In eliminating typing errors clue to cold agglutinins, one is helped by the failure of most of them to react at 37 C, but this does not help one in recognizing bacteriogenic hemagglutinins because they react readily at body temperature. Here too the best way to eliminate the source of error is to type the serum as well as the red cells and to remember that typing of red cells is only half of the job. Serum with bacteriogenic hemagglutinins will clump red cells of group O, which are normally not agglutinated by any serum. When one has reason to suspect that bacteriogenic panagglutination has developed, the way to prove it is to test the cells with serum of the same individual or with serum of group AB known to be free of cold agglutinins and to type the serum of the unknown blood specimen with red cells of known groups. Several bactericidal and bacteriostatic agents have been found which prevent development of bacteriogenic hemagglutination. Recent studies indicate that about 90 per cent of intragroup transfusion reactions following isoimmunization either by repeated transfusions or by fetal blood during pregnancy occur in Rh individuals. Unfortunately not all cases can be detected by the demonstration of anti Rh agglutinins. In many cases it must be assumed that the anti Rh antibody is fixed to the tissue cells of the reticuloendothelial system. To prevent intragroup transfusion accidents, all Rh patients should receive blood from Rh donors. Also the modified cross matching test, i. e. incubation of patient's serum and donor's cells at 37 C. for fifteen to thirty minutes, should be carried out. Whenever anti Rh agglutinins could be demonstrated, they frequently behave like warm agglutinins, in contrast to those which react best at 20 C. or lower temperature.Occasionally an Rh patient immunized by the Rh factor may have several atypical agglutinins, as demonstrated by varying specificities at different temperatures. In such cases the compatibility tests should be carried out at 37 C, while incompatibilities detectable at lower temperature are probably of less significance. Rarely, however, atypical agglutinins acting at low temperature may cause transfusion reactions. In my opinion these are apt to occur in patients immunized either by repeated transfusions or by the fetus, but by blood factors other than Rh. In these instances, as in the exceptional cases of Wiener and Peters, i. e. cold anti Rh agglutinins, one cannot be certain whether the demonstrable antibodies or tissue antibodies are responsible for the transfusion reactions. This view does not conflict with the claim of Landsteiner and Levine that the atypical agglutinins present in 3 per cent of all normal individuals probably do not cause transfusion reactions. In these instances the atypical agglutinins inactive at 37 C. are physiologic for these individuals, in contrast to the atypical immune agglutinins mentioned. An appeal can be made to abandon the nomenclature of the blood groups by numbers. The letters O, A, B and AB indicate the correct theory of...
