Kingella kingae Skeletal Infections in Children

Abstract & Commentary

By Hal B. Jenson, MD, FAAP, Chair, Department of Pediatrics, Director, Center for Pediatric Research, Eastern Virginia Medical School and Children’s Hospital of the King’s Daughters, Norfolk, VA, is associate editor of Infections Disease Alert

Dr. Jenson is on the speaker’s bureau of Merck.

Synopsis: Kingella kingae is increasingly recognized as a cause of skeletal infections among children. The first reported outbreak of K. kingae disease, among 3 children at a childcare center, is described.

Source: Kiang KM, et al. Outbreak of Osteomyelitis/Septic Arthritis Caused by Kingella kingae Among Child Care Center Attendees. Pediatrics 2005;116:e206-213.

Two definite (culture-confirmed), and one probable, cases of K. kingae invasive disease were reported in Minnesota in October 2003, among children attending the same toddler classroom of a childcare center. The first case was a 21-month-old boy diagnosed with femoral neck osteomyelitis and suppurative arthritis of the hip. The temperature was 103º F, WBC 17,200 cells/mm3, ESR 51 mm/hr, and CRP < 0.5 mg/dL (normal). Synovial and bone cultures showed K. kingae after 3 days of incubation. He was successfully treated with 3 weeks of intravenous piperacillin-tazobactam, followed by 2 weeks of oral amoxicillin-clavulanate. The second case was a 20-month-old girl who had recently completed a course of amoxicillin-clavulanate for otitis media. She developed ankle and subtalar suppurative arthritis.

The temperature was 101.6º F, WBC 7700 cells/mm3, and ESR 38 mm/hr. K. kingae was cultured after 4-5 days of incubation. She was successfully treated with 4 weeks of oral amoxicillin-clavulanate. The third case was a 17-month-old boy diagnosed with otitis media and reactive arthritis. The temperature was 102ºF, WBC 12,500 cells/mm3, and the CRP 1.27 mg/dL (mildly increased). He was treated initially with oral amoxicillin. His limp continued, and MRI 16 days later revealed distal tibial osteomyelitis. No cultures were obtained.

All 3 children had preceding or concurrent symptoms of upper respiratory tract infection. Oropharyngeal cultures from 115 children (94%) and 29 staff (97%) at the childcare center showed that 15 children (13%) were colonized with K. kingae, including 9 (45%) children in the classroom of the 3 affected children. No staff or children < 16 months of age were colonized. All 9 children who were colonized were given rifampin prophylaxis using the regimen recommended for meningococcus (4 doses, every 12 hours for 2 days); 3 (33%) remained positive on reculture 10--14 days later.


The past 15 years has seen the dramatic decline of Haemophilus influenzae type b infections, including skeletal infections resulting from universal vaccination with the conjugate vaccine. Use of the conjugate pneumococcal vaccine will have the same impact on Streptococcus pneumoniae infections. In the milieu of these seismic changes, less dramatic changes are also occurring, including the increasing recognition of K. kingae as a cause of childhood invasive disease. Conjugate vaccines not only reduce the incidence of invasive disease, but also decrease the rate of nasopharyngeal carriage. This effect may provide an opportunistic niche for nasopharyngeal carriage of less virulent organisms such as K. kingae.

This is the first reported outbreak of K. kingae infection, and emphasizes the underappreciation of K. kingae as a cause of childhood skeletal infections. This report offers several insights into pediatric K. kingae infections. K. kingae frequently colonizes the oropharynx and is most likely transmitted via upper respiratory tract secretions, saliva, and potentially oral contact with contaminated fomites. This cluster supports the oropharyngeal transmission of the organism. As in this outbreak, most reported cases are among children 6-24 months of age and occur in the fall and winter months, perhaps reflecting close quarters during the colder months. Skeletal infections caused by K. kingae present with low-grade fever and only modest elevation of WBC, ESR, and CRP but are clinically indistinguishable from those caused by Staphylococcus aureus and group A streptococcus, the most common causes of childhood skeletal infections. Culture is required for confirmation. K. kingae is susceptible to many antimicrobial agents, with low MICs to penicillin, azithromycin, and rifampin. The attempt to eliminate nasopharyngeal carriage was an interesting approach; unfortunately, it was only modestly successful (67%). It may be that the regimen used for H. influenzae (4 doses, every 24 hours for 4 days) would be more successful. The impact of prophylaxis on invasive disease is unknown.