PubMed Health⌕ Search

Biomedical subjects

R F Schell

Publications and source records attributed to R F Schell.

135 records · Page 8Linked to original sources

Detection of nonspecific resistance to Listeria monocytogenes in rabbits infected with Treponema pallidum.

Several lines of evidence suggest that cell-mediated immunity (CMI) is suppressed in the early stages of infection caused by Treponema pallidum and becomes activated at the time that latency is induced. In the studies reported in this paper, rabbits were infected intravenously with T. pallidum and subsequently challenged with Listeria monocytogenes. Enhanced ability to suppress the growth of Listeria was detected in their livers between 3 and 5 weeks after infection with T. pallidum, corresponding to the onset and regression of the generalized syphilitic eruption. A second infection of T. pallidum 4 weeks after the first, at a time when suppression was beginning to wane, prolonged the listericidal activity. These observations support the hypothesis that infection by T. pallidum stimulates CMI, which, in turn, may play a role in inducing latency.

Animals↗

Amikacin levels in the human biliary tract.

The concentrations of amikacin in serum, gallbladder, and common duct bile, and gallbladder tissue in patients undergoing surgery of the biliary tract were investigated. Patients received 500 mg amikacin intravenously or intramuscularly from 1 to 11 hours before surgery. Another group had T-tubes inserted and blood and bile levels were studied serially postoperatively. One half hour after 500 mg amikacin, serum levels were high and bile levels were 30 per cent of the serum levels, with tissue levels less than 19 per cent of the serum levels. At 6 hours, serum levels were 37 per cent of the 1-hour levels; however, bile levels were 34 per cent of the simultaneous serum levels. At 11 hours, both postdose serum and bile amikacin levels were low. However, simultaneous bile levels were higher than serum levels. No patient suffered from any side effects from amikacin.

Adult↗

Influence of hydroxyethyl starch on humoral and cell-mediated immune responses in mice.

The immunotoxicity of hydroxyethyl starch (HES), a reagent used in leukocytapheresis or as a plasma expander, was assessed. HES did not significantly alter host resistance to Listeria monocytogenes or Streptococcus pneumoniae. HES (4-32 ml/kg), as well as a physiological saline solution (32 ml/kg), did inhibit the in vitro lymphoproliferation of spleen cells from mice intravenously injected 1 hour prior to removal of the spleens; the proliferation induced by a T-cell and B-cell mitogen was suppressed. However, this suppression was transient, in that, HES and saline injections given 4 and 24 hours prior to removal of the spleens produced no significant inhibition. Unlike the HES effects on lymphoproliferation, HES did suppress the in vivo humoral immune response to sheep erythrocytes (SRBC) when given 24 hours prior to antigen, but this inhibition was obtained only with the 32 ml per kg dose. Interestingly, a similar dose of mouse albumin significantly enhanced the response. In vitro analysis of humoral and cell-mediated immune responsiveness with in vivo treated spleen cells produced results that were not dose dependent. Although HES was more suppressive than saline, both saline and HES were inhibitory. The lack of a dose-dependent effect suggests that the in vitro analysis of in vivo treated cells was not a good index of their in vivo reactivities. The greater variability and apparent sensitivity of the in vitro analysis probably reflect the transient effects of in vivo dilution of serum factors by relatively large intravenous injections and/or the transient effects of injection trauma.

Animals↗

In vitro and clinical evaluation of ceforanide.

Ceforanide, a new cephalosporin antibiotic with a long half-life (three hours), was evaluated for its antimicrobial activity, pharmacology, and clinical efficacy. Fifty-two patients with 56 infections due to susceptible organisms received ceforanide, 0.5 g, 1 g, or 2 g, intramuscularly or intravenously every 12 hours for four to 60 days (average: 14.1 days). The in vitro studies of our clinical isolates showed that 12.0 micrograms/ml or less of ceforanide inhibited all Streptococcus pneumoniae, beta hemolytic streptococci group A, B, F, Staphylococcus aureus, Staphylococcus epidermidis, Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis and Hemophilus influenzae. After a 1 gram intramuscular dose, the mean peak serum concentration at one hour was 44.0 micrograms/ml, and at 12 hours was 3.8 micrograms/ml. After a 1 gram intravenous dose, the mean peak serum concentration was 65.0 micrograms/ml, and the mean trough serum concentration at 12 hours was 9.6 micrograms/ml. The infections treated included ten pneumonias, ten urinary tract infections, seven bacteremias, two osteomyelitis, and 35 skin-soft tissue infections. Of the 56 evaluable infections treated, 52 had a clinical cure with only four failures. Ceforanide was well tolerated, with no patients developing thrombophlebitis, or liver or renal abnormalities. Three patients developed abnormal Coombs' reactions and one had diarrhea.

Adolescent↗

The effect of C3 depletion on resistance of hamsters to infection with the yaws spirochete.

The role of complement in humoral-mediated resistance to frambesial infection (yaws) needs to be defined. The level of serum C3 was reduced shortly after infection of hamsters with Treponema pallidum subspecies pertenue. Five weeks after frambesial infection, the serum C3 level began to increase and by week 7 no difference was detected between infected and uninfected hamsters. When C3 was depleted in hamsters by injection of 20 units of cobra venom factor (CoVF), two alterations in host resistance to frambesial infection occurred. Depletion of C3 abrogated the ability of immune serum to confer complete protection on normal hamsters against infection with the yaws spirochete. In all hamsters receiving immune serum but not CoVF, lesions failed to develop and lymph nodes weighed significantly less (P less than or equal to 0.1) than those of controls. Furthermore, no treponemes were detected in the lymph nodes of passively immunized animals. Second, depletion of C3 increased the susceptibility of hamsters to frambesial infection. The onset and progression of frambesial lesions were enhanced as compared with frambesial-infected hamsters not treated with CoVF. Finally, CoVF treatment did not reduce the ability of frambesia-immune hamsters cured of disease with penicillin to resist reinfection. These results demonstrate that complement influences the pathogenesis of yaws.

Animals↗

Synergistic effect of macrophage activation and immune serum, especially IgG2, on resistance to infection with Treponema pallidum ssp. endemicum in hamsters.

Experimental studies have indicated that macrophages are involved in the pathogenesis of syphilis. Whether macrophages alone or with immune serum are ultimately responsible for killing of treponemes is disputed. We have demonstrated that BCG-vaccinated hamsters administered normal serum contained fewer treponemes in the inguinal and popliteal lymph nodes than did the nonvaccinated controls. When BCG-vaccinated hamsters were injected with syphilitic immune serum and challenged with Treponema pallidum ssp. endemicum, treponemicidal activity was enhanced. Treponemicidal activity was also detected in BCG-vaccinated hamsters challenged with treponemes treated in vitro with immune serum and its immunoglobulin fractions, especially IgG2. The immune IgG2 fraction had more treponemicidal activity than did the immune IgG1 fraction and the unfractionated immune serum. Our observations indicate an important synergistic role for macrophages and immune serum, especially IgG2, for elimination of T. pallidum ssp. endemicum from the host.

Adult↗