Low-grade schistosome infection is often well tolerated, except for the danger of ectopic lesions; the risk of life-threatening pathology increases with rising worm burdens. At present, quantitative stool or urine egg counts do not reliably measure individual infection intensity, especially in adult patients, and more precise methods are needed on which to base therapeutic decisions. Timely schistosomicidal treatment will prevent or improve bilharzial lesions, often dramatically, but can not reverse established liver pipe stem fibrosis. Pathological studies in Ibadan and Cairo have shown that in schistosomiasis haematobia the frequency of obstructive uropathy increases in relation to the egg load in urinary tissues. Obstruction, in turn, predisposes to bacterial superinfection and is a significant cause of renal failure and death in highly endemic populations. Urinary bilharzial lesions are most active in the young and tend to become inactive in older patients. Urinary tissue egg burdens first rise, plateau, and ultimately decrease with age, most sharply after the fifth decade. The relationship between tissue egg burden and 24-hr urinary egg output varies according to stage of activity, while the severity of disease depends on egg burden regardless of stage. Therefore, during the inactive stage, severe pathology can coexist with a minimal urinary egg output. Both clinical and autopsy statistics show a correlation between the frequency and the intensity of bilharzial infection. Most of the severe pathology occurs in population groups with an autopsy frequency above a threshold of 30%. The clinical and epidemiological implications of these findings are discussed.