Bone and joint infection BJI is a potentially devastating disorder with a high incidence of severe and long-lasting sequelae, particularly in growing children. Improving patient management requires determining the causative agent to prevent the risk of long-term disabilities [8]. Staphylococcus aureus is the most common pathogen in acute BJI, being identified in 70 to 90% of culture positive cases. In our study, Staphylococcus aureus was the main causative agent of infections recovered at 82.2% on a positive culture. However, we showed that 59.1% of samples (65 of 110) remained culture negative. Dodwell has reported that no organism is identified in up to 55% of pediatric BJI cases, even if appropriate samples had been obtained [9].
Recently, molecular diagnosis has significantly increased positive results, especially among K. kingae infections. In countries where K. kingae-specific real-time PCR (RT-PCR) assays are routinely employed this organism is recognized as the main agent of BJI in young children [10, 11]. In fact, to date, little is known on the epidemiology of K. kingae BJIs in children in the African continent. To the best of our knowledge, we report the first study of K. kingae BJI among Moroccan children population. We revealed that K. kingae was the leading cause (58.7%) of culture-negative BJIs in young children. This rate are higher than 36.07 and 45% reported in France [10, 12], or 25.93% in Ottawa [13]. K. kingae infections seem to be closely correlated to children’s ages. In a meta-analysis, Wong et al. reported 47.6% of patients under 48 months of age were diagnosed with K. kingae BJI infections [4]. In this study, 55.6% of children were aged 6 to 48 months, and 14.8% (4/27) were under 6 months, 2 of them were aged < 1 month, with no history of trauma or unusual infections, and no warning signs of immunosuppression were found. Also, 29.6% (8/27) of children were over 48 months (5 years and older (5–8.2 years), close contact with younger children or siblings is very likely, which may explain this results. This finding is not corroborating with the classic representation of K. kingae BJI, which occurs in children between 6 months and 4 years old. Shahrestani et al. [14] and more recently, Ceroni et al. have established the possibility of K. kingae osteoarticular infections in older immunocompetent children [15]. Also, we diagnosed a large proportion of K. kingae patients during the fall to winter season. Wong et al. have reported that this seasonal variation is likely associated with respiratory viral infections and stomatitis, allowing for passage of the colonizing agent through the breached epithelium [4]. Concerning the site of infection, K. kingae are responsible of septic arthritis with variable of 45 to 69% [8, 10, 12, 16]. We recorded 21 cases of septic arthritis (77.8%), 4 osteomyelitis (14.8%) and 2 spondylodiscitis. Similarly to published data, our finding confirms that infection tends to affect the lower extremity the most, and the knee is often involved [16], and almost all cases present a moderate clinical picture with normal to slightly elevated inflammatory markers [6]. in fact, chronic osteomyelitis and orthopedic sequelae seem to be uncommon in K. kingae BJI in young children [2, 8].
Unfortunately, we were unable to establish an antimicrobial susceptibility pattern, because all culture was negative despite inoculation into blood culture vials. It has been recognized that K. kingae is most often sensitive to many classes of antibiotics (beta-lactams, macrolides, aminoglycosides, fluoroquinolones, tetracyclins) [13]. For managing BJI in our ward, empirical antibiotic therapy is started with intravenous antibiotics (clavulanic-acid/amoxicillin and gentamycin), and after discharge, treatment continues orally by 10 days to 3 weeks according to the judgment of the attending physician. In the case of documented K. kingae BJI, the antibiotic treatment consisted of oral clavulanic-acid/amoxicillin for 14 to 21 days. Several authors have suggested switching to trimethoprim-sulfamethoxazole once K kingae infection was identified [6, 14].
For PCR analysis, we targeted the groEL gene (also known cpn60), a housekeeping gene encoding a chaperone protein recognized as a universal bacterial marker [17]. Recently, El Houmani et al. provided evidence that kkgroEL gene could discriminate even K. kingae from K. negevensis [14].
Our study had several limits, the first of which was the one site of study and the small sample size. Despite this, we recorded 58.7% K. kingae BJI, providing evidence that K. kingae is circulating in our region as well. Also, we could not define antimicrobial susceptibility patterns in our region because no K. Kingae was growing in culture media even we inoculated joint samples into aerobic blood vials. Further studies are required to determine the prevalence of K. kingae carriage and BJI in other Moroccan sites.