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Across 12 consecutive influenza seasons in Utah, medically-attended visits for laboratory-confirmed influenza infection peaked first among older children (12–18 years). Peak activity in older children preceded that of children 0–4 years by more than 2 days and that of peak activity among adults ≥65 years by more than 6 days. [ABSTRACT FROM PUBLISHER]

Background Following widespread use of the Haemophilus influenzae serotype b (Hib) vaccine, H. influenzae serotype a (Hia) has emerged as an important pathogen in children. Rates of Hia disease are particularly high in Utah. We describe the clinical features and molecular epidemiology of invasive Hia disease in children in Utah over 11 years. Methods Cases of invasive Hia disease in children less than 18 years were identified through electronic clinical and microbiology records. Demographic data and clinical outcomes were abstracted from the medical record for all cases. Available Hia isolates were collected for molecular analysis. Isolates were genotyped by multi-locus sequence typing (MLST) and clonal division was determined using sodC PCR. Presence or absence of the putative virulence-associated IS 1016-bexA duplication-deletion was evaluated. Results We identified 51 children with invasive Hia between 2007 and 2017. Median age was 11.3 months. The average annual incidence was 1.7 cases per 100,000 children aged <5 years (95% CI 1.2–2.2). Incidence was highest among children less than one year of age (4.8/100,000; 95% CI 3.1–6.9). Incidence rates were similar by race and ethnicity, although the confidence intervals were wide. The annual number of cases was similar over the 11-year study period (figure). The most common clinical manifestation was meningitis (54%; half had intracranial complications, 25% suffered hearing loss), followed by pneumonia (14%), and arthritis (14%). Twenty-two children (44%) required ICU care and one child died. Twenty-eight isolates (56%) were available for molecular analysis. ST62, clonal division II isolates caused 75% (21/28) of disease. No isolates contained the virulence-associated IS 1016 - bexA duplication-deletion. Conclusion Hia is an important cause of severe invasive bacterial infection in Utah. Molecular analyses revealed that a majority of infections were caused by ST62 isolates, a clonal division II Hia type lacking the IS 1016 - bexA duplication-deletion. Hia ST62 has not been commonly reported in other settings, suggesting a unique molecular epidemiology in our population. Disclosures All authors: No reported disclosures. [ABSTRACT FROM AUTHOR]