Abstract
With 4 out of 5 human cords taken from acute cases of poliomyelitis at autopsy the virus was successfully transmitted to Macacus rhesus monkeys. All 5 individuals had died of respiratory paralysis in the acute stage of the disease. Histopathological study showed intense infiltration and considerable nerve cell destruction.
The first of these, strain B, was obtained from a child who died of bulbar paralysis, 5 days after the onset of paralysis, during an outbreak in Montreal, in 1931. More than 3 years later, during which interval the cord and tonsils were left in glycerine, at ice box temperature, a single intracerebral and intraperitoneal injection of each tissue was given to a monkey. The cord produced paralysis in 13 days and the animal was prostrate 4 days later, while the tonsil gave complete paralysis within 6 days.
The second strain, 1049, from a case occurring in New York in 1933, and had been in glycerine for a year when tested, was given in combined intracerebral and intraperitoneal inoculations over 3 consecutive days and produced a paralysis 5 days later. Repeated intracerebral and intraperitoneal injections of liver, spleen, mesenteric and submaxillary glands, and kidneys failed to show the presence of virus.
The third strain, J, from a case who had died of bulbar involvement on the 6th day of progressive paralysis, had been in glycerine a year prior to inoculation. A combined intracerebral and intraperitoneal injection brought on paralysis in 8 days. Of special interest was the rapid rise of infectivity during 3 serial passages in monkeys and then its sudden drop.
In Table I, the M.C.P. (minimal completely paralyzing dose) of this strain during these monkey transmissions is compared with the infectivity of the fixed monkey strain.
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