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Four hundred consecutive autopsy cases were examined in Cairo, Egypt. Sixty percent of cases had Schistosoma haematobium eggs in the tissues and 25% also were infected with S. mansoni. Only a quarter of S. haematobium infections were active, while nearly two-thirds of S. mansoni cases remained active. Adult S. haematobium and S. mansoni were effectively recovered from the mesenteric circulation by a combination of perfusion and dissection. Quantitative recovery from the genitourinary system was reasonably complete, although small numbers of worms were missed in the dissection of these organs.

Further analysis of the data obtained from 190 unselected autopsies at the University of Cairo (Faculty of Medicine) hospitals reinforces our conclusion that a high prevalence of urinary schistosomiasis leads to infection intensity causing severe uropathy and mortality, both directly and by way of complications and sequelae. Based on histological study, two stages of urinary schistosomiasis must be considered in epidemiological work: "active disease", characterized by significant egg excretion; and "inactive disease", in which eggs are excreted rarely. The proportion between active and inactive cases is progressively reversed with advancing age, while mean tissue egg burdens rise, plateau, and ultimately decrease, most sharply beyond 50 years of age. A model of the progression of active disease has been derived from the relations of individual organ egg burdens to overall infection intensity, showing that both the onset and the termination of oviposition probably begin in the urinary bladder and spread centrifugally. Therefore, extravesical activity may persist longer than bladder activity. Severe uropathy and mortality occur at all stages of the disease and depend principally, but not exclusively, on egg burden, i.e., on infection intensity. Correlations of infection intensity with degree of uropathy show that severe disease is quantitatively separable from incidental disease by its tissue egg burdens and lesions. However, the factors determining death from urinary schistosomiasis are only partly understood. They include bilateral upper obstructive uropathy and, probably, focal egg concentrations leading to rapid obstruction, such as aberrantly high egg burdens in the left ureter relative to those in the bladder. Analysis of epidemiologically homogeneous population groups reveals close mutual relationships between the total frequency of infection (active plus inactive), the intensity of infection, and the frequency of severe uropathy. A statistical model predicts that any rise in frequency beyond a 30% threshold will result in a linear increase in the frequency of severe disease, whereas below that threshold the bulk of infections will be incidental. These insights, applicable only to pathological material, must be complemented by efforts to establish clinical and laboratory criteria defining the severity and stages of urinary schistosomiasis in living patients, and to examine their population dynamics, so that effects of therapeutic and preventive measures may be evalulated more precisely.

Adult Schistosoma hematobium and S. mansoni were recovered at autospy. The number of eggs of both species present in the tissues and passed in the excreta was related to the number of female worms (worm pairs) recovered. Only 26% of the S. hematobium infections were active at the time of necropsy. 47% of S. hematobium females were in the mesenteric circulation and 52% were in the genitourinary organs. S. hematobium worm pairs were sedentary laying eggs in single sites for prolonged periods. In addition the worm pairs seemed to be clustered in active genitourinary lesions. S. hematobium eggs calcified and accumulated in the tissues and a geometric mean of 600000 eggs/worm pair was found. Large numbers of eggs remained in inactive cases. There was a significant increase in eggs/female worm in older persons. The relative contribution of egg accumulation (increasing the numerator) and worm death (decreasing the denominator) to this phenomenon are not known. In contrast S. mansoni eggs were not retained in the tissues to the degree exhibited by S. hematobium. There was an apparent equilibrium between egg deposition and egg excretion or destruction. A geometric mean of 15900 eggs/worm pair was present and did not change with age. The total number of eggs/female worm and the relative proportion of eggs in the lungs liver and intestines were similar to those seen in Brazilian cases of S. mansoni infection. The number of eggs/female worm found in feces was lower than that noted in Brazil. S. hematobium infections were much heavier in cases also infected with S. mansoni than in those with pure S. hematobium infection. No pure S. mansoni infections were seen. S. mansoni infection appeared unaffected by S. hematobium infection except for calcification and accumulation of S. mansoni eggs in the genitourinary system. (authors)

In a series of 32 unselected consecutive autopsies of Egyptian male adults, we found a significant prevalence of schistosomal obstructive uropathy (SOU) and of precursor lesions of stenosis, fibrosis and induration of the ureters (62.5%). Lower urinary tracts with obstructive uropathy had a significantly higher total egg burden (TEB) than did lower urinary tracts with any other type of gross lesion (i.e., benign prostatic hypertrophy, other urethral outlet obstruction, or SOU precursor lesions). In turn, lower urinary tracts with any type of gross change had higher egg burdens than did tracts which appeared grossly normal. Lower urinary tracts with any type of gross lesion had significantly larger seminal vesicles than did tracts which were grossly normal. Moreover, relative weight of seminal vesicles could be correlated with the S. haematobium egg burdens in the seminal vesicles. In a series of lower urinary tracts taken from unselected consecutive American autopsies, seminal vesicle weight could be correlated with increase in prostatic weight in those tracts with prostatic hypertrophy; the same correlation could not be found in tracts without prostatic hypertrophy. Thus, seminal vesicle hypertrophy appears to correlate with obstructive uropathy in general, not solely obstructive uropathy of schistosomal origin. Digital evaluation of seminal vesicle size may be useful in the clinical evaluation of such patients.

Further analysis of the data obtained from 190 unselected autopsies at the University of Cairo (Faculty of Medicine) hospitals reinforces our conclusion that a high prevalence of urinary schistosomiasis leads to infection intensity causing severe uropathy and mortality, both directly and by way of complications and sequelae. Based on histological study, two stages of urinary schistosomiasis must be considered in epidemiological work: “active disease,” characterized by significant egg excretion; and “inactive disease,” in which eggs are excreted rarely. The proportion between active and inactive cases is progressively reversed with advacing age, while mean tissue egg burdens rise, plateau, and ultimately decrease, most sharply beyond 50 years to age. A model of the progression of active disease has been derived from the relations of individual organ egg burdens to overall infection intensity, showing that both the onset and the termination of oviposition probably begin in the urinary bladder and spread centrifugally. Therefore, extravesical activity may persist longer than bladder activity. Severe uropathy and mortality occur at all stages of the disease and depend principally, but not exclusively, on egg burden, i.e., on infection intensity. Correlations of infection intensity with degree of uropathy show that severe disease is quantitatively separable from incidental disease by its tissue egg burdens and lesions. However, the factors determining death from urinary schistosomiasis are only partly understood. They include bilateral upper obstructive uropathy and, probably, focal egg concentrations leading to rapid obstruction, such as aberrantly high egg burdens in the left ureter relative to those in the bladder. Analysis of epidemiologically homogeneous population groups reveals close mutual relationships between the total frequency of infection (active plus inactive), the intensity of infection, and the frequency of severe uropathy. A statistical model predicts that any rise in frequency beyond a 30% threshold will result in a linear increase in the freqency of severe disease, whereas below that threshold the bulk of infections will be incidental. These insights, applicable only to pathological material, must be complemented by efforts to establish clinical and laboratory criteria defining the severity and stages of urinary schistosomiasis in living patients, and to examine their population dynamics, so that effects of therapeutic and preventive measures may be evaluated more precisely.

In a series of 32 unselected consecutive autopsies of Egyptian male adults, we found a significant prevalence of schistosomal obstructive uropathy (SOU) and of precursor lesions of stenosis, fibrosis and induration of the ureters (62.5%). Lower urinary tracts with obstructive uropathy had a significantly higher total egg burden (TEB) than did lower urinary tracts with any other type of gross lesion (i.e., benign prostatic hypertrophy, other urethral outlet obstruction, or SOU precursor lesions). In turn, lower urinary tracts with any type of gross change had higher egg burdens than did tracts which appeared grossly normal. Lower urinary tracts with any type of gross lesion had significantly larger seminal vesicles than did tracts which were grossly normal. Moreover, relative weight of seminal vesicles could be correlated with the S. haematobium egg burdens in the seminal vesicles. In a series of lower urinary tracts taken from unselected consecutive American autopsies, seminal vesicle weight could be correlated with increase in prostatic weight in those tracts with prostatic hypertrophy; the same correlation could not be found in tracts without prostatic hypertrophy. Thus, seminal vesicle hypertrophy appears to correlate with obstructive uropathy in general, not solely obstructive uropathy of schistosomal origin. Digital evaluation of seminal vesicle size may be useful in the clinical evaluation of such patients.

The distribution of S. haematobium eggs in urinary bladders containing tumors and removed at surgery has been studied; the majority of these tumors are well differentiated squamous cell carcinomas. The same three anatomic patterns of egg accumulation described in part I of this series (noncancerous lower urinary tracts) were found in these cancerous bladders, but, in addition, most of the tumors were surrounded by a collar of heavy S. haematobium egg deposition. The egg burdens in these collars were, on the average, twice the average egg burden in the remainder of the urinary bladder. These collars do not seem to be artifacts created by growth of the tumor and subsequent displacement of the adjacent normal tissue, creating a region of heavy egg concentrations; rather, these heavy S. haematobium egg concentrations seem to act as promoters of urothelial carcinogenesis.

We performed 400 consecutive autopsies in Cairo, Egypt. The intensity of schistosome infection in these cases was measured by counting adult worms recovered by perfusion and dissection and by counting eggs in the tissues of infected cases. Symmers' clay pipestem fibrosis of the liver was clearly related to the presence and intensity of Schistosoma mansoni, but not S. haematobium, infection. Morphologic findings in cases with Symmers' fibrosis were comparable to those in Brazilian cases, and the intensity of S. mansoni infection associated with Symmers' fibrosis was similar in Brazil and Egypt. The fine bilharzial periportal fibrosis described by Hashem was not identified in our material, and Symmers' fibrosis was present in all cases of portal hypertension caused by schistosomiasis. Schistosome eggs were found concentrated in areas of portal fibrosis of cases with Symmers' fibrosis. In the absence of Symmers' fibrosis, eggs did not concentrate in large portal areas regardless of the intensity of infection or the presence of lesser degrees of portal fibrosis. We thus feel it unlikely that Symmers' fibrosis is formed by the fusion of fibrotic granulomas around the schistosome eggs.