pneumonia

pneumoniajourn

Vol7SpecialIssueforweb

EuroPneumo Special Issue / pneumonia 2015 Oct 21;7:I–72

respectively (p = 0.07). Colonised 0–8-week-old children were more likely to have a nontypeable pneumococcus than

colonised 6–60-month-old children, with 33% (32/98 [95% CI 23.5–42.9%]) versus 14.1% (60/425 [95% CI 11–17.8%];

p < 0.0001). Infants in the pre-immunisation age group have a significantly lower prevalence of pneumococcal carriage

than vaccine age-eligible children; the youngest colonised children were more likely to have a nontypeable strain than

the older children. This may be due to factors such as inter-serotype competition for the nasopharyngeal niche, passively

transmitted serotype-specific maternal immunity, or differential exposure.

Funding: This study is funded by Gavi, The Vaccine Alliance

P1.21

Phosphoenol-pyruvate phospho-transferase A interactions with putative

host target receptors and their derived peptides during Streptococcus

pneumoniae adhesion

Tatyana Kushnir, Marilous Shagan, Anat Shahar, Raz Zarivach, Natali Elia, Ron Dagan, Yaffa

Mizrachi Nebenzahl

Ben Gurion University of the Negev, Beer Sheva, Israel

Streptococcus pneumoniae is a commensal pathogen and the major cause of life threatening diseases, including otitis

media, pneumonia, bacteraemia and meningitis. Adhesion of S. pneumoniae to the host mucosal cells is prerequisite

for disease development. In previous studies several proteins with known enzymatic functions were localised also

to the cell wall, and were found to function as adhesins. Current study focuses on one such adhesin, Phosphoenolpyruvate

phospho-transferase A (PtsA), which is the first enzyme of the PTS systems. Putative PtsA target receptors

were identified using combinatorial peptide library expressed in filamentous phage followed by a homology based

search of the human genome. Immunostaining proved 5 out of 6 PtsA putative target receptors to reside in the lung

derived epithelial cells. Microscale thermophoresis (MST) assay confirmed the specificity of rPtsA interaction with

each of the 5 putative target receptors derived peptides, yielding affinities in the micro-molar range, in accordance

with their inhibitory concentration range in adhesion. To decipher the precise mechanism of PtsA interactions with its

putative target receptors and their derived peptides, the 3D structure of PtsA is being resolved using X-ray diffraction.

In vivo experiments also exhibited lower bacterial load in mice infected with S. pneumoniae preincubated with putative

receptor derived peptides, indicating the essential role of PtsA in bacterial adhesion and infection. With respect to the

increasing antibiotic resistance of S. pneumoniae, the putative target receptor derived peptides are currently considered

as candidates for alternative effective therapeutics.

P1.22

Contribution of a temperate bacteriophage to the virulence of a

Streptococcus pneumoniae serotype 1 strain

Martin Norman 1, 2 , Anna Syk 1, 2 , Sarah Browall 1, 2 , Birgitta Henriques-Normark 1, 2

1

Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden; 2 Dep. of Clinical Microbiology, Karolinska University

Hospital, Stockholm, Sweden

Temperate bacteriophages are frequently found in the genomes of clinical isolates of Streptococcus pneumoniae.

Currently there is a lack of knowledge on how, if at all, these genetic elements affect the virulence of pneumococcal

strains. In our study we investigated the effect on virulence of a temperate phage in an invasive clinical isolate of a

highly virulent serotype 1 strain of sequence type (ST) 217 by using a mouse model of invasive disease. We found

that the presence of the phage was associated with increased virulence and the effect was linked to a gene encoding

a phage tail protein, which in S. mitis has been described as pblB. In S. mitis the pblB platelet binding locus has been

shown to mediate binding to platelets and increase virulence in an endocarditis model. We found that in S. pneumoniae

pblB is required for sustained bacteraemia during invasive disease. Further studies are needed to elucidate the exact

mechanisms by which bacteriophages contribute to pathogenesis.

pneumonia 2015 Volume 7

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