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The influence of in vitro fitness defects on pneumococcal ability to colonize and to cause invasive disease

BMC Microbiology
Springer (Biomed Central Ltd.)
Publication Date
DOI: 10.1186/1471-2180-8-65
  • Research Article
  • Biology
  • Medicine

Abstract ral ss BioMed CentBMC Microbiology Open AcceResearch article The influence of in vitro fitness defects on pneumococcal ability to colonize and to cause invasive disease Jenny Fernebro1,2, Christel Blomberg1,2, Eva Morfeldt1, Hans Wolf-Watz3, Staffan Normark1,2 and Birgitta Henriques Normark*1,2 Address: 1Swedish Institute for Infectious Disease Control, 171 82 Solna, Sweden, 2Dep. of Microbiology, Tumor and Cell Biology, Karolinska Institutet, 171 77 Stockholm, Sweden and 3Dep. of Molecular Biology, Umeå University, 901 87 Umeå, Sweden Email: Jenny Fernebro - [email protected]; Christel Blomberg - [email protected]; Eva Morfeldt - [email protected]; Hans Wolf-Watz - [email protected]; Staffan Normark - [email protected]; Birgitta Henriques Normark* - [email protected] * Corresponding author Abstract Background: Streptococcus pneumoniae is a genetically diverse major human pathogen, yet a common colonizer of the nasopharynx. Here we analyzed the influence of defects affecting in vitro growth rate, on the ability of S. pneumoniae to colonize and to cause invasive disease in vivo. Results: Of eleven different clinical isolates one serotype 14 carrier isolate showed a significantly longer generation time as compared to other isolates, and was severely attenuated in mice. To directly investigate the impact of growth rate on virulence, a panel of mutants in five non-essential housekeeping genes was constructed in the virulent TIGR4 background by insertion-deletion mutagenesis. Three of these mutants (ychF, hemK and yebC) were, to different degrees, growth defective, and showed a reduced invasiveness in an intranasal murine challenge model that correlated to their in vitro growth rate, but remained capable of colonizing the upper airways. The growth defect, as well as virulence defect of the hemK insertion-deletion mutant, was mediated by polarity effects on the downstream yrdC gene, encoding a probable

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