Second Attacks of Poliomyelitis

1. It was found in forty rhesus monkeys that intracerebral, intraocular, intracutaneous, intraperitoneal, intraspinal, and neural inoculations of poliomyelitis virus produced no lesions in the olfactory bulbs despite the fact that the animals contracted pronounced paralyses. This indicated that the virus could be restricted to certain neuronal systems. 2. Similarly intranasal inoculation of seven animals produced no lesions in the ciliary ganglia. 3. Two monkeys convalescent from an intracutaneous and an intracerebral inoculation respectively had further paralyses after intranasal inoculation of heterologous virus. A third animal convalescent from an intranasal inoculation showed extension of lesions after intranasal and intraocular inoculation with heterologous virus. 4. Two spinal animals in which an attack of poliomyelitis was limited to an isolated segment of spinal cord, contracted typical paralyses in the previously uninvaded portions of the CNS following intranasal inoculation of homologous virus. 5. Four of six convalescent monkeys showed extension of lesions but no clinical signs after homologous virus inoculation through a previously un-invaded portal. 6. Four animals convalescent from a unilateral intranasal inoculation showed evidence of new invasion in the opposite olfactory bulb but no extension of paralyses following a second inoculation of homologous virus into the appropriate nostril. 7. Two animals had second attacks after heterologous second inoculations. The intranasal portal was employed for both exposures. 8. It thus seems apparent that in the rhesus monkey a second attack of poliomyelitis, whether paralytic or not, seems to depend upon the strains of virus used and the degree to which virus is disseminated through the neuraxis during the first exposure. 9. The above experimental data emphasize the difficulty of utilizing the rhesus monkey for experiments seeking to elucidate the mechanisms of immunity in man and suggest that human immunity to poliomyelitis does not result from immunization of the nervous system but rather is the result of some process which prevents infective quantities of active virus from reaching nervous tissue.