1. Repeated non-traumatic exposures to poliomyelitis virus of the mucous membranes of the upper respiratory tract and of various portions of the alimentary tract in 5 cynomolgus monkeys, extending over a period of 9 to 14 months, were followed by a definite, though limited resistance to intracerebral inoculation to the homologous strain of virus in 4 of them. Only one monkey developed paralysis (20 per cent incidence) and the other 4 remained free of signs and symptoms of the disease. 92 per cent of 25 previously untreated monkeys developed paralysis with the same strain after intracerebral inoculation.

2. Microscopic examination of the central and peripheral nervous systems of the 4 non-paralytic cases revealed in all instances typical lesions in the central nervous system descending from the level of inoculation into the brain-stem but in only 2 into the spinal cord and then only in limited, small areas. Lesions were found in the peripheral ganglia in all animals which corresponded in distribution with the surface membranes previously exposed to virus. No lesions were found in the central nervous system indicative of invasion preceding the intracerebral inoculation.

3. Our observations point to the acquisition by the immune animal, as a result of surface exposure, of the power to limit the spread of infection in the central nervous system rather than of the capacity entirely to prevent implantation and multiplication of virus.

4. This limitation of spread, it is suggested, resembles the tendency so commonly seen in human poliomyelitis of the disease to "halt" at some stage of its evolution, resulting in the various clinical gradations in extent and severity of involvement (subclinical, abortive, non-paralytic, mild paralytic forms, etc.)

5. The experimental methods of exposure, previous to intracerebral inoculation, employed in our study are compared with the natural exposures of human beings during the course of life, which, as age advances, lead to increasing resistance to poliomyelitis and to an increasing incidence of specific neutralizing antibodies in the blood.

6. The mechanism of resistance is obscure. It may be related to the continuing presence of infection in the peripheral ganglia but this is as yet unproved.

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