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Reactions of the connective tissue in chickens to Plasmodium gallinaceum and Plasmodium lophurae. I. Histopathology during initial infections and superinfections



Reactions of the connective tissue in chickens to Plasmodium gallinaceum and Plasmodium lophurae. I. Histopathology during initial infections and superinfections



Journal of Infectious Diseases 97(2): 99-136



Connective tissue changes were studied in various tissues taken from chickens at closely spaced intervals throughout the course of infection and superinfection with P. gallinaceum and with P. lophurae. The changes took place chiefly in the spleen and to a lesser extent in the liver, bone marrow and bursa Fabricii. Little or no reaction occurred in other tissues. All activities were roughly correlated with the rise and fall of the parasitemia in initial infections and superinfections and chiefly involved (1) the phagocytosis of parasitized red cells, parasites and parasite debris including malarial pigment by macrophages, chiefly of the spleen, liver and bone marrow; (2) the destruction of red cells, lymphocytes and other lymphoid cells, macrophages and granulocytes; (3) the mitotic proliferation of lymphoid cells in lymphatic and myeloid tissues and the production of granulocytes and red cells chiefly in the bone marrow and spleen; (4) the marked increase of abnormally large lympho- cytes by mobilization from reticular cells and mitotic proliferation, (5) the development of plasma cells, and (6) the production of macrophages homoplastically from reticular cells and hetero-plastically from lymphocytes (and hemocytoblasts) and mono-cytes. All of these activities were more stereotyped in mild than in intense persisting initial infections and were initiated more rapidly in superinfections. Special attention was paid to the role of the mesenchymal reserves (both fixed and free cells) in the immune reactions. Among the free mesenchymal reserves there was an interplay between the loss and production of lymphoid cells, especially in the spleen and bone marrow. Thus, during the first part of initial infections, a progressive depletion of lymphocytes in the spleen reached its maximum in terminal lethal infections and was associated with the degeneration of many lymphocytes and the development of others into macrophages. Production of lymphocytes, which began early, compensated for this loss and produced a lymphoid hyperplasia during the late acute rise in mild infections and during the developed infection in persisting infections. The over-all lymphoid activities were reflected in a remarkable manner by the number of nodules in the spleen. Very large lymphocytes frequently developed into plasma cells and appeared to be a primitive free cell which often migrated to various tissues and played a major role in the development of various connective tissue cells associated with malarial immunity and repair. After superinfection, lymphoid depletion and lymphoid hyperplasia were initiated sooner and subsided more rapidly. Less pronounced changes occurred in erythropoietic and myelopoietic centers.

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Accession: 023464122

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PMID: 13263639

DOI: 10.1093/infdis/97.2.99


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