Draft Genome Sequences of Five Multilocus Sequence Types of Nonencapsulated Streptococcus pneumoniae

Keller, Lance E.; Thomas, Jonathan C.; Luo, Xinsong; Nahm, Moon H.; McDaniel, Larry S.; Robinson, D. Ashley

doi:10.1128/genomea.00520-13

Cited by 16 publications

(23 citation statements)

References 13 publications

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“…During nasopharyngeal carriage, other functions of PspC have been indicated by previous reports showing its importance in adherence (16,17,(20)(21)(22)(23)40). In addition, our observation that PspC binding of factor H by unencapsulated strains had no effect on complement resistance may help in understanding the loss of PspC in naturally occurring unencapsulated S. pneumoniae strains (41,42). Other gene products in the naturally occurring unencapsulated strains, such as the PspC-like protein PspK, were shown to play a role in colonization and adherence but did not bind factor H (43)(44)(45).…”

Section: Discussionsupporting

confidence: 64%

Streptococcus pneumoniae PspC Subgroup Prevalence in Invasive Disease and Differences in Contribution to Complement Evasion

et al. 2018

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The pneumococcal capsular serotype is an important determinant of complement resistance and invasive disease potential, but other virulence factors have also been found to contribute. Pneumococcal surface protein C (PspC), a highly variable virulence protein that binds complement factor H to evade C3 opsonization, is divided into two subgroups: choline-bound subgroup I and LPxTG-anchored subgroup II. The prevalence of different PspC subgroups in invasive pneumococcal disease (IPD) and functional differences in complement evasion are unknown. The prevalence of PspC subgroups in IPD isolates was determined in a collection of 349 sequenced strains of isolated from adult patients. deletion mutants and isogenic switch mutants were constructed to study differences in factor H binding and complement evasion in relation to capsule thickness. Subgroup I was far more prevalent in IPD isolates than subgroup II The presence of capsule was associated with a greater ability of bound factor H to reduce complement opsonization. Pneumococcal subgroup I PspC bound significantly more factor H and showed more effective complement evasion than subgroup II PspC in isogenic encapsulated pneumococci. We conclude that variation in the PspC subgroups, independent of capsule serotypes, affects pneumococcal factor H binding and its ability to evade complement deposition.

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Section: Discussionsupporting

confidence: 64%

Streptococcus pneumoniae PspC Subgroup Prevalence in Invasive Disease and Differences in Contribution to Complement Evasion

et al. 2018

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“…Furthermore, recent studies have revealed that a subset of non‐encapsulated isolates form a distinct phyletic group basal to other pneumococcal strains (Croucher et al ., ; Valentino et al ., ). Thus, we added isolates from this group, ending up with 32 pneumococcal genomes (Antic et al , unpublished) (Keller et al ., ) (light blue, Supporting Information Table S1). Finally, for the MAST, we added seven genomes from isolates from eye infections and non‐encapsulated strains that are distributed throughout the phylogenetic tree (Antic et al ., under review).…”

Section: Methodsmentioning

confidence: 99%

A novel streptococcal cell–cell communication peptide promotes pneumococcal virulence and biofilm formation

Cuevas

Eutsey

Kadam

et al. 2017

Molecular Microbiology

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Streptococcus pneumoniae (pneumococcus) is a major human pathogen. It is a common colonizer of the human respiratory track, where it utilizes cell-cell communication systems to coordinate population-level behaviors. We reasoned that secreted peptides that are highly expressed during infection are pivotal for virulence. Thus, we used in silico pattern searches to define a pneumococcal secretome, and analyzed the transcriptome of the clinically important PMEN1 lineage to identify which peptide-encoding genes are highly expressed in vivo. In this study, we characterized virulence peptide 1 (vp1), a highly expressed Gly-Gly peptide-encoding gene in chinchilla middle ear effusions. The vp1 gene is widely distributed across pneumococcus as well as encoded in related species. Studies in the chinchilla model of middle ear infection demonstrated that VP1 is a virulence determinant. The vp1 gene is positively regulated by a transcription factor from the Rgg family and its cognate SHP (short hydrophobic peptide). In vitro data indicated that VP1 promotes increased thickness and biomass for biofilms grown on chinchilla middle ear epithelial cells. Further, the wild-type biofilm is restored with the exogenous addition of synthetic VP1. We conclude that VP1 is a novel streptococcal regulatory peptide that controls biofilm development and pneumococcal pathogenesis.

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“…This included all unencapsulated nasopharyngeal genomes in Croucher et al . 19 (16 genomes) and 8 draft genomes of nasopharyngeal isolates currently available from either the NCBI GenBank or European Nucleotide Archive (ENA), including 5 genomes newly deposited to NCBI GenBank 70 . When available, we maximized the diversity of this set by downloading several representatives, spanning various dates of isolation, or when additional information on strain diversity was available (e.g.…”

Section: Methodsmentioning

confidence: 99%

Unencapsulated Streptococcus pneumoniae from conjunctivitis encode variant traits and belong to a distinct phylogenetic cluster

et al. 2014

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Streptococcus pneumoniae, an inhabitant of the upper respiratory mucosa, causes respiratory and invasive infections as well as conjunctivitis. Strains that lack the capsule, a main virulence factor and the target of current vaccines, are often isolated from conjunctivitis cases. Here we perform a comparative genomic analysis of 271 strains of conjunctivitis-causing S. pneumoniae from 72 postal codes in the US. We find that the vast majority of conjunctivitis strains are members of a distinct cluster of closely related unencapsulated strains. These strains possess divergent forms of pneumococcal virulence factors (such as CbpA and neuraminidases) that are not shared with other unencapsulated nasopharyngeal S. pneumoniae. They also possess putative adhesins that have not been described in encapsulated pneumococci. These findings suggest that the unencapsulated strains capable of causing conjunctivitis utilize a pathogenesis strategy substantially different from that described for S. pneumoniae at other infection sites.

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Draft Genome Sequences of Five Multilocus Sequence Types of Nonencapsulated Streptococcus pneumoniae

Cited by 16 publications

References 13 publications

Streptococcus pneumoniae PspC Subgroup Prevalence in Invasive Disease and Differences in Contribution to Complement Evasion

Streptococcus pneumoniae PspC Subgroup Prevalence in Invasive Disease and Differences in Contribution to Complement Evasion

A novel streptococcal cell–cell communication peptide promotes pneumococcal virulence and biofilm formation

Unencapsulated Streptococcus pneumoniae from conjunctivitis encode variant traits and belong to a distinct phylogenetic cluster

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