In vivo microscopic observations have elucidated the pathophysiology of hepatosplenic schistosomiasis mansoni in the mouse. Numerous schistosome eggs trapped in the interlobular portal venules partially or completely obstruct flow. Each egg is capable of obstructing blood flow to about 10 functional hepatic units (defined in text). In mice with severe hepatosplenic disease and portal hypertension, egg loads may reach 10,000 per gram of liver, but they block blood flow to only 6% of the total number of functional units. The host's granulomatous and fibrotic reaction to the eggs, which more than doubles the weight of the liver, imposes an extensive presinusoidal block to liver blood flow. Neovascular formation occurs in the scar tissue and provides a bridge between the presinusoidal vasculature and the sinusoids. The rapidity of the blood flow in these new vessels suggested that they were arterial; this was confirmed when ligation of the hepatic artery resulted in cessation of blood flow not only in the scar tissue but also in the adjacent sinusoids and central venules. On the basis of these studies, the pathophysiology of hepatosplenic schistosomiasis mansoni may be summed up as follows: schistosome eggs and the granulomatous inflammation and scar tissue around them gradually shut down portal venous flow. This results in portal hypertension, congestive splenomegaly, and the development of portal-systemic collateral circulation. Compensatory arterialization occurs through neovascular formation and this maintains sinusoidal perfusion and liver function within relatively normal limits.
Professor, Department of Anatomy.
On leave of absence from Cairo University, United Arab Republic: Lecturer of Clinical Tropical Medicine. Supported by the Rockefeller Foundation. Present address: Department of Medicine, Howard University, Washington, D. C.
Associate Professor, Department of Medicine and Preventive Medicine. Research Career Development Award number 5K03-AI 814-08 of the National Institutes of Health.