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Schistosomiasis: Epidemiology and clinical manifestations

Schistosomiasis: Epidemiology and clinical manifestations
Literature review current through: Jan 2024.
This topic last updated: May 31, 2023.

INTRODUCTION — Schistosomiasis is a disease caused by infection with parasitic blood flukes. It is also known as "bilharziasis" after Theodor Bilharz, who first identified the parasite in 1852.

The parasites that cause schistosomiasis live in certain types of freshwater snails. Emergence of cercariae (the infectious form of the parasite) from the snail leads to contamination of the water. Individuals can become infected when skin comes in contact with contaminated water and is penetrated by cercariae.

The epidemiology, pathogenesis, and clinical features of schistosomiasis will be reviewed here. The diagnosis, treatment, and prevention of schistosomiasis are discussed separately. (See "Schistosomiasis: Diagnosis" and "Schistosomiasis: Treatment and prevention".)

MICROBIOLOGY AND PHYLOGENY — Seven schistosome species can cause infection in humans. The three major species are Schistosoma mansoni (Africa and South America), Schistosoma haematobium (Africa and Middle East), and Schistosoma japonicum (East Asia). In general, S. mansoni and S. japonicum cause intestinal tract disease, while S. haematobium causes genitourinary tract disease. The four minor species are Schistosoma mekongi (Laos, Cambodia), the closely related Schistosoma malayensis, and the rare Schistosoma intercalatum and Schistosoma guineensis (West and Central Africa). Phylogenetically, the latter two are closely related to S. haematobium [1]. All four are tropic for the intestines and liver. S. mansoni infection occurs primarily among humans as well as some primates. S. japonicum, S. mekongi, and S. intercalatum are primarily zoonotic species with a broad spectrum of mammalian hosts [2]. Mixed infection has been observed among humans in some regions, predominantly with S. mansoni and S. haematobium [3,4].

Hybridization and introgressive gene transfer among phylogenetically related mammalian schistosome species occurs occasionally in areas where distinctive species and susceptible snail hosts coexist. As an example, hybrid species of S. haematobium with Schistosoma bovis or Schistosoma curassoni (related schistosome species with intestinal tropism infecting cattle) have been identified among humans in northern Senegal and Mali [5-8], and hybrids of S. haematobium and Schistosoma mattheei, a species found in cattle, have been reported in South Africa, both in autochthonous populations and in travelers [9,10]. Hybridization between S. haematobium and S. guineensis has changed the epidemiology of human schistosomiasis in coastal Cameroon [11].

EPIDEMIOLOGY

Geographic distribution — The prevalence of schistosomiasis is highest in sub-Saharan Africa. Worldwide, it has been estimated that more than 200 million people are infected [12,13], with considerable morbidity and mortality [14,15].

The geography of schistosomiasis affecting humans is as follows [16-19]:

S. mansoni occurs in most of sub-Saharan Africa, the western part of South America (mainly Brazil), and some of the South Caribbean islands.

S. haematobium infection occurs in foci throughout sub-Saharan Africa, the Middle East along the Tigris and Euphrates, and southern parts of the Arabian Peninsula.

S. japonicum occurs along the Yangtze River Basin in China, the southern and eastern islands of the Philippines, and in pockets in central Sulawesi, Indonesia.

S. intercalatum and S. guineensis occur in limited foci in the Congo, Gabon, and Cameroon in Central Africa.

S. mekongi occurs in the Mekong River Basin (and tributaries) in Laos and Cambodia, and its closely related species S. malayensis is endemic in peninsular Malaysia.

Infection tends to occur in rural areas; urban areas usually lack the freshwater conditions needed for the snail intermediate host to thrive [20]. Wet rice culture is an important source of exposure in East Asia, where the water buffalo acts as an important zoonotic reservoir, and parts of West Africa. In Africa, schistosomiasis is limited to altitudes <1800 m because a minimum water temperature is required to complete the parasite cycle in the snail intermediate host. An outbreak of acute infection was reported after a brief exposure to a high-altitude (1630 m) crater lake in Uganda [21].

Children acquire the infection by bathing in freshwater ponds, lakes, and rivers contaminated with cercarial larvae. Among children in endemic areas, worm burden increases gradually and culminates during adolescence [22,23]. Most individuals have a mild to moderate parasite load with limited morbidity [24,25]; heavy infection with significant consequence for disease occurs among relatively few individuals in a population [26].

Infection can be acquired by travelers following a single exposure. There have been numerous outbreaks of acute schistosomiasis in association with tourism [10,27-29]. Occasionally, human schistosomiasis can be introduced in nonendemic regions harboring the suitable intermediate hosts. As an example, an outbreak due to a S. haematobium-S. bovis complex species originating in Senegal occurred among bathers in the Cavu River in Corsica, France [30].

Infection is not uniformly distributed within communities; this may be attributable to differences in exposure patterns, age-related and acquired resistance, and distribution of infected mollusks [26].

Each human schistosome species requires a specific snail (mollusk) species:

S. mansoniBiomphalaria spp

S. haematobium and S. intercalatumBulinus spp

S. japonicumOncomelania spp

S. mekongiTricula spp

These mollusk species require specific environmental conditions and rarely coexist. Their distribution largely defines the local endemicity of the individual schistosome species. Occasionally, nonendemic invasive mollusk species may intervene in transmission [31].

Life cycle — The life cycle of schistosomiasis is complex and requires both intermediate and definitive hosts (figure 1).

Human contact with fresh water is required for transmission of schistosomiasis. The life cycle begins with seeding of eggs into fresh water through urine (S. haematobium and S. haematobium-S. bovis hybrids) or feces (S. mansoni, S. intercalatum, S. guineensis, S. mekongi, S. malayensis and S. japonicum, and occasionally S. haematobium-S. bovis hybrids) from infected humans or animal reservoirs. The eggs hatch and release miracidia, which are viable for up to seven days until they penetrate snail intermediate hosts. The stages in the snail include two generations of sporocysts followed by production of cercariae, which are released from the snail into the water after four to six weeks. Cercariae can survive up to two days in water but are most infectious to humans during the first few hours after release from the snail [22]. Cercariae penetrate human skin, shed their tails, and become schistosomulae, which migrate through the blood circulation until they reach the liver where they mature into adults over two to four weeks.

The adult worms migrate against portal blood flow to the mesenteric venules of the small and large intestine (S. japonicum and S. mekongi), the mesenteric venules of the colon (S. mansoni, S. intercalatum), or the vesical venous plexus (S. haematobium). The male schistosome forms a groove in which the female resides. After one to three months, the female worms (7 to 20 mm) deposit eggs in the small venules of the mesenteric or perivesical systems. The eggs move toward the lumen of the intestine (S. mansoni, S. intercalatum, S. japonicum, and S. mekongi) or bladder and ureters (S. haematobium) and are eliminated in feces or urine, respectively. The adult worms usually survive for 5 to 7 years but can persist for up to 30 years [32].

PATHOGENESIS — Most infected individuals do not develop symptomatic illness. The natural course of the infection depends on the age of primary exposure, the intensity of ongoing exposure, development of immunity against repeat infection, and genetic susceptibility [22,33]. In general, the intensity of infection rises during the first two decades of life and subsequently declines to very low levels in adults, presumably due to development of acquired immunity [34-37]. Repeated administrations of mass treatment substantially diminishes schistosome-associated disease and accelerates the acquisition of a protective immunity [38].

In general, clinical disease is caused by the host immune response to migrating eggs [39]. Adult worms absorb host proteins and coat themselves with host antigens, allowing prolonged residence in the bloodstream with evasion of immune attack [40].

Migration of eggs through tissues can be associated with entrapment, inflammation, and subsequent fibrosis [22]. Eggs are carried via the splanchnic venous system and may embolize to the liver, lungs, spleen, brain, or spinal cord; less common sites of embolization include the skin and peritoneal surfaces [41]. The trapped eggs secrete proteins and carbohydrates that induce a host Th-2 immune response, leading to an eosinophilic granulomatous reaction [42]:

In the bowel, inflammation can result in ulceration, blood loss, and scarring [43,44].

In the liver, periportal fibrosis (known as Symmers' pipestem fibrosis) can lead to portal hypertension and subsequent esophageal varices [45,46].

In the bladder, the eggs provoke granulomatous inflammation, ulcerations, and development of pseudopolyps in the vesical and ureteral walls, which may mimic malignancy. In addition, chronic inflammation due to schistosomiasis has been associated with bladder cancer.

Ectopic migration of adult worms and subsequent egg deposition in brain and spinal cord rarely occurs but causes serious morbidity. (See 'Neuroschistosomiasis' below.)

Eradication of adult worms in the setting of recently acquired schistosomiasis usually leads to complete remission of urinary and intestinal lesions [47-51].

CLINICAL MANIFESTATIONS — In general, manifestations of acute schistosomiasis syndrome (Katayama syndrome) are observed among individuals not living in endemic areas, such as travelers; this is likely because these individuals have not yet developed immunity associated with early exposure [52,53]. Swimmer's itch is observed among travelers as well as individuals in endemic areas. Manifestations of chronic infection are generally observed among individuals with ongoing exposure in endemic regions.

Most individuals with schistosomiasis infection are asymptomatic and have a low parasite burden [24].

Acute infection

Swimmer's itch — Skin penetration by cercariae usually goes unnoticed. Some individuals develop an itchy rash ("swimmer's itch") soon after swimming in fresh water; this is a localized dermatitis that can result in a pruritic papular or urticarial rash at the site of larval entry [53,54]. The rash is a hypersensitivity reaction that occurs with repeat exposure (never with initial exposure); it typically develops on the feet or lower legs.

Individuals can develop swimmer's itch in regions where human schistosome species are endemic and/or in regions where transmission of avian or mammalian (nonhuman) schistosome species occurs.

Acute schistosomiasis syndrome — Acute schistosomiasis syndrome (also known as Katayama syndrome, originally described following infection with S. japonicum) is a systemic hypersensitivity reaction to schistosome antigens and circulating immune complexes that occurs three to eight weeks after infection [55]. Acute schistosomiasis occurs at the time of initial infection with S. haematobium, S. mansoni, S. intercalatum, and S. mekongi; it can reappear after subsequent infection with S. japonicum. The onset of clinical manifestations usually appears 3 to 10 weeks after infection and coincides with the beginning of egg production, a period of rapid increase in antigen burden. The syndrome occurs almost exclusively among nonimmune hosts such as travelers and may be observed in more than half of infected individuals [53,56,57]. Activities associated with acute schistosomiasis syndrome include bathing and swimming in fresh water, scuba diving, water skiing, and rafting [58].

Clinical manifestations of acute schistosomiasis syndrome include sudden onset of fever, urticaria and angioedema, chills, myalgias, arthralgias, dry cough, diarrhea, abdominal pain, and headache [59-63]. Only one or a few of the above symptoms may be observed, and fever is not an essential component of the illness [64]. The symptoms are usually relatively mild and resolve spontaneously over a period of a few days to a few weeks. Occasionally persistent manifestations are observed including weight loss, dyspnea, and chronic diarrhea. In rare cases, neurologic symptoms suggestive of encephalitis can occur [65].

An elevated eosinophil count (>750/microL) is often observed within a few days after onset of symptoms [10,66]. Patients with cough and/or dyspnea may have patchy infiltrates on chest radiograph [55,63,67].

The diagnosis and treatment of acute schistosomiasis syndrome is discussed separately. (See "Schistosomiasis: Treatment and prevention" and "Schistosomiasis: Diagnosis".)

Chronic infection — Chronic infection related to schistosomiasis is most common among individuals in endemic areas with ongoing exposure. However, chronic infection can also occur in individuals with brief exposure such as travelers [58,68,69]. The severity of disease is related to the number of eggs trapped in tissues, their anatomic distribution, the duration and intensity of infection, and the host immune response [22,70].

Symptoms of chronic infection often begin insidiously [25]. The nature of clinical manifestations depends on the organ tropism of the infecting species. Major organs with potential involvement include the intestinal tract, liver, spleen, genitourinary tract, lungs, and central nervous system.

Other clinical manifestations that have been observed in association with schistosomiasis include anemia, malnutrition, growth retardation, and general disability [71,72].

Intestinal schistosomiasis — Intestinal schistosomiasis is caused by infection due to S. mansoni, S. japonicum, S. intercalatum, S. mekongi, and occasionally, with S. haematobium-S. bovis hybrids [8]. The most common symptoms include chronic or intermittent abdominal pain, poor appetite, and diarrhea. In heavy infection, chronic colonic ulceration may lead to intestinal bleeding and iron deficiency anemia [73-75]. Intestinal polyps and dysplasia can arise due to granulomatous inflammation surrounding eggs deposited in the bowel wall (picture 1) [76,77]. Bowel strictures can also develop. In rare cases, an inflammatory mass can lead to obstruction or acute appendicitis [78,79].

Hepatosplenic schistosomiasis — Hepatosplenic schistosomiasis is caused by infection due to S. mansoni, S. japonicum, S. intercalatum, S. mekongi, and, occasionally, S. haematobium. Hepatosplenic schistosomiasis consists of two phases depending on age and duration of infection.

Among children and adolescents, the predominant pathological process consists of nonfibrotic granulomatous inflammation around trapped eggs in the presinusoidal periportal spaces of the liver. The left liver lobe is enlarged with a sharp edge, and splenomegaly may extend below the umbilicus and into the pelvis in some cases [43,80,81]. There are generally no apparent signs of liver dysfunction. Ultrasonography demonstrates widened periportal spaces, which are more pronounced in heavily infected individuals. At this stage, the changes are largely reversible with treatment [82].

Among adults with chronic infection, the predominant pathologic process consists of collagen deposition in the periportal spaces by activated hepatic stellate cells, which causes periportal fibrosis (also known as Symmers' pipestem fibrosis) [25,81,83]. This leads to occlusion of the portal veins, portal hypertension with splenomegaly, portocaval shunting, and gastrointestinal varices. On physical examination, the liver is firm and nodular. Hepatocellular liver function is not impaired. The interaction of schistosome egg antigens and hepatic stellate cell activation is complex. Several host regulators of fibrosis, both inhibitory and enhancing, have been identified [84]. This partially explains why only few infected individuals progress towards hepatic fibrosis [85].

Ultrasonography may demonstrate periportal fibrosis around portal vein tributaries in the setting of late S. japonicum and S. mansoni infections [86-88]. Splenomegaly, portal vein dimensions, and the presence of collateral vessels may also be observed. Computed tomography (CT) and magnetic resonance imaging (MRI) demonstrate heterogeneity of hepatic parenchyma, periportal fibrosis, and the presence of venous collateral pathways [89]. (See "Noncirrhotic portal hypertension", section on 'Schistosomiasis'.)

Pulmonary complications — Pulmonary manifestations of schistosomiasis may be seen in the early infection stages but occur most frequently among patients with hepatosplenic disease due to chronic infection with S. mansoni, S. japonicum, or S. haematobium [90]. Lesions may resolve after treatment or even spontaneously [91]. Development of presinusoidal portal hypertension can lead to development of portosystemic collateral vessels, allowing a path for embolization of schistosome eggs into the pulmonary circulation. Eggs can lodge in pulmonary arterioles (diameter 50 to 100 micrometer) and produce a granulomatous pulmonary endarteritis, with subsequent development of pulmonary hypertension and cor pulmonale [92]. Progression of disease may be associated with cardiac enlargement and pulmonary artery dilatation. These manifestations represent end-stage disease and are generally irreversible.

Dyspnea is the primary clinical manifestation [93]. Chest radiography demonstrates fine miliary nodules. Echocardiography is useful screening tool for pulmonary hypertension in patients with hepatosplenic schistosomiasis [94].

In some cases, antischistosomal therapy may precipitate embolization of adult worms to the lungs, resulting in coughing, wheezing, and pulmonary infiltrates on chest radiography [95]. The mechanism may involve an immunologic response to exposed or released antigens from dead worms [96]. These manifestations are generally self-limited and antischistosomal therapy may be continued.

Genitourinary schistosomiasis — Genitourinary schistosomiasis is caused by infection due to S. haematobium, and occasionally, by S. haematobium-S. bovis and S. haematobium-S. mattheei hybrids [97-102]. It can result in infertility and increased risk for HIV transmission [103,104].

In early infection, eggs are excreted in the urine and patients present with microscopic or macroscopic hematuria and/or pyuria [48,105-107]. Blood is usually seen at the end of voiding ("terminal hematuria"), although in severe cases hematuria may be observed for the entire duration of voiding [22]. Men may present with hemospermia [107].

In early chronic infection, the eggs provoke granulomatous inflammation, ulcerations, and development of pseudopolyps in the vesical and ureteral walls, which may be observed on cystoscopy and mimic malignancy (picture 1) [48,105,106]. Biopsy of such lesions in the setting of suspected malignancy can lead to unexpected visualization of schistosome eggs [108]. Ultrasonography findings of the urinary tract generally correlate well with burden of infection [109]. Urinary tract lesions are largely reversible with treatment prior to onset of fibrosis and calcification [110-114].

In longstanding infection, dysuria and increased urinary frequency are common symptoms. At this stage, the bladder wall is fibrosed and may calcify, producing a characteristic radiographic image (image 1). Intravenous pyelogram (IVP) or CT urography may demonstrate ureteral stricture(s) [115]. Ultrasonography of the kidneys and bladder may demonstrate bladder wall irregularities due to granulomas. Hydronephrosis, bladder polyps, and tumors can also be detected.

Bladder neck obstruction, hydroureter, and hydronephrosis can ensue, leading to renal failure [105,108,116,117]. Bacterial superinfection can cause acute pyelonephritis. Longstanding infection may also be associated with development of bladder cancer, particularly in combination with other carcinogenic exposures such as tobacco [118]. (See "Epidemiology and risk factors of urothelial (transitional cell) carcinoma of the bladder".)

Female genital manifestations may include hypertrophic and ulcerative lesions of the vulva, vagina, and cervix [113,119,120]. Involvement may also include the ovaries or fallopian tubes, which can lead to infertility. Male genital manifestations may include involvement of the epididymis, testicles, spermatic cord, or prostate. Genital lesions may be partially reversible with treatment.

Genital schistosomiasis may be an independent risk factor for HIV infection [121-123]. (See 'HIV infection' below.)

Glomerular disease — Infection due to any schistosomal species can be associated with immune complex glomerulopathy, leading to proteinuria and the nephrotic syndrome. This is discussed separately. (See "Schistosomiasis and glomerular disease".)

Neuroschistosomiasis — Schistosomiasis can cause serious neurologic complications, even among individuals with a relatively low burden of infection, and occasionally in travelers during the acute phase of infection [124,125]. Neuroschistosomiasis can involve the spinal cord (causing an acute myelopathy) and/or the brain (image 2 and image 3); myelopathy is more common than cerebral disease [108,126-131]. Embolization of adult worms to the spinal cord or cerebral microcirculation with subsequent release of eggs leads to an intense inflammatory granulomatous reaction with local tissue destruction and scarring [132].

Schistosomiasis accounts for 1 to 4 percent of spinal cord lesions in sub-Saharan Africa and is probably underestimated in endemic populations [130,133]. Spinal cord involvement consists of a rapidly progressive transverse myelitis. It is usually intramedullary but occasionally includes extramedullary involvement, mainly affecting the conus medullaris and the cauda equine and may be missed [134,135]. Patients may present with lower limb pain, lower motor dysfunction, bladder paralysis, and bowel dysfunction [136].

Schistosomiasis of the brain may cause single or multiple intracerebral lesions and presents with a wide variety of symptoms including seizures, motor and/or sensory impairment, or a cerebellar syndrome [137]. Cerebral involvement may occur more frequently than suspected clinically [138].

In rare cases, schistosomiasis can cause a multifocal encephalopathy with features similar to acute vasculitis; this may occur as a result of eosinophil-mediated toxicity [65]. Cerebral vasculitis associated with schistosomiasis in the absence of eosinophilia has also been described [139].

Neuroschistosomiasis is a medical emergency; diagnosis and treatment are discussed separately. (See "Schistosomiasis: Diagnosis", section on 'Neuroschistosomiasis' and "Schistosomiasis: Treatment and prevention", section on 'Neuroschistosomiasis'.)

LABORATORY FINDINGS — Eosinophilia is observed in 30 to 60 percent of patients [140-142]. Eosinophilia is very common among patients with acute schistosomiasis infection syndrome, a hypersensitivity that occurs most frequently among travelers with new infection [53,64,143]. The degree of eosinophilia depends on the stage, intensity, and duration of infection [144].

Eosinophils may be observed in the cerebrospinal fluid (CSF) among patients with neurologic involvement; one review including 231 patients with spinal cord involvement noted presence of CSF eosinophils in 41 percent of cases [136].

Anemia may be observed in patients with blood loss due to chronic intestinal or urinary tract schistosomiasis. A fecal occult blood test may be positive in intestinal schistosomiasis if there is a heavy burden of infection [145].

Thrombocytopenia may be observed in patients with portal hypertension due to hepatosplenic schistosomiasis secondary to splenic sequestration in an enlarged spleen.

Liver enzymes are rarely elevated, even in established hepatic fibrosis due to schistosomiasis.

Hematuria and/or leukocyturia are common in the setting of S. haematobium infection [146-150].

Diagnostic laboratory tests for schistosomiasis are discussed further separately. (See "Schistosomiasis: Diagnosis".)

ASSOCIATED INFECTIONS

Bacteremia and bacteriuria — Egg migration through tissues can cause inflammation of the colon or urinary tract, leading to bacteremia and/or bacteriuria [66]. Infection with any bacterial organism can occur, including recurrent infection due to Salmonella [151].

HIV infection — Schistosome infections appear to have little to no association with HIV infection [152,153]. Infection due to S. haematobium may be associated with increased risk of HIV transmission since eggs can induce inflammation leading to development of ulcerative lesions in the female reproductive tract [154-156]. In addition, schistosomiasis may interfere with the host immune response, increasing susceptibility to HIV infection [121,157]. Coinfection with HIV and schistosomiasis may facilitate HIV replication and cytokine dysregulation [158]. It has also been suggested that HIV infection may be associated with increased susceptibility to repeat infection with schistosomes [159,160].

Symptomatic schistosomiasis has also been described in the setting of immune reconstitution syndrome in a patient receiving antiretroviral therapy [161].

Viral hepatitis — Individuals with hepatitis B and schistosomiasis caused by S. mansoni or S. japonicum have more severe disease and worse prognosis than those infected with either pathogen alone [162].

Individuals with hepatitis C virus (HCV) and schistosomiasis appear to have more severe liver disease than those with HCV monoinfection [163,164]. This may be related to alteration of cellular immune responses to HCV antigens that is modulated by schistosomiasis infection, leading to increased levels of HCV RNA and more rapid progression of liver disease [165].

Malaria — Malaria and schistosomiasis are co-endemic in many areas. Studies have shown coinfection may increase morbidity in hepatosplenic schistosomiasis and alter the host immune response to schistosome antigens [157,166]. In addition, development of hepatocellular carcinoma may be potentiated in coinfected individuals [167].

However, coinfection may be protective in urinary schistosomiasis; one study among children (four to eight years of age) with asymptomatic urinary schistosomiasis noted delayed onset to first clinical malaria infection, fewer malarial episodes, and a lower mean parasite density at initial infection compared with children who did not have S. haematobium infection [168].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Schistosomiasis".)

SUMMARY

Schistosomiasis is a disease caused by infection with parasitic blood flukes. The three major schistosome species that cause infection in humans are Schistosoma mansoni (Africa and South America), Schistosoma japonicum (East Asia), and Schistosoma haematobium (Africa and the Middle East). (See 'Microbiology and phylogeny' above.)

The prevalence of schistosomiasis is highest in sub-Saharan Africa. Children acquire the infection by bathing in fresh water contaminated with cercariae (the infectious form of the parasite). Worm burden gradually increases to culminate during adolescence. Most individuals have a mild to moderate parasite load with limited morbidity; heavy infection with significant consequence for disease occurs among relatively few individuals in a population. (See 'Epidemiology' above.)

The life cycle of schistosomiasis is complex and requires both intermediate and definitive hosts (figure 1). Cercariae released from snails in fresh water penetrate human skin and migrate to the liver, where they mature into adults. The adult worms migrate to the mesenteric venules of the intestine (S. japonicum and S. mekongi), the colon (S. mansoni), or the vesical venous plexus (S. haematobium). The female worms deposit eggs in the portal or perivesical systems, which migrate to the lumen of the intestine (S. mansoni and S. japonicum) or bladder (S. haematobium) and are excreted via stool or urine, respectively. The eggs hatch and release miracidia, which penetrate snail intermediate hosts; subsequently cercariae are produced. (See 'Life cycle' above.)

Manifestations of acute infection are generally observed among individuals not living in endemic areas, such as travelers; this is likely because these individuals do not present with hypersensitivity at first exposure. Acute infection can present with "swimmer's itch" and/or acute schistosomiasis syndrome (Katayama syndrome), a systemic hypersensitivity reaction to schistosome antigens and circulating immune complexes. (See 'Acute infection' above.)

Manifestations of chronic infection are generally observed among individuals with ongoing exposure in endemic regions. Disease is caused by the host immune response to migrating eggs. In the bowel, inflammation can result in ulceration, blood loss, and scarring. In the liver, periportal fibrosis (Symmers' pipestem fibrosis) can lead to portal hypertension and subsequent esophageal varices. In the bladder, granulomatous inflammation can result in development of pseudopolyps and/or urinary tract obstruction leading to renal failure. (See 'Chronic infection' above and 'Pathogenesis' above.)

Schistosomiasis can cause serious neurologic complications, even among individuals with a relatively low burden of infection, including travelers. Neuroschistosomiasis can involve the spinal cord (causing an acute myelopathy) and/or the brain. (See 'Neuroschistosomiasis' above.)

ACKNOWLEDGMENTS — The UpToDate editorial staff acknowledges Karin Leder, MD, and Peter Weller, MD, who contributed to an earlier version of this topic.

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Topic 5717 Version 30.0

References

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