ERIK, a low-frequency red cell antigen of the MNS blood group system associated with Sta.

A new low-frequency red cell antigen, ERIK (MNS37), is associated with the Sta antigen of the MNS system. Four ERIK+ propositi have been identified: all are St(a+). Thirteen other St(a+) samples, including one of the Mz type, and over 200 St(a-) samples were ERIK-. In two of the propositi ERIK is associated with an abnormal trypsin-resistant M antigen; in the others it is associated with N, which is shown to be expressed weakly in one family. Immunoblotting with an antibody to an epitope common to glycophorin A (GPA) and glycophorin B (GPB) gave identical results with St(a+) ERIK+ and St(a+) ERIK- cells, revealing GPA, GPB, an abnormal structure GPSta and aggregates of these components. In the propositi with trypsin-resistant M, GPSta carries the unusual M antigen, whereas in the M-N+ERIK+ individual analysed by immunoblotting GPSta carries N. Immunoblotting with anti-Sta and anti-ERIK showed that Sta is located on GPSta but that ERIK is located on GPA, presumably the GPA molecule encoded by the GYPA gene contiguous to the gene encoding GPSta.

Nosocomial epidemic of Serratia marcescens septicemia ascribed to contaminated blood transfusion bags.

Two cases of transfusion-related Serratia marcescens bacteremia prompted extensive epidemiologic investigations in three independent hospitals. Test tubes and plasma from donors whose blood was drawn into bags from a single production batch were cultured. Analysis of the ribotype of S. marcescens isolates was performed. For comparison, a strain from the production plant and eight other, unrelated bacteremia isolates were examined. In addition, a retrospective national survey was carried out. S. marcescens was cultured from 11 (0.73%) of 1515 blood units, and an additional (third) bacteremic patient was identified. The clinical isolates from three patients, the three units of blood transfused, and the plant-derived strain shared a unique ribotype. The incident is interpreted as a sporadic, bacterial contamination of blood bags with the S. marcescens epidemic strain, occurring during the manufacturing or packaging. A similar incident has not previously been reported. Attention is drawn to the possibility of significant contamination during the complex production of multiple-bag blood collection systems. Guidelines for improved registration and handling of transfusion complications in wards are suggested. Manufacturers should be encouraged to provide blood packs with sterile exteriors, in appropriate, single, outer packages.

The Haakestad antigen is identical with the Hov antigen.

The rare blood group antigen previously referred to as the 'Haakestad antigen' is shown to be identical with the Hov antigen (numerical designation: 700.038). Family studies add AB0 and HLA to the systems already known to segregate independently from Hov. Among 2,021 Danish blood donors, 4 Hov+ persons were found. Anti-Hov activity has been demonstrated in several 'multiple-antibody sera'.

Incidence of rhesus immunisation after genetic amniocentesis.

Of 655 Rh negative women without anti-D antibody in their serum at genetic amniocentesis, 361 delivered a Rh positive infant. Prophylactic treatment with anti-D immunoglobulin was not given at amniocentesis. The women were followed prospectively, being given a screening test for antibody after amniocentesis, at delivery, and six months later. Five of these 361 women yielded a positive test result due to anti-D antibody. The immunisation rate after genetic amniocentesis was no higher than the spontaneous immunisation rate during pregnancy. Four women who had two amniocenteses in the same pregnancy and 34 women who had amniocentesis in two consecutive pregnancies with Rh positive fetuses were not immunised. Among six women with anti-D antibody in their serum before amniocentesis the titre of antibody increased in three. Amniocentesis may have worsened the outcome of these pregnancies. These results suggest that the risk of immunisation in Rh negative women is small.

Correlation between donor cytomegalovirus immunity and chronic graft-versus-host disease after allogeneic bone marrow transplantation.

Chronic graft-versus-host disease (GvHD) in bone marrow allograft recipients is frequently preceded by a cytomegalovirus (CMV) infection. To elucidate whether an immune reaction of transplanted donor cells against CMV was involved in the pathogenesis of chronic GvHD, the effect of donor pretransplant CMV immune status on chronic GvHD incidence was analyzed. In 43 bone marrow recipients at risk, the 2-yr cumulative chronic GvHD probability was 55% when the donor was immune, in contrast to 16.5% when the donor was non-immune (p less than 0.002). No correlation between recipient pretransplant CMV immunity and chronic GvHD was observed. Donor CMV immunity did not correlate with acute GvHD or posttranplant CMV infection and seemed to predispose for chronic GvHD regardless of donor and recipient age. However, the proportion of CMV immune donors increased with increasing donor and recipient age. This may account for the higher incidence of chronic GvHD in older patients. The present study suggests that chronic GvHD may be mediated by a reaction of immune donor cells against CMV infected recipient cells.

Studies on Cob (Colton) antigen and anti-Cob.

Using a reliable and strong reacting antiserum of the rare anti-Cob specificity, it was shown that the Cob antigen was fully developed at birth. Gene dosage effect could not be demonstrated. The frequency of Co(b+) persons in the Danish population (7.8%) was found not to differ from other Caucasian populations. The antibody belonged to immunoglobulin class IgG without ability of fixing complement in vitro.

Antibody suppression and antiallotype antibodies. I. Failure of antibody to suppress antibody formation in rabbits possessing antiallotype anantibodies.

Antibody formation in rabbits against sheep erythrocytes (SRBC) was suppressed after injection of anti-SRBC IgG. Suppression did not occur, however, if the injected IgG had an allotypic marker to which the rabbits possessed circulating antibody.

Antibody suppression and antiallotype antibodies. II. Interference of circulating antiallotype antibodies with prophylactic treatment against Rh sensitization.

Sera from Rh-sensitized women representing presumable failure of the prophylactic treatment with IgG anti-D (Rh) have been examined for activity against allotype markers on IgG1. Antiallotype antibodies were found with increased frequency compared with a nonsensitized control. In general, however, interference of antiallotype antibodies is not considered to be a great risk of Rh prophylaxis at present. Some requirements which, in this context, may be of importance to the composition and dose of the IgG anti-D-containing preparations used are stressed.