Pediatric bone and joint infections (BJIs) encompass acute hematogenous osteomyelitis, septic arthritis and mixed forms, defined by bacterial invasion of the bone and/or joint and typically presenting with fever, pain and functional impairment of the affected limb [1][2]. They are distinguished from chronic or inflammatory conditions, such as tuberculosis, Lyme disease or inflammatory arthropathies by their acute onset, infectious context and the risk of rapid destruction of the growth cartilage in the absence of timely management [1][3]. Pathophysiologically, most pediatric BJIs arise from transient bacteremia in otherwise healthy children, facilitated by the particular vascular anatomy of the metaphysis and synovium, which favors septic embolization [1][3]. The principal pathogens are Staphylococcus aureus (methicillin-susceptible or methicillin-resistant) and Kingellakingae in infants and preschool children, alongside β-hemolytic streptococci, Streptococcus pneumoniae and, more rarely, Gram-negative bacilli according to age and underlying conditions [1]-[4].

Epidemiological data from North American, Latin American and European cohorts indicate that BJIs constitute a significant cause of pediatric hospitalization, with an incidence estimated between 10 and 80 cases per 100,000 children, depending on age, vaccination status and geographical setting, with a peak between 6 months and 4 years and a male predominance [1][2][4]. The widespread use of MRI, now regarded as the reference modality for diagnosis and assessment of disease extent, has enabled earlier detection of bone and joint involvement, particularly in deep-seated or pauci-symptomatic forms [2][5][6]. In parallel, the deployment of molecular biology techniques, especially K.kingae-targeted PCR on osteoarticular samples and oropharyngeal swabs, has substantially improved microbiological yield in preschool children and highlighted often subtle clinical presentations linked to this pathogen [3][4][6].

These diagnostic advances have driven major changes in therapeutic strategies. Current recommendations underline the necessity of prompt treatment while avoiding unnecessary invasiveness [2][4]-[6]. Protocols now favour limited drainage procedures rather than extensive surgery, shortened courses of intravenous antibiotics followed by early oral switch, and, in carefully selected low-risk cases, exclusive oral therapy from the outset, provided adherence and follow-up are optimal [2][4][5]. Empirical regimens are designed to cover the dominant pathogens (MSSA, locally prevalent MRSA and K.kingae), then refined according to culture and susceptibility results, with an effort to minimise exposure to very broad-spectrum agents in immunocompetent children [1]-[4][6]. In this context, our study aims to evaluate the adequacy of empirical antibiotic choices with local microbiology and to analyse concordance between empirical and targeted therapy, in order to optimise antibiotic stewardship in paediatric BJIs.

This study, conducted in a tertiary center in Casablanca between 2020 and 2023, provides original data on antibiotic adaptation in pediatric bone and joint infections. The population included 161 children with a mean age of 6.38 years, with a predominance of the 1 - 9-year age groups. These results are in line with major pediatric series in which BJIs occur mainly in preschool and school-aged children, although other cohorts dominated by Kingellakingae report an earlier peak around 2 - 4 years [7]-[9], and higher ages in series focusing on acute hematogenous osteomyelitis [10]-[13]. The low rate of comorbidities and the rarity of bone or tumor history in our series are similar to cohorts including otherwise healthy children [7][9][13].

From a diagnostic standpoint, the distribution between arthritis, soft-tissue collections, subperiosteal abscesses and osteomyelitis mirrors the diversity of presentations described in large mixed series [7]-[9][12]-[14]. The microbiological approach was highly systematic, with sampling performed in 99.4% of patients, a rate higher than in several studies where 25% - 30% of children have no microbiological investigation [10][12]. Despite this strategy, almost half of samples remained sterile, a result comparable to that reported in acute hematogenous osteomyelitis when molecular techniques are not routinely used [11]-[13]. By contrast, teams that have widely implemented K.kingae-specific PCR or other molecular tools report higher documentation rates above 60%, with K.kingae predominating in younger children [7]-[9]. This heterogeneity highlights the degree to which the available technical platform influences the ability to refine antibiotic adaptation.

This focused empirical strategy, centered on a limited number of standard combinations, differs from the more varied approaches described in other pediatric series. In several European cohorts, first-line treatment is most often based on an antistaphylococcal beta-lactam (such as co-amoxiclav, cloxacillin or cefazolin), sometimes combined with an aminoglycoside and adapted to the child’s age [7][9][12][13]. In contrast, many North American teams routinely include empirical coverage of methicillin-resistant Staphylococcus aureus (MRSA) with clindamycin or vancomycin, reflecting a non-negligible prevalence of MRSA infections in children [10][11][15]. In those studies, S. aureus frequently represents more than half of all isolates, with a substantial proportion of MRSA that justifies broader empirical regimens [10]-[13]. Conversely, in series where Kingellakingae and methicillin-susceptible S. aureus (MSSA) predominate, a more targeted empirical regimen is generally sufficient, with very good agreement between empirical treatment and susceptibility profiles [7][9][15]. Our results, characterized by the apparent absence of MRSA and the central place of standard regimens, fall within this second pattern and are in line with a restrained use of reserve antibiotics.

A key message from our work is the excellent match between the standard empirical regimen and the definitive targeted therapy. Among children who initially received amoxicillin-clavulanic acid combined with gentamicin (AC + G), more than 96% remained on this same combination after adaptation, and only 3.5% required escalation to a broadened regimen. This remarkable stability contrasts with reports in which the first-line treatment is frequently revised, either because microbiological documentation reveals resistant organisms or because the clinical response is deemed insufficient [12][14].

Musso et al. reported a change in intravenous regimen in half of their cases [12], while Cohen et al. described modification of empirical treatment in almost one quarter of children with septic arthritis, mainly within the first three days of hospitalization [14]. Conversely, the studies by Lemoine et al. and Filleron et al. show, as in our work, excellent adequacy between relatively simple empirical regimens (co-amoxiclav, cloxacillin, cefamandole) and susceptibility profiles, with very few necessary adaptations and clinical cure rates close to 100% [7][9]. Taken together, these converging data suggest that, in settings with low MRSA prevalence, a standardized empirical strategy based on a beta-lactam, with or without an aminoglycoside, provides a solid foundation for subsequent targeted adjustment.

Our analysis also shows a strong association between the initial use of a “broad” empirical regimen (third-generation cephalosporin-based schemes, metronidazole and/or vancomycin) and the continuation of broadened targeted antibiotic therapy (OR 40.8; 95% CI 11.5 - 144.4; p < 0.0001). In our setting, the use of an initially broad-spectrum antibiotic regimen appears less as simple “over-treatment” and more as a clinical marker of infections that are more severe or complex, in which the subsequent need for prolonged and expanded coverage is ultimately confirmed once microbiological data become available. This pattern is similar to that reported in cohorts where broad regimens are deliberately reserved for complicated presentations, suspected methicillin-resistant Staphylococcus aureus infection, or the most critically ill children [10]-[12].

Our two-by-two analyses further show that the documentation of a pathogen is significantly associated with the prescription of a broadened targeted regimen, whereas the mere presence of an identified organism is not significantly linked to the initial decision to start with a broad-spectrum empirical treatment. In other words, it is mainly the microbiological result, obtained a posteriori, that leads to broadening antibiotic therapy rather than clinical suspicion alone. These findings echo those of Mobayed et al., who emphasis the value of a disease-specific antibiogram to safely support relatively focused empirical regimens [15], and those of Hu et al. and Roversi et al., who underline the importance of local ecology for calibrating empiricism and guiding subsequent adaptation [8][11].

Finally, our study has several practical implications for antibiotic adaptation in pediatric BJIs. The strong concordance between empirical AC + G and targeted therapy, combined with the rarity of MRSA, supports maintaining a relatively narrow first-line regimen, in line with series demonstrating the efficacy of shorter treatments with early oral switch [9][12]. The high proportion of sterile cultures and the absence of targeted PCR techniques nonetheless suggest a potential underestimation of hard-to-culture pathogens, particularly K.kingae in younger children [7]-[9]. The gradual integration of molecular tools, regular updating of the local antibiogram, and clear clinical criteria for the use of broad-spectrum regimens should further optimize the balance between infection control, prevention of resistance, and rational antibiotic use in pediatrics.

Although nearly half of microbiological samples were sterile, this did not appear to negatively affect clinical outcomes. The vast majority of children, including those with sterile cultures, evolved favorably under the standard empirical regimen based on amoxicillin-clavulanic acid and gentamicin. This suggests that, in our setting, the most likely uncultured pathogens are effectively covered by this regimen. Similar findings have been reported in other series, where favorable outcomes were achieved despite limited microbiological documentation, particularly in the absence of routine molecular diagnostics. These results support the safety of a narrow-spectrum empirical approach when adapted to local epidemiology, even in the context of a high rate of culture-negative infections.

Despite the limitations related to the monocentric and retrospective design, the internal consistency of our results and their concordance with several major international series [7]-[15] suggest that the Casablanca approach—centered on a standardized AC + G regimen with targeted adaptation based on microbiological results and clinical course—is a relevant strategy for managing pediatric bone and joint infections in a setting with low prevalence of highly resistant organisms.

In our center, pediatric osteoarticular infections are managed mainly with a standardized empirical antibiotic regimen based on amoxicillin-clavulanic acid and gentamicin, which proves appropriate in the vast majority of cases, with limited use of broader-spectrum protocols. Isolation of a pathogen and the empirical use of broad-spectrum agents are strongly associated with continuation of extended antibiotic therapy, highlighting the risk of unjustified prolongation of such treatments. These findings support an antibiotic stewardship strategy based on narrow-spectrum empirical regimens tailored to local ecology, combined with systematic microbiological sampling and targeted adjustment rather than empirical broadening of therapy.

Pediatric bone and joint infections (BJIs) are common emergencies that expose children to a risk of cartilage destruction, functional sequelae and systemic complications in the absence of timely management. Bone and joint infections in children are most often due, depending on age, to Staphylococcus aureus (both methicillin-susceptible and methicillin-resistant strains) and Kingellakingae. Published series show wide variation between countries in the choice of empirical antibiotic therapy: some teams favor relatively focused antistaphylococcal beta-lactams, while others use combinations that include glycopeptides or third-generation cephalosporins, especially in regions where methicillin-resistant S. aureus is common. This heterogeneity highlights the importance of tailoring therapeutic protocols to local microbiological patterns and of avoiding unnecessary exposure to broad-spectrum antibiotics, in line with rational antibiotic use and stewardship principles.

Our work provides the first detailed data, from a tertiary center in Casablanca, on antibiotic adaptation in pediatric BJIs, based on an exhaustive cohort of 161 children followed over four years. It shows that a standardized empirical strategy centered on amoxicillin-clavulanic acid plus gentamicin remains appropriate in the vast majority of cases, with a very low rate of escalation after microbiological documentation. The analysis shows that starting treatment with a so-called broad empirical regimen is strongly linked to the subsequent maintenance of an expanded-spectrum therapy, while it is chiefly the identification of a causative pathogen that significantly prompts later extension of the antibiotic spectrum. Taken together, these findings provide solid local arguments in favor of initiating therapy with narrow-spectrum regimens tailored to the Moroccan microbiological context, coupled with systematic microbiological sampling and careful, evidence-based adjustment of treatment, rather than routine empirical broadening of antibiotic coverage.

Salma Bouchti, KhadijaEssafi: ensured study design, data collection, statistical analysis and manuscript drafting.

HasnaDarouich, Kaoutar El Fakhr, SamiraKalouch: provided scientific supervision, methodological oversight, critical revision and final approval of the manuscript.