We recognize that this study has several limitations. Although the study cohort is, to our knowledge, the largest sample of fatal infl uenza cases in children and young adults, the analysis has limited statistical power to detect associations because of small sample sizes, especially when examining subsamples. We had access to limited information about racial and ethnic background of casepatients. Clinical data were obtained primarily from a US surveillance system and were not validated with medical chart review. Although we were able to infer truncated haplotypes for MBL2, haplotype information for TNF was unavailable. Despite these shortcomings, the possibility that specifi c variants of the MBL2 gene known to infl uence serum MBL levels appear to be associated with severe bacterial co-infection is an intriguing fi nding deserving of additional study, especially given the prevalence of co-infection among case-patients who died of pandemic (H1N1) 2009 virus infection (38) and observations that children co-infected with infl uenza and S. aureus may have higher case-fatality rates (39) .