FATE OF NASALLY INSTILLED POLIOMYELITIS VIRUS IN NORMAL AND CONVALESCENT MONKEYS WITH SPECIAL REFERENCE TO THE PROBLEM OF HOST TO HOST TRANSMISSION

With a method of intranasal instillation of poliomyelitis virus that brings about infection of all M. rhesus monkeys subjected to it, a study was undertaken of the fate of nasally instilled virus in normal and convalescent, immune animals. Control experiments revealed that nasal mucosa of normal monkeys contained no observable antiviral factors and that when five or ten minimal cerebral infective doses were added to the mucosa, virus could be detected by the employed procedure. In the olfactory bulbs even a single infective dose could be recovered, since suspensions of both bulbs could be transferred to the brain of a monkey without any loss of material. After nasal instillation of virus in normal monkeys, it disappeared quickly (4 hours or less) and could be recovered neither from the excised nasal mucosa nor from the olfactory bulbs during the first 48 hours. At 72 hours, just before or coincident with the first rise of temperature, virus was found in very small amounts in the nasal mucosa and for the first time also in the olfactory bulbs. At 96 hours, at least 3 days before the appearance of nervous signs, and later, while virus continued to be present in considerable amounts in the olfactory bulbs (and presumably elsewhere in the central nervous system), none was detected in the nasal mucosa. In convalescent, immune animals receiving the same strain of virus intranasally which caused the original infection, none could be recovered from the nasal mucosa or central nervous system at 4 hours, 1, 2, 3, 4, 5, and 7 days. The bearing of these observations on the problem of host to host transmission of poliomyelitis virus is discussed.

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LOCALIZATIONS OF THE VIRUS OF POLIOMYELITIS IN THE CENTRAL NERVOUS SYSTEM DURING THE PREPARALYTIC PERIOD, AFTER INTRANASAL INSTILLATION

Journal of Experimental Medicine ◽

10.1084/jem.57.6.933 ◽

1933 ◽

Vol 57 (6) ◽

pp. 933-954 ◽

Cited By ~ 30

Author(s):

Harold K. Faber ◽

Louis P. Gebhardt

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Olfactory Bulbs ◽

Parietal Lobes ◽

The Central Nervous System ◽

Olfactory Cells ◽

The Brain ◽

Intranasal Instillation ◽

Initial Focus ◽

Experimental Disease

1. About 4 days after intranasal instillation, the virus of poliomyelitis establishes its initial focus, within the central nervous system, in the olfactory bulbs. It apparently reaches this structure through the axons of the olfactory nerves after primarily infecting the olfactory cells of the nasal mucosa. 2. From this initial focus, the virus spreads (on the 5th and 6th days) through the olfactory tracts and their connections in the brain stem. A secondary focus in the hypothalamus is first established. From this, two main channels can be discerned: first, to the medulla; second, to the thalamus and midbrain. 3. On the 7th day, virus can first be detected in the spinal cord. It is widespread but is found in larger amounts in the cervical than in the lumbar segments. It is present in both the anterior and posterior horns, either in equal amounts or in slightly larger amounts in the posterior. It is also present in the intervertebral ganglia. The surmise is presented that the main route of infection of the cord is not from the medulla (which had been infected as early as the 5th day) but along the sensory tracts, presumably from the thalamus (spinothalamic tracts). 4. Certain portions of the central nervous system were never found to contain demonstrable quantities of virus: these were the cortex of the frontal and parietal lobes (neopallium), and the cerebellum. The olfactory (archipallial) cortex (hippocampus) was only once found to contain virus; this occurred on the 7th day and in small amounts, and presumably had its source in the olfactory bulbs. 5. The experiments of the 7th day suggest that virus had died out in areas previously infected (in the hypothalamus and thalamus, particularly), while continuing, apparently undiminished, in the midbrain and medulla, and spreading to the cord. These observations are in harmony with the general contentions of Fairbrother and Hurst that virus is better adapted to survival in the lower portions of the cerebrospinal axis than in the higher. 6. The conception here presented of the manner of entrance and routes of propagation of the virus of poliomyelitis in the experimental animal appears to be in essential agreement with the clinical and pathological characteristics of the disease in man. Both the experimental disease and the disease as it occurs in man appear to present the features of an infection spread through nervous tissue only. It is unnecessary to assume that at any stage of its progress, during the incubation period or later, systemic or general extranervous infection is present.

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MULTIPLICATION AND SPREAD OF THE VIRUS OF ST. LOUIS ENCEPHALITIS IN MICE WITH SPECIAL EMPHASIS ON ITS FATE IN THE ALIMENTARY TRACT

Journal of Experimental Medicine ◽

10.1084/jem.85.6.647 ◽

1947 ◽

Vol 85 (6) ◽

pp. 647-662 ◽

Cited By ~ 7

Author(s):

John L. Peck ◽

Albert B. Sabin

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Intestinal Tract ◽

Antiviral Agent ◽

Nerve Fibers ◽

Human Beings ◽

Poliomyelitis Virus ◽

Virus Content ◽

The Central Nervous System ◽

The Brain

1. Beginning at 24 hours after intravenous injection of about 10 million intracerebral LD50 of virus there was evidence of simultaneous, progressive multiplication in the brain and intestinal tract. 2. When the virus was introduced directly into the brain or the nasal cavities and mouth, none was found in the intestinal tract until there was general centrifugal spread from the central nervous system during the last stages of the infection at 96 or 120 hours after inoculation when the virus in the entire brain had reached a concentration of about 3 billion LD50. 3. Centrifugal spread began when the virus in the brain reached a concentration of about 400 million LD50 and virus appeared in the pharynx, tongue, and adrenals before it was demonstrable in the intestinal tract, blood, or viscera such as the spleen, liver, and kidneys. 4. Despite the high concentrations of virus which developed in the intestinal tract following intravenous inoculation, it was not demonstrable in the stools, differing in this respect from Theiler's virus in mice and poliomyelitis virus in human beings and monkeys. 5. No antiviral agent was found in the stools, but the urine of normal mice having a pH of 5.6, inactivated large amounts of St. Louis encephalitis virus. 6. There was no evidence of multiplication in the nasal mucosa of mice which succumbed with encephalitis following nasal instillation of the virus, the course of events being comparable in this respect to the behavior of the M.V. poliomyelitis virus in rhesus monkeys. 7. At the terminal stage of infection the virus content per milligram of tissue was as great in the leg muscles as in the sciatic nerves. Since this was also true for the urinary bladder, heart, lungs, and tongue among other tissues, and since the amount in the blood was too negligible to account for it, it would appear that the virus either accumulated in these tissues by diffusion from the nerve fibers, along which it was spreading from the central nervous system, or that it multiplied in some constituent other than the nerve fibers.

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CLIPPERS. Three clinical cases and review

Bulletin of Siberian Medicine ◽

10.20538/1682-0363-2019-4-256-265 ◽

2020 ◽

Vol 18 (4) ◽

pp. 256-265

Author(s):

L. N. Prakhova ◽

A. S. Parfyonova ◽

Zh. I. Savintseva ◽

A. G. Ilves ◽

E. V. Bubnova ◽

...

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Literature Review ◽

Diagnostic Criteria ◽

Inflammatory Disease ◽

Present Moment ◽

The Central Nervous System ◽

First Time ◽

The Brain ◽

Clinical Cases

CLIPPERS (Chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids) is a rare inflammatory disease of the central nervous system, during which the pons of the brain is damaged. This disease was described for the first time in 2010 by S.J. Pittock et.al. At present, there have been around 50 described cases of the disease. Up to the present moment, there are difficulties diagnosing this disease. In the article, a literature review and three clinical cases are presented. Furthermore, the necessity of further research is shown for improving the accuracy and specificity of the diagnostic criteria, as well as for defining biomarkers and developing algorithms of effective therapy.

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The brain of Brycon orbignyanus (Valenciennes, 1850) (Teleostei: Characiformes: Bryconidae): gross morphology and phylogenetic considerations

Neotropical Ichthyology ◽

10.1590/1982-0224-20150051 ◽

2016 ◽

Vol 14 (3) ◽

Cited By ~ 6

Author(s):

Thiago N. A. Pereira ◽

Ricardo M. C. Castro

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Brain Morphology ◽

Future Studies ◽

The Central Nervous System ◽

First Time ◽

The Brain ◽

Detailed Protocol

ABSTRACT The brain of Brycon orbignyanus is described as a model for future studies of the gross morphology of the central nervous system in Characiformes. The study of brain gross morphology of 48 distinct taxa of Characiformes, one of Cypriniformes, two of Siluriformes and two of Gymnotiformes, allowed us to propose, for the first time, six putative brain synapomorphies for the Characiformes and also two possibly unique gross brain morphology characters for the Siluriformes. A detailed protocol for the extraction of the brain in Characiformes is also provided.

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THE GROWTH CURVE OF THE LANSING STRAIN OF POLIOMYELITIS VIRUS IN THE CENTRAL NERVOUS SYSTEM OF THE MOUSE

Journal of Experimental Medicine ◽

10.1084/jem.95.1.1 ◽

1952 ◽

Vol 95 (1) ◽

pp. 1-7 ◽

Cited By ~ 4

Author(s):

John D. Ainslie

Keyword(s):

Spinal Cord ◽

Central Nervous System ◽

Nervous System ◽

Growth Curve ◽

Clinical Signs ◽

Virus Suspension ◽

Poliomyelitis Virus ◽

The Central Nervous System ◽

Infectivity Titer ◽

The Brain

After intracerebral inoculation of mice with a 10 per cent suspension (approximately 2000 LD50) of the Lansing strain of poliomyelitis virus, the infectivity titer in the brain decreased for approximately 6 hours. It then rose rapidly for 12 to 18 hours to reach titers of over 10–4. The rise in titer in the spinal cord closely paralleled that in the brain for 18 hours, after which the titer surpassed that in the brain by as much as one log. The infectivity titers in the central nervous system of unparalyzed mice remained between 10–3.5 and 10–4.2 for at least 7 days. With the onset of paralysis it was found that the titer was consistently and significantly higher in the spinal cords of paralyzed mice than in their brains or in the brains or cords of unparalyzed mice. After inoculation of 1 per cent virus suspension the increase in titer occurred about 9 hours later than after the inoculation of 10 per cent virus suspension, and the onset of clinical signs of illness was also delayed. Once the titers began to rise, the rate was the same after the inoculation of either concentration of virus, and the maximal levels reached were the same. With both concentrations of virus, maximal infectivity titers in non-paralyzed mice were reached about 9 hours before the onset of signs of poliomyelitis. The significance of these findings is discussed.

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NON-PARALYTIC POLIOMYELITIS IN THE CHIMPANZEE

Journal of Experimental Medicine ◽

10.1084/jem.81.3.255 ◽

1945 ◽

Vol 81 (3) ◽

pp. 255-274 ◽

Cited By ~ 23

Author(s):

David Bodian ◽

Howard A. Howe

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Pathological Process ◽

Paralytic Poliomyelitis ◽

Local Resistance ◽

Cerebral Lesions ◽

Olfactory Bulbs ◽

Homologous Virus ◽

The Central Nervous System ◽

The Brain

1. Thirteen cases of non-paralytic poliomyelitis infection in chimpanzees are described. Nine of these animals were excreting virus in. their stools at periods of from 3 days to 8 weeks following inoculation. 2. All animals killed during the acute stage showed lesions in the brain distributed in centers usually involved in, and compatible with the presence of, poliomyelitic infection. In 2 chimpanzees typical cord lesions were also present. No lesions were found in the brains of 4 control chimpanzees which had had no virus contact as far as known. The occurrence of a purely systemic or peripheral form of poliomyelitis, without lesions in the central nervous system, has thus not been established. 3. Four instances of arrest of the pathological process near the portal of entry into the brain, indicating partial resistance, are included in this series. One was a chimpanzee inoculated intranasally (A1-75) who had severe tuberculosis at the time of inoculation. The second was an animal convalescent after intracerebral inoculation (A1-74), who sustained a second infection limited to the olfactory bulbs when inoculated intranasally 2 months later with homologous virus. The third (A5-01) was inoculated orally with human stool, but contammation of the olfactory area resulted with infection of the olfactory bulbs and of the forebrain; virus was present in the stools of this animal. The fourth chimpanzee (A48) had suffered an initial non-paralytic attack after stomach tube inoculation, followed by a second attack about 9 months later after oral inoculation with part of the same virus-containing pool (human stools). The second attack consisted of a facial paralysis, with arrest of the pathological process near the facial nucleus. 4. Although cerebral lesions were light in some of the non-paralytic and inapparent infections, their presence in all indicates the action of virus on the central nervous system with the possibihty of production of at least partial local resistance. It is not unreasonable to assume that this may occur in inapparent human cases, although the point is, of course, not susceptible to critical proof in man. 5. The degree of severity of pathological involvement in non-paralytic cases varies from a fully developed distribution of lesions in brain and spinal cord in some chimpanzees, to mild and scattered lesions in the brains of others. This suggests that if the extent of pathological reaction is an indicator of subsequent local resistance to reinfection, the degree of protection afforded by a non-paralytic attack of poliomyelitis to even homologous virus must be variable.

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Glucuronyl 3-sulfate occurs exclusively on distal unmyelinated terminals of selected sensory neurons in the peripheral nervous system

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100141160 ◽

1995 ◽

Vol 53 ◽

pp. 958-959

Author(s):

S.S. Spicer ◽

B.A. Schulte

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Cerebral Cortex ◽

Peripheral Nervous System ◽

Sensory Neurons ◽

Sensory Nerves ◽

Tissue Antigens ◽

The Central Nervous System ◽

The Brain ◽

Leu 7

Generation of monoclonal antibodies (MAbs) against tissue antigens has yielded several (VC1.1, HNK- 1, L2, 4F4 and anti-leu 7) which recognize the unique sugar epitope, glucuronyl 3-sulfate (Glc A3- SO4). In the central nervous system, these MAbs have demonstrated Glc A3-SO4 at the surface of neurons in the cerebral cortex, the cerebellum, the retina and other widespread regions of the brain.Here we describe the distribution of Glc A3-SO4 in the peripheral nervous system as determined by immunostaining with a MAb (VC 1.1) developed against antigen in the cat visual cortex. Outside the central nervous system, immunoreactivity was observed only in peripheral terminals of selected sensory nerves conducting transduction signals for touch, hearing, balance and taste. On the glassy membrane of the sinus hair in murine nasal skin, just deep to the ringwurt, VC 1.1 delineated an intensely stained, plaque-like area (Fig. 1). This previously unrecognized structure of the nasal vibrissae presumably serves as a tactile end organ and to our knowledge is not demonstrable by means other than its selective immunopositivity with VC1.1 and its appearance as a densely fibrillar area in H&E stained sections.

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Central Nerve System Impairment, AMA Guides, Sixth Edition: An Overview

Guides Newsletter ◽

10.1001/amaguidesnewsletters.2018.janfeb03 ◽

2018 ◽

Vol 23 (1) ◽

pp. 10-13

Author(s):

James B. Talmage ◽

Jay Blaisdell

Keyword(s):

Spinal Cord ◽

Central Nervous System ◽

Nervous System ◽

Neurological Impairment ◽

Sixth Edition ◽

Central Nerve System ◽

The Central Nervous System ◽

The One ◽

Nerve System ◽

The Brain

Abstract Injuries that affect the central nervous system (CNS) can be catastrophic because they involve the brain or spinal cord, and determining the underlying clinical cause of impairment is essential in using the AMA Guides to the Evaluation of Permanent Impairment (AMA Guides), in part because the AMA Guides addresses neurological impairment in several chapters. Unlike the musculoskeletal chapters, Chapter 13, The Central and Peripheral Nervous System, does not use grades, grade modifiers, and a net adjustment formula; rather the chapter uses an approach that is similar to that in prior editions of the AMA Guides. The following steps can be used to perform a CNS rating: 1) evaluate all four major categories of cerebral impairment, and choose the one that is most severe; 2) rate the single most severe cerebral impairment of the four major categories; 3) rate all other impairments that are due to neurogenic problems; and 4) combine the rating of the single most severe category of cerebral impairment with the ratings of all other impairments. Because some neurological dysfunctions are rated elsewhere in the AMA Guides, Sixth Edition, the evaluator may consult Table 13-1 to verify the appropriate chapter to use.

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