Fibrotic hepatic schistosomiasis caused by S. mansoni usually develops in around 5–15 years, while it can take less time for S. japonicum. Symptoms may include:
Esophageal varices (can cause life-threatening esophageal variceal bleed)
Ascites (end-stage)
Caput medusae
Enlarged spleen and liver
Complications may include:
Neuroschistosomiasis due to portosystemic anastomoses from portal hypertension
Pulmonary Schistosomiasis due to portosystemic anastomoses from portal hypertension

Pulmonary schistosomiasis
Portal hypertension secondary to hepatosplenic schistosomiasis can cause vessel connections between the portal (liver and gut) circulation and systemic circulation to develop, which creates a pathway for the eggs and worms to travel to the lungs. The eggs can be deposited around the alveolar capillary beds and causes granulomatous inflammation of the pulmonary arterioles followed by fibrosis. This leads to high blood pressure in the pulmonary circulation system (pulmonary hypertension), increased pressure in the right heart, enlargement of the pulmonary artery and right atria, and thickening of the right ventricular wall.Symptoms of pulmonary hypertension may include:

Shortness of breath
Chest pain
Feeling tired
Fainting during physical exertion

Urogenital schistosomiasis
The worms of S. haematobium migrate to the veins around the bladder and ureters where they reproduce. S. haematobium can produce up to 3000 eggs per day, these eggs migrate from the veins to the bladder and ureter lumens, but up to 50 percent of them can become trapped in the surrounding tissues causing granulomatous inflammation, polyps formation, and ulceration of bladder, ureter, and genital tract tissues. This can lead to blood in the urine 10 to 12 weeks after infection. Over time, fibrosis can lead to obstruction of the urinary tract, hydronephrosis, and kidney failure.
Life Cycle
The excretion Schistosome eggs in urine or feces depending on species
The hatching of the eggs leading to release of the free-swimming, ciliated larvae called miracidia
Miracidia find and penetrate the snails, which are the intermediate hosts (specific species of snails is dependent on the species of schistosoma)
Within the snails, two successive generations of sporocysts occur
Sporocyts gives rise to the infective free-swimming larvae with forked tails called cercariae, and they leave the snails to enter the water
Cercariae finds the human hosts and penetrate their skin
Upon entrance into the human hosts, cercariae lose their tails and become schistosomulae
The schistosomulae travels to the lungs and heart via the venous circulation
They migrate to the portal venous system of the liver where they mature into the adult form with two separate sexes
The adult male and female are paired together, exits the liver via portal venous system, and travel to the venous systems of the intestines or bladder (species dependent) and produce eggs
S. japonicum - superior mesenteric veins (but can also inhabit inferior mesenteric veins)
S. mansoni - inferior mesenteric veins (but can also inhabit superior mesenteric veins)
S. haematobium - vesicular and pelvic venous plexus of the bladder (occasionally rectal venules)
S. intercalatum and S. guineensis - inferior mesenteric plexus (lower portion of the bowels compared to S. mansoni)Schistosomes can live an average of 3–5 years, and the eggs can survive for more than 30 years after infection. Other hosts
Schistosomiasis is also a concern of cattle husbandry and mice. O-methyl-threonine is weakly effective in mouse schistosomiasis but is not in use.