Takeshi Kumanomido

Clinical and virological observations on swine experimentally infected with Getah virus

The pathogenicity of Getah virus for swine was examined. All 8 pigs (4 adults and 4 piglets) inoculated with Strains MIP-99 and MI-110 developed pyrexia ranging from 39.4 to 40.7 degrees C and anorexia. Mild depression and diarrhea were observed in 2 of the 4 piglets. These clinical signs were transient. Viremia occurred 1-2 days post-inoculation (p.i.) and the maximum titer was 10(3.0) TCID50 0.1 ml-1. The virus was recovered from a piglet autopsied on Day 3 p.i. from spleen and various lymph nodes. The maximum titer of virus (10(3.75) TCID50 0.1 g-1) was detected in the inguinal lymph node. Seroconversion was demonstrated in all the pigs on Day 6 p.i. These results suggest that Getah virus is mildly pathogenic for swine, which may play a role as an amplifying host in nature.

Pathogenicity for horses of original sagiyama virus, a member of the Getah virus group

Sagiyama virus is a member of the Getah virus group. Its pathogenicity for horses was examined. All the horses infected with the original 4 strains of Sagiyama virus (M6/Mag 33, Mag 121, Mag 132 and Mag 258) developed pyrexia ranging from 39.0 to 40.0 degrees C. Other clinical signs, characterized by eruptions, edema in the hind legs, enlargement of the submandibular lymph node and mild leukopenia, were also manifested. Viremia occurred 1-4 days post-inoculation (p.i.). Virus was recovered from spleen, liver, lung and various lymph nodes of a horse autopsied on Day 4 p.i. The maximum titer of virus (10(6.0) TCID50 g-1) was detected in the inguinal lymph node. Seroconversion was demonstrated in all the infected horses on Day 5 p.i. These clinical signs and virological findings were similar to those of horses infected naturally. The results indicate that Sagiyama virus has pathogenicity for horses and is similar to that of Getah virus.

Transplacental infection in mice inoculated with Getah virus

Transplacental transmission was demonstrated in pregnant mice subcutaneously inoculated with Getah virus. Viremia was shown in the infected dams, and high-titered virus was detected in the placenta and later in the fetus, suggesting virus invasion of the fetus through hematogenous infection of the placenta. High-titered virus was shown in the fetal brain and muscle and in the brain of the young dying soon after birth. Intrauterine infection resulted in a reduction of the litter size, number of young born alive and survival rate to 1 week of age. These results were further corroborated by necropsy performed several days after virus inoculation. The stage of gestation at the time of virus inoculation greatly influenced these results. Dams inoculated at 12 days of gestation delivered all dead babies, whereas virus inoculation at 5 days of gestation had no effect on the number of young born alive. The dams inoculated at 8 days of gestation had reduced litter sizes and those inoculated at 16 days of gestation produced slightly fewer live babies. Gestational stage at the time of virus inoculation also influenced viral growth in fetuses and placentas. The infection rate was low in dams inoculated at 5 days of gestation, high in dams inoculated at 8 or 16 days of gestation and 100% in dams inoculated at 12 days of gestation. High-titered virus was shown in placentas and fetuses of the dams inoculated at 8, 12 or 16 days of gestation. These results suggest that Getah virus may readily cross the placental barrier through hematogenous infection of the placenta in mice.