1. The effects of viremia on the CNS of cynomolgus monkeys were studied by comprehensive histological examination following inoculations of approximately equal amounts of the same strain of poliomyelitis virus into the femoral vein, carotid artery, and vertebral artery, respectively, of four animals in each case. 2. The intravenous injections failed to produce lesions in the CNS, indicating that an effective mechanism exists for the removal of virus from the blood stream. While not absolute, the degree of protection of the CNS afforded by this mechanism appears to be of major importance. 3. Inoculations into the carotid artery failed to produce significant lesions in the CNS in two animals; only a few minor lesions in one; and bulbar paralysis in one. The neuronal areas supplied by the carotid artery are in general those of low susceptibility to poliomyelitis virus. 4. Inoculations into the vertebral artery, which supplies neuronal areas of high susceptibility, produced in all four animals severe symmetrical and widely distributed lesions in the brainstem, chiefly the motor centers of the pons, medulla, and cord, and maximal in the cord. Involvement of all of the various affected areas appeared to be simultaneous. 5. Viremic invasion of the CNS appears to occur at many points by direct passage of virus from capillary to neuron, and not at a single area of specialized vascular permeability. 6. Comparison of the two routes of arterial inoculation indicates that: (a) the localizations of CNS lesions from viremia depend largely upon the susceptibilities of exposed nerve cells in a given region; (b) in areas of high neuron susceptibility the blood-neuron "barrier" does not present an obstacle of importance to the passage of virus. 7. Invasion of the CNS from the blood results in a notable difference in the initial localization of lesions from that produced by invasion by way of the peripheral nerves, the latter tending to occur in isolated nuclear groups, usually in the lower brainstem, related to the regional supply.

Animals↗

PubMed1954

Studies on entry and egress of poliomyelitic infection. VII. Early lesions in peripheral ganglia after simple feeding; with comments on the possible value of immunization in preventing neural entry.

At 56, 60, and 72 hours after simple feeding of poliomyelitis virus, typical, discrete lesions were found in the ganglia supplying the mouth and pharynx, which were most numerous and severe in the Gasserian ganglia. Lesions were also found in the nerve bundles adjacent to the infected ganglia. The character, localizations, and time of appearance of lesions point to nerve-conducted entry of infection from the mucosa of the mouth and pharynx. The possibility is suggested that under natural conditions of exposure, in which only small amounts of virus are involved, artificially induced immunity, active and probably passive, may block primary neural entry at the oropharyngeal portal by virtue of antibodies in the overlying mucus.

Disease↗

PubMed1953

Studies on entry and egress of poliomyelitic infection. V. Entry after simple feeding: with notes on viremia.

Poliomyelitis virus, when ingested by cynomolgus monkeys in their regular food, infected peripheral ganglia (nodose) as early as the 3rd day, as shown by recovery of the virus. Conditions on the 2nd and 4th days were not investigated, but on the 5th and 6th days, virus was recovered from the Gasserian and nodose ganglia, and from the superior cervical sympathetic and celiac ganglia. The findings indicate that the method of oropharyngeal swabbing used in a study already reported and the method of simple feeding used in the present study produce comparable results. Viremia, noted in the present study, was contemporaneous with virus recoveries from the ganglia. Reasons are presented why the peripheral ganglia are the most probable source of viremia since these are the only known site of early lesions (which are typical and appear as early as the 2nd day after oral infection) and no lesions are known to occur in extraneural tissues. Invasion of the CNS occurred in 3 animals out of 11; one on the 5th and 2 on the 6th day. Whether this was due to viremia or to centripetal extension along axonal channels is not clear.

Animals↗

PubMed1953

Studies on entry and egress of poliomyelitic infection. VI. Centrifugal spread of the virus into peripheral nerve with notes on its possible implications.

We have demonstrated a progressive centrifugal migration of poliomyelitis virus from the CNS into various peripheral ganglia and into peripheral nerves, including their distal portions. This phenomenon appears to be a regular occurrence in experimental animals, and is similar to that found in two other neurotropic infections, rabies and Borna disease. Viremia appears to be secondary to primary neural infection. The presence of virus in the lumen of the alimentary tract appears to be secondary to primary neural infection and not to viremia, and to be associated with the centrifugal spread of virus in peripheral nerves. The presence of virus in "extraneural" tissues is not per se referable to infection of their constituent cells but rather to infection of their supplying nerves or, in some instances, to their content of virus-bearing blood. The finding of virus in the vagus nerve may throw light on some of the electrocardiographic changes noted in certain cases of human poliomyelitis. The presence of virus in peripheral nerves may throw light on the etiology of the most frequent clinical manifestations of human poliomyelitis, localized pain and tenderness.

Animals↗

PubMed1953

Virucidal activity of some common surface antiseptics, with special reference to poliomyelitis.

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Anti-Infective Agents, Local↗

PubMed1953

Poliocidal activity of some common antiseptics with special reference to localized paralysis.

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Anti-Infective Agents, Local↗