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Kingella kingae is being increasingly recognized as the most common etiology of septic arthritis, osteomyelitis, and spondylodiscitis in young children.
Kingella kingae is a fastidious, facultative anaerobic, β-hemolytic member of the Neisseriaceae family that appears as pairs or short chains of gram-negative coccobacilli with tapered ends ( Fig. 220.1 ).
K. kingae is asymptomatically carried in the posterior pharynx. Colonization usually starts after age 6 mo, reaches a prevalence of 10% between 12 and 24 mo, and decreases in older children. Pharyngeal colonization plays a crucial role in the transmission of the organism through intimate contact between siblings and playmates. Daycare attendance increases the risk for colonization and transmission, and clusters of invasive infection have been reported in childcare facilities.
The species elaborates 4 different polysaccharide capsules (a-d),which appear to represent important virulence factors. Colonizing K. kingae strains differ in their invasive potential. Whereas certain clones are commonly found as respiratory colonizers but are seldom isolated from sites of disease, other clones, usually expressing polysaccharide capsule a or b, readily penetrate into the bloodstream and disseminate to the skeletal system or the endocardium, sites for which the organism has a particular tropism.
Invasive K. kingae disease is most frequently diagnosed in otherwise healthy children between ages 6 mo and 3 yr, coinciding with the peak prevalence of pharyngeal carriage ( Fig. 220.2 ). In contrast, older children and adults with K. kingae infections often have underlying chronic diseases, immunosuppressing conditions, malignancy, or cardiac valve pathology. An annual incidence of 9.4 per 100,000 culture-proven invasive infections among Israeli children <5 yr old has been estimated, but because of the suboptimal culture recovery of K. kingae organisms, this figure can be considered only a minimal estimate.
The pathogenesis of K. kingae disease begins with adherence of the organism to the pharyngeal epithelium, mediated by pili and a nonpilus adhesin. K. kingae secretes a potent Repeats-in-Toxin (RTX) toxin that exhibits deleterious activity to respiratory epithelial cells, macrophages, and synoviocytes, suggesting that it may play a role in disrupting the respiratory mucosa, promoting survival of the bacterium in the bloodstream, and facilitating invasion of skeletal system tissues. Children with K. kingae disease frequently present with symptoms of an upper respiratory infection, hand-foot-and-mouth disease, herpetic stomatitis, or buccal aphthous ulcers, suggesting that viral-induced damage to the colonized mucosal surface facilitates invasion of the bloodstream.
Septic arthritis is the most common invasive K. kingae infection in children, followed by bacteremia, osteomyelitis, and endocarditis ( Table 220.1 ). The organism is the most frequent etiology of skeletal system infections in children 6 mo to 3 yr old in at least some countries. With the exception of patients with endocarditis, the presentation of invasive K. kingae infections is frequently mild, and a body temperature <38°C (100.4°F), a normal C-reactive protein (CRP) level, and a normal white blood cell (WBC) count are common, requiring a high index of clinical suspicion.
CLINICAL DISEASE | FREQUENCY |
---|---|
SKELETAL SYSTEM | +++ |
Septic arthritis | +++ |
Osteomyelitis | ++ |
Spondylodiscitis | + |
Tenosynovitis | ± |
Dactylitis | ± |
Bursitis | ± |
Bacteremia with no focus | +++ |
CARDIAC | + |
Endocarditis | + |
Pericarditis | ± |
Meningitis | ± |
Peritonitis | ± |
Cellulitis | ± |
Soft tissue abscesses | ± |
LOWER RESPIRATORY TRACT | ± |
Laryngotracheobronchitis | ± |
Pneumonia | ± |
Pleural empyema | ± |
OCULAR | ± |
Keratitis | ± |
Corneal abscess | ± |
Endophthalmitis | ± |
Eyelid abscess | ± |
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