1921
Volume s1-27, Issue 3
  • ISSN: 0002-9637
  • E-ISSN: 1476-1645
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Abstract

Summary and Conclusions

It has been demonstrated that experimental tsutsugamushi disease in Swiss mice and monkeys in the terminal stages is pathologically similar to the terminal stages of the disease in man. It is a disease in which there is widespread involvement of tissues of mensenchymal origin, an involvement that depends on lymphoid-macrophage proliferation, mobilization, and invasion. The lymphoid elements show signs of hyperplasia early in the disease. In Swiss mice, the spleen is the first organ to react, increased mitotic activity being noted on the second or third day post inoculation followed by hyperplasia. One or two days later the generalized systemic involvement begins, manifested by the appearance of the lymphoid-macrophage cells in the stroma of the various organs. Endothelial stickiness is prominent early in mice and monkeys but gradually subsides in the monkey as the convalescent period is reached. In neither experimental animals or man is the endothelium destroyed, but sometimes it appears swollen and hypertrophied. Likewise the blood vessel walls may be infiltrated with lymphoid-macrophage cells, but only rarely is the reaction severe enough to cause tissue necrosis. Perivascular cell collections increase in number and size as the disease progresses and persist during the healing period. Small focal necroses in the parenchyma of the various organs may be seen in the advanced stage of the disease particularly in the vicinity of the large cell collections. However, because of the lack of truly pathognomonic lesions, diagnosis of the disease should depend not only on tissue changes, but should include observations on the history of exposure to the mite vector, demonstration of the presence of the organism by blood or ground spleen passage to animals and by staining of organ impression smears, and finally, by observation of the trend of Proteus OX-K agglutination titers.

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/content/journals/10.4269/ajtmh.1947.s1-27.245
1947-05-01
2017-11-24
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