Schistosomiasis

Also known as: Bilharzia, Snail fever

Schistosomiasis is a chronic parasitic infection caused by trematode flukes of the genus Schistosoma, acquired through skin contact with fresh water containing infective cercariae released by an intermediate snail host.

It remains a major cause of chronic morbidity in many parts of sub-Saharan Africa, the Middle East, South America, and parts of Asia.

The three species of greatest clinical significance differ in their primary organ tropism: Schistosoma haematobium predominantly affects the urinary and genital tract, while Schistosoma mansoni and Schistosoma japonicum predominantly affect the intestinal tract and, via portal venous migration, the liver, causing periportal fibrosis and portal hypertension over time.

Cercarial dermatitis ("swimmer's itch") may occur at the point of skin penetration, typically within hours to days of exposure, causing a transient, itchy papular rash.
Acute schistosomiasis (Katayama fever) occurs weeks after heavy primary exposure, particularly in previously unexposed travelers to endemic areas, and presents with fever, urticaria, myalgia, cough, hepatosplenomegaly, and eosinophilia, reflecting an acute immune response to migrating and newly egg laying worms.
Chronic urinary schistosomiasis (S. haematobium) presents with terminal hematuria (blood at the end of micturition, a relatively distinctive feature), dysuria, and, over years, progressive bladder wall fibrosis and calcification, hydronephrosis, and an important, well established association with squamous cell carcinoma of the bladder.
Chronic intestinal and hepatic schistosomiasis (S. mansoni, S. japonicum) presents with abdominal pain, diarrhea (sometimes bloody), and, over years, hepatosplenomegaly and progressive periportal fibrosis leading to portal hypertension, with, notably, relatively preserved hepatocellular synthetic function compared to cirrhosis of other causes, since the fibrosis is presinusoidal rather than reflecting diffuse parenchymal injury.
Female genital schistosomiasis, an under-recognized manifestation of S. haematobium infection, causes genital lesions and is associated with increased susceptibility to HIV acquisition, an important public health consideration in co-endemic regions.

Microscopy for ova in urine (for S. haematobium, ideally on a terminal, concentrated urine sample, sometimes collected around midday when egg excretion peaks) or stool (for S. mansoni and S. japonicum) is the traditional diagnostic method, though sensitivity is imperfect, particularly in light infection.
Serology can support diagnosis, particularly useful in travelers or in acute Katayama fever presentation before eggs become detectable, though it cannot reliably distinguish active from past, treated infection.
Eosinophilia is a common and useful supportive finding, particularly prominent in acute Katayama fever.
Urinary tract ultrasound assesses for bladder wall thickening, hydronephrosis, and other structural sequelae in chronic S. haematobium infection. Abdominal ultrasound assesses hepatic periportal fibrosis and splenic size in intestinal and hepatic disease, with characteristic imaging patterns described for hepatic involvement.
Cystoscopy with biopsy may be needed to assess bladder pathology or investigate for malignant transformation in longstanding urinary schistosomiasis.

Differentials include other causes of hematuria, other causes of chronic diarrhea, and other causes of hepatosplenomegaly and portal hypertension, particularly cirrhosis of other etiology.

Praziquantel is the treatment of choice across all schistosome species, typically given as a single day's treatment (often split into two doses a few hours apart), highly effective against adult worms though notably less effective against immature, migrating schistosomula, which is relevant in acute Katayama fever, where a repeat dose some weeks later is often given to treat any worms that have since matured.
Acute Katayama fever may additionally benefit from a short course of corticosteroids to dampen the acute immune reaction, alongside praziquantel, particularly in more severe presentations.
Established chronic complications, such as periportal fibrosis with portal hypertension or urinary tract structural damage, are managed according to their own specific principles, since praziquantel treats the active infection but does not reverse established fibrotic damage.
Prevention centers on avoiding contact with potentially infected fresh water in endemic areas, alongside broader public health measures including snail control, improved sanitation, and mass drug administration programs in highly endemic communities.

Referral: infectious disease or tropical medicine for diagnostic confirmation and treatment guidance, particularly in returning travelers; urology for structural urinary tract complications; gastroenterology or hepatology for portal hypertension and its complications.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Meningococcal Meningitis

Meningitis caused by Neisseria meningitidis, a gram negative diplococcus, notable both for its capacity to cause explosive, rapidly fatal disease within hours of symptom onset and for its outbreak potential, particularly within the "meningitis belt" of sub-Saharan Africa where large epidemics have historically occurred, predominantly with serogroup A, though the epidemiology has shifted with vaccination programs. Serogroups A, B, C, W, and Y account for the large majority of invasive disease globally, with regional variation in the dominant serogroup.

Follows the general meningitis pattern detailed in that entry, but with a specific and important additional feature: meningococcal disease frequently presents with, or rapidly progresses to, meningococcemia, a bloodstream infection causing a characteristic non-blanching petechial or purpuric rash (test with a glass tumbler, a true non-blanching rash does not fade under pressure), which can evolve rapidly from a few scattered petechiae to widespread purpura fulminans.

Meningococcal septic shock, with or without overt meningitis, is a distinct and even more rapidly fatal presentation, featuring hypotension, poor peripheral perfusion, and disseminated intravascular coagulation, and can occur without significant meningeal signs, particularly in young children.

Waterhouse-Friderichsen syndrome (bilateral adrenal hemorrhage causing acute adrenal insufficiency superimposed on septic shock) is a recognized, catastrophic complication.

The presence of a non-blanching rash in a febrile, unwell patient should prompt immediate empirical antibiotic treatment before any further diagnostic workup, given the speed of potential deterioration; diagnostic confirmation should never delay treatment in this scenario.

Once treatment is initiated, blood cultures, CSF analysis (via lumbar puncture where safe to perform, see Meningitis entry for specific contraindications and timing considerations), and PCR of blood or CSF (particularly valuable where antibiotics have already been given and culture yield may be reduced) confirm the diagnosis and serogroup.

Immediate IM or IV benzylpenicillin (or, if unavailable, ceftriaxone) should be given in the pre-hospital or primary care setting on clinical suspicion of meningococcal disease, without waiting for hospital transfer, given the mortality benefit of even a short delay reduction; in hospital, empirical treatment follows the general bacterial meningitis approach detailed in the Meningitis entry (typically IV ceftriaxone 2 g bd), continued and rationalized once meningococcus is confirmed and sensitivities (where relevant, though resistance remains uncommon) are available
Septic shock or meningococcemia requires the full sepsis and septic shock resuscitation approach detailed in those entries: aggressive fluid resuscitation, vasopressor support as needed, and consideration of corticosteroid therapy for refractory shock, alongside correction of the coagulopathy that frequently accompanies severe meningococcal sepsis
Chemoprophylaxis for close contacts is essential given the risk of secondary cases: ciprofloxacin 500 mg PO as a single dose (adults; weight-based dosing in children) is commonly used, with rifampicin (600 mg PO bd for 2 days in adults, weight-based in children) or ceftriaxone (single IM dose) as alternatives, particularly in pregnancy where ciprofloxacin and rifampicin carry specific considerations
Public health notification is mandatory given the outbreak potential, with contact tracing and, in outbreak settings, mass vaccination campaigns using the relevant serogroup-specific vaccine
Vaccination: conjugate meningococcal vaccines (covering various combinations of serogroups A, C, W, Y, and, separately, a specific serogroup B vaccine) form part of many routine national immunization schedules, and post-exposure vaccination of close contacts may be considered in addition to chemoprophylaxis depending on the specific serogroup and local protocol

Referral: this is a maximum medical emergency requiring immediate treatment, ICU involvement for shock or significant compromise, and public health notification for contact tracing and prophylaxis coordination.

Schistosomiasis

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management