Serotype 14 variants of the Spanish penicillin-resistant serotype 9V clone of Streptococcus pneumoniae arose by large recombinational replacements of the cpsA-pbp1a region.
The high prevalence of penicillin resistance among Streptococcus pneumoniae isolates from Uruguay has been associated with the emergence of a penicillin-resistant clone of serotype 14. Isolates of this clone were identical by multilocus sequence typing to members of the Spanish penicillin-resistant serotype 9V clone and possessed indistinguishable forms of the penicillin-binding protein 2b and 2x genes. Their pbp1a genes were also identical, except at the 3' end. The serotype 14 isolates were shown to be a variant of the Spanish serotype 9V clone which arose by a 22.2 kb recombinational replacement that introduced the capsular biosynthetic locus, and part of the neighbouring pbp1a gene, from a serotype 14 isolate. One end of the recombinational replacement was within the first gene of the capsular polysaccharide operon, cpsA, as the sequence of the upstream dexB gene, through most of cpsA, was identical in the penicillin-resistant serotype 9V and 14 isolates, but the sequences differed in the rest of cpsA and in cpsB. The other recombinational junction was at the end of the divergently transcribed pbp1a gene, which is approximately 11.6 kb downstream of the capsular biosynthetic locus. Isolates of this serotype variant were also detected in Spain and Denmark. Penicillin-resistant serotype 14 isolates from Poland were also closely related to the penicillin-resistant serotype 9V clone, but have emerged independently, as one end of the recombinational replacement was upstream of dexB and the other was within pbp1a, but at a different position from that in the serotype 14 variants from Uruguay, Spain and Denmark. Serotype 14 variants of the Spanish serotype 9V clone have therefore arisen on more than one occasion by large recombinational replacements that extend from the start of the cps region into the pbp1a gene.
Coffey
Tracey J
TJ
Wellcome Trust Centre for the Epidemiology of Infectious Disease, Department of Zoology, University of Oxford, Oxford OX1 3FY, UK.
Daniels
Margaret
M
Molecular Microbiology Group, School of Biological Sciences, University of Sussex, Brighton BN1 9QG, UK.
Enright
Mark C
MC
Wellcome Trust Centre for the Epidemiology of Infectious Disease, Department of Zoology, University of Oxford, Oxford OX1 3FY, UK.
Spratt
Brian G
BG
Wellcome Trust Centre for the Epidemiology of Infectious Disease, Department of Zoology, University of Oxford, Oxford OX1 3FY, UK.
D016667:Bacterial Capsules / Q000235:genetics / Q000378:metabolism; D001426:Bacterial Proteins; D001483:Base Sequence; D002268:Carboxypeptidases / Q000235:genetics*; D002352:Carrier Proteins; D005798:Genes, Bacterial; D014644:Genetic Variation; D006602:Hexosyltransferases / Q000235:genetics*; D008969:Molecular Sequence Data; D009097:Multienzyme Complexes / Q000235:genetics*; D002267:Muramoylpentapeptide Carboxypeptidase; D010403:Penicillin Resistance / Q000235:genetics*; D046915:Penicillin-Binding Proteins; D010458:Peptidyl Transferases / Q000235:genetics*; D011995:Recombination, Genetic; D012703:Serotyping; D013296:Streptococcus pneumoniae / Q000145:classification / Q000187:drug effects / Q000235:genetics*
D001426:Bacterial Proteins; D002352:Carrier Proteins; D009097:Multienzyme Complexes; D046915:Penicillin-Binding Proteins; D010458:Peptidyl Transferases; D006602:Hexosyltransferases; D002268:Carboxypeptidases; C095874:CpsA protein, Sulfolobus solfataricus; D002267:Muramoylpentapeptide Carboxypeptidase