Studies on entry and egress of poliomyelitis infection. III. Excretion of the virus during the presymptomatic period in parenterally inoculated monkeys

Abstract

Excretion of poliomyelitis virus has been demonstrated in monkeys after four different parenteral routes of inoculation. Virus has been found in both the pharyngeal secretions and the stools after infraorbital nerve dip and after inoculation of the Gasserian ganglion; in the pharyngeal secretions after intrathalamic inoculation; and in the stools after inoculation of the celiac ganglion. Excretion began as early as the 2nd and as late as the 7th day after inoculation, in all instances before the onset of symptoms. The immediate source of the excreted virus appeared to be infected peripheral ganglia with neural connections to the mucous membranes of the upper and lower portions of the alimentary tract, notably the pharynx. Primary infection of the body surfaces was excluded in the experiments and therefore could not account for the excretion of virus. The mode of elimination was probably by centrifugal spread through axons of peripheral nerve fibers and not by way of the blood stream or lymphatics. Evidence was obtained that when excretion of virus has once occurred, reinvasion from the implicated surface to other, previously uninfected peripheral ganglia ensues, thus providing new sources for excretion and other potential pathways for invasion of the CNS. It is suggested that such reinvasion may occur serially until the immunological defenses come into play. Our experiments lend support to the view that during the initial stage of poliomyelitis, and perhaps throughout its course in some cases, e.g. the asymptomatic and the mild cases without central nervous symptoms, infection is confined to the peripheral nervous system. Involvement of the CNS when it occurs is a secondary phase of the infective process and is not a necessary prelude to elimination of the virus. Excretion is explainable on the basis of the established neurocytotropism and axonal conduction of the virus without resort to the hypothesis of extraneural infection.