ABSTRACT
Chuzan virus at 2 to 3 passage levels in cell cultures after isolation was inoculated intravenously into 15 seronegative pregnant cows at 89 to 150 days of gestation. All of the cows developed viremia a few days after inoculation and antibodies 2 weeks after inoculation. No clinical signs, except leukopenia, were observed throughout the experimental period. These 15 cows delivered 15 calves after normal gestation. One of the calves which was born to a dam inoculated at 120 days of gestation, showed impairment of movement, and the remaining 14 were healthy. Postmortem examination revealed that this calf had hydranencephaly- cerebellar hypoplasia (HCH) syndrome and that the remaining calves were normal. Two of the 15 calves, including the one that had HCH syndrome, had antibody to Chuzan virus in their precolostral sera. These findings provide additional evidence that Chuzan virus is the etiological agent of an epizootic of congenital abnormalities with HCH syndrome of calves in Japan, 1985 to 1986. We propose to name the HCH syndrome caused by Chuzan virus infection Chuzan disease.
Subject(s)
Anencephaly/veterinary , Animals, Newborn , Cattle Diseases/etiology , Cerebellum/abnormalities , Hydranencephaly/veterinary , Reoviridae Infections/veterinary , Animals , Cattle , Cattle Diseases/congenital , Cattle Diseases/pathology , Female , Hydranencephaly/etiology , Pregnancy , Reoviridae/classification , Reoviridae/pathogenicity , Reoviridae Infections/congenital , Reoviridae Infections/etiology , Reoviridae Infections/pathologyABSTRACT
Indirect immunoperoxidase (IP) staining was evaluated for sensitivity and specificity in detecting Colorado tick fever (CTF) virus antigen in infected cell cultures and infected mouse tissues, and then was applied to a study of congenital CTF infection in mice. The sensitivity of IP staining was comparable to that of immunofluorescence staining in detecting CTF antigen in infected cell cultures. Endogenous peroxidase activity of mouse tissues caused nonspecific reactivity in the IP system, but this could be abolished by treatment with sodium azide and hydrogen peroxide without destroying CTF antigen. Offspring of mice infected with CTF virus during the 2nd week of pregnancy showed a highly significant increase in the incidence of stillbirths and neonatal deaths as compared with offspring of uninfected controls. CTF antigen or virus was demonstrable in only a low proportion (7%) of embryos, ill newborns or stillborns examined, but a high proportion of mice examined at a time when maternal antibody would be lost (6 and 12 weeks) showed CTF antibody, indicating a higher incidence of infection. IP staining showed potential for use in studies of viral pathogenesis in the mouse model.
