Anti-pneumococcal antibody levels three to seven years after first booster immunization in children with sickle cell disease, and after a second booster.

We measured pneumococcal antibody levels in 55 patients (ages 7 to 20 years) with sickle cell disease 3 to 7 years after the first booster immunization. Only 6 of the children had protective levels of antibodies (> 300 ng/ml) against all 12 serotypes tested. Thirty-two children (58%) had suboptimal levels against 1 to 3 serotypes; 17 had suboptimal levels against 4 to 10 serotypes. Ten patients from the latter group (ages 13 to 17 years) received a second booster 6 to 8 years after the first booster immunization, and had a marked increase in antibody levels against all serotypes with the exception of serotypes 3 and 4 in two patients and serotype 6A in one patient.

Immunodeficiency in long-term survivors of acute lymphoblastic leukemia treated with Berlin-Frankfurt-Münster therapy.

OBJECTIVE: To determine whether the immune systems of long-term survivors of acute lymphoblastic leukemia (ALL) have persistent immune defects after Berlin-Frankfurt-Münster (BFM) treatment. STUDY DESIGN: We evaluated the cellular and humoral immune responses of 13 children with ALL in complete remission and off modified protocol treatment for 2 or more years. All patients had received complete immunizations for measles, mumps, rubella, and poliovirus before ALL developed. They were challenged with Haemophilus influenzae type B (Hib) and Pneumococcus vaccines after baseline serum samples were obtained. We also determined in vivo humoral immune responses to bacteria and viruses that cause common pediatric diseases. RESULTS: Compared with age-matched control subjects, the long-term survivors of ALL had a significant difference in the presence of protective antibodies to measles (p < 0.0001) and polioviruses (p < 0.0001) in their baseline sera; more than half had no protective antibodies to one or more previously administered vaccines or related infections. Most produced protective concentrations of specific antibody after reimmunization, but some were repeatedly unable to make protective antibodies, or mount a normal antibody response, despite natural disease and/or revaccination. Four children had significant infections. CONCLUSIONS: Long-term survivors of ALL who had BFM treatment may have persistent immune defects with respect to common childhood bacterial and viral diseases they previously had, or vaccines they received.

Minimal role for the spleen in antibody responses of C57BR/cdj mice to pneumococcal polysaccharide antigens.

The role of the spleen in antibody production and in susceptibility to pneumococcal infections remains poorly understood. Recently we showed that in A/J mice high antibody responses to polysaccharide antigens depend upon dosage, antigenic structure, interval between immunization and assay and the presence of the spleen. To investigate the possibility of alternative patterns of response, intact and splenectomized (Sx) C57BR/cdj mice were assayed for antibody responses to two structurally different pneumococcal polysaccharides, type 3 (SIII) and type 14 (SXIV). After 50 or 100 ng of SIII, intact C57BR/cdj mice produced uniformly low antibody responses that were further suppressed by splenectomy, but after 1,000 ng of SIII, C57BR/cdj mice, regardless of whether they were intact or Sx, produced antibody responses as high as those of intact A/J mice. Following SXIV, a spleen-dependent antigen, C57BR/cdj mice produced consistently lower antibody responses than A/J mice. Antibody responses to 500 or 5,000 ng of SXIV were totally obliterated in Sx C57BR/cdj mice; but unlike A/J mice, responses to 10,000 ng were similar regardless of whether C57BR/cdj mice were intact or Sx. The inability of intact C57BR/cdj mice to produce elevated responses to SIII or SXIV suggests that C57BR/cdj mice may lack the subset of spleen cells necessary for a vigorous response to these antigens. The data suggest that these mice could provide useful animal models for studying host variability in antibody responses to pneumococcal polysaccharides.

Decline of serum antibody in splenectomized children after vaccination with pneumococcal capsular polysaccharides.

Asplenic persons are at increased risk of overwhelming sepsis caused by Streptococcus pneumoniae. Vaccination with polyvalent pneumococcal polysaccharide has been shown to stimulate a nearly normal antibody response in these individuals, indicating that active vaccination might prevent pneumococcal disease in this population. To obtain information on the duration of protective levels of pneumococcal antibody, 33 asplenic children were vaccinated and antibody levels were measured at intervals for up to 4 1/2 years after vaccination. Significant antibody decline was observed in children who had undergone splenectomy because of trauma, but antibody decline was not observed in children whose spleens had been removed because of hereditary spherocytosis. There was a highly significant difference in rates of antibody decline among the 12 antibody serotypes measured: types 1, 4, 6A, 7F, 8, 19F, and 23F showed the greatest decline. Based on measured rates of antibody decline, subprotective antibody levels (antibody nitrogen less than 300 ng/ml) for types 7F, 8, and 19F would be reached 1 to 2 years after vaccination; type 6A never reached the protective level; and antibodies against the remaining eight types either were within the protective range initially or did not show significant decline. Asplenic children may benefit from revaccination with certain antigen types (7F, 8, and 19F) 1 to 2 years after initial vaccination.