Mice with mild prolonged infection with Schistosoma mansoni showed a considerable variation in the appearance of the hepatic granulomas appearing around mature eggs in the course of infection. An earlier large, necrotic, exudative-proliferative lesion turned later into small, rounded granulomas composed of a few histiocytes and fibroblasts. This was interpreted as morphological expression of hypersensitivity and immunity developing in the course of prolonged infection. Gradual resorption of older granulomas and a more effective and economical response to new eggs were the principal mechanisms by which the host protected itself more efficiently. The mild prolonged infection was accompanied by portal inflammation and later also by fibrosis, which was similar to the early “pipe-stem” fibrosis as seen in human beings. Whether this was a late sequela of earlier changes or a progressive lesion due to the infection was not determined.
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Andrade et al. (1964) studied this question.
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