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Please use this identifier to cite or link to this item: http://hdl.handle.net/10466/2874

Title: Cerebrospinal Nematodiasis as a Provoking Factor in Japanese Encephalitis : An Experimental Approach (II)
Authors: MOCHIZUKI, Hiroshi
Issue Date: 31-Dec-1959
Publisher: University of Osaka Prefecture
Citation: Bulletin of the University of Osaka Prefecture. Ser. B, Agriculture and biology. 1959, 9, p.93-105
Abstract: The present study has been carried out chiefly to answer the question whether morphological evidence for the provocation of Japanese encephalitis by the migration of Toxocara canis larvae can be obtained or not. For this purpose the author examined the brains of mice infected with the worm eggs alone and those infected with the virus after feeding of the eggs. The intracerebral migration and leptomeningeal hemorrhage took place 2.5 days after feeding of eggs, and thereafter the number of larvae in the brain increased rapidly. The rate of the number of larvae in the brain to the number of eggs fed was nearly over 5% on and after the 5th day, and showed no tendency to decrease until the 17th day. Cerebral changes caused by the larval migration were found chiefly in parietofrontal parts of the cerebral hemispheres and each layer of the cerebellum. They were consisted of minute foci of hemorrhage, hemosiderosis, disappearance of nerve cells, perivascular cuffings and nodular or somewhat diffuse proliferation of microglia, being accompanied with eosinophilic infiltration. According to the time of injury, they were divided into two categories: 1) those derived from the lesions which were brought about at the time of larval penetration of the brain from blood stream, and 2) those caused by larval movement after the penetration of the brain had been completed. The formers were various in the extent according to the number of migrating larvae, causing early death in severely infected cases, while the latters were very slight and rare on account of the minuteness of the larvae. All cases which died or were killed under encephalitic symptoms, had typical encephalitic lesions all over the brain. The parasitic lesions, however, were very slight and were covered with the viral changes. Out of 32 encephalitic cases, 4 showed conspicuous changes of viral encephalitis in the predilection sites of the larval lesions. Most of the cases, however, did not show such a marked correspondence of the viral foci to the predilection sites of the parasitic lesions. Thus the author could not obtain morphological evidence sufficient to explain the provocation of clinical infection of Japanese encephalitis by the larval migration. Though unknown factors might lie concealed in the provocation, the cerebral lesions caused by the larval migration seemed to deserve consideration of the damage of the blood-brain barrier. In a mouse, polynucleate PURKINJE cells were found in considerable number close to the parasitic lesions.
URI: http://hdl.handle.net/10466/2874
Appears in Collections: Vol.9

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