SCHISTOSOMIASIS: REVIEW OF AN IMMUNE COMPLEX DISEASE

BACKGROUND: Morbidity due to human schistosomiasis is associated with host immune responses which result in immune based inflammation, granuloma formation and fibrotic lesions. MATERIALS AND METHODS: This is a review of the literature on the immunology of schistosomiasis and the description of the immunopathogenesis of the disease. Relevant articles were retrieved using electronic search and hand search of published literature. RESULTS: Host responses which include immune based inflammation, granuloma formation and fibrotic lesions are aimed at destroying schistosome ova lodged in the liver, intestinal and bladder walls, and other tissues. At the site of the infection, ‘swimmers’ itch is due to physical damage to the skin by proteases and other toxic substances secreted by cercaria. During intestinal Schistosomiasis, the parasitic ova are lodged in the liver provoking fibrogenesis, while during urinary schistosomiasis pathology is attributed to the formation of granuloma along the urinary tract, there is fibrosis which lead to strictures, calcification and urodynamic abnormalities. The classic descriptions of schistosomiasis-related morbidity focus on pathologies unique to schistosome infection: periportal fibrosis for intestinal schistosomiasis and bladder deformity and h y d r o n e p h r o s i s


INTRODUCTION
Schistosomiasis is a cause of significant parasitic morbidity and mortality in endemic countries.It is also known as bilharziasis after Theodor Bilharz who discovered the causative agent in Egypt in 1851.The disease has a relatively low mortality but high morbidity; causing severe debilitating illness in millions of people.It is caused by an infection with Schistosoma species of helminthic flat worms known as flukes belonging to the class Trematoda of the 1 phylum Platyhelminthes .The parasite 2 3 afflict at least 243 million people , Most infections are subclinical but may progress to chronic forms characterized by the presence of liver, intestinal and kidney 4 involvement .Schistosoma parasites display considerable 5 biodiversity in habitat there are two major forms of schistosomiasis: intestinal caused by four main species S.mansoni, S.japonicum, S. mekongi, S. guineensis and S. intercalatum while urogenital form of the disease is caused 1, 4 by S. haematobium

METHODS
Information for this review were from the comprehensive search of titles related to the immunology of schistosomiasis using PUBMED and other bibliographic data bases between 1985 and 2016 using key words, i m m u n o l o g y, i m m u n o p a t h o g e n e s i s , epidemiologic trends and pathology of schistosomiasis.Relevant websites such as that of the World Health Organization (WHO) were also searched.

LIFE CYCLE
Infection is initiated by the infectious cercariae which burrow into the skin, transform into schistosomulae and then enter the vasculature, migrate to the portal system where they cross the endothelium and basement membrane of the vein and traverse the intervening tissue, basement membrane and epithelium of the intestine (S. mansoni, S. japonicum and other associated species) or bladder (S. haematobium).Adult male and female worms mate and produce fertilized eggs in the veins of their human hosts where they live for an average of between 3-19 years, with longevity records that extend for There is no sex predilection to infection both s e x e s a r e e q u a l l y s u s c e p t i b l e t o schistosomiasis; different local, cultural and social practices may predispose either sex to higher infection.

Immunopathogenesis
The mechanism of pathogenicity of Schistosoma is attributable to the antigenic secretions of the parasites which perturbs the immune system of the host; including type I confront , the challenges posed stimulate humoral and cellular responses.The life cycle stages which express antigens include juvenile worms, adult worm and egg: p e n e t r a t i n g c e r c a r i a e , m i g r a t i n g schistosomulae, adult worm and eggs 15,16 produced by the adult worm.There is an overriding differential pattern in the host's immune responses against wormderived antigens when compared to egg 17 derived antigen.This is seen as early high level responses to soluble egg antigen (SEA) 18, that decreases as infection becomes chronic.

19, 20
However responses to soluble worm antigen preparations (SWAP) rises early in the course of infection and continues to be expressed 21 throughout the chronic stage of infection.During infection with any Schistosoma species, chronic disease is the result of the ongoing host response to accumulating tissue-trapped eggs.In, S. mansoni and S. japonicum infections, the liver is the principal site that is affected because, many of the eggs are carried by the blood into this organ and the sinusoids are too narrow for the eggs to traverse.This is a dead end for the eggs which eventually die within the tissue.Symmers' fibrosis of the liver which may result in portal hypertension and congestive splenomegaly is the most severe is extremely slow; due to the following hypotheses: i) that dying worms are the main source of protective antigen which is delayed 29 by the long parasite lifespan; ii) exposure to certain threshold level of antigen is required 30 before protective response is stimulated.Despite the long time to taken to develop some degree of protective immunity, it rarely 27 results in sterile immunity.In acute schistosomiasis, after initial infection with S.mansoni, S.japonicum or S. haematobium, a serious illness accompanied by high fever (Katayama fever) may be seen.This is due to the release of soluble parasite antigen into the circulation as the worms 1 mature and begins to release eggs.
Katayama fever is commonly associated with S.japonicum infection and is probably due to larger number of eggs released by the species.The onset of symptoms is about 20-40 days after exposure.This fever is less common in S.mansoni and rare with S. haematobium CONCLUSION This review is summary of the immunology of schistosomiasis which reflects the pathogenesis of the disease in humans.Host i m m u n e r e s p o n s e s t o t h e v a r i o u s developmental stages of the parasite produce cell mediated responses, granulomatous reaction and fibrosis.

REFERENCES:
1 14and type IV hypersensitivity reactions.Life cycle stages of the parasite express several antigens that the host immune system15 16