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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.

Ectopic Bilharziasis is discussed and two cases of ectopic pharyngeal affections are reported. The five theories advocated to explain how ectopic lesions can develop outside the portol-caval system are discussed. The clinical picture, age, diagnosis and follow-up of such lesions are mentioned.

A village, 20 miles north of Cairo, with a census population of 2010, was surveyed in 1976 by the Center of Disease Control (CDC) and the Egyptian Ministry of Health for hepatitis B surface antigen (HBsAg). Ninety individuals (47 males and 43 females were positive for HBsAg (a prevalence rate of 4.5%). Forty-two of the 47 males were the subject of this study. They were admitted to the Naval Medical Research Unit Hospital 2 years later. They all had active Schistosoma mansoni infection. Nineteen of the 42 were carrying HBsAg and the remaining 23 were negative for hepatitis antigen at this time of investigation. Histological examination of percutaneous liver biopsies showed chronic-active hepatitis in five of 17 HBsAg carriers including two with additional cirrhosis. Two others with clinical evidence of cirrhosis could not safely have biopsies taken. Two of these 19 persons died and three became incapacitated over 2 years of further observation. Of the 23 individuals who had transient HBsAg in 1976 and equally heavy S. mansoni infection, evaluation in 1978 showed chronic active hepatitis in one, and at re-evaluation 2 years later, one had become unable to work but none had died. Ten other individuals (military recruits) from different villages of the Nile Valley who had no schistosomiasis but were carriers of HBsAg, were symptom free and liver biopsy showed chronic active hepatitis in one individual and no morbidity or mortality in 2 years. Morbidity of chronic hepatitis B infection in S. mansoni infected persons appears to be unusually severe compared with hepatitis B infection in other populations.

Liver biopsies of four patients with hepatosplenic schistosomiasis, two patients with schistosomiasis and chronic active hepatitis, two patients with chronic active hepatitis and four control patients with no clinical evidence of either disease, were examined by standard light microscopic techniques, electron microscopy and immunocytochemical staining for collagen type I, III and B. Pure schistosomiasis showed the classical "clay-pipe stem fibrosis" and granulomata composed of eosinophils, macrophages and lymphocytes. In that group, the hepatocellular damage was less conspicuous than in the groups with chronic hepatitis and was usually confined to the granulomatous or fibrotic areas. Destruction of the normal architecture and infiltration by macrophages and lymphocytes with severe damage of hepatocytes was found only in the cases of chronic active hepatitis, with or without associated schistosomiasis. Increased collagen deposits were demonstrated in all three groups. Types I, III and B were found in the enlarged portal triads and fibrotic septa. The intranodular or intralobular collagen stained negatively for type I and strongly positive for types III and B.

Thirty-five male patients with decompensated hepatosplenic schistosomiasis were longitudinally studied and divided into 3 Groups; with hepatitis B surface antigen (HBsAg) or antibody (anti-HBs) and a control group negative to both. Patients with HBsAg were persistently carrying the antigen as estimated by radioimmunoassay (RIA) for up to 3 years and when compared with the other 2 groups, they had significantly higher serum glutamic transaminases, their liver biopsy showed more destructive liver cell lesions in the form of chronic active hepatitis or liver cirrhosis, they were refractory to diuretic treatment and had higher mortality rate (64% in 3 years compared to 22% and 33% in the other 2 groups). The majority of patients with dual infection are at greater risk in spreading hepatitis B as they proved to carry the 'e' antigen.

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.

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.

We determined collagen synthetic rates and utilization of key amino acid precursors of collagen in slices of wedge liver biopsy specimens obtained at required surgery from 9 patients with hepatosplenic schistosomiasis and from 4 control patients. The liver specimens from the patients with schistosomiasis showed advanced fibrosis, with histologic evidence of schistosomiasis alone in four, and both schistosomiasis and chronic active hepatitis in five cases. Liver slices were incubated with radioactive proline, arginine and glutamine, using quantitative assay conditions validated earlier for murine schistosomiasis. Collagen peptide synthesis in slices from all nine fibrotic liver specimens was 4- to 25-fold greater than normal and correlated positively with liver collagen content, which was 2- to 5-fold greater than normal. Free proline, an amino acid that may contribute to regulation of collagen peptide synthesis, was increased in six of the nine fibrotic liver specimens, and proline was actively formed from arginine in liver slices from all specimens. These measurements of the initial steps of collagen biosynthesis in fibrotic human liver are quantitatively similar to those previously made of the same processes in experimental animals.

Kidneys were studied by light microscopy in 246 consecutive autopsies in Cairo, Egypt. Glomerulonephritis was not related to the presence or intensity of either S. haematobium or S. mansoni infection, and mesangial thickening and proliferation were also unrelated to schistosome infection. Acute and chronic pyelonephritis were also unrelated to the presence of schistosome infection.