Based on our case’s characteristics, we identified three potentially interconnected factors: first, the A2063G mutation-mediated macrolide resistance enabled persistent infection [19]; second, tNGS revealed polymicrobial infection with M. pneumoniae (10,008 sequence reads), Streptococcus pneumoniae (7,377 reads), and Staphylococcus aureus (2,267 reads), correlating with a dramatic CRP rise from 9.6 mg/L to 66.1 mg/L within 3 days (689% increase); third, despite distinct pathogenic mechanisms, both PB and KD involve excessive inflammatory responses and immune dysregulation [14, 17]. Here, CRP is linked to infection.