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Review
. 2015 Jan;28(1):54-79.
doi: 10.1128/CMR.00028-14.

Kingella kingae: carriage, transmission, and disease

Affiliations
Review

Kingella kingae: carriage, transmission, and disease

Pablo Yagupsky. Clin Microbiol Rev. 2015 Jan.

Abstract

Kingella kingae is a common etiology of pediatric bacteremia and the leading agent of osteomyelitis and septic arthritis in children aged 6 to 36 months. This Gram-negative bacterium is carried asymptomatically in the oropharynx and disseminates by close interpersonal contact. The colonized epithelium is the source of bloodstream invasion and dissemination to distant sites, and certain clones show significant association with bacteremia, osteoarthritis, or endocarditis. Kingella kingae produces an RTX (repeat-in-toxin) toxin with broad-spectrum cytotoxicity that probably facilitates mucosal colonization and persistence of the organism in the bloodstream and deep body tissues. With the exception of patients with endocardial involvement, children with K. kingae diseases often show only mild symptoms and signs, necessitating clinical acumen. The isolation of K. kingae on routine solid media is suboptimal, and detection of the bacterium is significantly improved by inoculating exudates into blood culture bottles and the use of PCR-based assays. The organism is generally susceptible to antibiotics that are administered to young patients with joint and bone infections. β-Lactamase production is clonal, and the local prevalence of β-lactamase-producing strains is variable. If adequately and promptly treated, invasive K. kingae infections with no endocardial involvement usually run a benign clinical course.

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Figures

FIG 1
FIG 1
Timeline of milestone research studies on K. kingae.
FIG 2
FIG 2
(A) Typical Gram stain of K. kingae organisms, depicting short Gram-negative coccobacilli with tapered ends arranged in pairs or short chains. (B) Gram stain of K. kingae small-colony variant, showing atypical long chains.
FIG 3
FIG 3
Electron microscope picture of K. kingae organisms, showing sequential formation of outer membrane vesicles.
FIG 4
FIG 4
Prevalence of pharyngeal K. kingae colonization among children aged 0 to 36 months.
FIG 5
FIG 5
Age distribution of 143 patients with culture-proven K. kingae infections detected in southern Israel between 1988 and 2013.
FIG 6
FIG 6
Spatial distribution of K. kingae clones carried in a Bedouin neighborhood as determined by PFGE with restriction enzyme EagI. Each star represents a positive pharyngeal culture, while the different colors represent distinct clones. Red ovals depict geographic clusters of identical strains.
FIG 7
FIG 7
Clinical syndrome in 143 consecutive patients with K. kingae infections diagnosed in southern Israel between 1988 and 2013. LRTI, lower respiratory tract infection; SA, septic arthritis; OM, osteomyelitis; AB, abortive; TS, tenosynovitis.
None

References

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