Sequence type 1 group B Streptococcus, an emerging cause of invasive disease in adults, evolves by small genetic changes.
The molecular mechanisms underlying pathogen emergence in humans is a critical but poorly understood area of microbiologic investigation. Serotype V group B Streptococcus (GBS) was first isolated from humans in 1975, and rates of invasive serotype V GBS disease significantly increased starting in the early 1990s. We found that 210 of 229 serotype V GBS strains (92%) isolated from the bloodstream of nonpregnant adults in the United States and Canada between 1992 and 2013 were multilocus sequence type (ST) 1. Elucidation of the complete genome of a 1992 ST-1 strain revealed that this strain had the highest homology with a GBS strain causing cow mastitis and that the 1992 ST-1 strain differed from serotype V strains isolated in the late 1970s by acquisition of cell surface proteins and antimicrobial resistance determinants. Whole-genome comparison of 202 invasive ST-1 strains detected significant recombination in only eight strains. The remaining 194 strains differed by an average of 97 SNPs. Phylogenetic analysis revealed a temporally dependent mode of genetic diversification consistent with the emergence in the 1990s of ST-1 GBS as major agents of human disease. Thirty-one loci were identified as being under positive selective pressure, and mutations at loci encoding polysaccharide capsule production proteins, regulators of pilus expression, and two-component gene regulatory systems were shown to affect the bacterial phenotype. These data reveal that phenotypic diversity among ST-1 GBS is mainly driven by small genetic changes rather than extensive recombination, thereby extending knowledge into how pathogens adapt to humans.
Department of Pediatrics and Molecular Virology and Microbiology, MD Anderson Cancer Center, Houston, TX 77030;
Anthony R
AR
Flores
Department of Infectious Diseases, Infection Control and Employee Health, MD Anderson Cancer Center, Houston, TX 77030;
Jessica
J
Galloway-Peña
Department of Infectious Diseases, Infection Control and Employee Health, MD Anderson Cancer Center, Houston, TX 77030;
Pranoti
P
Sahasrabhojane
Department of Infectious Diseases, Infection Control and Employee Health, MD Anderson Cancer Center, Houston, TX 77030;
Miguel
M
Saldaña
Department of Bioinformatics and Computational Biology, MD Anderson Cancer Center, Houston, TX 77030;
Hui
H
Yao
Department of Bioinformatics and Computational Biology, MD Anderson Cancer Center, Houston, TX 77030;
Xiaoping
X
Su
The Alkek Center for Metagenomics and Microbiome Research, Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX 77030;
Nadim J
NJ
Ajami
The Alkek Center for Metagenomics and Microbiome Research, Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX 77030;
Michael E
ME
Holder
The Alkek Center for Metagenomics and Microbiome Research, Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX 77030;
Joseph F
JF
Petrosino
DNA Sequencing Facility, MD Anderson Cancer Center, Houston, TX 77030;
Erika
E
Thompson
Novartis Vaccines, 53100 Siena, Italy;
Immaculada
I
Margarit Y Ros
Novartis Vaccines, 53100 Siena, Italy;
Roberto
R
Rosini
Novartis Vaccines, 53100 Siena, Italy;
Guido
G
Grandi
Department of Infectious Diseases, Infection Control and Employee Health, MD Anderson Cancer Center, Houston, TX 77030;
Nicola
N
Horstmann
Public Health Ontario, Toronto, ON, Canada M5G 1M1;
Sarah
S
Teatero
Department of Microbiology, Mount Sinai Hospital, Toronto, ON, Canada M5G 1X5; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada MG5 1M1; and.
Allison
A
McGeer
Public Health Ontario, Toronto, ON, Canada M5G 1M1; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada MG5 1M1; and.
Nahuel
N
Fittipaldi
Novartis Vaccines, 53100 Siena, Italy; rino.rappuoli@novartis.com sshelburne@mdanderson.org.
Rino
R
Rappuoli
Department of Pediatrics and Molecular Virology and Microbiology, MD Anderson Cancer Center, Houston, TX 77030; The Alkek Center for Metagenomics and Microbiome Research, Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX 77030;
Carol J
CJ
Baker
Department of Infectious Diseases, Infection Control and Employee Health, MD Anderson Cancer Center, Houston, TX 77030; Department of Genomic Medicine, MD Anderson Cancer Center, Houston, TX 77030 rino.rappuoli@novartis.com sshelburne@mdanderson.org.
Samuel A
SA
Shelburne
D000220:Adaptation, Biological / Q000235:genetics*; D000328:Adult; D001483:Base Sequence; D005075:Biological Evolution; D016000:Cluster Analysis; D021821:Communicable Diseases, Emerging / Q000453:epidemiology* / Q000382:microbiology*; D016680:Genome, Bacterial / Q000235:genetics; D006801:Humans; D016013:Likelihood Functions; D008957:Models, Genetic; D008969:Molecular Sequence Data; D009864:Ontario / Q000453:epidemiology; D010802:Phylogeny; D020641:Polymorphism, Single Nucleotide / Q000235:genetics; D017422:Sequence Analysis, DNA; D065288:Serogroup; D013045:Species Specificity; D013292:Streptococcus agalactiae / Q000235:genetics*; D013781:Texas / Q000453:epidemiology
Streptococcus agalactiae; evolution; pathogenesis; single nucleotide polymorphisms; surface protein