Genetic relationship between Streptococcus pneumoniae isolates responsible for a case of meningitis and for asymptomatic carriage in children attending a day-care centre in Lisbon
Abstract number: o167
Figueiredo T., Ramirez M., Santos-Sanches I., Nunes S., Brito-Avô A., Barros R.M., Peres I., de Lencastre H.
Colonisation of the nasopharyngx by Streptococcus pneumoniae although asymptomatic, is a prerequisite for the development of a clinical infection. However, the underlying mechanisms that turn the benign state of colonization into clinical disease are poorly understood. Thus, in order to understand the molecular mechanisms that define the virulence of S. pneumoniae, a clear picture of the genetic relationship between invasive and carried pneumococci is needed.
We characterised 2 pneumococcal strains recovered from the blood and cerebrospinal fluid (CSF) of a child with meningitis and 23 nasopharyngeal isolates from asymptomatic carriers attending the same room in a day care centre (DCC), using antimicrobial susceptibility profiling, serotyping, PFGE and MLST. We also investigated the presence of lysogenic phage since these were shown to be associated with virulence determinants in other streptococci.
Strains recovered from the sick child and seven carriage isolates were fully susceptible, expressed serotype 6B and belonged to a new clone by PFGE and MLST (ST896). However, there was a band difference in the PFGE pattern of the isolates from the CSF and carriage. The in vivo loss of a lysogenic phage in the CSF isolate accounted for this difference and suggested an involvement of the phage in the transition between colonization and disease. However, the localization of the attB in an intergenic region and the putative functions of the adjacent genes do not support this hypothesis. The remaining 16 isolates recovered from asymptomatic carriers belonged to other clones including internationally clones previously found associated with invasive disease (e.g. Spain23F-1).
The same pneumococcal clone was simultaneously responsible for carriage and for invasive disease in different hosts. The in vivo loss of a lysogenic prophage, between the isolate recovered from the blood and the one from the CSF, suggested an involvement of the bacteriophage in this transition. The localization of the attB site in an intergenic region and the suggested functions of the adjacent genes do not support this hypothesis.
|Session name:||XXIst ISTH Congress|
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