional clinical syndromes, including involvement of skin, lungs, brain, muscles, adrenal glands, genitalia, and eyes. CNS involvement can result in transverse myelitis (best described for S haematobium and S mansoni) and/or cerebral disease (most common with S japonicum infection). Local tissue invasion of eggs brings about the release of toxins and enzymes and provokes a TH-2–mediated immune response.[22]

Etiology

Human beings become infected with schistosomiasis when larval forms of the parasite, released by freshwater snails, penetrate their skin during contact with infested water. In the body, the larvae develop into adult schistosomes. Adult worms live in the blood vessels, where the females release eggs. Some of the eggs are passed out of the body in the feces or urine to continue the parasite life cycle. Others become trapped in body tissues, causing an immune reaction and progressive damage to organs.

Two major forms of schistosomiasis exist: intestinal and urogenital. These are caused by 5 main species, listed in Table 1.

Table 1. Parasitic Species and Geographical Distribution of Schistosomiasis[1, 8]



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See Table

Life cycle

The geographic distribution and etiology of schistosomiasis reflect the unique life cycle of Schistosoma species. Schistosomes infect susceptible freshwater snails in endemic areas, usually with specific species of schistosomes infecting specific species of snails. The infected snails release cercariae 4-6 weeks after infection. The cercariae are fork-tailed, free-swimming larvae approximately 1mm in length. They can survive in fresh water up to 72 hours, during which time they must attach to human skin or to that of another susceptible host mammal or die.

Successful cercariae attach to human hosts, utilizing oral and ventral suckers. They then migrate through intact skin to dermal veins and, over the next several days, to the pulmonary vasculature. During this migration, the cercariae metamorphose, shedding tails and outer glycocalyces while developing double-lipid-bilayer teguments that are highly resistant to host immune responses.

The organisms, now called schistosomula, incorporate host proteins, including major histocompatibility complexes (MHCs) and blood group antigens, into their integuments. Their metabolism shifts to glycolysis. The worms then migrate through the pulmonary capillaries to the systemic circulation, which carries them to the portal veins, where they mature. The adult worms are small, 12-26mm long and 0.3-0.6mm wide, and vary with the different species.

Within the portal vasculature, male and female adults pair off, with the thin female entering and remaining in the gynecophoric canal of the stockier 8mm male worm. Together they migrate along the endothelium, against portal blood flow, to the mesenteric (S mansoni, S japonicum) or vesicular (S haematobium) veins, where they begin to produce eggs.

The microscopic appearance of the egg allows diagnostic differentiation of the 5 species. An adult S haematobium produces 20-200 round, terminally spined eggs per day (see the image below); S mansoni produces 100-300 ovoid, laterally spined eggs per day; and S japonicum produces 500-3500 small, round, laterally spined eggs per day. The eggs of S intercalatum have prominent, terminal spines, and those of S mekongi have small, lateral spines.



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Egg of Schistosoma hematobium, with its typical terminal spine.

The eggs, which are highly antigenic and can induce an intense granulomatous response, migrate through the bowel or bladder wall to be shed via feces or urine. During this time (approximately 10d), the organisms begin to mature into miracidia.

Eggs that are not shed successfully may remain in the tissues or be swept back to the portal circulation (from the mesenteric vessels) or to the pulmonary circulation (from the vesicular vessels via the inferior vena cava). Eggs can end up in the skin, brain, muscle, adrenal glands, and eyes. As the eggs penetrate the urinary system, they can find their way to the female genital region and form granulomas in the uterus, fallopian tube, and ovaries. CNS involvement occurs because of embolization of eggs from the portal mesenteric system to the brain and spinal cord via the paravertebral venous plexus.[5, 6]

The free-swimming miracidia that are shed into fresh water survive 1-3 weeks, during which time they must infect a susceptible snail to complete the life cycle. Within the infected snail, 2 generations of sporocysts multiply, mature into free-swimming cercariae, and exit the snail to seek a human host and begin a new cycle.

In the case of S japonicum, which may be the species with the highest risk of complications, the life cycle may include domesticated animals (eg, cattle) and wild animals (including rodents). This creates a complex and durable reservoir of disease that often thwarts control efforts based on treating human infection and reducing snail populations.

Epidemiology

Occurrence in the United States

Acute and chronic schistosomiasis infections are not common in the United States. Although it is estimated that 400,000 infected persons have immigrated to this country, neither susceptible snail species nor chronically infected human reservoirs sufficient to infest fresh water exist. However, pathogenic schistosomes can survive and replicate in human hosts for years and even decades. Therefore, persons who have traveled or immigrated may present to EDs with active cases of acute or chronic schistosomiasis and/or associated end-organ complications. Most infected patients remain asymptomatic. Acute symptoms are more common in nonimmune travelers. This is because of a severe immune response following exposure.

International occurrence

Globally, schistosomiasis is a major source of morbidity and mortality. The unique schistosomal life cycle limits endemic areas to tropical and subtropical zones, but these areas exist around the world and may even increase with some agricultural practices. Although freshwater lakes and streams are usually identified as the source of the disease, man-made reservoirs and irrigation systems are increasingly implicated in some countries. Indeed, geographic spread continues because of water resource engineering issues in developing countries and the migration of infected populations.

Intestinal schistosomiasis caused by S mansoni occurs in 52 nations, including Caribbean countries (ie, Saint Lucia, Antigua, Montserrat, Martinique, Guadeloupe, Dominican Republic, Puerto Rico), eastern Mediterranean countries, South American countries (ie, Brazil, Venezuela, Surinam), and most countries in Africa.[23]

Other Schistosoma species that can cause intestinal symptoms and diseases include S intercalatum, S japonicum, and S mekongi.S intercalatum is found in 10 countries within the rain forests of central Africa. S japonicum is endemic in 4 countries in the western Pacific region (ie, China, Philippines, Indonesia, Thailand). S mekongi infection occurs in the Mekong River area of Southeast Asia (ie, Kampuchea, Laos, Thailand). Urinary schistosomiasis caused by S haematobium affects 54 countries in Africa and the eastern Mediterranean.

More than 207 million people in at least 74 countries have active schistosomal infection.[24] Of this population, approximately 60% have disease symptoms, including organ-specific complaints and problems related to chronic anemia and malnutrition from the infection; more than 20 million are severely ill. Disease prevalence is heterogeneous in vulnerable locales and tends to be worse in areas with poor sanitation, increased freshwater irrigation usage, and heavy schistosomal infestation of human, animal, and/or snail populations.

However, targeted interventions combining snail control, improved water supply quality, and treatment of infected persons, particularly children, have shown success in diverse endemic areas, including China, Brazil, Egypt, and some areas of sub-Saharan Africa. Interventions based on treating infections annually in humans and domesticated animals while controlling snail populations have decreased disease burden in some areas by an order of magnitude in the last 50 years, but these efforts have plateaued.

A controlled study of enhanced community intervention performed in rural Chinese villages demonstrated significant improvements in human, snail, and wild mouse schistosomiasis infection rates. Along with the preexisting programs for the annual treatment of farmers and cattle, efforts were made to optimize animal grazing sites, sewage management, drinking water supplies, and health education with regard to schistosomiasis.[25, 26]

According to the World Health Organization (WHO), the global distribution of schistosomiasis has changed in that it has been eradicated from Japan and the Lesser Antilles islands; transmission has been stopped in Tunisia; and transmission is very low in Morocco, Saudi Arabia, Venezuela, and Puerto Rico.

Nevertheless, the human cost of schistosomal infections remains high, and the disease contributes to comorbidity with other infections, including hepatitis, human immunodeficiency virus (HIV), and malaria, in endemic regions.[27]

Race-related demographics

The frequency of infection among individuals of specific races is based on the geographic distribution of endemic schistosomiasis in large tropical and subtropical regions of Africa, Asia, the Middle East, and the Caribbean. However, all humans appear equally susceptible if exposed to infested fresh water.

The frequency of some complications appears to vary geographically during infection with the same worm species (eg, ascites is more common in the Middle East than in Brazil).

Sex-related demographics

Schistosomiasis is more common in males, most likely because of increased exposure to infected water via bathing, swimming, and agricultural activities. S haematobium causes genital lesions in 30% of women who are infected. Vulval lesions may increase the risk of HIV transmission.

Age-related demographics

The prevalence and severity of schistosomal infections vary with age. Children and adolescents are infected most often and are infested most heavily. Infection rates and severity may vary with gender-specific activity at all ages. (Congenital infection has been defined; Schistosomiasis has been detected in the placenta and newborns have been diagnosed with the disease, thus confirming congenital infection.[4] )[28]

Globally, infections peak in individuals aged 10-19 years. In some areas, the prevalence in this group may approach 100%.

In persons older than age 19 years living in endemic areas, the prevalence of active infection and egg counts slowly declines. (End-stage complications may persist or worsen.) This decline in active infection may reflect that individuals have an increasing host immune response or a decreasing exposure to contaminated water as they age. Reinfection, particularly after high exposure, is possible.

Age distribution differs somewhat in infected travelers, with young adults most likely to be exposed and infected.

Prognosis

Early disease usually improves with treatment. Surprisingly, patients with hepatic and urinary disease, even with fibrosis, may improve significantly over months or years following therapy. Renal and intestinal pathology also improves with treatment, as, usually, do brain lesions (depending on their location and size).[29]

Hepatosplenic schistosomiasis carries a relatively good prognosis because hepatic function is preserved until the end of the disease (unless variceal bleeding occurs).

Although treatment is indicated for patients with end-stage complications of portal hypertension and severe pulmonary hypertension, these patients are much less likely to benefit from it. Indeed, cor pulmonale usually does not improve significantly with treatment.

Spinal cord schistosomiasis carries a guarded prognosis. Praziquantel should be administered as soon as possible. Praziquantel can safely be given to pregnant and lactating women; it decreases the disease burden and improves pregnancy and fetal outcomes. Programs targeting women during reproductive years will improve their reproductive life and well-being.[30, 29]

Co-infection of schistosomiasis along with hepatitis, HIV, and malaria can raise the risk of hepatocellular carcinoma and increase the risk of mortality.

Patients with heavier worm burdens are less likely to improve and are more likely to require re-treatment.

Morbidity and mortality

Acute schistosomiasis is associated with a mortality rate of up to 25% in some series. Although most individuals with chronic schistosomiasis have few or no symptoms, significant morbidity can develop.

Complaints are difficult to quantitate because of the geographic distribution of this infection in developing nations and the frequency of comorbid conditions such as viral hepatitis. Hepatosplenic disease with portal hypertension is the most common long-term, serious outcome, followed by cardiopulmonary involvement, obstructive nephropathy, bacteremia, and malignancy. Female genital infection can contribute to pregnancy complications, including reports of related ectopic pregnancy. Urogenital schistosomiasis is considered to be a risk factor for HIV infection, especially in women.[1]

End-stage hepatosplenic disease with variceal bleeding, pulmonary hypertension with cor pulmonale, and central nervous system disease are associated with high mortality rates. Carcinoma of the urinary tract, liver, and gallbladder may cause death. Although effective antihelminthic treatment exists, it may not reverse fibrosis and may not be readily available in endemic areas.

Reinfection is extremely common in persons who live in, or return to, endemic areas. Repetitive treatment is necessary to prevent disease progression in this situation.

Acute schistosomiasis (Katayama syndrome)

Tissue migration of schistosomal larvae may cause a hypersensitivity reaction. Any species of Schistosoma can cause it. Although most clinical manifestations are benign, some are severe and may require hospitalization. If acute schistosomiasis is not suspected clinically and treated appropriately, it can result in severe morbidity or death. Nonimmune travelers are especially prone to this disease manifestation. It was found, for example, that after a single exposure to a freshwater pond in Tanzania, 86% of tourists developed acute schistosomiasis. Symptoms include cough, fever, and fatigue.[31] Symptoms usually appear 2-12 weeks after exposure.

Chronic schistosomiasis

Most patients are asymptomatic or mildly symptomatic and do not require medical attention. Only a small proportion of an endemic population harbors a heavy worm burden that later leads to clinical complications.

Gastrointestinal schistosomiasis

The most common complication of GI schistosomiasis is periportal fibrosis, also termed Symmers pipestem fibrosis. This leads to portal hypertension and GI hemorrhage. Liver failure is uncommon, except in persons with concomitant chronic hepatitis or cirrhosis. Among persons with S mansoni, S japonicum, and, possibly, S mekongi, 4-8% develop hepatosplenic disease.[20]

People co-infected with either hepatitis B or C and S mansoni have been shown to have rapid progression of liver disease.

Urinary tract schistosomiasis

This can lead to renal failure due to obstructive uropathy, pyelonephritis, or bladder carcinoma (occurring usually 10-20y after the initial infection). In addition, immune complexes that contain worm antigens may deposit in the glomeruli, leading to glomerulonephritis and amyloidosis.

Female genital schistosomiasis

S haematobium causes lesions in the female lower genital tract (ie, cervix, valva, vagina). Female genital schistosomiasis has been identified as a major social and medical problem that may facilitate the spread of some sexually transmitted diseases, such as HIV and human papillomavirus (HPV).[32]

Coexistence of sexually transmitted infection and urogenital schistosomiasis

One study found that among women with S haematobium infection in Madagascar, 35% may have co-existing sexually transmitted infections, such as Neisseria gonorrhoeae, Chlamydia trachomatis, Mycoplasma genitalium, or Trichomonas vaginalis, as compared with 17% of the men. This is found to be more common in younger populations (aged 15-24 y) than in older populations. The association became stronger with greater parasite burden.[33] Increased HIV replication and cytokine dysregulation occurs when schistosomiasis is present in HIV-positive individuals. In patients on antiretroviral treatment, immune restoration syndrome has been described with symptomatic schistosomiasis.

Pulmonary arterial hypertension in schistosomiasis

This is an important complication that develops in about 7.7% of patients with hepatosplenic disease in S mansoni, S japonicum, and possibly S mekongi infections.[20] The prevalence of the disease worldwide is estimated to exceed 270,000 individuals.[20]

CNS schistosomiasis

Because of its smaller egg size, S japonicum causes 60% of all Schistosoma brain infections,[34] with CNS involvement occurring in 2-4% of all S japonicum infections. One million people in China are estimated to be infected with S japonicum.[35] Nodular, enhancing cerebellar lesions can occur as well with this species.[35]

However, CNS schistosomiasis can also occur with other species. Spinal schistosomiasis usually presents as transverse myelitis and is primarily due to S mansoni infection because of the larger egg size.[34] S haematobium can infect the brain or spinal cord.[34]

The distribution of S mekongi is limited to the Mekong River basin in Laos and Cambodia, where some 140,000 people are estimated to be at risk for this infection. Temporal mass causing paraesthesias of the arm and leg with dysphasia has been described with S mekongi infection.[6] Neurologic symptoms can develop months after the infection. Cauda equina syndrome, anterior spinal artery syndrome, and quadriparesis can occur. Most of the lower spinal cord is affected.[34]

Schistosomiasis in pregnancy

This has been associated with anemia and low birth weight.[13]

History

Acute manifestations

Individuals who have been exposed to fresh or salt water may develop a pruritic rash due to cercarial dermatitis (also called swimmer's itch). This has been described in North America as occurring via nonhuman avian schistosomes.

Patients with acute schistosomiasis (Katayama fever) present usually 4-8 weeks after contact with infested water. It occurs 2-8 weeks after exposure to S japonicum or S mansoni. Katayama fever is common in heavily infested areas where there is S japonicum. Wading and swimming in fresh water in tropical regions causes schistosomal trematodes to enter the body. Fever, lethargy, malaise, and myalgia are the most common symptoms of Katayama syndrome. Less common symptoms include cough, headache, anorexia, and rash (urticarial or papular). Right upper quadrant pain and bloody diarrhea may also occur.[36]

These symptoms mimic any acute viral, bacterial, or malarial illness. The distinguishing features from malaria include generalized urticaria, pruritic rash at the site of cercarial penetration (often the legs), eosinophilia, and lymphadenopathy. Consequently, acute illness is often missed unless schistosomiasis is suspected.

In acute schistosomiasis, patients may present with focal neurological deficits.

Obtaining a careful travel history, including drinking water sources and recreational activities, is important. Symptoms are likely secondary to immune complex formation following egg deposition in tissues; the illness resembles serum sickness.

Chronic manifestations

Patients with symptomatic chronic schistosomiasis may present months to years after primary exposure. A complete lifelong travel history is often essential for diagnosis. Many patients do not have a clear history of acute schistosomiasis and many individuals have few or mild symptoms. Individuals with symptoms may present with nonspecific complaints reflecting their level of infection, the immune response to the eggs, the primary location of egg production for the schistosomal species involved (eg, mesenteric, bladder wall), the extent of hepatosplenic involvement, the extent of cardiopulmonary involvement, and the presence of ectopic sites (eg, CNS). Typically, disease onset is insidious.

S mansoni, S mekongi, S intercalatum, and S japonicum cause intestinal tract and liver disease. S haematobium only rarely causes intestinal or liver disease but characteristically causes urinary tract disease.[37] S hematobium can also cause genital involvement. In men, schistosomiasis can cause involvement of the epididymis, spermatic cord, testicles, and prostate.

In the early stage of hepatic schistosomiasis, dyspepsia, flatulence, and pain are present in the left hypochondrium due to spleen enlargement. Anemia or cor pulmonale may cause generalized pain, weakness, and shortness of breath. In the later stages, abdominal distention, lower limb edema, hematemesis, and melena can occur. Symptoms of liver failure are rare unless other infectious, toxic, or malignant causes of hepatitis are present.[38]

In patients with intestinal schistosomiasis, the following symptoms may occur:

In patients with urinary schistosomiasis, the following symptoms may occur:

Cardiopulmonary schistosomiasis may cause larval pneumonitis with a cough, mild wheezing, and a low-grade fever, while in schistosomal cor pulmonale, easy fatigability, palpitations, dyspnea on exertion, and hemoptysis are present.

CNS schistosomiasis causes the following:

Dizziness, nausea, and increased intracranial pressure can occur with cerebellar schistosomiasis.[35] Visual scintillation from occipital mass has been described.[39]

Female genital schistosomiasis can involve the following symptoms:

Physical Examination

Physical findings vary with the stage of illness, worm burden, worm location, and end-organ involvement.

Findings with acute schistosomiasis may include the following:

Findings with chronic schistosomiasis may include the following:

Approach Considerations

Blood tests are occasionally useful in supporting the diagnosis or assessing the severity of schistosomal infection. Serologies and polymerase chain reaction (PCR) assay–based testing can confirm a diagnosis.[40, 41] Considerations in laboratory testing include the following:

Acute illness is often associated with eosinophilia in the blood and tissues. With chronic illness, peripheral eosinophilia may be minimal or absent, while tissue eosinophilia persists.

Urinary and fecal microbiology

Urinary microbiology is key when diagnosing vesicular infection from S haematobium. Gross and microscopic hematuria is common. Concentration methods may be necessary, and a rough determination of egg load can be obtained. However, this should not be used as a firm measure of disease severity, as egg counts can vary markedly between specimens in a single patient.

Fecal microbiology, usually on thick smears, is essential when diagnosing schistosomiasis with primary bowel infection. Stool specimens may be positive for heme or grossly bloody. Concentration methods will be needed to identify light infestations. Rough quantitation can also be performed in these specimens with the same limitation as above.

In an experienced lab, morphologic details and staining can identify single and mixed schistosomal species in an infected individual.

PCR assay

Using patient urine samples, polymerase chain reaction (PCR) assay was 94.4% sensitive and 99.9% specific for the diagnosis of schistosomiasis.[40] PCR can detect and quantify schistosome deoxyribonucleic acid (DNA) in stool or urine.[42]

Stool or Urinary Analysis

Identify and speciate the eggs in the stool or urine. Quantification of the egg excretion is calculated by collecting 24-hour urine or stool, homogenizing the sample, and counting the eggs in a measured sample. Urine or stool egg count in a 24-hour collection quantitates the severity of the infection. (However, urinary excretion of eggs is not uniform. The urine is most likely to be positive for S hematobium from 10 am until 2 pm.[43] )

Fewer than 100 eggs per gram of stool or 10mL of urine indicates a light infection; 100-400 eggs per gram of stool or 10mL of urine indicates a moderate infection, and more than 400 eggs per gram of stool or 10mL of urine indicates a heavy infection.

Determination of the intensity of infection is an important tool in endemic areas, as many of the complications of schistosomiasis are related to the parasite burden. Intensity determination is made via quantitative sampling of 20-50g of stool (Kato-Katz technique) or a standardized volume of urine through a Nuclepore membrane.[44]

Egg Viability Test

This test is important for assessing the effectiveness of treatment. Because persons with inactive infection may continue to shed dead eggs into stool and urine for months, tests for egg viability, such as egg hatching or microscopic examination of eggs for the movement of flame cells, should be performed.

Viability testing requires mixing the stools or urine with room-temperature distilled water and observing for hatching miracidia. An active infection produces viable eggs, while treated or past infection results in nonviable eggs and an absence of miracidia.

Urinary Schistosomiasis

The following tests are performed in the diagnosis of urinary schistosomiasis:

Intestinal and Liver Schistosomiasis

Points to consider in testing for intestinal and liver schistosomiasis include the following:

Liver function test results usually are within the reference range until the end stage of disease. Mild elevation of alkaline phosphatase and gamma-glutamyl transferase levels may occur. If liver function test results are abnormal, look for other co-infections or diseases.

Serology

Antibody testing is epidemiologically useful but cannot be used to differentiate active and past illness. It also does not allow quantification of egg burden.

Serologic findings can be used to reach a diagnosis in a patient from a nonendemic area, because a negative antibody test result would be expected.

Detection of antibodies to S mansoni, S haematobium, and S japonicum adult worm microsomal antigens (ie, mansoni adult worm microsomal antigen [MAMA], haematobium adult worm microsomal antigen [HAMA], japonicum adult worm microsomal antigen [JAMA]) has been reported to be highly specific for all 3 species when the Falcon assay screening test (FAST), enzyme-linked immunoassay (ELISA), and immunoblot assays have been used.[45]

The sensitivity and specificity of ELISA tests currently in use are generally reported to be greater than 90% and 95%, respectively. Western blot tests are often used to confirm ELISA results.[46]

Antibody tests are generally negative during the acute presentation of Katayama syndrome, although serology often becomes positive before eggs become detectable. Seroconversion generally occurs 4-8 weeks after infection.

Antigen Tests

Because these tests measure parasite antigen as opposed to host antibody response, they reflect active infection. The tests are still investigational. With effective treatment, a reduction in antigenemia is expected.

The 2 proteoglycan, gut-associated antigens that appear most promising are circulating anodic antigen (CAA) and circulating cathodic antigen (CCA). These antigens can be found in urine or serum.[47]

Studies are underway to evaluate the sensitivity and specificity of these investigational antigen tests. A reagent strip using monoclonal antibodies to detect somatic schistosome antigens in urine has a sensitivity of more than 85% and is suitable for use in the field.[48]

Antigen titers also correlate well with the determination of infection intensity by egg counts and with clinical severity of disease.[49]

Antigen titers can be used to assess treatment efficacy posttherapy, since loss of circulating antigens indicates cure. Antigen tests may become negative as early as 5 to 10 days posttreatment.[47]

Imaging Studies

Ultrasonography (US) is a sensitive means of assessing hepatosplenic disease with periportal fibrosis or urinary obstruction. It can demonstrate periportal fibrosis, splenomegaly, portal collaterals, periportal adenopathy, ureteral obstruction, and obstructive nephropathy.

Echocardiography and/or invasive hemodynamic studies can demonstrate pulmonary hypertension and cor pulmonale, if present.[20]

Chest radiographs may show patchy infiltrates in acute schistosomiasis and can indicate pulmonary hypertension and cor pulmonale in end-stage chronic infection, if present.

Computed tomography (CT) or magnetic resonance imaging (MRI) scanning may be useful in the evaluation of CNS disease or in the detection of periportal fibrosis.

Acute schistosomiasis

With acute schistosomiasis, a chest radiograph sometimes demonstrates a generalized increase in vascular and interstitial marking and mild lymphadenopathy.

Urinary schistosomiasis

Imaging tests for urinary schistosomiasis can include the following:

Liver and intestinal schistosomiasis

Imaging tests for liver and intestinal schistosomiasis can include the following:

Lung schistosomiasis

Imaging tests for lung schistosomiasis include the following:

CNS schistosomiasis

A CT or MRI scan of the brain and spinal cord may show lesions in CNS schistosomiasis. Nodular and ring-enhancing lesions with surrounding edema are seem on CT and MRI brain scans. Eggs reach the lower spinal cord through the Batson plexus with S haematobium and S mansoni infection. These produce granulomatous lesions of the cauda equine and conus medullaris.

Biopsy and Other Procedures

Biopsy is helpful when stool sample findings are negative or in light infection. Mucosal biopsy is effective for visualizing eggs. Obtain multiple biopsy samples and crush them between slides to increase egg-detecting sensitivity. In one study, 61% of patients had eggs detected on rectal biopsy, whereas only 39% of patients had ova detected in stool.[51]

Liver biopsy has also been used for egg detection and may be appropriate in patients with unclear diagnoses or suspected co-infections.

Procedures used in the diagnosis of schistosomiasis include the following:

Approach Considerations

Prehospital care should include treating acute complications, such as acute intestinal bleeding. Stabilize patients who have acute complications. If appropriate, include schistosomiasis as one of the differential diagnoses.

Send urine or stool samples to the parasitology laboratory with a special request to look for eggs indicative of schistosomiasis.

Patients with severe complications, such as GI bleeding, GI obstruction, renal failure, cardiac failure, bacteremia due to Salmonella, and CNS complications, need inpatient care.

Acute schistosomiasis and Katayama fever

Patients should receive antischistosomal drugs and corticosteroids, especially if acutely ill. Steroids reduce inflammation and help suppress changes that result from killing of the parasites. As maturing schistosomes are less susceptible to therapy than adult worms, a second course of treatment is necessary. This is given several weeks after the first course of therapy.

The drug of choice for treating all species of schistosomes is praziquantel. Cure rates of 65-90% have been described after a single treatment with praziquantel. In individuals not cured, the drug causes egg excretion to be reduced by 90%.[55] Praziquantel affects the membrane permeability of the parasite, which causes vacuolation of the tegument. It paralyses the worm and exposes it to attack by the host immune system. However, as praziquantel is ineffective on developing schistosomula, it may not abort early infection. Praziquantel can be used in pregnant and lactating women.[56] Resistance to praziquantel occurs in the field and is well defined.[57, 58] Adverse effects include dizziness, headache, nausea, vomiting, diarrhea, abdominal discomfort, bloody stool, urticaria, and fever following initiation of treatment. These are usually mild and last about 24 hours. These are reactions from dying worms.

Neurologic disease

Treatment of schistosomiasis affecting the CNS consists of praziquantel with glucocorticoids. In CNS disease, corticosteroids are used to reduce inflammation and edema around eggs. If patients present with seizures, anticonvulsant therapy may also be needed. Observe patients with suspected or known cysticercosis as they may develop seizures or neurologic effects from dying cysticerci.

Surgical care

Surgical care includes removal of tumor masses, ligation of esophageal varices, and porta-caval shunt surgeries. Large granulomas in urinary bladder or lungs may warrant surgical extirpation.

Consultations

Appropriate consultations depend on the suspected complications but may include an infectious disease physician, urologist, gynecologist, or gastroenterologist.

Corticosteroids

The symptoms of Katayama syndrome often require administration of corticosteroids to suppress the inflammatory process, but no consensus exists regarding proper antihelminthic treatment. Prednisolone 40mg daily for 5 days can be used for the hypersensitivity reaction. Treatment is essentially supportive.

Persons with CNS involvement should be given corticosteroids to prevent inflammation and edema around eggs. Repeated courses of corticosteroid therapy may be warranted to suppress recrudescent neurologic symptoms.

Outpatient Care

Response to treatment is evaluated by counting the amount of decrease in egg excretion. In the initial 2 weeks after treatment, the egg count may not decrease, because eggs laid before the treatment require 2 weeks to be shed. Viable eggs can be excreted for 6-8 weeks after treatment.

When measured 5-10 days after treatment, newer tests that measure antigens may help to assess therapeutic response. Persistent circulating antigen and the excretion of eggs indicate residual infection. These patients should be retreated with praziquantel.

Follow-up

Antischistosomal drugs inhibit egg-laying by adult worms. Therefore, patients’ stool and urine should be tested for 6 months after treatment. Treatment is repeated for those excreting eggs. If symptoms recur, hematuria occurs, or eosinophilia is noted, repeat parasite investigation should be performed. However, serology can remain positive for years.

Pregnancy

Schistosomiasis affects the uterine environment during pregnancy. These pregnant women develop severe anemia, have low ̶ birth-weight infants, and are at increased risk for infant and maternal mortality. Schistosomiasis has been found in placenta, and newborns have been diagnosed with this condition, thus confirming congenital infection.[4] Infected pregnant women have a higher rate of spontaneous abortions and a higher risk for ectopic pregnancies. In addition, increased pelvic blood flow during pregnancy is thought to increase the infection load. WHO recommends giving praziquantel to pregnant and lactating women to decrease the disease burden and improve the pregnancy and fetal outcomes.[30]

A retrospective study of 88 women with schistosomiasis who received praziquantel during pregnancy, in a mass treatment campaign, did not show an increase in the rate of abortion, preterm deliveries, or congenital abnormalities compared with untreated women.[59]

Starting treatment after the first trimester may be advisable.[60] Praziquantel is excreted in human breast milk. No adverse effects of praziquantel administration during lactation have been reported.[60, 61]

Deterrence and Prevention

No vaccine or prophylactic chemotherapy for schistosomiasis is currently available. However, clinical trials involving human volunteers are underway to develop an effective vaccine against schistosomiasis. Moreover, clinical studies show that artemether may be used as a prophylactic agent if given once every 2-4 weeks.[62]

Travelers to endemic areas should avoid contact with fresh water. Suspect acute schistosomiasis in a setting of recent contact with fresh water and treat early if diagnostic test results are positive or clinical suspicion is high. Early treatment after high-risk exposures should minimize morbidity.

People returning from endemic areas with history of exposure to fresh water should be screened by serologic testing for schistosomiasis. Many infections are silent and may remain asymptomatic. Urine and stool screening should be obtained in patients with positive serologies for species identification.[60] Rates of schistosomiasis seropositivity have been recorded as 44% and 23% in African refugees.[63]

Topical lipid formulations of N,N-diethyl-m-toluamide (DEET), such as LipoDEET, are effective in killing schistosome cercariae. Minimal absorption, low cost, and a range of activity against insects and schistosomes make this compound an excellent prophylactic agent against human and animal schistosomiasis, especially for travelers.[64]

Endemic regions

Controlling schistosomiasis in an endemic area should include the following:

Medication Summary

The aim of chemotherapy is 2-fold. The first goal is to cure the disease or at least minimize morbidity. The second goal is to control transmission of the parasite in the endemic areas. Praziquantel and oxamniquine (no longer available in the United States) are used commonly, but praziquantel is the treatment of choice for all species of schistosomiasis. Clinical studies show that artemether, which is used as antimalarial treatment, is also active against all 3 major schistosome parasites (mainly schistosomula).[62]

In addition, the combination of artemether and praziquantel can kill schistosomula during the first 3 weeks of infection and is synergistic with praziquantel in killing adult worms.[66] The high efficacy of mefloquine-artesunate against S haematobium warrants further investigation. Individuals co-infected with Plasmodium and Schistosoma who are treated with a mefloquine-artesunate combination against malaria may experience a dual benefit: clearance of malaria parasitemia and reduction of schistosomiasis-related morbidity.[67]

Praziquantel (Biltricide)

Clinical Context:  Praziquantel is usually well tolerated. It is used for the treatment of individual patients and for mass community treatment programs. The drug's mechanism of action is complex; it induces ultrastructural changes resulting in increased permeability to calcium ions. Calcium ions accumulate in the parasite cytosol, leading to muscle contractions and ultimate paralysis of adult worms. The worm's tegument membrane (the natural covering of the worm body) is damaged, exposing the worm to the patient's immune response, which leads to worm death. The cure rate with praziquantel is 85% or greater. In persons not cured, the egg burden is markedly decreased.

Oxamniquine (Vansil)

Clinical Context:  Oxamniquine is no longer available in the United States. Its mechanism of action is complex. The drug is metabolized into an ester by schistosomes. It damages the tegument of male schistosome worms so that the patient's immune system is able to kill the organisms. It also stops female worms from producing eggs. Oxamniquine is effective only against S mansoni. The cure rate with the drug is 60-90%.

Class Summary

Parasite biochemical pathways are sufficiently different from the human host to allow selective interference by chemotherapeutic agents in relatively small doses.

What is schistosomiasis (bilharzia) and how common is it?How was schistosomiasis (bilharzia) discovered?What causes schistosomiasis (bilharzia)?What is the pathophysiology of schistosomiasis (bilharzia)?What are the intermediate hosts of Schistosoma?Which populations are at risk for schistosomiasis (bilharzia)?Which age groups are likely to be infected with schistosomiasis (bilharzia)?What are the possible complications of schistosomiasis (bilharzia)?What is acute schistosomiasis (Katayama syndrome)?What is the prognosis of acute schistosomiasis (Katayama syndrome)?What are the symptoms of schistosomiasis (bilharzia)?What is the pathogenesis of chronic schistosomiasis (bilharzia)?What is the disease progression of chronic schistosomiasis (bilharzia)?What is the role of periportal fibrosis in the pathophysiology of chronic schistosomiasis (bilharzia)?What is the prevalence of pulmonary hypertension in schistosomiasis (bilharzia)?What are the possible complications of S haematobium schistosomiasis (bilharzia)?What is the role of ectopic egg deposition in the pathogenesis of schistosomiasis (bilharzia)?How is schistosomiasis transmitted?What are the major forms of schistosomiasis (bilharzia)?What is the life cycle of Schistosoma species?How do Schistosoma species migrate through the body?What is the role of histocompatibility complexes and blood group antigens in the pathophysiology of schistosomiasis (bilharzia)?What is the microscopic appearance of Schistosoma species eggs in the human body?How do Schistosoma species infect a snail host?What is the life cycle of Schistosoma japonicum?What is the prevalence of schistosomiasis (bilharzia) in the US?What is the global prevalence of schistosomiasis (bilharzia)?What is the geographical distribution of Schistosoma species?What is the global prevalence of active schistosomiasis (bilharzia) infection?What is the efficacy of enhanced community intervention for reducing the incidence of schistosomiasis (bilharzia)?How does the incidence of schistosomiasis (bilharzia) vary by race?How does the incidence of schistosomiasis (bilharzia) vary by sex?How does the prevalence and severity of schistosomiasis (bilharzia) vary by age?What is the prognosis of schistosomiasis (bilharzia)?What is the prognosis of hepatosplenic schistosomiasis?What is the prognosis of patients with end-stage complications of hepatosplenic schistosomiasis?What is the prognosis of spinal cord schistosomiasis (bilharzia)?What may increase the risk of mortality in schistosomiasis (bilharzia)?Which patients with schistosomiasis (bilharzia) have a poor prognosis?What is the mortality rate of acute schistosomiasis (Katayama syndrome)?What are the possible complications of schistosomiasis (bilharzia)?Which factors increase the mortality rate of schistosomiasis (bilharzia)?Which factors increase the risk of schistosomiasis (bilharzia) reinfection?What are the symptoms of acute schistosomiasis (Katayama syndrome)?What are the symptoms of chronic schistosomiasis (bilharzia)?What complications may occur in GI schistosomiasis?What are the possible complications of urinary tract schistosomiasis?What are the possible complications of genital schistosomiasis in females?What is the prevalence of comorbid sexually transmitted diseases and urogenital schistosomiasis?What is the prevalence of pulmonary arterial hypertension in schistosomiasis (bilharzia)?What is the prevalence of CNS schistosomiasis?What are the complications of schistosomiasis (bilharzia) during pregnancy?What are acute manifestations of schistosomiasis (Katayama syndrome)?How is acute schistosomiasis (Katayama syndrome) differentiated from malaria?What should be the focus of the history in suspected acute schistosomiasis (Katayama syndrome)?What history is needed to diagnose suspected chronic schistosomiasis (bilharzia)?What are the possible manifestations of chronic schistosomiasis?What are the signs and symptoms of hepatic schistosomiasis?What are the symptoms of intestinal schistosomiasis?What are the symptoms of urinary schistosomiasis?What are the symptoms of cardiopulmonary schistosomiasis?What are the symptoms of CNS schistosomiasis?What are the symptoms of cerebellar schistosomiasis?What are the symptoms of female genital schistosomiasis?What factors affect the variance of physical findings in schistosomiasis (bilharzia)?Which physical findings suggest acute schistosomiasis (Katayama syndrome)?Which physical findings suggest chronic schistosomiasis (bilharzia)?Which differential diagnoses might be suggested by hematuria in the evaluation of schistosomiasis (bilharzia)?Which differential diagnoses might be suggested by intestinal and liver symptoms in the evaluation of schistosomiasis (bilharzia)?Which differential diagnoses might be suggested by seizures and focal neurologic symptoms in the evaluation of schistosomiasis (bilharzia)?What conditions should be considered in the differential diagnoses of schistosomiasis (bilharzia)?What are the differential diagnoses for Schistosomiasis (Bilharzia)?What is the role of lab testing in the diagnosis of schistosomiasis (bilharzia)?What does a finding of eosinophilia indicate in the workup of schistosomiasis (bilharzia)?What is the role of urinary microbiology in the diagnosis of schistosomiasis (bilharzia)?What is the role of fecal microbiology in the diagnosis of schistosomiasis (bilharzia)?How are single and mixed schistosomiasis (bilharzia) species identified?What is the role of polymerase chain reaction (PCR) assay in the diagnosis of schistosomiasis (bilharzia)?How is a stool or urinary analysis performed in the evaluation of schistosomiasis (bilharzia)?How is the intensity of infection determined in the evaluation of schistosomiasis (bilharzia)?What is the role of an egg viability test in the diagnosis of schistosomiasis (bilharzia)?How is viability testing performed for schistosomiasis (bilharzia)?How is urinary schistosomiasis (bilharzia) diagnosed?How is intestinal and liver schistosomiasis (bilharzia) diagnosed?What are the limitations of antibody testing in the diagnosis of schistosomiasis (bilharzia)?What is the role of serologic testing in the diagnosis of schistosomiasis (bilharzia)?What is the sensitivity and specificity of ELISA tests in the diagnosis schistosomiasis (bilharzia)?What are expected antibody test results during acute schistosomiasis (Katayama syndrome)?What is the role of antigen tests in the diagnosis of schistosomiasis (bilharzia)?Which antigen tests appear most promising for in diagnosing schistosomiasis (bilharzia)?What could antigen titers reveal in the evaluation of schistosomiasis (bilharzia)?What is the role of ultrasonography (US) in the diagnosis of schistosomiasis (bilharzia)?What is the role of cardiovascular testing in the diagnosis of schistosomiasis (bilharzia)?What is the role of chest radiography in the diagnosis of schistosomiasis (bilharzia)?What is the role of CT scanning and MRI in the diagnosis of schistosomiasis (bilharzia)?Which chest radiograph findings suggest acute schistosomiasis (Katayama syndrome)?What is the role of imaging studies in the diagnosis of urinary schistosomiasis?What is the role of imaging tests in the diagnosis of liver and intestinal schistosomiasis?What is the role of imaging tests in the diagnosis of lung schistosomiasis?What is the role of imaging studies in the diagnosis of CNS schistosomiasis?What is the role of biopsy in the diagnosis of schistosomiasis (bilharzia)?Which procedures are used in the diagnosis of schistosomiasis (bilharzia)?What is prehospital care for schistosomiasis (bilharzia)?How should urine or stool samples be evaluated for schistosomiasis (bilharzia)?When is inpatient care indicated for treatment of schistosomiasis (bilharzia)?What is the treatment for acute schistosomiasis (Katayama syndrome)?What is the role of praziquantel in the treatment of acute schistosomiasis (Katayama syndrome)?What is the treatment for CNS schistosomiasis?What are the surgical options for schistosomiasis (bilharzia)?Which specialist consultations are needed for the treatment of schistosomiasis (bilharzia)?What is the indication for corticosteroids in the treatment of schistosomiasis (bilharzia)?How is response to treatment evaluated in schistosomiasis (bilharzia)?What monitoring is needed following treatment of schistosomiasis (bilharzia)?How does schistosomiasis (bilharzia) affect pregnancy?What is the efficacy of treatment for schistosomiasis (bilharzia) during pregnancy?Is a vaccine available for schistosomiasis (bilharzia)?How can schistosomiasis (bilharzia) be prevented?How is schistosomiasis (bilharzia) controlled in an endemic area?What are the goals of drug treatment in schistosomiasis (bilharzia), and what is the medication of choice?Which medications in the drug class Anthelmintics are used in the treatment of Schistosomiasis (Bilharzia)?

Author

Shadab Hussain Ahmed, MD, AAHIVS, FACP, FIDSA, Professor of Clinical Medicine, The School of Medicine at Stony Brook University Medical Center; Adjunct Clinical Associate Professor, Department of Medicine, New York College of Osteopathic Medicine of New York Institute of Technology; Attending Physician, Department of Medicine, Division of Infectious Diseases, Director of HIV Prevention Services, Administrative HIV Designee, Nassau University Medical Center

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD, David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America; Fellow of the Royal College of Physicians, London

Disclosure: Nothing to disclose.

Acknowledgements

Joseph F John Jr, MD, FACP, FIDSA, FSHEA Clinical Professor of Medicine, Molecular Genetics and Microbiology, Medical University of South Carolina; Associate Chief of Staff for Education, Ralph H Johnson Veterans Affairs Medical Center

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

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Egg of Schistosoma hematobium, with its typical terminal spine.

Granuloma in the liver due to Schistosoma mansoni. The S mansoni egg is at the center of the granuloma.

Egg of Schistosoma hematobium, with its typical terminal spine.

Egg of Schistosoma hematobium, with its typical terminal spine.

Granuloma in the liver due to Schistosoma mansoni. The S mansoni egg is at the center of the granuloma.

Species Geographical distribution
Intestinal schistosomiasis Schistosoma mansoni



(mesenteric venules of the colon)



Africa, the Middle East, the Caribbean, and South America
Schistosoma japonicum



(mesenteric venules of the small intestine)



Asia only: China, Indonesia, the Philippines, and Thailand
Schistosoma mekongi



(mesenteric venules of the small intestine)



Several districts of Cambodia and the Lao People’s Democratic Republic. 200-km area of Mekong river basin; now extending toward northern provinces
Schistosoma intercalatum



(mesenteric venules of the colon) and related S guineensis



Rain forest areas of Central and West Africa
Urogenital schistosomiasis Schistosoma haematobium



(vesical venous plexus)



Africa, the Middle East, India, and Turkey