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Biomedical subjects

J R Baringer

Publications and source records attributed to J R Baringer.

At least 73 records · Page 4Linked to original sources
PubMed1977

Subacute measles encephalitis complicating Hodgkin's disease in an adult.

A progressive neurological illness characterized by myoclonus, motor and sensory deficits, and lethargy occurred in a patient with Hodgkin's disease and was fatal within two months. A focal inclusion cell encephalitis was demonstrated by immunohistological means to be due to measles virus. Measles encephalitis must be considered a potential opportunistic agent in the immune-compromised host.

Antibodies, Viral↗
PubMed1976

Experimental herpes simplex virus encephalitis. Effect of corticosteroids and pyrimidine nucleoside.

The effects of methylprednisolone sodium succinate and cytarabine have been examined in an experimental herpes simplex virus-induced encephalitis in rabbits. In this model herpes simplex virus (HSV) is normally cleared from the brains of untreated animals. Infected animals treated with large doses of methylprednisolone showed a slight delay in the rate of clearance of virus, and a minimal reduction in the inflammatory process, but did not otherwise differ from untreated controls. Animals treated with cytarabine displayed a notable rise in viral titers in brain at a time when virus had been cleared from untreated controls. Cytarabine-treated animals also showed persistence of intranuclear inclusions in the lesions, and moderate diminution in the extent of inflammatory response. Thus, while methylprednisolone appears to have little adverse effect on the encephalitic process, cytarabine, perhaps because of its immunosuppressive properties, results in a failure of normal clearance of virus from nervous system lesions.

Animals↗
PubMed1976

The neuropathology of progressive rubella panencephalitis of late onset.

The clinicopathological changes in a case of progressive rubella panencephalitis of late onset have been presented. The prominent pathological findings in the brain included diffuse destruction of white matter with perivascular inflammatory cells and gliosis, moderate neuronal loss, numerous amorphous vascular deposits in the white matter and severe generalized cerebellar atrophy. These changes are compared and contrasted with those found in congenital rubella and other latent viral illnesses.

Adult↗
PubMed1976

Persistence of neuroadapted mumps virus in brains of newborn hamsters after intraperitoneal inoculation.

Neuroadapted mumps virus produces systemic infection in newborn hamsters after intraperitoneal inoculation. Virus is disseminated via a low-level viremia and appears to enter the central nervous system by passage through the choroid plexus. At such sites, choroidal and ependymal epithelial cells are productively infected and become a source for further viral spread throughout the brain parenchyma. The development of neutralizing and hemagglutination-inhibiting antibodies in serum correlates with the clearance of virus from most systemic sites. However, peristence of virus in both brain and kidney is demonstrated late in this infection.

Animals↗
PubMed1976

Ultrastructure of mumps virus replication in organotypic cultures of hamster choroid plexus.

Organotypic cultures of newborn hamster choroid plexus were inoculated with equal titre doses of newly isolated or hamster adapted strains of mumps virus. The ultrastructure of virus replication in choroid epithelial cells of the cultures was compared. No qualitative differences were observed; however, the adapted strain produced significantly greater numbers of virions and earlier destruction of the cultures. These findings are consistent with previous in vivo observations of the ultrastructure of the replication of these strains in the newborn hamster central nervous system. This in vitro study leads further support to the hypothesis that differences in the in vivo biological effects of the virus strains are primarily the result of virus-cell rather than virus-host interactions.

Animals↗
PubMed1975

Progressive rubella panencephalitis. Late onset after congenital rubella.

In children with congenital rubella infection the deficits remain stable; neurologic deterioration after the first few years of life is not believed to occur. We have encountered three patients with a definite or presumptive diagnosis of congenital rubella, in whom a progressive neurologic illness developed that began in the second decade and was characterized by spasticity, ataxia, intellectual deterioration, and seizures. High antibody titers to rubella virus in serum and spinal fluid were present in two, and all had increased cerebrospinal-fluid protein and gamma globulin. Extensive attempts to recover a virus from brain and body fluids were unsuccessful. The brains of two patients showed a widespread, progressive, subacute panencephalitis mainly affecting white matter. These data suggest that rubella virus may be a cause of progressive panencephalitis.

Adolescent↗
PubMed1975

Acquired toxoplasmosis. A neglected cause of treatable nervous system disease.

The neurological manifestations of six cases of acquired central nervous system toxoplasmosis are compared with the 39 well-documented cases from the literature. Half of the patients had underlying systemic diseases (18 malignant neoplasms, two renal transplants, three collagen vascular diseases) treated with intensive immunosuppressive therapy. The remainder had primary toxoplasmosis. Three major neurological patterns were seen: (1) diffuse encephalopathy with or without seizures, (2) meningoencephalitis, and (3) singular or multiple progressive mass lesions. Routine neurological diagnostic studies were not helpful. The Sabin-Feldman dye test or IgM indirect fluorescent antibody test or both were effective in confirming the diagnosis. Twenty-seven patients died without a clinical diagnosis of toxoplasmosis. The diagnosis was made terminally in four additional patients. Thirteen of fourteen patients who received a full course of sulfadiazine or pyrimethamine or both did well. Toxoplasmosis should be considered in the immunosuppressed patient who appears with neurological involvement.

Adult↗