Characterizing the Novel CRP, IP-10, and TRAIL Host-Response Protein Signature in Pediatric Kingella kingae Infections—A Retrospective Cohort Study

Background: Kingella kingae is a primary cause of pediatric osteoarticular infections. Diagnosis is challenging due to mild clinical presentations and fastidious culture growth, often mimicking viral illnesses. The MeMed BV™ assay measures C-reactive protein (CRP), interferon gamma-induced protein 10 (IP-10), and Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL) to differentiate bacterial from viral infections, but its utility in K. kingae has not been evaluated. Objectives: To characterize the CRP, IP-10, and TRAIL profiles in pediatric patients with confirmed K. kingae infections compared to viral and classical bacterial cohorts. Methods: This retrospective study analyzed 19 children with microbiologically confirmed K. kingae. Controls included viral (n = 20), pneumococcal (n = 17) and Gram-negative (n = 7) cohorts. Serum concentrations of the three host-response proteins were compared. Results: The median age of the K. kingae cohort was 11.0 months (IQR, 9.0–12.0 months). Compared to viral controls, K. kingae elicited significantly lower IP-10 levels (median: 100.0 pg/mL [IQR, <100.0–399.0] vs. 632.5 pg/mL [IQR, 346.3–1375.8]; p = 0.004) and a downward trend in TRAIL levels (median: 75.0 pg/mL [IQR, 66.0–95.0] vs. 169.5 pg/mL [IQR, 76.5–205.0]; p = 0.066), aligning with a bacterial profile. Conversely, K. kingae induced significantly lower inflammatory and host-response markers than typical bacterial infections; its median CRP (18.8 mg/L [IQR, 10.0–50.0]) and MeMed BV™ score (28 [IQR, 11–61]) were markedly lower than those observed in the pneumococcal cohort (CRP: 94.0 mg/L [IQR, 39.5–182.5]; MeMed BV: 89 [IQR, 51–98.5]) and the alternative bacterial cohort (CRP: 106.0 mg/L [IQR, 32.0–250.0]; MeMed BV: 73.0 [IQR, 67.0–99.0]). Conclusions: Kingella kingae infections elicit a distinct host-response fingerprint characterized by mild CRP elevation, leukocytosis, and uniquely suppressed IP-10 levels. Utilizing this three-protein signature may help distinguish K. kingae from viral mimics, preventing diagnostic delays and optimizing antibiotic stewardship.