Further studies on the immunology of the infant rat experimental model of Haemophilus influenzae type B meningitis.

An age-related acquisition of anticapsular (AC) antibodies to b (HIb) did not occur in rats; this result corrects a previous spurious observation from this laboratory. Purified HIb polysaccharide was found to be totally non-immunogenic over a wide range of doses in infant and adult rats, with or without booster immunizations. Killed HIb was also totally non-immunogenic. Only about one-quarter of survivors of infantile HIb disease made an AC antibody response. In an attempt to observe “immune paralysis”, survivors of infantile HIb disease were immunized with live HIb at age 8 weeks. This immunization resulted in significantly fewer AC antibody responders in the survivors than in the controls. However, immunization of survivors with killed HIb produced significantly greater responders in survivors than in controls. In order to determine whether passive protection from HIb disease could be achieved by non-capsular antibodies, survivors' offspring were studied and found to be protected from infantile HIb disease due to bactericidal (BA) antibodies that were probably not directed at the capsular polysaccharide. Using the BA assay, differences were observed between two HIb strains, presumably due to differences in non-capsular antigens. The infant rat experimental model of HIb disease appears to have only limited value in the study of AC antibody responses since infant rats differ from infant humans in several respects. The model may be more useful in studying the immunology of non-capsular HIb antigens including their role in protective immunity and possible differences in these antigens among strains of HIb.