<i>Schistosoma mansoni </i>Nephropathy in Syrian Golden Hamsters: Effect of Dose and Duration of Infection

Abstract

In this work, 180 golden hamsters were infected with Schistosoma mansoni and 30 hamsters matched for age and sex served as controls. According to the number of injected cercariae, infected hamsters were divided into six main groups (20, 50,100,150, 200 and 250 cercariae). Each group was divided into five subgroups, according to the duration of infection after which animals were sacrificed (4,6,8,12 and 24 weeks). Control and infected hamsters were subjected to laboratory evaluations (serum creatinine, blood urea nitrogen, cholesterol, albumin, total protein and urine protein concentration) and histopathologic examinations of kidney and liver tissues. A significant proteinuria, hypoalbuminemia and hypercholesterolemia was observed in schistosome infected (50 cercariae or more) but not in the controls and the group infected with 20 cercariae. There was a significant correlation between these changes and duration of infection and the number of adult worm recovered from the mesenteric circulation at the end of the experiments. Histopathologic evaluation showed appearance of the circulating schistosome antigens, circulating anodic antigen (CAA) and circulating cathodic antigen (CCA), and of IgG glomerular deposits by the 6th week following infection; mesangial hypercellularity appeared early after infection (6–8 weeks), renal amyloid deposition appeared later (8–12 weeks). Egg antigens were not detected in the renal glomeruli. There was a significant correlation between the pathologic changes and duration of infection and the number of recovered adult worms from the mesenteric circulation. No histopathologic lesions were detected in controls and the group injected with 20 cercariae. A significant correlation was found between hepatic periportal fibrosis, amyloidosis and immune complex, deposition in the renal glomeruli. Hamsters did not tolerate infection with 150 cercariae or more for more than 12 weeks, and 20 cercariae caused no detectable glomerular disease. From this study, we concluded that S. mansoni infection causes nephropathy in the Syrian golden hamster. The disease became biochemically and histopathologically manifest by the 6th week following infection. Both immune complex deposition and renal amyloidosis stand as major pathogenic mechanisms. CAA and CCA are the major responsible antigens. Hepatic disease has an impact on the kidney lesion. 50 cercariae are the best dose to produce disease without early death of the animal. There is a significant correlation between the kidney disease and the duration and the load of S. mansoni infection.

Localization by Immunoelectron Microscopy of Schistosoma mansoni Antigens in the Glomerulus of the Hamster (Mesocricetus auratus) Kidney

“…Although our model is not the one suggested by Sobh et al [9], in which the animals developed a protracted and, therefore, prolonged infection, our light microscopy findings using methacrylate-embedded sections agree with their results. Mesangial cell hypercellularity was seen during the late phase of the experiment and did not affect all the glomeruli in animals infected with cercariae.…”

“…The use of the Syrian golden hamster as a model of experimental schistosomal nephropathy was initially studied by Hillyer and Lewert [8], but was more extensively explored by Sobh et al [9, 10]. These investigators demonstrated mesangial hypercellularity in hamsters infected 6–8 weeks before with 50 cercariae accompanied by IgG glomerular deposits.…”

“…Significant proteinuria, hypoalbuminemia, and hypercholesterolemia were observed in the infected animals. These findings were significantly correlated with the duration of infection and the number of adult worms recovered from the mesenteric circulation at the end of the experiment [9]. …”

“…Hillyer and Lewert [8] and, more recently, Sobh et al [9, 10] demonstrated that hamsters infected with S. mansoni also develop renal lesions due to exposure to the parasite.…”

Cryoglobulinaemic vasculitis and glomerulonephritis associated with schistosomiasis: a case study

“…Unlike antigen/antibodyinduced schistosomal glomerulopathy, where schistosomal antigen is deposited in the glomeruli complexed to IgG (15), renal damage and vasculitis associated with cryoglobulinaemia are independent of antigen deposition (4,5,10). Notably, rabbits infected with S. japonicum suffered cryoglobulinaemia and glomerulonephritis in the absence of schistosomal antigen deposition in the glomerular lesions (10).…”