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H K FABER

Publications and source records attributed to H K FABER.

At least 19 recordsLinked to original sources
PubMed1958

Pediatrics.

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Child↗
PubMed1955

Studies on entry and egress of poliomyelitic infection. VIII. The relation of viremia to invasion of the central nervous system.

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↗
PubMed1951

Studies on entry and egress of poliomyelitic infection. IV. Atraumatic oral entry distribution of lesions and virus during the incubation period with notes on asymptomatic poliomyelitis.

Within 48 hours after simple oropharyngeal exposures of cynomolgus monkeys to poliomyelitis virus, histological signs of infection were found in ganglia supplying the exposed mucous membranes. At 3 days, virus was found in the Gasserian, petrosal-nodose, and superior cervical sympathetic ganglia. Lesions were most extensive and severe in the Gasserian. Virus continued to be detected daily from the 3rd to the 8th day, inclusive, in the Gasserian but not on the 9th; from the 3rd to the 6th day, inclusive, in the petrosal-nodose but not on the 7th, 8th, or 9th; on the 3rd and 6th days only, in the superior cervical sympathetic; and on the 5th day only, in the celiac. In all the ganglia examined, the histological signs of infection increased to a maximum on the 5th day, and thereafter declined. In the sympathetic ganglia, a secondary late increase was observed on the 7th day. During the first 7 days, no signs of infection were found in the CNS in 84 per cent of the animals examined, and in the remainder such lesions as were found were probably not significant. In control animals permitted to survive, the median period before the onset of symptoms of poliomyelitis, when these occurred, was 9 days (range 7 to 16 days), and in the animals with symptoms typical extensive lesions were found in the CNS. In two control animals failing to show symptoms and sacrificed at 26 and 30 days respectively, histological signs of infection were present in the Gasserian and other ganglia but none in the CNS.

Animals↗
PubMed1950

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

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.

Animals↗