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Background Varicella-zoster virus (VZV) infection is known to occur in 13-55% of patients within the first year after hematopoietic stem cell transplant (HSCT). The dynamics of recovery of VZV-specific T cell- mediated immunity (CMI) and its role for prevention and control of VZV reactivation are rarely reported in pediatric allogenic HSCT recipients. Methods From April 2019 to February 2020, subjects aged younger than 19 years who underwent allogenic HSCT with at least 1 year of follow up at Asan Medical Center Children`s Hospital were prospectively enrolled. All of them underwent VZV-specific enzyme-linked immune absorbent spot (ELISPOT) assays just before HSCT and then at 1, 3 months following HSCT. Extension study, which measures VZV-specific CMI before and after VZV vaccination at 24 months post-HSCT, is currently underway. Results A total of 32 HSCT recipients with a median age of 11years were enrolled. 37.5% underwent haploidentical HSCT and VZV R+ were in 78.1%. Antiviral prophylaxis was applied to all HSCT recipients, of which 65.6% were applied up to 365 days after HSCT. During this study period, only 1 patient (3.1%) experienced herpes zoster at 23 months following HSCT, whose VZV-specific ELISPOT assay showed 0, 1, and 0 spot-forming cells (SFC)/2.0x105 cells before HSCT, 1 and 3 months following HSCT, respectively. The presence of VZV-specific CMI ≥ 1 SFC/ 2.0 × 105 cells was observed in 62.5 % before HSCT, 65.6 % at 1 month, 59.4 % at 3 months, and 70% at 24 months after HSCT, respectively. However, only 18.8 % ,12.5 % and 21.9 % recovered VZV-specific CMI with ≥ 5 SFC/ 2.0 × 105 cells at 1, 3 and 24 months following HSCT. Meanwhile, all the 4 recipients who got the 1st VZV vaccination at 24 months following HSCT showed recovery of VZV-specific CMI with ≥ 5 SFC/ 2.0 × 105 cell. Recovery of VZV-specific CMI after HSCT was not associated with VZV serostatus, chickenpox history, type of HSCT, conditioning regimens, and GVHD. Conclusion Only a few pediatric allogenic HSCT recipients recovered VZV-specific CMI with ≥ 5 SFC/ 2.0 × 105 cell up to 2 years following HSCT. In addition, the association between VZV-specific CMI and VZV reactivation could not be analyzed because no one experienced VZV reactivation within 1 year after HSCT. More long-term large-scale multicenter study is mandatory to supplement these parts. Disclosures All Authors: No reported disclosures.

Background Methicillin-resistant Staphylococcus aureus (MRSA) colonization pressure (CP) is a useful indicator for measuring the extent of MRSA reservoir in healthcare settings. The purpose of this study is to determine the MRSA colonization rate and invasive MRSA infection rate in severely ill pediatric patients requiring pediatric intensive care unit (PICU) stay, and to evaluate the association between MRSA CP and MRSA acquisition/invasive infection. Methods From January 2016 to December 2020, pediatric patients admitted to 2 PICUs with a total of 25 beds were retrospectively analyzed. Routine nasal and/or endotracheal cultures were performed on MRSA at the time of PCIU admission and thereafter, every week. MRSA CP was defined as the ratio of the monthly MRSA positive number of patients to 100 patient days. Among MRSA colonizers, MRSA obtained after 2 days of PICU admission was defined as an acquired colonizer, and imported colonizer was defined when it was confirmed as an MRSA colonizer at the time or within 2 days of entry. When MRSA was cultured in a normally sterile body fluids, it was defined as an invasive MRSA infection. Results Of the total 6,907 patients admitted to the PICUs during this study period, 8.4% (487/6,907) were MRSA colonizers; 30% (139/487) were acquired colonizers, and invasive MRSA infections occurred in 3.3% (16/487). During the stay in the PICUs, the MRSA acquisition rate was 4.1%. A total of 22 invasive MRSA infections occurred during this study period, with an incidence rate of 3.1/1,000 patient days, of which 72.7% (n=16) occurred to the patients with MRSA colonization. Invasive MRSA infection occurred in 2.4% (8/348) of imported colonizers, and 5.2% (8/139) of acquired colonizers (p=0.108). The median duration from the time of colonization to invasive infection was 24 days(IQR; 2.25-49.75). Although MRSA CP was not correlated with the incidence of invasive MRSA infection (p=0.101), MRSA CP itself affected MRSA acquisition in PICU (p< 0.001). Conclusion MRSA CP influenced the new acquisition of MRSA during PICU stay, and newly acquired colonizers are more likely to experience invasive MRSA infection. Continuous multi-faceted efforts to minimize MRSA CP can provide opportunities for reducing MRSA colonization and infections rates in PICU settings. Disclosures All Authors: No reported disclosures.

Background Haemophilus influenzae is known to develop resistance to β-lactam antibiotics by either producing β-lactamase or modifying structure of penicillin-binding protein 3 (PBP3) by ftsI gene mutation. Since 2017, H. influenzae with ceftriaxone resistance has been continuously appearing in our hospital, and the genotypic characteristics of these strains was analyzed. Methods Among a total of 69 H. influenzae isolated from the patients who admitted to Asan Medical Center Children’s Hospital from March 2014 to April 2019, 23 isolates resistant to ceftriaxone by EUCAST disk diffusion method were included. The ceftriaxone MIC was checked again with the E-test and ceftriaxone MIC ≤ 0.125 mg/L were categorized as susceptible. As test for β-lactamase production, the cefinase test and PCR amplification for blaTEM-1 and blaROB-1 were performed. The sequencing of the ftsI encoding PBP3 amplified by PCR was performed, and amino acid sequences were compared with H. influenzae Rd KW20. Results Among total 23 ceftriaxone-resistant isolates by disk diffusion method, 21 isolates restored for further molecular characterization were included, and 19% (4/21) were reported as susceptible by E-test. Among the 21 ceftriaxone-resistant isolates, 76.2% (16/21) were non-susceptible to amoxicillin/clavulanate, and one of them were resistant to meropenem. The prevalence of b-lactamase-producers was 57.1% (12/21), all of which were positive for blaTEM-1. For ftsI gene sequencing, either R517H or N526K amino acid substitution was observed, and none had both. The number of isolates having S385T was 17, of which 15 isolates accompanied with both M377I and L389F. The median ceftriaxone MIC of 3 isolates with only N526K was 0.012 ug/ml (range 0.008-0.125 ug/ml), and 12 isolates with N526K, M377I, S385T, and L389F was 0.19 ug/ml (0.19-0.25 ug/ml). Lastly, the three isolates with R517H, M377I, S385T, and L389F showed the highest median ceftriaxone MIC with 0.25 ug/ml (0.19-0.75 ug/ml). Conclusion Ceftriaxone-resistant H. influenzae isolates in Korea seems to be related to the combination of R517H, M377I, S385T, and L389F by ftsI gene mutation. Although clinical concerns about treatment failure may be low, continuous monitoring of the emergence of highly resistant strains is necessary. Disclosures All Authors: No reported disclosures.