Targeting The Kingella Kingae Groel Gene Is A Reliable Method For The Molecular Diagnosis Of K-Kingae Infection And Carriage

Khatami et al. recently reported a zero-prevalence rate of oropharyngeal Kingella kingae carriage in healthy children younger than 4 years of age in Sydney, Australia, using suboptimal culture methods.1 These findings strongly contrast with the current, modern literature that demonstrated a rate of oropharyngeal K. kingae carriage reaching up to 23% in similar paediatric populations by means of specific molecular tools.2 Kingella kingae is notoriously reluctant to grow on classical cultures and its isolation from the dense, competing oropharyngeal microbiota is difficult and requires the use of an appropriate selective blood–agar medium enriched in vancomycin.3 Thus, the huge discrepancy in the determination of prevalence rates reported by Khatami et al. may be primarily explained by the deficient microbiological methods used by the authors to disclose the organism. To overcome this barrier, the use of real-time polymerase chain reaction assays targeting the groEL (cpn60) gene of K. kingae has significantly contributed to the recognition of K. kingae as a major pathogen of infantile osteoarticular infections world-wide, including in the Western Pacific region.2, 4 Although Khatami et al. emphasise that this molecular tool is currently limited for detecting the viability of microorganisms,1 we highlight that this is absolutely not an issue for specifying the rate of oropharyngeal K. kingae carriage in large-cohort, transversal studies. Indeed, in such context, the calculated prevalence is the result of analysis obtained at a specific point in time with no dynamic assessment that may interfere the final outcomes. Importantly, phylogenetic analysis of the housekeeping groEL gene from more than 40 genomes of K. kingae strains and closely related species indicated its presence in all K. kingae strains with a maximum of nucleotide sequence similarity ranging from 85 to 82% with that of Kingella negevensis and Neisseria lactamica, respectively (El Houmami, unpublished data). This low nucleotide similarity of orthologous groEL genes, combined with the extremely weak risk of lateral gene transfer for a such gene5 make of the groEL gene a target of choice for the molecular detection of K. kingae from both normally sterile and polymicrobial, oropharyngeal specimens. Finally, while the targeting of two independent genes for the molecular diagnosis of K. kingae infections was previously assessed with the groEL and rtxA genes,4, 6 we point out that this diagnostic strategy is costly and showed no substantial advantage in comparison with the targeting of groEL alone.