ABSTRACT
Encephalomyocarditis virus (EMCV) was isolated for the rst time in 1945 in Miami, Florida, from a captive chimpanzee and a gibbon that died suddenly of pulmonary edema and myocarditis [1]. Mice inoculated with a ltered edema uid from the gibbon or the chimpanzee displayed paralysis of the posterior members and myocarditis followed by death in a week. The pathogenic agent was at that time given the name of EMCV. The virus had probably been transmitted from wild rats living in proximity to the monkeys, as nearly 50% of the captured rats had antibodies against EMCV. In 1948, in the Mengo district of Uganda, Dick et al. [2] isolated Mengo virus from a captive rhesus monkey that had developed a posterior member paralysis. In 1949, cross-neutralization studies showed that Mengo virus, EMCV, Columbia-SK (discovered in 1939), and MM (discovered in 1943) were antigenically indistinguishable but differed from Theiler’s murine encephalomyelitis virus (TMEV) [3]. Following the Panama epizooty of 1958, Murnane et al. [4] described the isolation of EMCV from swine for the rst time. Since then, the virus has been isolated in many countries, in swine and in wild animals.
