Julian J Weiss1,2, Tuki N Attuquayefio3, Elizabeth B White4, Fangyong Li5, Rachel S Herz6, Theresa L White7,8, Melissa Campbell1,9, Bertie Geng10, Rupak Datta1, Anne L Wyllie4, Nathan D Grubaugh4, Arnau Casanovas-Massana4, M Catherine Muenker4, Adam J Moore4, Ryan Handoko10, Akiko Iwasaki11,12, Richard A Martinello1,13,14, Albert I Ko1,4, Dana M Small3,15, Shelli F Farhadian1,2. 1. Department of Medicine, Section of Infectious Diseases, Yale School of Medicine, New Haven, Connecticut, United States of America. 2. Department of Neurology, Yale School of Medicine, New Haven, Connecticut, United States of America. 3. Department of Psychiatry, Yale School of Medicine, New Haven, Connecticut, United States of America. 4. Department of Epidemiology of Microbial Diseases, Yale School of Public Health, New Haven, Connecticut, United States of America. 5. Yale Center for Analytical Sciences, Yale School of Public Health, New Haven, Connecticut, United States of America. 6. Department of Psychiatry and Human Behavior, Alpert Medical School of Brown University, Providence, Rhode Island, United States of America. 7. Department of Psychology, Le Moyne College, Syracuse, New York, United States of America. 8. SUNY Upstate Medical University, Syracuse, New York, United States of America. 9. Center for Outcomes Research and Evaluation, Yale-New Haven Health, New Haven, Connecticut, United States of America. 10. Yale School of Medicine, New Haven, Connecticut, United States of America. 11. Department of Immunobiology, Yale School of Medicine, New Haven, Connecticut, United States of America. 12. Howard Hughes Medical Institute, Chevy Chase, Maryland, United States of America. 13. Department of Pediatrics, Yale School of Medicine, New Haven, Connecticut, United States of America. 14. Department of Infection Prevention, Yale-New Haven Health, New Haven, Connecticut, United States of America. 15. Department of Psychology, Yale University, New Haven, Connecticut, United States of America.
Abstract
INTRODUCTION: Healthcare workers (HCW) treating COVID-19 patients are at high risk for infection and may also spread infection through their contact with vulnerable patients. Smell loss has been associated with SARS-CoV-2 infection, but it is unknown whether monitoring for smell loss can be used to identify asymptomatic infection among high risk individuals. In this study we sought to determine if tracking smell sensitivity and loss using an at-home assessment could identify SARS-CoV-2 infection in HCW. METHODS AND FINDINGS: We performed a prospective cohort study tracking 473 HCW across three months to determine if smell loss could predict SARS-CoV-2 infection in this high-risk group. HCW subjects completed a longitudinal, behavioral at-home assessment of olfaction with household items, as well as detailed symptom surveys that included a parosmia screening questionnaire, and real-time quantitative polymerase chain reaction testing to identify SARS-CoV-2 infection. Our main measures were the prevalence of smell loss in SARS-CoV-2-positive HCW versus SARS-CoV-2-negative HCW, and timing of smell loss relative to SARS-CoV-2 test positivity. SARS-CoV-2 was identified in 17 (3.6%) of 473 HCW. HCW with SARS-CoV-2 infection were more likely to report smell loss than SARS-CoV-2-negative HCW on both the at-home assessment and the screening questionnaire (9/17, 53% vs 105/456, 23%, P < .01). 6/9 (67%) of SARS-CoV-2-positive HCW reporting smell loss reported smell loss prior to having a positive SARS-CoV-2 test, and smell loss was reported a median of two days before testing positive. Neurological symptoms were reported more frequently among SARS-CoV-2-positive HCW who reported smell loss compared to those without smell loss (9/9, 100% vs 3/8, 38%, P < .01). CONCLUSIONS: In this prospective study of HCW, self-reported changes in smell using two different measures were predictive of SARS-CoV-2 infection. Smell loss frequently preceded a positive test and was associated with neurological symptoms.
INTRODUCTION: Healthcare workers (HCW) treating COVID-19 patients are at high risk for infection and may also spread infection through their contact with vulnerable patients. Smell loss has been associated with SARS-CoV-2 infection, but it is unknown whether monitoring for smell loss can be used to identify asymptomatic infection among high risk individuals. In this study we sought to determine if tracking smell sensitivity and loss using an at-home assessment could identify SARS-CoV-2 infection in HCW. METHODS AND FINDINGS: We performed a prospective cohort study tracking 473 HCW across three months to determine if smell loss could predict SARS-CoV-2 infection in this high-risk group. HCW subjects completed a longitudinal, behavioral at-home assessment of olfaction with household items, as well as detailed symptom surveys that included a parosmia screening questionnaire, and real-time quantitative polymerase chain reaction testing to identify SARS-CoV-2 infection. Our main measures were the prevalence of smell loss in SARS-CoV-2-positive HCW versus SARS-CoV-2-negative HCW, and timing of smell loss relative to SARS-CoV-2 test positivity. SARS-CoV-2 was identified in 17 (3.6%) of 473 HCW. HCW with SARS-CoV-2 infection were more likely to report smell loss than SARS-CoV-2-negative HCW on both the at-home assessment and the screening questionnaire (9/17, 53% vs 105/456, 23%, P < .01). 6/9 (67%) of SARS-CoV-2-positive HCW reporting smell loss reported smell loss prior to having a positive SARS-CoV-2 test, and smell loss was reported a median of two days before testing positive. Neurological symptoms were reported more frequently among SARS-CoV-2-positive HCW who reported smell loss compared to those without smell loss (9/9, 100% vs 3/8, 38%, P < .01). CONCLUSIONS: In this prospective study of HCW, self-reported changes in smell using two different measures were predictive of SARS-CoV-2 infection. Smell loss frequently preceded a positive test and was associated with neurological symptoms.
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