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Infect Immun. 1974 December; 10(6): 1315-1320
Copyright © 1974 American Society for Microbiology. All Rights Reserved.

Opsonin System of the Group B Streptococcus

^a Streptococcal Disease Section, Center for Disease Control, Fort Collins, Colorado 80521

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.

¹ Present address: Vector-Borne Diseases Branch, Center for Disease Control, P.O. Box 2087, Fort Collins, Colo. 80521.

² Present address: Regional Parasite Research Laboratory, U.S. Department of Agriculture, Auburn, Ala. 36830.

³ Present address: Central Health Management Division, State Health Agency, State of New Mexico, Santa Fe, N. M. 87501.