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Background Strongyloides stercoralis is a nematode endemic to the tropical and subtropical regions. In the United States, it is mostly found at southeastern states. Most infections are asymptomatic but disseminated and fatal infections have been reported in immunocompromised patients. At our institution, universal screening through Strongyloides antibody detection in serum among solid-organ transplant candidates began since 2010 and all seropositive candidates are treated before transplantation. We previously determined our incidence to be about 5%. The aim of this study was to determine demographic characteristics and risk factors that can be used for more cost-effective targeted screening. Methods We performed a retrospective cohort study of patients who underwent transplant evaluation from 2014 to 2016. A total of 228 charts were reviewed for Strongyloides serology status, eosinophilia, demographics and risk factors. Chi-square and Fisher exact tests were used to do a comparative analysis between Strongyloides seropositive and seronegative cohorts. Results We identified 113 seropositive (SP) patients and 115 seronegative (SN) patients. There were more males in the seropositive group (79%) compared with seronegative group (62%) (P = 0.005). Caucasians predominated in both groups (SP 71% vs. SN 57%; P = 0.286). No significant difference was found between both groups with regards to occupation with soil or water contact (SP 38% vs. SN 30%; P = 0.281), birthplace outside USA or travel outside of United States (SP 31% vs. SN 36%; P = 0.732). Eosinophilia occurred less in the seropositive group compared with the seronegative group (SP 16% vs. SN 30%; P = 0.030). Conclusion The study did not find any statistically significant difference in the demographic characteristics or risk factors that can be used for prediction of Strongyloides seropositivity among solid-organ transplant candidates. Hence, our institution will continue universal screening for Strongyloides stercoralis for all our transplant candidates. Our findings further question donor screening for Strongyloides that uses a similar questionnaire which may not be reliable to identify those infected with this parasite. This would put recipients at risk for a donor-transmitted infection. Disclosures All authors: No reported disclosures. [ABSTRACT FROM AUTHOR]

Clostridioides difficile, the primary cause of nosocomial antibiotic-associated diarrhea, has a complex relationship with antibiotics. While the use of broad-spectrum antibiotics disrupts the gut microbiota and increases the risk of C. difficile infection (CDI), antibiotics are also the primary treatment for CDI. However, only a few antibiotics, including vancomycin, fidaxomicin, and rifaximin, are effective against CDI, and resistance to these antibiotics has emerged recently. In this study, we report the identification of two RT027 C. difficile clinical isolates (TGH35 and TGH64) obtained from symptomatic CDI-diagnosed patients in Tampa, Florida in 2016. These two strains showed an elevated minimum inhibitory concentration (MIC) of vancomycin (MIC = 4 μg/mL, compared to the EUCAST breakpoint of 2 μg/mL) and contained a vanR Cd 343A>G mutation resulting in a Thr115Ala substitution in the VanR Cd response regulator. This mutation was absent in the vancomycin-sensitive control epidemic strain RT027/R20291. TGH64 was also resistant to rifaximin (MIC ≥ 128 μg/mL) and carried the previously reported Arg505Lys and Ile548Met mutations in RpoB. Furthermore, we report on the antimicrobial resistance (AMR) and genomic characterization of additional C. difficile isolates, including RT106/TGH120, RT017/TGH33, and RT017/TGH51, obtained from the same patient sample cohort representing the highly prevalent and regionally distributed C. difficile ribotypes worldwide. Considering that the VanR Cd Thr115Ala mutation was also independently reported in seven C. difficile clinical isolates from Texas and Israel in 2019, we recommend epidemiological surveillance to better understand the impact of this mutation on vancomycin resistance. IMPORTANCE 343A>G) that causes a Thr115Ala substitution and is linked to an increased MIC of vancomycin in clinical isolates of C. difficile obtained from Florida in 2016. Understanding the mechanisms of AMR, especially those of newly evolving strains, is essential to effectively guide antibiotic stewardship policies to combat antibiotic resistance as well as to discover novel therapeutic targets.vanR Cd 343A>G) that causes a Thr115Ala substitution and is linked to an increased MIC of vancomycin in clinical isolates of C. difficile obtained from Florida in 2016. Understanding the mechanisms of AMR, especially those of newly evolving strains, is essential to effectively guide antibiotic stewardship policies to combat antibiotic resistance as well as to discover novel therapeutic targets., Competing Interests: The authors declare no conflict of interest.