scholarly journals INDUCED RESISTANCE OF THE CENTRAL NERVOUS SYSTEM TO EXPERIMENTAL INFECTION WITH EQUINE ENCEPHALOMYELITIS VIRUS

1944 ◽  
Vol 80 (3) ◽  
pp. 197-211 ◽  
Author(s):  
R. Walter Schlesinger ◽  
Peter K. Olitsky ◽  
Isabel M. Morgan
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Guinea Pigs ◽  
Early Stage ◽  
Neutralizing Antibody ◽  
Challenge Dose ◽  
Abortive Infection ◽  
Encephalomyelitis Virus ◽  
The Central Nervous System ◽  
Western Equine Encephalomyelitis Virus

Although vaccination of guinea pigs with formalin-inactivated Western equine encephalomyelitis virus rendered them specifically immune to an intracerebral challenge dose of 1,000 M.L.D. of Western virus, it failed to protect their central nervous system against the initial effects of the virus: the intracerebral challenge dose was followed by an abortive infection of 20 to 30 hours' duration characterized by fever and histopathological changes which simulated the response at that early stage of non-vaccinated control animals. During the abortive infection of immune animals, virus could occasionally be demonstrated in their brains; indeed, it was detected with about the same frequency it was isolated from brains of similarly inoculated, non-immune guinea pigs during corresponding early phases of the infection. About one week after the abortive infection there was found a marked transitory accumulation of specific neutralizing antibody in the brain tissue. See PDF for Equation equalled at this time 1:1 to 1:10 instead of the value of about 1:300 found under physiological conditions. Guinea pigs which had recovered from an abortive infection with Western virus were resistant for a limited period of time to the effects of intracerebral inoculations of the immunologically distinct viruses of Eastern equine encephalomyelitis or vesicular stomatitis.

scholarly journals Development of the Cerebrospinal Fluid in Early Stage after Hemorrhage in the Central Nervous System

Life ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 300
Author(s):  
Petr Kelbich ◽  
Aleš Hejčl ◽  
Jan Krejsek ◽  
Tomáš Radovnický ◽  
Inka Matuchová ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Early Stage ◽  
Rank Test ◽  
Signed Rank ◽  
Signed Rank Test ◽  
The Central Nervous System ◽  
Poor Outcomes ◽  
Molecular Patterns

Extravasation of blood in the central nervous system (CNS) represents a very strong damaged associated molecular patterns (DAMP) which is followed by rapid inflammation and can participate in worse outcome of patients. We analyzed cerebrospinal fluid (CSF) from 139 patients after the CNS hemorrhage. We compared 109 survivors (Glasgow Outcome Score (GOS) 5-3) and 30 patients with poor outcomes (GOS 2-1). Statistical evaluations were performed using the Wilcoxon signed-rank test and the Mann–Whitney U test. Almost the same numbers of erythrocytes in both subgroups appeared in days 0–3 (p = 0.927) and a significant increase in patients with GOS 2-1 in days 7–10 after the hemorrhage (p = 0.004) revealed persistence of extravascular blood in the CNS as an adverse factor. We assess 43.3% of patients with GOS 2-1 and only 27.5% of patients with GOS 5-3 with low values of the coefficient of energy balance (KEB < 15.0) in days 0–3 after the hemorrhage as a trend to immediate intensive inflammation in the CNS of patients with poor outcomes. We consider significantly higher concentration of total protein of patients with GOS 2-1 in days 0–3 after hemorrhage (p = 0.008) as the evidence of immediate simultaneously manifested intensive inflammation, swelling of the brain and elevation of intracranial pressure.

Coxsackievirus Group B Antibodies in the Ventricular Fluid of Infants with Severe Anatomic Defects in the Central Nervous System

PEDIATRICS ◽  
1985 ◽  
Vol 76 (1) ◽  
pp. 64-68
Author(s):  
Charles J. Gauntt ◽  
Richard J. Gudvangen ◽  
Yves W. Brans ◽  
Arthur E. Marlin
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Newborn Infants ◽  
Neutralizing Antibody ◽  
Detectable Level ◽  
Immunoglobulin M ◽  
Congenital Infections ◽  
The Central Nervous System ◽  
Group B

Ventricular fluids from four of 28 newborn infants who were initially seen with severe congenital anatomic defects in the central nervous system contained neutralizing antibody to at least one serotype of coxsackieviruses group B. Two of the four infants with anticoxsackieviruses group B antibody in the ventricular fluid did not have a detectable level of the same antibody(ies) in their serum. The ventricular fluid of one of the infants had immunoglobulin M neutralizing antibody directed against coxsackievirus B6. Of 11 mother-infant pairs that had neutralizing antibody to coxsackieviruses group B in both sera, nearly half had antibodies directed against more than one serotype. These data suggest the possibility of an association between congenital infections with coxsackieviruses group B and rare severe CNS defects.

scholarly journals A PARALYTIC DISEASE OF GUINEA PIGS DUE TO THE TUBERCLE BACILLUS

1929 ◽  
Vol 50 (3) ◽  
pp. 365-370 ◽  
Author(s):  
Richard E. Shope ◽  
Paul A. Lewis
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Tuberculous Meningitis ◽  
Guinea Pigs ◽  
Tuberculous Infection ◽  
Tubercle Bacillus ◽  
Herpes Encephalitis ◽  
Subsequent Publication ◽  
The Central Nervous System ◽  
Rule Out

The experimental data collected during this study of a transmissible type of paralysis developing in tuberculous guinea pigs indicate the condition to be a true tuberculous meningitis. We have been able to rule out the possibility that it is due to a non-tuberculous infection of the central nervous system caused by Roemer's virus, or by an atypical herpes virus, or by some bacterium other than the tubercle bacillus. Roemer's virus and herpes could be eliminated from consideration when Berkefeld N filtrates of infectious brain emulsions proved incapable of reproducing the disease. Furthermore, rabbits could be infected as they cannot with Roemer's virus, and the disease elicited in rabbits bears no semblance to herpes encephalitis. No organism other than the tubercle bacillus could be obtained on culturing brain or brain emulsions from experimental cases, and no others were seen in examining fresh smear preparations from the central nervous system. In a modified Noguchi medium a tubercle bacillus possessing atypical staining properties was obtained. This organism was capable of producing the typical paralytic disease when injected intracerebrally into guinea pigs, and also generalized tuberculosis in animals inoculated subcutaneously with it. Typical tuberde bacilli were readily demonstrable in sections of the meninges from animals with the disease, and culture of pieces of brain on Dorset's egg medium usually yielded a growth of tubercle bacilli. Only in the first of the experimental passages, on the other hand, was it possible to demonstrate acid-fast organisms in fresh smear preparations from the central nervous system. This fact and the attributes of the atypically staining organisms encountered in the cultures in Noguchi media will be considered more fully in a subsequent publication. In view of the much discussed question of the filtrability of the tubercle bacillus our observations concerning the failure of this organism to pass a Berkefeld N filter are of interest. No animal in our series inoculated intracerebrally with brain emulsion from either a "spontaneous" or experimental case of tuberculous meningitis failed to develop meningitis, and that rather acutely, while no animal in our series injected with a Berkefeld filtrate of brain emulsion has developed tuberculous meningitis or any other form of tuberculosis. In connection with this observation it must be recalled that the organism was atypical in respect to its staining qualities at least.

scholarly journals Aino Virus Antigen in Brain Lesions of a Naturally Aborted Bovine Fetus

1998 ◽  
Vol 35 (5) ◽  
pp. 409-411 ◽  
Author(s):  
Y. Noda ◽  
Y. Uchinuno ◽  
H. Shirakawa ◽  
S. Nagasue ◽  
N. Nagano ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Brain Lesion ◽  
Neutralizing Antibody ◽  
Virus Antigen ◽  
Brain Lesions ◽  
Significant Feature ◽  
The Central Nervous System ◽  
The Brain

A bovine fetus aborted at 187 days of gestation was serologically and immunohistopathologically examined. Serum and cerebrospinal fluid samples had high titers of virus-neutralizing antibody for Aino virus. A severe necrotizing encephalopathy was noted. Aino virus antigen was demonstrated in neuroglial cells within the brain lesion. The destruction of developing neuronal cells appeared to be a significant feature of the pathogenesis of lesions due to Aino virus infection in the central nervous system.

scholarly journals Epitope-Tagged L* Protein of Theiler's Murine Encephalomyelitis Virus Is Expressed in the Central Nervous System in the Acute Phase of Infection

2002 ◽  
Vol 76 (24) ◽  
pp. 13049-13054 ◽  
Author(s):  
Kunihiko Asakura ◽  
Harunobu Murayama ◽  
Toshiki Himeda ◽  
Yoshiro Ohara
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Acute Phase ◽  
Wild Type Virus ◽  
Theiler's Murine Encephalomyelitis Virus ◽  
L Protein ◽  
Theiler’S Murine Encephalomyelitis Virus ◽  
Encephalomyelitis Virus ◽  
The Central Nervous System ◽  
Resistant Strains

ABSTRACT TO subgroup strains of Theiler's murine encephalomyelitis virus (TMEV) synthesize L* protein from an alternative initiation codon. We first demonstrated L* expression in the central nervous system (CNS) of TMEV-infected mice during the acute phase of infection by immunoprecipitation and immunoblotting with anti-L* antibody. In addition, we generated mutant viruses which synthesize FLAG or 3xFLAG epitope-tagged L* protein. With a mutant virus expressing 3xFLAG epitope-tagged L*, designated DA/3xFLAGL*, we investigated L* in the CNS in the acute phase of infection. DA/3xFLAGL* did not change the virus tropism in comparison with wild-type virus, and L* was clearly identified in the CNS in both susceptible and resistant strains of mice. Double immunolabeling studies showed that L* is colocalized with TMEV polyprotein and exclusively expressed in neurons.

scholarly journals Neuropathogenesis caused by Trypanosoma brucei, still an enigma to be unveiled

2021 ◽  
Vol 8 (4) ◽  
pp. 73-76
Author(s):  
Katherine Figarella
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Immune Responses ◽  
Trypanosoma Brucei ◽  
Late Stage ◽  
Early Stage ◽  
Tropical Diseases ◽  
The Central Nervous System ◽  
The Impact ◽  
The Brain

Trypanosoma brucei is one of the protozoa parasites that can enter the brain and cause injury associated with toxic effects of parasite-derived molecules or with immune responses against infection. Other protozoa parasites with brain tropism include Toxoplasma, Plasmodium, Amoeba, and, eventually, other Trypano-somatids such as T. cruzi and Leishmania. Together, these parasites affect billions of people worldwide and are responsible for more than 500.000 deaths annually. Factors determining brain tropism, mechanisms of in-vasion as well as processes ongoing inside the brain are not well understood. But, they depend on the par-asite involved. The pathogenesis caused by T. brucei initiates locally in the area of parasite inoculation, soon trypanosomes rich the blood, and the disease enters in the so-called early stage. The pathomecha-nisms in this phase have been described, even mole-cules used to combat the disease are effective during this period. Later, the disease evolves towards a late-stage, characterized by the presence of parasites in the central nervous system (CNS), the so-called meningo-encephalitic stage. This phase of the disease has not been sufficiently examined and remains a matter of investigation. Here, I stress the importance of delve into the study of the neuropathogenesis caused by T. brucei, which will enable the identification of path-ways that may be targeted to overcome parasites that reached the CNS. Finally, I highlight the impact that the application of tools developed in the last years in the field of neuroscience will have on the study of neglect-ed tropical diseases.

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