Schistosomiasis

Infection with parasitic blood flukes. Two types of schistosomes are found in Malawi: urinary schistosomiasis (S. haematobium) and intestinal schistosomiasis (S. mansoni). S haematobium is endemic in many areas, particularly around the lake shore. S. mansoni mainly occurs in the central and Southern Highlands, Likoma Island and in the Lower Shire Valley

Clinical presentation

Cercarial dermatitis

Within hours after infection
Worms enter and migrate under the skin. “Swimmers itch” and maculopapular rash.

Acute schistosomiasis syndrome (Katayama fever)

Ca. six weeks after infection
Systemic hypersensitivity syndrome
Symptoms can include: fever (not an essential component), urticaria, angioedema, cough, abdominal pain, hepatosplenomegaly.
Usually self-limiting. More frequent in individuals who do not live in endemic setting, hence not common in Malawians.

Organ manifestations

Months or years after infection (most frequent presentation in endemic areas with ongoing exposure)
Adult worms live in the veins of the bowel or bladder and shed eggs. Eggs get trapped in tissue and cause damage through granulomatous inflammation, tissue scarring and calcification.
Disease severity depends on anatomic distribution of the trapped eggs, worm burden & duration of infection, severity of the host immune response, egg laying sites of the adult worms, and co-infections (e.g. HIV or malaria).

Unspecific symptoms: microcytic anaemia, malnutrition, fatigue, growth retardation, cognitive delay and disability

Urogenital Schistosomiasis

Acute:

Painless micro/macrohaematuria may persist for months. Dysuria. Mild fever.

Chronic:

Urinary tract infections
Fibrosis and calcification of the bladder
Obstructive uropathy (hydronephrosis), perineal fistula
Renal failure
Bladder cancer
Vaginal (bloody) discharge, genital itching, dyspareunia
Infertility/subfertility
Granulomas of uterine cervix, pelvic pain

Intestinal Schistosomiasis

Acute:

Diarrhoea, abdominal pain

Chronic:

Periportal fibrosis and hepatomegaly (palpable, nodular and hard liver), Splenomegaly
Hypersplenism secondary to portal hypertension
Complications of portal hypertension: oesophageal varices, ascites
Liver function usually preserved

Complications of both types

Parasite burden correlates with the likelihood of complications
Hypertension with cor-pulmonale (tricuspid regurgitation and right sided heart failure)
Neuroschistosomiasis: result of embolization of adult worms to the spinal cord or cerebral microcirculation. Causes cerebral disease or, more commonly, myelopathy.
If treated promptly patients might fully recover. Might account for up to 4% of spinal cord lesions in SSA

Investigations

Microscopy of stools or urine (eggs): Diagnostic golden standard (Stool needs concentration techniques, Kato Katz - specify your request on the lab form). Ideally second urine of the day, aim for large volume
Urine dipsticks can detect haematuria (+/- proteinuria) in urinary Schistosomiasis
USS abdomen - kidneys, bladder, liver (periportal fibrosis in S. mansoni infections)
PCV
Peripheral blood smear may show eosinophilia
Others: Antigen-tests (Point of care-urinary CCA has been useful to assess burden of S.mansoni in epidemiological studies), Serology. Molecular tests. Not routinely available
MRI of brain and spine

Treatment

A single dose of Praziquantel (40 mg/kg PO to nearest 1/4 tablet. Tablets of 600 mg) is curative in 85% of cases and reduces parasite burden in the remaining. Give before sleep (side effects are dizziness and GI disturbance).
Repeat course after 4 weeks if still symptomatic
Give a three day course of up to 60mg/kg if severely sick
Steroids for neuroschistosomiasis and Katayama Fever, refer to literature

Prevention

Minimize contact with fresh water containing infectious cercarial larvae
Water sanitation programmes and Praziquantel mass treatment

Reference:

CDC - See http://www.cdc.gov/parasites/schistosomiasis/health_professionals/index.html
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Lectures of tropical medicine and hygiene at LSTM