Oral or intraperitoneal inoculation of suspensions of liver from fatal human cases of infectious hepatitis in Nigeria was found to cause a subclinical disease in patas and some other species of West African monkeys; a few animals became ill and a very few died. The disease was maintained in serial monkey-to-monkey passage by the oral or intraperitoneal inoculation of infected monkey livers. It appeared to increase in severity on passage. The most frequently observed signs of the disease were neutropenia and liver lesions. The neutropenia was rapid in onset after the oral, but slower after the intraperitoneal inoculation of infected liver. It was modified when concurrent bacterial infection occurred in the 2nd and subsequent weeks. The liver lesions varied in severity and frequency of occurrence. Usually they consisted of small foci in which the liver and Kupffer cells showed an increase in nucleolar and cytoplasmic basophilia. Necrosis was rare. These foci and the portal tracts were infiltrated with inflammatory cells. In some animals the changes were absent and in others they were slight and difficult to detect. In a few animals they became widespread throughout the liver. Because there was neither swelling nor necrosis of liver cells, tests for liver function showed values within the limits of normal. Electron microscopy of the liver showed irregularity of the nuclear membrane, increased numbers of mitochondria, hypertrophy of the Golgi complex and internal structures within the lysosomes. No virus-like particles were seen. The infective agent was stable to heating at 56°C for 30 min. and exposure to ether and freezing. It passed through bacteria-stopping filters. It was not isolated in artificial media or tissue cultures and did not cause clinical disease in laboratory animals other than monkeys.


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