The Contemporary Microbiology of Osteoarticular Infections in Young Children

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We have read with interest the article of Branson et al1 about the etiology of the osteoarticular infections (OAIs) in Houston, Texas. We would like to discuss the differences of epidemiology between countries and settings. We performed a retrospective chart review between February 2013 and February 2016 at the Pediatric University Hospital La Paz (Spain). Inclusion criteria were children younger than 14 years with a diagnosis of osteomyelitis (OM) confirmed with magnetic resonance imaging or bone scintigraphy or of septic arthritis (SA) microbiologically confirmed or when the joint fluid had more than 40,000 cells/mm3. A total of 90 OAIs were included (41 OM, 7 spondylodiscitis, 31 SA and 11 osteoarthritis). The microbiology was defined in 15 of them: Streptococcus pyogenes was isolated in 2 cases (OM, blood culture), Streptococcus pneumoniae in 1 case of SA (synovial fluid culture) and Kingella kingae in 12 (10 SA and 2 OM) cases.
K. kingae was the most frequently identified agent in our series comprising up to 80% of microbiologically confirmed cases [3 blood cultures, 2 synovial fluid culture and 7 polymerase chain reaction (PCR) in synovial fluid]. The mean age of our total cohort was 28 months, and children with K. kingae infection were 15 months of mean age (range, 6–25). The average erythrocyte sedimentation rate was 72 mm/h (range, 20–120) and the C-reactive protein 27 mg/L (range, 2–82). The average white blood cell count was 164,160 ± 75,380/mm3 (range, 58,800 to 288,000). All patients received antibiotics, and arthrocentesis was performed when necessary. None of them needed surgery.
K. kingae is a Gram-negative coccobacillus and a common colonizer of the upper respiratory tract. As several recent studies describe, in some countries, K. kingae has become the most frequent causal agent of OAI in children younger than 4 years.2,3 It has been shown that infections caused by K. kingae yield a lower C-reactive protein value than other agents and probably a less severe inflammatory process.3 According to the latest publications, short intravenous treatment (2–4 days) followed by oral therapy for 2–3 weeks is a safe option in this selected group of patients.4 These patients often should be treated with arthrocentesis and joint lavage avoiding arthrotomy.
Diagnosing Kingella by routine culture is challenging because specific methods such as blood agar or chocolate agar are required. Direct inoculation of synovial fluid into the blood culture bottle is recommended because microbiologic recovery is better than that in solid medium. Furthermore, specific PCR has improved the microbiologic yield of this pathogen, especially in young patients 6 months to 3–4 years of age in whom this agent can be the leading cause of infection.
It is well established that OAI caused by K. kingae can have no significant increase of acute-phase reactants.4 Probably, the mean age of our cohort and the routine use of PCR might explain the high percentage of K. kingae. Recognizing and identifying the etiology of OAI infections is important for implementing comprehensive management of these cases, possibly with a less aggressive treatment. In the light of our findings, we recommend performing specific K. kingae PCR to improve the diagnosis of this agent, especially in children younger than 5 years.
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