To the Editors: The pathogenesis of Kingella kingae invasive infections remains unclear, even if there is evidence that K. kingae first colonizes the oropharynx before penetrating the bloodstream and invading distant organs.1 The density of the oropharyngeal carriage may thus be suspected to play a role in the pathogenesis of invasive K. kingae infections, as it is the case with many other pathogens of the oropharyngeal flora, such as Streptococcus pneumoniae or Haemophilus influenzae.2–7 In the current study, we explored whether there was a modification in the density of K. kingae oropharyngeal bacterial load that might modify the risk of invasive infections during the first years of life in children. We quantified the oropharyngeal colonization density of 117 positive oropharyngeal swabs, analyzed with a rtPCR assay targeting the toxin-encoding gene rtxB. As we have previously demonstrated that there is no difference in the density of oropharyngeal K. kingae colonization between children with osteoarticular infections and asymptomatic carriers,8 throat swabs of all children were considered together. All participants’ parents provided written consent, and the protocol was approved by the institutional ethics committee. For baseline characteristics, variables are reported as mean ± standard deviation. Pearson coefficient was used to establish correlation between continuous variables. Between January 2008 and December 2012, 117 children with positive K. kingae rtPCR assays on oropharyngeal swabs were included and investigated in this study (71 asymptomatic oropharyngeal carriers and 46 children with suspected or proven osteoarticular infections due to K. kingae). The mean age of the children was 22.8 ± 10.1 months (range: 8-48 months). The oropharyngeal colonization density was estimated by the number of cycles needed to detect the DNA target. The mean number of cycles for detection was 33 ± 4.5 cycles. The Pearson’s correlation coefficient (r) between oropharyngeal colonization density and age of the children was –0.050 (P = 0.592), demonstrating no statistically significant correlation between the 2 variables (Fig. 1). Similarly to S. pneumoniae, H. influenzae type b or Neisseria meningitidis, K. kingae resides in the mucosal surface and is able to penetrate the bloodstream, disseminate and invade distant organs.9–11 Colonization of the respiratory tracts by these organisms is, therefore, a prerequisite for later invasion. For most of these microoorganisms, such as S. pneumoniae or H. influenzae,2–7 there are evidences that the bacterial load varies in the nasopharynx with the age of subjects, and that higher nasopharynx colonization densities play major roles in the development of invasive infections.2–7 For K. kingae, there are currently no data about the K. kingae oropharyngeal colonization density during the first years of life. This study is thus the first, to the best of our knowledge, to demonstrate that the pharyngeal colonization density is very stable during the first 4 years of life, and that this parameter must thus play a minor role in the development of invasive infection. In conclusion, the density of the K. kingae oropharyngeal carriage does not vary during the first 4 years of life and seems thus to play no role in the development of invasive infections, as it is the case with many other pathogens present in oropharyngeal flora, such as S. pneumoniae or H. influenzae. Dimitri Ceroni, MD Victor Dubois-Ferriere, MD Rebecca Anderson Della Llana, MD Pediatric Orthopedic Service University Hospitals of Geneva Omar Kherad, MD Internal Medicine Department University of Geneva Hôpital de la Tour Pierre Lascombes, MD Pediatric Orthopedic Service University Hospitals of Geneva Gesuele Renzi, MD Clinical Microbiology Laboratory Service of Infectious Diseases University Hospitals of Geneva Sergio Manzano, MD Pediatric Emergency Division University Hospitals of Geneva Abdessalam Cherkaoui, PhD Clinical Microbiology Laboratory Service of Infectious Diseases University Hospitals of Geneva Jacques Schrenzel, MD Clinical Microbiology Laboratory Genomic Research Laboratory Service of Infectious Diseases University Hospitals of Geneva Geneva, Switzerland
Read full abstract