In:
Infection and Immunity, American Society for Microbiology, Vol. 10, No. 6 ( 1974-12), p. 1315-1320
Abstract:
The opsonization by polymorphonuclear leukocytes of group B streptococcal serotypes associated with neonatal sepsis and delayed meningitis was studied. A specific BIa opsonizing antibody (not related to the antipolysaccharide typing antibody) was present in only 10% of the population tested. Serotype BIa was not opsonized in the absence of this specific antibody. BIa antibody specificity was demonstrated by macroagglutination and absorption with BIa streptococci and extracts, but not by gel diffusion. The binding of complement by the BIa opsonin increased the mean phagocytic activity by 60%; complement was manifested via the classic and/or alternate C3-related pathway, but seldom by both concurrently. Serotypes BIb, BIc, BII, and BIII were naturally and nonspecifically opsonized in 95% of the human and baboon sera or plasma tested. Although similar levels of opsonization were present in hyperimmune rabbit sera, heat inactivation and homologous bacterial absorption did not reduce the level of phagocytic activity in the rabbit, human, or primate groups studied. These immunological studies confirmed previous findings that serotype BIa presents a serious hazard for neonatal sepsis, with a nearly 100% mortality. Exclusive isolation of BIII in delayed meningitis suggests that ingestion and subsequent killing by polymorphonuclear leukocytes of type III may differ from the other serotypes.
Type of Medium:
Online Resource
ISSN:
0019-9567
,
1098-5522
DOI:
10.1128/iai.10.6.1315-1320.1974
Language:
English
Publisher:
American Society for Microbiology
Publication Date:
1974
detail.hit.zdb_id:
1483247-1
