Alterations in T, B, and null cells in children with autoimmune diseases.
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Biomedical subjects
Publications and source records attributed to V Schauf.
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Group B streptococci are uniformly susceptible to penicillin or ampicillin. Nevertheless, morbidity and mortality in newborn infants infected with group B streptococci is a major clinical problem. Bacteriologic determinants in the outcome of this infection were studied. Streptococcal killing kinetics were studied for ampicillin alone and in combination with gentamicin. In all cases killing was accelerated by the combination. The practice of discontinuing administration of the aminoglycoside antibiotic when group B streptococcal infection is confirmed should be re-evaluated.
The distribution of immunoglobulin bearing (Ig+), T, and null lymphocyte subpopulations and the lymphocyte response to phytohaemagglutinin (PHA) and pokeweed mitogen (PWM) were determined in three infants with cytomegalovirus (CMV) infection. These infants had significantly decreased percentages of T cells (13%, 29% and 40%) compared to age-matched controls (61 +/- 2%). Compensatory increases in the percentages of Ig+ and null cells occurred. Decreased lymphocyte reactivity to PHA and PWM occurred in two patients. Purified T cells from these patients had normal reactivity indicating a disproportion of T cells in the peripheral blood. These abnormalities may result from CMV infection of lymphocytes and could be responsible for prolonged CMV viruria.
Group B beta hemolytic streptococcal infection of the newborn, acquired from the maternal genital tract, has emerged as an important cause of morbidity and mortality. In that the risk to the infant for colonization and infection may relate to the degree of streptococcal exposure, a semiquantitative determination of genital tract colonization was made in 210 pregnant women. Twelve women (6%) were colonized with 10(0) to 10(5) colonies of streptococci per sample. Among colonized women, 70% had used oral contraceptives in the year prior to pregnancy, whereas only 35% of uncolonized women gave such a history (P less than .05). There was an inverse relation between colony count and duration of pregnancy. Six of 9 untreated, colonized women had 1 to 3 repeat cultures which were negative for streptococci indicating that treatment for carriers, if available, would not be necessary much of the time.
The effects of specific immunotherapy with allogeneic cells transformed by Schmidt-Ruppin Rous sarcoma virus (SR-RSV), of treatment with BCG, and of surgery on the growth of SR-RSV-induced sarcomas in white-lipped marmosets were studied. Tumor incidence, tumor progression, and survival did not differ between control and treated animals. Animals immunized with BCG developed lymphocyte reactivity to tuberculin, which remained until the animals died. BCG was isolated from the spleen of one tumor-bearing animal.
Eight white-lipped marmosets immunized with BCG and 3 sham-immunized marmosets were studied after inoculation with Herpesvirus saimiri (HVS). BCG immunization had no significant influence on the incidence of infection by HVS, incidence of fatal malignant lymphoma, time of leukemia onset, development or titer of HVS antibodies, or average survival time. One BCG-immunized, HVS-infected marmoset failed to develop malignant lymphoma, whereas the remaining 10 HVS-infected marmosets died of malignant lymphoma. Prolonged survival occurred also in 1 marmoset immunized with BCG 100 days after HVS inoculation. The development and disappearance of lymphocyte reactivity to tuberculin were followed in 4 BCG-immunized marmosets.
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Normal rat kidney (NRK) cells, NRK cells infected with Rauscher murine leukemia virus, and NRK cells infected with Kirsten murine sarcoma-leukemia virus (NRK-K) were synchronized by a double thymidine block. At intervals after release from thymidine blockage, the cells were examined for the presence of viral antigens in the cytoplasm and on the cell surface by immunofluorescent microscopy by using goat anti-Rauscher murine leukemia virus and goat anti-Moloney leukemia virus (Tween-ether disrupted) sera. Detection of viral antigens in the cytoplasm was periodic during the cell cycle. Antigens were detected first during the S phase, increased during the G2 phase, and disappeared during the M and G1 phases. A similar pattern of surface immunofluorescence was observed. Infectious virus was detected in culture fluids from synchronized cells during the M phase. Surface immunofluorescence was detected in NRK-K cells with anti-Rauscher murine leukemia virus and may represent the presence of group-specific antigens on the cell surface. Control, uninfected NRK cells, which did not normally fluoresce, showed weak immunofluorescence during the S and G2 phases after synchronization. Synchronization can be used to amplify latent oncornavirus expression.
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