Experimental Animals Infected with Japanese Encephalitis Virus. Report　IV. Effect of Pertussis Vaccine Inoculation to Mice Infected Subcutaneously with JE Virus. On Formation of Focal Rarefation Necrotic Foci in Histopathological Changes of JE..

It is well recognized that pertussis vaccine (Pt-V) has adjuvant property and causes transient damages to the blood-brain-barrier. Histopathological findings of Japanese encephalitis (JE) in laboratory animals are relatively simple in comparison with those of human cases as shown in the previous report. So, to intensify histopathological change of JE in the experimental animals and also to produce the similar focal rarefaction necrotic foci to those seen in human cases, pt-v was administered to mice (4 to 7 weeks old) together with JE virus inocculation. JE virus (JaTH 160 strain) was subcutaneously inoculate and pt-v (standard vaccine for toxicity : 23 to 30 billion organisms/injection LD50) was intraperitoneally given to mice. The change of body weight, hemaggulutinin inhibition (HI) antibody levels, and virus recovery were observed during 21 days after inoculation of JE virus and pt-v administration. HI antibody levels in asymptomatic cases were varied from 1 : 20 to 1 : 640. There was no intimate correlation between the severity of pathological changes and antibody levels. However, virus recovery showed close relation to the severity of histopathological changes in general. When Pt-V was intraperitoneally given to mice with dose of 5 to 7.5bil./inj. at 24 to 48 hours after or before JE virus inocculation, onset and development of the clinical signs and death were rapid. In appearance, infectious levels of virus in those mice became 10^0.5 to 10^2.5 LD50 higher than that of Pt-V non-treated mice. Pathological changes of JE in mice which were treated with Pt-V administration were more severe comparing to those observed in the control mice, and the analogous figures to focal rarefaction necrotic foci and pseudolaminarily distributed cortical deterioration as observed in human cases were frequently encountered. In addition, distribution and forming site of these foci were also coincided with those of human cases of JE.. Administration of pt-v has some abilities to intensify the pathological changes of JE in mice, and this action is not the result of toxicity of pt-v itself but may be due to adjuvant effect. Production of the focal rarefaction necrosis around the small blood vessels may be the result of hyperpermiability due to pt-v administration. Furthermore, absence of morphological changes in the blood vessels suggests some functional alteration such as angiospasmus. From above mentiond findings, one of producing mechanisms of the focal rarefaction necrosis in human JE may have a relation to some modification or allergic reaction in addition to JE virus infection.