Schistosomiasis 

It is the most important helmenthic disease infecting 200 million people & killing 250,000 annually. 

Life cycle: Schistosomal larval, (cercaria) & penetrate human skin.  Ghycocalyx that protect the organism from osmotic is shed but it activates complement by alternative pathway. Schistosomes migrate into peripheral vasculature transverse to the lung and little in the portal venous system where they develop into adult male and female schistosomes. Females produce hundreds of eggs per day around which granulmas and fibrosis form the major manifestation in schistosomiasis. Some schist some eggs are passed from the portal veins through the intestinal wall into the colonic lumen are shed with the feces and released into fresh water, form to miracidia that infect the snail to complete the life cycle.

Pathogenesis 

1. S. mansoni eggs cause liver disease in multiple ways. The schistosoma eggs are direct hepatotoxicity.

2. Carbohydrate antigens of the eggs induce macrophage accumulation and granulomas formation mediated by TNF only TH¹ and TH²  helper cells.

TH² helper T-cells are responsible for eosinophilia mastocytosis and high level of serum in human schistosomiasis, because these cells secrete IL-3 and IL-4, which stimulate mastocytosis and IL-5, which is the growth factor for eosinophils. Resistance to reinfection by schistosomes after treatment correlates with IgE levels whereas, eosinophils major basic proteins may destroy larvae schistsomula.

3. Eggs release factors that stimulate lymphocytes to secrete a lymphokine that stimulate fibroblast proliferation and portal fibrosis the exuberant fibrosis which is out of proportion to the injury caused by the eggs and granucoma, occurs in 5% of persons infected with schistosomes and cause severe portal hypertension esophageal varicoses and ascites - the hallmark of severe schistosomiasis. 

Morphology: 

White granulomas scattered in the liver and gut. The center of the granuloma is the schistosoma eggs. The granuloma degenerate overtime and undergo fibrosis and calcification. The liver is darken by regurgitated pigments from the schistosoma gut which like malaria pigment are iron negative and accumulate in kuffer cells and splenic macrophages. 

Severe infection (s. mansoni & S. Japanicum) 

Colonic pseudopolyps 

Liver surface is bumpy and its cut section shows granuloma and wide spreading fibrous portal enlargement without distortion of the intervening parenchyma. 

Portal fibrosis (PIPE-stem fibrosis) many of  these portal triads lack a vein lumen causing perisinusoidal portal hypertension and severe congestive splenomegaly, esophageal varices. Schistome eggs diverted to the lungs through portal collateral may produce granulomatous pulmonary arteritis with intimal hyperplasia progressive arterial obstruction and ultimately heart failure (cor pulmonale). 

Patients with hepatosplenic Schistosomiasis have also increased frequency of mesangioproliferative glomerulonephritis or membranous glomerulonepritis in which glomeruli contain deposits of immunoglobulins and compliments but rarely schistosomal antigens.

S. hamatobium infection 

Massive egg depositions and early granuloma formation that when erode the vasculature (hamaturia). Latter the granuomas calcify and develop a sandy appearance and in severe cases, it causes concentric rim on the wall of the bladder forming calcified bladder on x- rays films.

When the urinary inflammation involves the ureteral orifices, it causes obstructive hydronephrosis and chronic pylonehphritis.  Urinary schistosomiasis is also associated with squamous cell carcinoma of the bladder that is commonly seen in Egypt.      

References

Bezabeh ,M. ; Tesfaye,A.; Ergicho, B.; Erke, M.; Mengistu, S. and Bedane,A.; Desta, A.(2004). General Pathology. Jimma University, Gondar University Haramaya University, Dedub University.