PEDIATRICS Vol. 64 No. 5 November 1979, pp. 787-794
This Article
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow E-mail this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My File Cabinet
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hill, H. R.
Right arrow Articles by Hemming, V. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hill, H. R.
Right arrow Articles by Hemming, V. G.

Neonatal Cellular and Humoral Immunity to Group B Streptococci

Harry R. Hill MD1, Ann O. Shigeoka MD1, Robert T. Hall MD1, and Val G. Hemming MD1

1 Division of Clinical Immunology and Allergy, Departments of Pediatrics and Pathology, University of Utah, Salt Lake City

The mechanisms of host resistance to group B streptococci have not been defined precisely. In the studies reported here we have assessed the contributions of both humoral and cellular factors in protection against strains of this group. With assays of specific opsonic activity based upon the production of polymorphonuclear leukocyte chemiluminescence and radiolabeled bacterial uptake, we have demonstrated that specific heat-stable antibody and the classic complement pathway are major factors in opsonization of these organisms. In the absence of specific antibody, fresh serum resulted in markedly reduced bacterial uptake indicating, at best, a minor role for the alternative complement pathway. Additional studies have indicated that strain-specific antiphagocytic factors as well as type-specific ones may play a role in the virulence of these organisms. Neonates who developed group B streptococcal sepsis usually lacked opsonic activity in their infecting strain. In addition, polymorphonuclear leukocytes from normal term and stressed neonates showed impaired metabolic activation as measured in the chemiluminescence assay following exposure to opsonized group B streptococci. These results suggest that neonates who develop group B streptococcal disease may have defects in both the humoral and cellular aspects of their acute inflammatory response which may contribute to the high mortality observed in this most fulminant of bacterial infections.




This article has been cited by other articles:


Home page
 Arch. Dis. Child. Fetal Neonatal Ed.Home page
J. Källman, J. Schollin, C. Schalèn, A. Erlandsson, and E. Kihlström
Impaired phagocytosis and opsonisation towards group B streptococci in preterm neonates
Arch. Dis. Child. Fetal Neonatal Ed., January 1, 1998; 78(1): 46F - 50.
[Abstract] [Full Text]