Renal changes in golden hamsters experimentally infected with Leishmania D. infantum on top of Schistosoma mansoni infection.

In Egypt, Schistosomiasis mansoni is one of the most important parasitic disease of man. Besides, in the last two decades, indigenous cases of infantile visceral leishmaniasis have been reported. These two parasites affect the kidney causing renal histopathological changes. Thus, it was aimed to study the concomitant infection of L. d. infantum on top of S. mansoni infection in Syrian golden hamsters, the model animal for both parasites. The results showed that the renal changes were more or less the same as infection with either parasite alone. Both parasites produce mesangial cell proliferation and mesangial matrix increase. Some glomeruli showed complete replacement of the capillary tuft with structureless homogenous material. In one S. mansoni positive control hamster Schistosoma eggs were seen within granulomas and atrophic glomeruli. However, the lesihmanial infection, more or less suppressed the schistosomal infection. The leishmanial infection itself became more prominent and the renal changes it caused appeared earlier and were more obvious.

The validity of AG-NOR profile in schistosomal lesions of the urinary bladder.

AG-NOR was determined in the nuclei of thirty-five urinary bladder lesions, varying between benign and malignant schistosomal lesions and non schistosomal ones. The results showed that the assessment of AG-NOR in urinary bladder lesions can be valuable in distinguishing benign from malignant lesions of the urinary bladder and can be used as a prognostic parameter.

Histopathological study of the bilharzial affection on the bladder and ureter.

This study was carried out on 68 cases (50 bilharzial stricture lower ureter, eight vesico-ureteral reflux cases and ten control). In cases of reflux associated with bilharziasis heavy ova-deposition was obvious all through the ureteral wall especially per-ureteral sheath. Also heavy deposition in the bladder wall involved the detrusor and trigonal muscle with fibrosis and obliteration of Waldeyer's space and atrophy and fasciculation of detrusor and trigonal muscle. This implies ureteral rigidity, impaired mobility and compression against a firm detrusor buttress.

Detrusor morphology and pathology in relation to bladder outflow obstruction in bilharzial patients.

The light and electron microscopic structure of detrusor muscle of trabeculated urinary bladder from patients with urodynamically proved bilharzial outflow obstruction had been compared with normal detrusor muscle. In bilharzial outflow obstruction, the detrusor muscle bundles were formed of relatively smaller smooth muscle cells widely separated by dense connective tissue, fatty infiltration, bilharzial ova, inflammatory cells and hyalinosis. No evidence of smooth muscle hyperplasia, mitosis, or fibroblastic proliferation. At the level of electron microscopy. The connective tissue infiltration was proved to be microfibriles apparently in continuity of the basal lamina of the smooth muscle. These pathological changes can explain both the morphological and urodynamic changes in bilharzial urinary bladder outflow obstruction.