Advanced

Virulence in mice of pneumococcal clonal types with known invasive disease potential in humans

Sandgren, Andreas; Albiger, Barbara LU ; Orihuela, Carlos J; Tuomanen, Elaine; Normark, Staffan and Henriques-Normark, Birgitta (2005) In Journal of Infectious Diseases 192(5). p.791-800
Abstract
Streptococcus pneumoniae isolates of serotypes 1, 4, 6B, 7F, 14, and 19F belonging to clonal types with known invasive disease potential in humans were used to infect C57BL/6 and BALB/c mice. Most isolates were able to colonize the nasopharynx for 7 days. One serotype 19F isolate of the clonal type ST162 had higher bacterial numbers than other isolates and clonal types of the same serotype. Serotype 4 clones caused the most-severe invasive disease, whereas serotype 1 clones caused low-level bacteremia without disease symptoms. BALB/c mice were more likely than C57BL/6 mice to develop meningitis. Disease kinetics varied significantly between clonal types. Although most induced a robust tumor necrosis factor response, some isolates of... (More)
Streptococcus pneumoniae isolates of serotypes 1, 4, 6B, 7F, 14, and 19F belonging to clonal types with known invasive disease potential in humans were used to infect C57BL/6 and BALB/c mice. Most isolates were able to colonize the nasopharynx for 7 days. One serotype 19F isolate of the clonal type ST162 had higher bacterial numbers than other isolates and clonal types of the same serotype. Serotype 4 clones caused the most-severe invasive disease, whereas serotype 1 clones caused low-level bacteremia without disease symptoms. BALB/c mice were more likely than C57BL/6 mice to develop meningitis. Disease kinetics varied significantly between clonal types. Although most induced a robust tumor necrosis factor response, some isolates of serotype 1 and 7F did not, suggesting that invasive disease caused by different clonal types may result in different degrees of host response. Capsular serotype, other clonal properties, and host factors are important for the development of pneumococcal disease. (Less)
Please use this url to cite or link to this publication:
author
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Infectious Diseases
volume
192
issue
5
pages
791 - 800
publisher
Oxford University Press
external identifiers
  • pmid:16088828
  • scopus:23944445632
ISSN
1537-6613
DOI
10.1086/432513
language
English
LU publication?
no
id
292fdf78-8576-4d8c-be0a-11504e0e5acf (old id 1132190)
date added to LUP
2008-06-30 13:56:25
date last changed
2017-10-01 04:36:07
@article{292fdf78-8576-4d8c-be0a-11504e0e5acf,
  abstract     = {Streptococcus pneumoniae isolates of serotypes 1, 4, 6B, 7F, 14, and 19F belonging to clonal types with known invasive disease potential in humans were used to infect C57BL/6 and BALB/c mice. Most isolates were able to colonize the nasopharynx for 7 days. One serotype 19F isolate of the clonal type ST162 had higher bacterial numbers than other isolates and clonal types of the same serotype. Serotype 4 clones caused the most-severe invasive disease, whereas serotype 1 clones caused low-level bacteremia without disease symptoms. BALB/c mice were more likely than C57BL/6 mice to develop meningitis. Disease kinetics varied significantly between clonal types. Although most induced a robust tumor necrosis factor response, some isolates of serotype 1 and 7F did not, suggesting that invasive disease caused by different clonal types may result in different degrees of host response. Capsular serotype, other clonal properties, and host factors are important for the development of pneumococcal disease.},
  author       = {Sandgren, Andreas and Albiger, Barbara and Orihuela, Carlos J and Tuomanen, Elaine and Normark, Staffan and Henriques-Normark, Birgitta},
  issn         = {1537-6613},
  language     = {eng},
  number       = {5},
  pages        = {791--800},
  publisher    = {Oxford University Press},
  series       = {Journal of Infectious Diseases},
  title        = {Virulence in mice of pneumococcal clonal types with known invasive disease potential in humans},
  url          = {http://dx.doi.org/10.1086/432513},
  volume       = {192},
  year         = {2005},
}