岡山医学会
Acta Medica Okayama
0030-1558
71
11-2
1959
Ectromelia virusに依る実験的肝炎の研究 第2編 電撃性肝炎の成因に関する二,三の考察
7841
7848
EN
Tatsuo
Tokiya
1. The greater is the amount of Extromelia virus incoculated intraperitoneally the earlier is the onset of the symptoms and death of mice, revealing a straight live rise in the erythrocyte agglutination value. In contrast to the serum affinity antigen-antibody reaction observable in the groups inoculated with a small amount of the virus, both groups inoculated with virus supernatant diluted 20-fold and 100-fold respectively show relatively or absolutely no reaction and die. 2. The toxicity of the so-called concomitant substance is trivial. 3. When the mice with incomplete immunity are reinfected with Extromelia virus, the pathological picture is controlled only by the quantity of the virus Inoculated. 4. When the mice infected with Extromelia virus are enforced to labor, these animals die at the early stage of the onset of symptoms and the recovery mechanism of pathologic changes is delayed. 5. Therefore, the principal cause of the electro-shock hepatitis lies in the toxicity of the virus and the quantity of virus inoculated and it is in no way associted with the incomplete immunity. Moreover, the enforcing labor seems only to aggravate the pathologic conditions of the animals, showing absolutely no process of recuperation and extremely little infiltration of round cells. 6. Histological changes are especially marked in the liver, spleen and bone marrow; and in the lung, hemorrhagic interalveolitis and nephro-nephritis can be recognized in the kidney. 7. Pathologic changes at the peak of the infection in the animals inoculated with a great quantity of Extromelia virus resemble closely to the histological changes of viscera in the human electro-schook hepatitis; and in the case inoculated with a relatively large amour. of the virus the changes resemble to the visceral histological changes at the peak in th. human hepatitis. Moreover, the histological picture of the liver during the period from the virus inoculation to the peak of the infection and the same in the animals escaped the death, taking the similar course as at peak of the human hepatitis observable by the biopsy, resemble the picture of the liver in the human hepatitis at the later stage of recuperation. 8. The pathological picture in the mice infected with Ectromelia virus closely resemble that in the humsn infectious hepatitis and both seem to revel mesenchymal tissue reaction as the basic histological changes.
No potential conflict of interest relevant to this article was reported.
岡山医学会
Acta Medica Okayama
0030-1558
71
11-2
1959
Ectromelia virusに依る実験的肝炎の研究 第1編 Ectromelia virus感染Mausの肝臓内Virus量の消長について
7831
7839
EN
Tatsuo
Tokiya
By inoculating a given amount of Extromelia virus to roups of mice, intrapeitoneally, orally, in toe foot, through the nasal passage, or subcutaneously (the back), and by preparing the suppernatant of the liver emulsion from these infected mice, the author performed erythrocyte agglutination tests (Hists's phenomenon); and obtained the fhllowing resnlts. 1. Juding from the changes in the agglutination values, the most vigorous proliferation of the virus seems to occur at the early stage of the infection and of the onset of symptoms in every group. 2. At the peark of the infection the erythrocyt agglutination value in every group falls rapidly, and this seems to be due to the antigen-antibody reaction. 3. The reticulo-endothelial system is not the necessary site for the infection of Extromelia virus nor doest it has any function as the stie of the antibody production. 4. It seems that the antigen-antibody reaction of Extromelia virus is the serum affinity antige-antibody reaction and it is represented by the changes in the blood vessel listem as its main symptoms. 5. The difference in the distribution of pathologic changes between the diffuse hapatic changes in ths group infected intraperitoneally or orally and localized changes in the group infected unber foot, via nasal passage or subcutaneously (the back) may be interpreted as not to be dependent on the reaction pattern of allergic inflammation bnt to be due to the anatomical difference in the infection route. 6. This interpretation will offer a certain theoretical basis in support of the assumptions made in ous department as regards the pattern of infectious hepatitis and the route of its infection.
No potential conflict of interest relevant to this article was reported.