Esquistosomiasis

Section Contents

Key Points
Background
Transmission & Life Cycle
Epidemiology
Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Prevention
Assessment: Did I Get It? (DIG-IT)
Other Media Resources (Optional)
References

Key Points

Schistosomiasis is a parasitic infection caused by the blood trematode Schistosoma, and it is acquired when larval forms (in freshwater) penetrate the skin.
Six species are known to cause human disease, but the biggest burden is due to: S. mansoni, S. haematobium & S. japonicum.
Unlike many other helminthiasis, most of the disease pathology is caused by the eggs and larval stages, and NOT from the adults.
Diagnosis is supported by microscopy, serology, or imaging.
Drug of choice for adult worms is praziquantel.

Background

Schistosomiasis (also known as “bilharzia”) is VERY COMPLEX! Please bear with us! This is a parasitic infection caused by the blood trematode of the genus Schistosoma. Schistosomiasis is a neglected tropical disease disproportionately affecting those in rural and impoverished communities in tropical and subtropical areas. Although around 200 million people are estimated to be infected, this number is likely an underestimation since most people have little to no symptoms and the diagnostic methods we have are not that great.

The most important species in humans are: S. mansoni, S. haematobium, and S. japonicum. Other species (S. mekongi, S. intercalatum, and its sister species S. guineensis) play a secondary role on the global burden of schistosomiasis and will only be briefly described in this module.

Main clinical syndrome	Genus and species	Distribution
Urogenital schistosomiasis	S. haematobium	Africa and Middle East
Intestinal schistosomiasis	S. mansoni	Africa, South America (Brazil, Venezuela, Suriname) & The Caribbean (Saint Lucia)
	S. japonicum	South East Asia (China, Philippines, Indonesia)
	S. mekongi	South East Asia (along Mekong River in Laos & Cambodia)
	S. guineensis & S. intercalatum	Africa (West & Central)

Table 1. Summary of clinical phenotypes of schistosomiasis and distribution by species

Transmission & Life cycle

Transmission: infection starts when humans come in contact with stagnant freshwater (never saltwater) containing larval stages (cercariae) and snails (intermediate hosts).

Life Cycle (general): cercariae penetrate the intact skin, and transform into another larval stage called schistosomulae. After ~2 days, schistosomulae migrate through the lungs and mature into adult worms in the portal system of the liver. The disease caused by the transit of schistosomulae through the body is called acute schistosomiasis. Mature adults "crawl" against the blood flow to its definitive habitat in a venous plexus [the type of venous plexus is different for each species- summarized in Table 2]. Once in the definitive habitat, adult females release eggs - which can be swept away to other organs (e.g., liver, intestine, bladder, genital tract) OR can penetrate the intestinal or vesical wall, allowing them to get released with feces (intestinal schistosomiasis) or with urine (urogenital schistosomiasis). After adults start producing eggs, the disease is referred to as chronic schistosomiasis. Eggs passed in feces or urine, hatch in freshwater, and release a larval stage called miracidia, which is capable of infecting the snail [intermediate] host, which is different for each species (please see Table 2). In the snail, miracidia transform back to cercariae, which can infect the human host, and re-start the cycle. Click on the figures below to see the life cycle for each species.

Figure 1. Life cycle of S. mansoni and S. japonicum

Figure 2. Life cycle of S. haematobium

Schistosoma spp	Intermediate host (snails)	Definitive venous plexus	Reservoirs	Distribution
*S. haematobium*	Bulinus spp.	Vesical plexus and veins draining the ureters	Monkeys	Africa and Middle East
*S. mansoni*	Biomphalaria spp.	Inferior mesenteric veins	Monkeys (Africa), Rodents (America)	Africa, South America (Brazil, Venezuela, Suriname) & The Caribbean (Saint Lucia)
*S. japonicum*	Oncomelania spp.	Superior mesenteric veins	Dogs, Cattle, Rodents	South East Asia (China, Philippines, Indonesia)

Table 2. Main differences betwen Schistosoma species

Epidemiology

Schistosomiasis is distributed across tropical and subtropical areas; although >85-90% of cases worldwide occur in Africa. For a map of the endemic areas of bilharzia, we recommend accessing this excellent article!

Risk factors for acquiring schistosomiasis:

Lack of access to clean water & poverty
Exposures to bodies of freshwater (e.g., washing clothing or dishes, recreational contact,
showers directly connected to lakes, work-related: agriculture, rice farmers)
Encroachment into irrigation canals
Living in close proximity to water
Children

Pathophysiology

Unlike many other helminthiasis, the pathology is NOT caused by the adult worms, but rather by the eggs or the larval stages. Let's understand how schistosomes cause disease:

Larval induced inflammation

Both cercariae and schistosomulae can cause pathology:

Cercarial dermatitis → when cercariae (shown in the picture to the right) penetrate the skin, it can induce an intense pruritic, papular response called cercarial dermatitis [more common among non-immune travelers].
Swimmer’s itch → this is a self-limiting subtype of cercarial dermatitis, caused by cercariae of avian schistosomes - ducks, swans, waterbirds. However, unlike human schistosomes, these larvae do not pass beyond the skin, do not transform into schistosomulae, and do not lead to schistosomiasis.
Acute schistosomiasis → it is caused by the transit of schistosomulae through the general circulation, and occurs 4-8 weeks after freshwater exposure. It is characterized by a hypersensitivity reaction responsible for symptoms we will describe in Clinical Presentation.

Egg induced inflammation

Eggs are highly antigenic and when they get retained in tissues, they induce a granuloma formation, which then leads to fibrosis around the retained eggs. Accumulation of eggs overtime is the cause of the disease seen in chronic schistosomiasis. A diagram summarizing the pathology in chronic schistosomiasis can be seen below.

Intestinal schistosomiasis → occurs when eggs of S. mansoni and S. japonicum pass through or get retained in the intestinal wall - leading to ulceration, micro-abscess, and pseudo-polyp formation.
Hepato-splenic schistosomiasis → occurs when S. mansoni and S. japonicum eggs are swept into the liver, and get retained in small branches of the portal vein. Granuloma formation leads to periportal fibrosis (also known as Symmer’s fibrosis), and portal hypertension.
Urinary schistosomiasis → occurs only in S. haematobium when eggs passing through or retained in the bladder and ureter - induce granulomatous inflammation, fibrosis - leading to pseudopolyps, urinary obstruction, hydroureter, hydronephrosis, and renal failure with nephrotic range proteinuria. Chronic inflammation can lead to squamous cell carcinoma of the bladder.
Genital schistosomiasis → retained eggs in the uterus, cervix, or lower genital tract lead to granuloma formation in the cervix, ectopic pregnancy, infertility, vulvo-vaginal disease, among others - collectively called as female genital schistosomiasis.
Pulmonary schistosomiasis → eggs retained in the lung capillaries induce granuloma formation and fibrosis - leading to pulmonary hypertension and cor pulmonale.
Neuro-schistosomiasis → occurs when eggs are carried into aberrant locations in the central nervous system. S. mansoni and S. haematobium eggs, which are larger, can be retained in the spinal cord - leading to transverse myelitis, and paralysis. S. japonicum eggs, which are smaller, can be retained in the brain, leading to epilepsy, and encephalopathy.

Figure 3. Pathophysiology of chronic schistosomiasis

Clinical Presentation

You're almost done with this lesson! Keep up the good work! One of the most challenging features of schistosomiasis is the many different phenotypes it can cause, and symptoms will depend on the stage of the disease:

Figure 4. Phases and timeline of schistosomiasis

Cercarial dermatitis

Once cercariae penetrates the skin, it induces a pruritic maculopapular rash a few hours after exposure. It is found in water-exposed areas and it is more severe in non-sensitized individuals (such as travelers or during primary infection).

Swimmer’s itch: as noted above, this is a self-limiting subtype of cercarial dermatitis caused by avian schistosomes (e.g., ducks, geese, seabirds, etc), but does not lead to disease beyond the skin. Subsequent exposures shorten the interval time between exposure and symptoms. It is more common in Northern Climates.

Acute schistosomiasis ("Katayama fever")

It occurs generally 4-8 weeks after freshwater exposure, and it is reflective of the hypersensitivity reaction caused by the transit of the schistosomulae. Patients may present with fever, malaise, urticaria, headaches, generalized myalgias, abdominal pain, dysentery, respiratory symptoms (cough, pulmonary infiltrates, pneumonitis - in ~70% of cases), hepatomegaly, splenomegaly (in ~30% of cases), or generalized lymphadenopathy - often with pronounced eosinophilia.

Note: During the acute phase, no egg production is made, and thus stool/urine microscopy will often be negative. Serology is variably positive.

Chronic schistosomiasis

Chronic schistosomiasis: it occurs after adults lay eggs, which get retained in small capillaries, inducing formation of granulomas and fibrosis. Symptoms are often apparent with chronic egg deposition and progressive tissue injury. Depending on the egg burden, some patients will remain asymptomatic, while others will exhibit distinct clinical syndrome depending on the location of the eggs:

Intestinal schistosomiasis: egg deposition in the intestinal mucosa, may cause intermittent abdominal pain, and sometimes dysentery. Predominantly seen with infections with S. mansoni, S. japonicum, and S. mekongi. Infections due to S. intercalatum, and S. guineensis tend to have less pronounced symptoms.
Hepato-splenic disease (5-10%): chronic egg deposition in the portal circulation leads to a type of periportal fibrosis called Symmer’s fibrosis, resulting in portal hypertension & hypersplenism. Individuals can present with gastrointestinal bleeding from esophageal varices.
Note: Symmer’s fibrosis ≠ Swimmer’s itch. Do not get them confused!
Urogenital schistosomiasis: (only in S. haematobium).
1. Urinary → Patients may develop hematuria, dysuria, frequency, and “UTI-like” symptoms. Inflammation may lead to ureteral fibrosis with obstructive uropathy and hydroureter, resulting in renal failure with nephrotic range proteinuria. More rarely, it can induce squamous cell carcinoma of the bladder.
2. Genital → Males can develop hematospermia. Females (called “Female Genitourinary Schistosomiasis”) can develop cervical and vaginal granulomas (described as “sandy patches”), which can result in bleeding, dyspareunia, chronic pelvic pain, and infertility. It increases the risk of HIV acquisition.
Pulmonary schistosomiasis: occurs because of egg deposition in the pulmonary vasculature, resulting in portacaval shunting, pulmonary hypertension, and cor pulmonale.
Neuro-schistosomiasis: rare but feared complication that occurs when ectopic eggs get retained in the central nervous system. S. mansoni & S. haematobium have bigger eggs, and are more likely to induce spinal inflammation; whereas S. japonicum’s eggs are smaller and thus more likely to get swept away more distantly to the brain. Can lead to transverse myelitis, focal neurologic signs, seizures, and/or encephalopathy

Diagnosis

As with all diseases, diagnosis starts with a clinical suspicion in the right epidemiological context (What is the presentation? Who is the host?). Definitive diagnosis can be supported through different modalities based on which phase of schistosomiasis you are suspecting:

Cercarial dermatitis & swimmer's itch

Acute schistosomiasis ("Katayama fever")

The diagnosis is greatly based on the clinical suspicion with signs/symptoms compatible with Katayama fever, PLUS pronounced peripheral eosinophilia. Remember that pulmonary infiltrates are common!

At this stage, eggs in stool or urine are rarely seen. Serology may be initially negative, but patients can seroconvert 4-12 weeks after the initial exposure.

Abdominal ultrasound may show hepatosplenomegaly, and or lymphadenopathy.

Chronic schistosomiasis

Microscopy/Tissue biopsy: detection of eggs in stool, urine, or seen in tissue biopsy, is the gold-standard. Unfortunately, sensitivity is <50%, so a negative urine or stool smear microscopy does not exclude diagnosis. Concentration techniques (i.e., Kato-Katz) are preferred.

For more information on the morphology of the eggs, please visit this amazing blog.

Serology: is useful when no egg production is detected. Just remember that seroconversion takes 4-12 weeks after exposure, and can be initially negative during acute infection. Its use is limited because it does not distinguish between present or previous infection. Sensitivity is lower in S. japonicum (<50%), compared to S. mansoni and S. haematobium (>95%).

Imaging:

1. Ultrasound: useful to detect periportal fibrosis, signs of portal hypertension, bladder wall abnormalities, obstructive uropathy, or hydronephrosis.
2. Cystoscopy/Pyelogram: useful to detect ureterovesical lesions or lesions in the bladder mucosa.
3. Neuroimaging (i.e., MRI): method of choice for neuroschistosomiasis.
4. Colposcopy: useful to evaluate cervical lesions in suspected female genitourinary schistosomiasis.

Figure 5. S. mansoni egg - lateral spine

Figure 6. S. haematobium egg - terminal spine

Figure 7. S. japonicum egg - no spine

Figure 8. Schistosoma egg in colon polyp in a patient from Cote D'Ivoire (courtesy of Stephen Lagana, MD)

Treatment & Management

Swimmer’s itch: symptomatic treatment (e.g.., antihistamines, topical steroids,
emollients) +/- systemic steroids.
Acute schistosomiasis: symptomatic treatment (similar to swimmer’s itch) +
praziquantel.

Note: Praziquantel only acts on adults (not on larval stages), so during acute infection treatment needs to be repeated 6-12 weeks later to kill newly developed adult worms.

3. Chronic schistosomiasis:

All clinical forms (except neuroschistosomiasis) → treat with praziquantel.
Neuroschistosomiasis → prednisone followed by praziquantel.

Condition	Treatment
Swimmer's itch	Symptomatic treatment +/- steroids
Cercarial dermatitis, Acute schistosomiasis	Symptomatic treatment +/- steroids; Praziquantel (may need retreatment)
Chronic schistosomiasis	Praziquantel; start with steroids in neuro-schistosomiasis

Please remember these management pearls:

Always screen for signs/symptoms of neuroschistosomiasis & neurocysticercosis before treating! Remember praziquantel can induce seizures, myelitis, eye damage in coinfected patients
In patients with positive microscopy at baseline, perform a test of cure (e.g., stool/urine microscopy) 3-6 months after treatment
If persistent eggs are seen, re-treat!
Treatment does NOT prevent re-infection

Prevention

If possible, implement integrated control measures, including:

Infection avoidance → counsel patients on avoiding recreational swimming in areas at risk, improved sanitation practices (i.e., if possible defecate/urinate in toilets), instruct on safe water practices. If contact with water unavoidable, use personal protection (i.e., boots).
Health education
Vector control → snail control and integrated control programs.
Chemoprevention → praziquantel is given periodically as part of mass drug administration programs in endemic areas with >10% prevalence.

Assessment: Did I Get It? (DIG-IT)

Assessment: Did I Get It? (DIG IT)

DIG ITs are online modules designed to reinforce key learning points for you! Please choose the best answer, then check all of the answer choices for more learning pearls

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Other Media Resources (Optional)

Podcast Recordings

References

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CDC Yellow Book 2024: Health Information for International Travel. Oxford University Press
Blumberg, L. et al. (2021) Oxford Handbook of Tropical Medicine. Oxford: Oxford University Press. Camilla Rothe, 57 - A 37-Year-Old Woman from Malawi With Haematemesis, Editor(s): Camilla Rothe, Clinical Cases in Tropical Medicine (Second Edition), Elsevier,2022,
Beeching, N. and Gill, G. (2014) Lecture notes tropical medicine, 7th edition. John Wiley & Sons.
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Friedman, JF., Olveda, RM., Mirochnick, Mark, B., Amaya L & Elliott, AM. (‎2018)‎. Praziquantel for the treatment of schistosomiasis during human pregnancy. Bulletin of the World Health Organization, 96 (‎1)‎, 59 - 65. World Health Organization.
Hewitt, R., & Willingham, A. L. (2019). Status of schistosomiasis elimination in the Caribbean region. Tropical Medicine and Infectious Disease, 4(1), 24
PAHO/WHO Schistosomiasis Regional Meeting. Defining a road map toward verification of elimination of schistosomiasis transmission in Latin America and the Caribbean by 2020 [Internet]. Pan American Health Organization. World Health Organization (2014)
WHO guideline on control and elimination of human schistosomiasis [Internet]. Geneva: World Health Organization; 2022. Summary of recommendations. Available from: https://www.ncbi.nlm.nih.gov/books/NBK578396/
Review of 2022 WHO guidelines on the control and elimination of schistosomiasis Lo, Nathan C et al. The Lancet Infectious Diseases, Volume 22, Issue 11, e327 - e335
Obonyo, C. O., Muok, E. M., & Were, V. (2019). Biannual praziquantel treatment for schistosomiasis. Cochrane Library.
Colley DG, Bustinduy AL, Secor WE, King CH. Human schistosomiasis. Lancet. 2014 Jun 28;383(9936):2253-64. doi: 10.1016/S0140-6736(13)61949-2. Epub 2014 Apr 1. PMID: 24698483; PMCID: PMC4672382

This lesson was last updated May 12 2025

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