Limits...
Nonencapsulated Streptococcus pneumoniae Cause Acute Otitis Media in the Chinchilla That Is Enhanced by Pneumococcal Surface Protein K.

Keller LE, Friley J, Dixit C, Nahm MH, McDaniel LS - Open Forum Infect Dis (2014)

Bottom Line: Deletion of PspK from an isolate significantly reduced bacterial loads.Furthermore, expression of PspK by an avirulent NESp resulted in virulence.The current study is the first report of a NESp-specific virulence factor.

View Article: PubMed Central - PubMed

Affiliation: Departments of Microbiology.

ABSTRACT

Background: Use of the pneumococcal conjugate vaccine has led to serotype replacement of carriage and acute otitis media (AOM) pneumococcal isolates. Increases in nonencapsulated Streptococcus pneumoniae (NESp) isolates have also occurred, and there are increasing reports of NESp-associated disease. Disease prevalence and virulence factors of NESp isolates have not been studied.

Methods: A chinchilla model of pneumococcal AOM was utilized, and disease was assessed through bacterial enumeration along with scoring visible signs of pathology. An adhesion-invasion assay using a human epithelial cell line was performed.

Results: Nonencapsulated Streptococcus pneumoniae strains containing pneumococcal surface protein K (PspK) were more likely to cause AOM and pathology upon infection. Deletion of PspK from an isolate significantly reduced bacterial loads. Increased epithelial cell adhesion correlated with increased virulence of NESp isolates naturally lacking PspK. Furthermore, expression of PspK by an avirulent NESp resulted in virulence.

Conclusions: The presence of PspK increased the disease potential of NESp. Pneumococcal surface protein K is not the only virulence factor of NESp in AOM. Expression of PspK in an avirulent NESp mediated the progression to pneumococcal disease. Genetic exchange between pneumococci may allow dissemination of PspK, increasing the potential of NESp disease. The current study is the first report of a NESp-specific virulence factor.

No MeSH data available.


Related in: MedlinePlus

Pneumococcal surface protein K (PspK) increases pneumococcal virulence in acute otitis media. Four days after intrabullar challenge, LEK01 (R36A PspK+) significantly increased in numbers compared with the parent strain R36A. Counts displayed as log colony-forming unit/bulla ± standard error. Data represent cumulative data of 2 independent bulla from 2 animals. *, P < .0001 by Student's t test.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4281809&req=5

OFU037F4: Pneumococcal surface protein K (PspK) increases pneumococcal virulence in acute otitis media. Four days after intrabullar challenge, LEK01 (R36A PspK+) significantly increased in numbers compared with the parent strain R36A. Counts displayed as log colony-forming unit/bulla ± standard error. Data represent cumulative data of 2 independent bulla from 2 animals. *, P < .0001 by Student's t test.

Mentions: Pneumococcal strain R36A, a laboratory-derived nonencapsulated D39 (serotype 2), does not effectively colonize the mouse nasopharynx. We have previously reported that LEK01 (R36A expressing PspK) has enhanced epithelial cell adherence and colonization in the mouse [7]. The expression of PspK in R36A significantly increased the number of bacteria in the bullae and resulted in increased pathology and biofilm formation (P < 0.0001) (Figure 4).Figure 4.


Nonencapsulated Streptococcus pneumoniae Cause Acute Otitis Media in the Chinchilla That Is Enhanced by Pneumococcal Surface Protein K.

Keller LE, Friley J, Dixit C, Nahm MH, McDaniel LS - Open Forum Infect Dis (2014)

Pneumococcal surface protein K (PspK) increases pneumococcal virulence in acute otitis media. Four days after intrabullar challenge, LEK01 (R36A PspK+) significantly increased in numbers compared with the parent strain R36A. Counts displayed as log colony-forming unit/bulla ± standard error. Data represent cumulative data of 2 independent bulla from 2 animals. *, P < .0001 by Student's t test.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4281809&req=5

OFU037F4: Pneumococcal surface protein K (PspK) increases pneumococcal virulence in acute otitis media. Four days after intrabullar challenge, LEK01 (R36A PspK+) significantly increased in numbers compared with the parent strain R36A. Counts displayed as log colony-forming unit/bulla ± standard error. Data represent cumulative data of 2 independent bulla from 2 animals. *, P < .0001 by Student's t test.
Mentions: Pneumococcal strain R36A, a laboratory-derived nonencapsulated D39 (serotype 2), does not effectively colonize the mouse nasopharynx. We have previously reported that LEK01 (R36A expressing PspK) has enhanced epithelial cell adherence and colonization in the mouse [7]. The expression of PspK in R36A significantly increased the number of bacteria in the bullae and resulted in increased pathology and biofilm formation (P < 0.0001) (Figure 4).Figure 4.

Bottom Line: Deletion of PspK from an isolate significantly reduced bacterial loads.Furthermore, expression of PspK by an avirulent NESp resulted in virulence.The current study is the first report of a NESp-specific virulence factor.

View Article: PubMed Central - PubMed

Affiliation: Departments of Microbiology.

ABSTRACT

Background: Use of the pneumococcal conjugate vaccine has led to serotype replacement of carriage and acute otitis media (AOM) pneumococcal isolates. Increases in nonencapsulated Streptococcus pneumoniae (NESp) isolates have also occurred, and there are increasing reports of NESp-associated disease. Disease prevalence and virulence factors of NESp isolates have not been studied.

Methods: A chinchilla model of pneumococcal AOM was utilized, and disease was assessed through bacterial enumeration along with scoring visible signs of pathology. An adhesion-invasion assay using a human epithelial cell line was performed.

Results: Nonencapsulated Streptococcus pneumoniae strains containing pneumococcal surface protein K (PspK) were more likely to cause AOM and pathology upon infection. Deletion of PspK from an isolate significantly reduced bacterial loads. Increased epithelial cell adhesion correlated with increased virulence of NESp isolates naturally lacking PspK. Furthermore, expression of PspK by an avirulent NESp resulted in virulence.

Conclusions: The presence of PspK increased the disease potential of NESp. Pneumococcal surface protein K is not the only virulence factor of NESp in AOM. Expression of PspK in an avirulent NESp mediated the progression to pneumococcal disease. Genetic exchange between pneumococci may allow dissemination of PspK, increasing the potential of NESp disease. The current study is the first report of a NESp-specific virulence factor.

No MeSH data available.


Related in: MedlinePlus