EXPOSURE OF CLINICAL ISOLATES OF ACINETOBACTER-BAUMANNII AND GENOSPECIES-3 TO DEFIBRINATED HUMAN BLOOD WITH AND WITHOUT ADDED HUMAN-NATURALOR (PATIENT)-IMMUNE ANTIBODIES

Fresh defibrinated blood (65% v/v) from 2 human donors failed to compl etely kill strains of Acinetobacter baumannii and genospecies 3, repre senting four serovars each. Although colony counts were reduced greate r than or equal to 90%, there invariably occurred rebound growth follo wing extended incubation. Neither selected serovar-specific or isolate -homologous (following experimental bacteremia) rabbit immune sera nor three intravenously applicable IgG preparations augmented the bacteri cidal activity of human blood against six selected strains of A. bauma nnii and genospecies 3, despite documented antibody contents of all se ra and IgG preparations employed. The majority of the sera from 22 pat ients who were early reconvalescent from systemic infection due to A. baumannii or genospecies 3, showed raised IgM antibody titers, and all sera demonstrated markedly elevated IgG antibody titers as determined with an enzyme-linked immunoassay. Defibrinated blood from donors B a nd T failed to completely kill the bacteria inocula of these 22 Acinet obacter isolates. Only one patient serum enhanced the bactericidal act ivity of human blood in the absence of antimicrobial drug(s), and only 1 patient serum with large amounts of detectable antimicrobial drug(s ) effected complete killing of the homologous bacterial inoculum.