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Life sciences · Journal article
Rheumatology International · September 26, 2026
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Abstract IgA vasculitis (IgAV) is the most common systemic vasculitis in childhood. Its seasonal distribution and frequent respiratory or gastrointestinal prodromes implicate environmental exposures. However, microbiological detection temporally proximate to disease onset is insufficient to establish causality in an individual patient. To critically evaluate infectious exposures associated with pediatric IgAV, we distinguished epidemiological associations from incidental detection and infectious mimics, and separate direct IgAV evidence from mechanisms extrapolated from IgA nephropathy or general mucosal immunology. PubMed and MEDLINE were searched from inception through 6 August 2026 and supplemented by backward and forward citation tracking. Controlled-vocabulary and free-text terms addressed IgAV, pediatric populations, infection, specific pathogens, microbiota, vaccination, and immune mechanisms. The broad query retrieved 1,174 records before deduplication. Because screening was not prospectively logged, deduplicated screening and full-text counts could not be reconstructed; accordingly, no systematic-review or PRISMA completeness claim is made. Comparative evidence was most consistent for group A streptococcal exposure and population-level circulation of seasonal respiratory bacteria. Evidence for Mycoplasma pneumoniae, Helicobacter pylori in selected phenotypes, SARS-CoV-2, and specific enteric or parasitic infections was of lower certainty and was frequently case-based. Pediatric vaccine studies did not demonstrate a consistent excess risk. Evidence supports convergence of mucosal IgA induction, IgA1-containing immune complexes, complement activation, FcαRI-mediated myeloid signaling, neutrophil extracellular traps, and endothelial injury. Causal attribution requires integrated assessment of temporality, anatomical source, microbiological specificity, background exposure prevalence, and alternative diagnoses. Infectious investigations should be restricted to circumstances in which identification of a treatable infection, persistent antigen source, or immunosuppression-related hazard would alter management.