In 1910, while studying experimental poliomyelitis in monkeys, Roemer and Joseph1 first called attention to a presumably spontaneous flaccid paralysis which occurred among approximately 5 per cent of their normal guinea pig stock. In the following year Roemer2 succeeded in transmitting this disease to normal guinea pigs by intracerebral injection of emulsions of the brains and spinal cords of spontaneously paralyzed guinea pigs. The causative agent was identified as a hitherto unknown filter-passing virus which proved glycerin resistant and could not be grown on artificial mediums. The pathologic condition in the central nervous system was described as meningomyeloencephalitis of lymphocytic nature, involving the pia mater and also the substance of the spinal cord, particularly in the lumbar levels. While stressing the dissimilar pathologic features, Roemer did not fail to emphasize the striking analogy between this paralysis of guinea pigs and Heine-Medin disease. Identification of the etiologic agent was
JUNGEBLUT CW, SANDERS M. TRANSMISSION OF A MURINE STRAIN OF POLIOMYELITIS VIRUS TO GUINEA PIGS AND RHESUS MONKEYS. JAMA. 1941;116(19):2136–2139. doi:10.1001/jama.1941.02820190012004
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