Getah virus as an equine pathogen.

Getah virus is a member of the genus Alphavirus in the family Togaviridae and has been frequently isolated from mosquitoes. Seroepizootiologic studies indicate that the virus is mosquito-borne and widespread, ranging from Eurasia to southeast and far eastern Asia, the Pacific islands, and Australasia. The natural host animal of the virus was not known until the first recognized occurrence of Getah virus infection among racehorses in two training centers in Japan in 1978. Outbreaks of clinical disease due to Getah virus infection occur infrequently, and only one outbreak has been reported outside Japan; this was in India in 1990. Clinical signs of the disease are mild and nonlife-threatening and are characterized by pyrexia, edema of the hind limbs, swelling of the submandibular lymph nodes, and urticarial rash, as reported in the 1978 epizootic. The morbidity was 37.9% (722 of 1903 horses) in one training center, with 96% of 722 affected horses making a full clinical recovery within a week without any significant sequelae. Antibodies against Getah virus were detected in 61.2% (172 of 281) and 55.8% (254 of 455) of horses at two training centers, respectively. Virus isolation can be attempted in VERO, RK-13, BHK-21, and many other cell lines as well as in suckling mouse brain. Blood plasma collected from suspect cases of infection at the onset of pyrexia is the specimen of choice. A diagnosis of Getah virus infection can also be confirmed serologically based on testing acute and convalescent phase sera by using SN, CF, HI, and ELISA tests. An inactivated vaccine is available for the prevention and control of Getah virus infection in horses in Japan.

Effect of viral inoculum size on appearance of clinical signs in equine Getah virus infection.

A study was performed to examine the effect of viral inoculum size on the appearance of clinical signs in equine Getah virus (GV) infection by intramuscular inoculation with 10(1.3) to 10(6.3) TCID50 of the MI-110 strain in 6 experimental horses. When inoculated with more than 10(3.3) TCID50 of the virus, every horse developed pyrexia, edema in the hind legs, serous nasal discharge, lymphopenia and viremia in the relatively early stage of disease. On the other hand, enlargement of the submandibular lymph node was observed only in horses inoculated with 10(5.3) and 10(6.3) TCID50 of the virus, while typical eruptions were developed in every horse inoculated with 10(4.3) TCID50 or less. These results demonstrated that the appearance of clinical signs in equine GV infection was dependent on viral inoculum size. Besides, it was assumed to be rare chance that eruptions and enlargement of the submandibular lymph node were developed simultaneously in a horse.

Intranasal infection of Getah virus in experimental horses.

Aerosol transmission in equine Getah virus (GV) infection was examined by intranasal inoculation with 10(3.0) to 10(7.0) TCID50 of the MI-110 strain in 7 experimental horses. The establishment of intranasal infection of GV was confirmed in all these horses by detecting serum neutralizing antibody against the MI-110 strain. Horses inoculated with more than 10(4.0) TCID50 of the virus manifested mild pyrexia, eruptions, serous nasal discharge, lymphopenia or monocytosis. Viremia ranging from 10(1.0) to 10(3.5) TCID50/0.2 ml occurred in horses inoculated with 10(5.0) TCID50, or more. Virus recovery from the nasal cavity was observed only in horses inoculated with 10(7.0) TCID50, and the viral titers recorded were 10(3.0) TICD50/ml or less. From these results, it is assumed that GV disseminated from the nasal cavity of naturally infected horses, except for intranasal infection with a lot of the virus, is probably very low in titer. So it seems to be rare that GV in natural cycles is spread from horse to horse by aerosol transmission.

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.

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.

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.

Equine Getah virus infection: isolation of the virus from racehorses during an enzootic in Japan.

A primary enzootic of equine Getah virus infection involving 722 of 1,903 racehorses occurred at a training center in Japan between September and November of 1978. Sixty-two viral agents were isolated from the plasma of 209 sick horses which exhibited pyrexia with rectal temperatures ranging from 38.5--40 degrees C, urticarial rash on various portions of the body, and edema of the hind legs. The viruses were antigenically related to the AMM 2021, Haruna, and Sagiyama strains of Getah virus. Infection and disease were produced experimentally in horses when inoculated by the intramuscular or intranasal routes.