Urogenital Schistosomiasis-History, Pathogenesis, and Bladder Cancer

Abstract

Schistosomiasis is the most important helminthiasis worldwide in terms of morbidity and mortality. Most of the infections occurs in Africa, which about two thirds are caused by Schistosoma haematobium. The infection with S. haematobium is considered carcinogenic leading to squamous cell carcinoma (SCC) and urothelial carcinoma of the urinary bladder. Additionally, it is responsible for female genital schistosomiasis leading to infertility and higher risk of human immunodeficiency virus (HIV) transmission. Remarkably, a recent outbreak in Corsica (France) drew attention to its potential re-mergence in Southern Europe. Thus far, little is known related to host-parasite interactions that trigger carcinogenesis. However, recent studies have opened new avenues to understand mechanisms on how the parasite infection can lead cancer and other associated pathologies. Here, we present a historical perspective of schistosomiasis, and review the infection-associated pathologies and studies on host-parasite interactions that unveil tentative mechanisms underlying schistosomiasis-associated carcinogenesis.

Keywords: bladder cancer; pathogenesis; schistosomiasis; squamous cell carcinoma.

Figure 1

(A) Cystoscopy view of the posterior bladder mucosa with UGS lesions, granulomas, ulcers and tumor. (B) Histology from the bladder mass biopsy showing S. haematobium ova (black circles) and SCC of the bladder (expression of sialyl-Le^a).

Figure 2

Metabolites identified in urine with UGS and UGS-associated SCC that were not present in urine of healthy individuals [65]. The metabolites were divided in three groups: catechol estrogen-like (green), catechol-estrogen-DNA adducts (red) and 8-oxodG derivatives (blue). The catechol estrogen-DNA adducts may be a consequence of interaction of catechol estrogen derivatives with host DNA. On other hand, 8-oxodG derivatives may be a result of liberation of nitrogenous bases from DNA and/or its oxidation.