Serotype III Streptococcus agalactiae from Bovine Milk and Human Neonatal Infections1

Although largely unrelated, many bovine type III GBS appear to share a common ancestor with an important human clone

MS

thesisSerotype III group B streptococci (GBS) have previously been sub-classified by restriction digest pattern (RDP) typing into three RDP type: III-3, III-2, and III-1. RDP type III-3 strains were previously found to cause the majority of neonatal invasive disease among a collection of isolates from Tokyo and Salt Lake City. The majority of asymptomatically colonizing isolates were RDP type III-2. The polysaccharide capsule of RDP type III-3 strains were found to contain more sialic acid and activate less serum complement than RDP type III-2 strains. The purpose of the studies reported here were to determine if insertional inactivation of the hyaluronidase (hylB) gene correlates with RDP typing of serotype II GBS strains. All RDP type III-3 and type III-1 strains lacked the presence of IS1548 within their genome while all RDP type III-2 strains were found to have an insertional interruption of the hylB gene by IS1548. All RDP type III-1 strains were found to express hyaluronidase. All RDP type III-2 strains failed to express hyaluronidase. IS1548 was also detected in some serotype II and some serotype V strains, but was not located within the hylB gene in these strains. These serotype II and serotype V strains expressed hyaluronidase. In-activation of the hylB gene by IS1548 and the resulting inability to express hyaluronidase appears to be specific for RDP type III-2 GBS strains. Additional studies were performed to determine if RDP typing of serotype III GBS correlates with the presence of alleles of the gene for translation initiation factor-2 (IF2). Alleles of the info gene encoding IF2 were used to separate GBS strains into phylogenetic lineages previously described by Hauge. RDP typing also correlated with the separation of GBS strains into phylogenetic lineages. All RDP type III-3 strains had infB allele "C." All RDP type III-2 and type III-1 strains had infB allele "A." Most GBS populations had infB allele "A." Fewer populations had infB alleles "B," "C," or "D." Allele "B" was found among the RDP type Ia-2 population. Allele "D" was restricted to a subpopulation of RDP type Ia-1. RDP type Ia-1 was the only population to have subpopulations with different infB alleles "E" and "F" were not detected in any of our GBS populations. A previously undescribed infB allele "G" was found only among the RDP type V-2 population. Phylogenetic analysis using RDP typing and infB allele classification to identify specific GBS populations may be an important step toward the clinical identification of GBS strains with enhanced pathogenic potential