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Bacterial genetics and human immunity to group B streptococci
E E Adderson1, S Takahashi, J F Bohnsack
1Department of Infectious Diseases, St. Jude Children's Research Hospital, 332 N. Lauderdale Street, Memphis, Tennessee 38105, USA.
Molecular Genetics and Metabolism
|September 26, 2000
Summary
Group B Streptococcus (GBS) type III-3 strains are linked to most neonatal infections. Genetic variations, including C5a-ase and sialic acid content, influence GBS virulence and immune evasion.
Area of Science:
- Microbiology
- Immunology
- Genetics
Background:
- Group B Streptococcus (GBS) type III is a leading cause of neonatal sepsis and meningitis.
- Genetic heterogeneity among GBS strains influences virulence and host immune responses.
Purpose of the Study:
- To classify type III GBS strains using DNA restriction patterns.
- To investigate genetic factors contributing to the virulence of specific GBS subgroups, particularly RDP type III-3.
Main Methods:
- Chromosomal DNA restriction digest patterns were used for GBS classification.
- Analysis of C5a-ase expression and functional activity in different GBS RDP types.
- Quantification of capsular sialic acid content in virulent and less virulent GBS strains.
Main Results:
- A subgroup of genetically related strains, RDP type III-3, was identified as responsible for the majority of type III GBS neonatal infections.
- Functional C5a-ase, an inhibitor of neutrophil chemotaxis, was present in 100% of less virulent strains (III-1, III-2) but only 63% of virulent III-3 strains.
- Virulent RDP type III-3 strains exhibited significantly higher capsular sialic acid content, which limits complement activation and contributes to invasiveness.
Conclusions:
- Genetic classification of GBS is crucial for understanding virulence.
- Differences in C5a-ase and capsular sialic acid content, regulated by genetic polymorphisms, contribute to GBS pathogenesis.
- These findings have significant implications for understanding and combating neonatal GBS infections.