Central nervous system infections. Etiologic and epidemiologic observations in New York State, 1975.
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Biomedical subjects
Publications and source records attributed to R Deibel.
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Cerebrospinal fluid (CSF) and sera from 129 patients of a study population of 139 were tested for antibody to herpes simplex, measles,and mumps viruses. Herpes simplex virus antibody was found in three of five patients with laboratory-confirmed herpes simplex infection and in eight patients without serological or virological evidence of current infection with this or other common neurotropic visuses. Eleven of the 139 patients were studied for antibody to lymphocytic choriomeningitis (LCM) virus. Eight of these had laboratory-confirmed LCM infection, and antibody was detected in the CSF of five of them. In one of these five, complement-fixing antibody appeared earlier in the CSF than in the blood. Assay of LCM virus antibody in the CSF may thus indicate infection with LCM virus more rapidly than serological and virological studies. The diagnostic and the possible prognostic significance of herpes simplex visus antibody in CSF remains to be ascertained.
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Laboratory evidence of recent or current lymphocytic choriomeningitis (LCM) virus infection was obtained in 60 patients. Twelve had diagnosis of central nervous system (CNS) infection: four of meningoencephalitis and eight of meningitis. Thirty-four patients had a grippe-like syndrome. Fifty-nine had had contact with pet hamsters. All of the 24 patients whose pets were studied had been exposed to one or more hamsters with serologic evidence of past LCM virus infection. The data implicate pet hamsters as a source of LCM in man. A continuous effective control of LCM virus in pet hamsters appears impractical. At present, the only feasible way to prevent further cases is the physician's special attention to the possibility of rodent contacts of patients with CNS disease and early laboratory confirmation of suspected cases of human LCM virus infections.
Chronic idiopathic polyneuropathy of a primary demyelinating type developed in a man who had had recurrent herpes simplex 2 for 10 years. A serum IgM kappa M-component was demonstrated on the myelin of individual sural nerve fibers by direct immunofluorescence microscopy. Marrow lymphocytosis and serum M-component increased with time. Attempts to confirm antibody activity of the M-component were negative. The evidence suggests that the attachment of M-component to nerve is a physical-chemical one. Interaction of M-component and nerve appears to have led to the neuropathy as an early manifestation of Waldenström's macroglobulinemia.
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During 1972 an apparently new enterovirus with characteristics of the Coxsackievirus group A was isolated from 11 residents of New York State, 10 of whom had central nervous system disease. The representative strain S/Albany 1/72 has the physical and chemical properties of an enterovirus and causes the pathology typical for Coxsackievirus group A in 1-day-old mice. Cross-neutralization tests indicated that the virus is distinct from currently recognized enteric viruses of man. Antibody levels to the representative strain were moderate to high in patients and were low to moderate in 26% of healthy individuals tested.
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White mice of the NYA: NYLAR strain were infected with coxsackie B1 or B4 virus and studied for persistence of virus, antibody conversion, histologic changes, and glucose tolerance during periods up to 13 months. Pancreatitis was observed during the acute phase of infection. Suggestions of subclinical diabetes were found during the first six months after virus inoculation. A normal glucose tolerance at 10 to 13 months suggestes that the functional lesion is temporary.
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