Schistosoma

Schistosoma species are dioecious blood flukes with a complex life cycle involving freshwater snails as intermediate hosts. Humans are infected when cercariae released from snails penetrate intact skin during freshwater exposure, causing an initial dermatitis (swimmer's itch). The larvae migrate through venous circulation to the lungs and liver, mature into adult worms, and pair up (male and female worms living together) in the mesenteric or vesical venous plexuses depending on species.

S. haematobium resides in the venous plexus of the bladder, causing hematuria, bladder wall fibrosis/calcification, and is a major risk factor for squamous cell carcinoma of the bladder. S. mansoni and S. japonicum inhabit the mesenteric veins, leading to granulomatous inflammation from egg deposition in the intestinal wall and liver, causing hepatosplenic disease, periportal ('pipestem') fibrosis, and portal hypertension without cirrhosis (leading to esophageal varices).

Pathophysiology is largely immune-mediated: eggs trapped in tissue provoke a granulomatous, Th2-driven response (eosinophils, IgE) that causes the fibrosis and organ damage, rather than the worms themselves. Chronic infection can lead to Katayama fever (acute serum sickness-like reaction) in early infection, and chronic complications like cor pulmonale (from egg embolization to lungs) or CNS granulomas.

Diagnosis is via microscopic identification of eggs in urine (S. haematobium - terminal spine) or stool (S. mansoni - lateral spine; S. japonicum - small rounded egg) or with serology/PCR. Treatment is praziquantel, which increases calcium influx into schistosome tegument causing paralysis and death of the worm.

High-yield associations: S. haematobium and bladder squamous cell carcinoma, portal hypertension without cirrhosis, eosinophilia in returning travelers, geographic distribution (S. haematobium - Africa/Middle East, S. mansoni - Africa/South America, S. japonicum - Asia).