Simultaneous occurrence of posttransfusion purpura due to anti-HPA-1a and a delayed transfusion reaction due to anti-Jk(b)
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to J L Swanson.
Explore the source record for details and available documents.
Receptor specificities of the three recognized variants of PapG, the major adhesin of uropathogenic Escherichia coli, have been deduced in part from the distinctive hemagglutination (HA) patterns these adhesins ostensibly exhibit with different erythrocytes. A comprehensive reevaluation of these HA patterns using sheep, rabbit, and diverse human erythrocytes revealed that the erythrocyte binding ranges of the three PapG variants are broader and more overlapping than generally recognized, suggestive of receptor specificities beyond those posited in the prevailing model. Experiments involving guinea pig erythrocytes artificially labeled with defined Gal(alpha1-4)Gal-containing glycolipids supported this hypothesis and further suggested that HA patterns with naturally occurring erythrocytes cannot be used to determine reliably an adhesin's glycolipid binding specificities. Finally, slide HA assays exhibited considerable interexperiment, interobserver, and intraobserver irreproducibility, limiting their usefulness for assessing either the receptor specificities of PapG variants or the PapG repertoire of wild-type E. coli strains.
Explore the source record for details and available documents.
BACKGROUND: Chloramphenicol-dependent antibodies are a rare cause of interference in pretransfusion serologic testing. Their presence can be confirmed by the testing of red cells in both the presence and absence of chloramphenicol. CASE REPORT: A 29-year-old, group A, Rh-positive man with no history of chloramphenicol exposure was found to have a chloramphenicol-dependent panagglutinin in his serum. The antibody was IgM with a titer of 8. It showed no blood group specificity when tested with common and rare red cell phenotypes, and it failed to react with platelets and granulocytes. Confirmation attempts using a chloramphenicol sodium succinate solution as the cell-suspending medium led to negative results. The antibody reacted serologically only in the presence of chloramphenicol, which arises from the succinate derivative by the action of blood esterases. CONCLUSION: This case is an additional example of a chloramphenicol-dependent antibody. It demonstrates how the laboratory investigation of drug-related phenomena is dependent on testing the drug from that reacts in vivo.
BACKGROUND: Patients with hemophilia B lack factor IX (F IX). These patients may become alloimmunized after the transfusion of F IX concentrates and may develop F IX inhibitors, which have been characterized as polyclonal IgG4 alloantibodies. Two cases in which F IX inhibitors caused difficulty in compatibility testing and antibody identification were encountered. It was hypothesized that, because F IX is present in normal plasma, it might be adsorbed by red cells in vivo and then be detected during antibody screening tests with serum containing F IX inhibitors. CASE REPORT: Sera from two African American half-brothers with hemophilia B were incompatible with all common and rare red cell phenotypes tested in the anti-human globulin test, but did not react with each other's red cells. The brothers' red cell antibodies were neutralized with both normal plasma and a commercially available F IX concentrate, which indicated that the red cell incompatibility was most probably caused by their F IX inhibitors. Red cells from an unrelated patient with hemophilia B and a very low titer of F IX inhibitor were tested against the half-brothers' sera and did not react. The compatible red cells from one of the half-brothers and the unrelated patient with hemophilia B adsorbed F IX from normal plasma or F IX concentrate after 37 degrees C incubation; this rendered them incompatible with the plasma containing F IX inhibitor from the other half-brother. CONCLUSION: F IX appears to be present on normal red cells and may be detected during compatibility and antibody identification procedures when serum or plasma containing F IX inhibitors is tested.
A study of 565 Puerto Rican patients with storage pool deficient (SPD) Hermansky-Pudlak syndrome (HPS) demonstrated that most HPS patients had minor bleeding episodes while others had repeated, severe hemorrhagic episodes requiring transfusion. The severity of bleeding in these latter patients could not be attributed to their SPD alone. As swine with SPD platelets and low von Willebrand factor antigen (vWF:Ag) have more severe hemorrhages than pigs with either defect alone, 146 albino patients and 46 normally pigmented patients were examined for their level of vWF:Ag. The risk of SPD HPS patients having severe, repeated bleeding episodes increased when vWF:Ag fell below 70 U/dL. Family studies indicated that low vWF:Ag levels were more frequently associated with O blood group than from a gene suppressing production or release of vWF1. HPS patients should be tested for vWF:Ag levels.
A mouse IgG1 monoclonal antibody (MAb) UMRh, was prepared by immunizing Balb/c mice with the Jurkat T cell acute lymphoblastic leukemia (T-ALL) cell line. The MAb UMRh is directed against a widely distributed Rh-related cell surface antigen, present on red blood cells (RBCs) expressing the more common Rh phenotypes. The antigen has reduced expression on RBCs of -D-, DCW-/DCW-, Rhmod and Rhnull phenotypes. UMR immunoblotted a unique pattern on RBC membrane preparations of two bands at 40 and 43 kD and a diffuse pattern extending upward to about 55 kD. The UMRh antigen is also present on peripheral blood mononuclear cells, granulocytes, platelets, leukemic cells of T cell, B cell and myeloid origins, hematopoietic stem cells, and two tumor lines (lung and colon carcinoma). The number of UMRh sites per RBC (CDe/ce) was determined to be 5,519 copies/cell, whereas the sites on a -D- phenotype RBC were 1,096 copies/cell. A T-ALL line (CEM) expressed 333,364 copies/cell and a myeloid line (KG-1) expressed 90,913 copies/cell. Several Rh-related murine MAbs have been described, but our data indicates that UMRh recognizes a previously uncharacterized Rh-related specificity.
Fishhook injuries rarely pose a true emergency, and only a few cases of posterior ocular injury from fishhooks have been described. We present a case of penetrating ocular, orbital, and cranial trauma produced by a broken fishhook. The morbidity and mortality as well as the initial emergency evaluation of penetrating foreign objects in the orbital-cranial region are discussed.
Whole egg white from pigeon, dove, and cockatiel eggs, as well as the ovomucoid fraction of pigeon egg white, exhibited strong P1 antigenic activities and inhibited agglutination of human P1 erythrocytes and of digalactoside-coated latex beads by P-fimbriated Escherichia coli strains. In contrast, chicken egg white exhibited only weak P1 antigenic activity and had little impact on P-fimbrial agglutination. These preparations did not affect hemagglutination by E. coli strains expressing mannose-resistant adhesins other than P fimbriae, i.e., Dr, F1845, and S adhesins. Human anti-P1 serum diminished the P-fimbrial inhibitory activities of pigeon egg white and pigeon ovomucoid. Pigeon ovomucoid was equipotent on a molar basis with globoside, and the pigeon, dove, and cockatiel egg white preparations were equipotent with each other in P-fimbrial inhibition. Incubation of p erythrocytes in whole egg whites or in pigeon ovomucoid did not render them agglutinable by P-fimbriated bacteria, whereas incubation in globoside did. These data demonstrate that whole egg whites (and their ovomucoid fraction) from members of the families Columbidae (pigeons and doves) and Psittacidae (parrots) specifically and potently inhibit P-fimbrial agglutination, probably by providing P1 antigen as a receptor for the P-fimbrial adhesin. Avian egg white preparations may facilitate adhesin characterization of wild-type uropathogenic strains and may useful in preventing upper urinary tract infections due to P-fimbriated E. coli.
Hyperacute rejection of organ xenografts is thought to be mediated by the reaction of naturally occurring antibodies and complement of the recipient with blood vessels in the donor organ. We have suggested previously that the pathogenesis of hyperacute rejection might involve the activation of endothelial cells in the graft. To evaluate the potential role of natural antibodies and complement in hyperacute xenograft rejection, sixteen human sera were tested for variation in the ability to activate porcine endothelial cells as manifested by the release of biosynthetically labeled heparan sulfate from the cells. It was then asked to which extent such variation might reflect differences in natural antibody titer and/or complement activity. The sera mediated release of 3.6-57% of endothelial cell-associated heparan sulfate. Heparan sulfate release correlated significantly with the titer, in the sera, of IgM antibodies that bound to cultured endothelial cells (P = 0.0008) or to a triad of glycoproteins believed to represent the major targets of natural antibodies in porcine to primate xenografts (P = 0.001); correlation was also observed with the total concentration of IgM (P = 0.0046). The release of heparan sulfate did not correlate with corresponding properties of serum IgG, with anti-swine hemagglutination or with isohemagglutination titers. Heparan sulfate release correlated with deposition on endothelial cells of iC3b (P = 0.0095), but not with serum complement activity. Our findings indicate that in the reaction between human serum and xenogeneic endothelial cells, it is the concentration of xenoreactive IgM and not differences in complement activity that limits the ensuing pathophysiologic events.
Red blood cell alloantibody production was studied in 90 neonates who received a mean of 14.1 transfusions (range 2-35) from an average of 8.9 donors during the first three months after birth. Standard antibody detection procedures were done with the use of a selected red blood cell panel. No unexpected alloantibodies were detected. These findings suggest, at a 99% confidence level, that neonates do not make red blood cell alloantibodies in response to transfusion, indicating that repeated compatibility testing is probably unnecessary. Thus, following initial antibody screening and compatibility tests, further compatibility testing can be eliminated.
Alloantibodies of A and B specificity were detected in the serum and on the red cells of 4 non-0 recipients of group 0 solid organ transplants. The antibodies were assumed to be produced by 'passenger' lymphocytes introduced at the time of transplant. Gm allotyping of donor serums, recipient serums and the unexpected antibodies was done. Gm typing was informative in 1 case, when the anti-A1 found in the serum of a liver transplant recipient was shown to be of phenotype Gm(fb) and the Gm phenotype of the recipient to be Gm(axg). Gm allotyping was not informative in the other 3 cases.
A C4-deficient patient with systemic lupus erythematosus had been transfused on several occasions. His red cells reacted with a proportion of anti-Rg (Rodgers) and anti-Ch (Chido) reagents, but this was due to a separable antibody that did not have anti-Rg or anti-Ch specificity. Eluates of anti-Rg and anti-Ch indicate his red cell phenotype to be Rg-Ch-. Anti-C4 has been identified in his serum that exhibits neither anti-Rg nor anti-Ch specificity, but has similar serological characteristics in reacting with C4- and C4d-coated red cells.
Dengue virus suspensions from mouse brain and cell culture were fractionated into three components by rate zonal centrifugation in sucrose gradients. Infectious virus sedimented in a single zone and possessed hemagglutinating (HA) and complement fixing (CF) activity. Electron micrographs showed the virion to be a spherical particle 48 to 50 nm in diameter with 7-nm spherical structures on its surface. Buoyant density in CsCl of virions from mouse brain was estimated at 1.22 g/cm(3) and from cell culture at 1.24 g/cm(3). During centrifugation of virions in CsCl, an additional HA component appeared with a buoyant density of 1.18 g/cm(3). It was shown in electron micrographs to consist of virion fragments. A noninfectious component with HA and CF activity sedimented in sucrose more slowly than intact virus, had a buoyant density of 1.23 g/cm(3) in CsCl, and appeared as "doughnut" forms measuring 13.8 to 14 nm in diameter. A third component, with CF activity and no HA activity, sedimented very little in sucrose gradients. Particles of the same size and shape as the spherical subunits on the surface of the virion were observed in electron micrographs.
Explore the source record for details and available documents.
Explore the source record for details and available documents.