Background

The presentation of coronavirus 2019 (COVID-19) overlaps with common influenza symptoms. There is limited data on whether a specific symptom or collection of symptoms may be useful to predict test positivity.

Methods

An anonymous electronic survey was publicized through social media to query participants with COVID-19 testing. Respondents were questioned regarding 10 presenting symptoms, demographic information, comorbidities, and COVID-19 test results. Stepwise logistic regression was used to identify predictors for COVID-19 positivity. Selected classifiers were assessed for prediction performance using receiver operating characteristic (ROC) curve analysis.

Results

A total of 145 participants with positive COVID-19 testing and 157 with negative results were included. Participants had a mean age of 39 years, and 214 (72%) were female. Smell or taste change, fever, and body ache were associated with COVID-19 positivity, and shortness of breath and sore throat were associated with a negative test result (p < 0.05). A model using all 5 diagnostic symptoms had the highest accuracy with a predictive ability of 82% in discriminating between COVID-19 results. To maximize sensitivity and maintain fair diagnostic accuracy, a combination of 2 symptoms, change in sense of smell or taste and fever was found to have a sensitivity of 70% and overall discrimination accuracy of 75%.

Conclusion

Smell or taste change is a strong predictor for a COVID-19-positive test result. Using the presence of smell or taste change with fever, this parsimonious classifier correctly predicts 75% of COVID-19 test results. A larger cohort of respondents will be necessary to refine classifier performance.

Objective

To identify differentiation features of chemosensory dysfunction in COVID-19 infection and their primary drivers.

Study design

Cross-sectional cohort comparison.

Methods

A national anonymous survey was used to query participants regarding nasal symptoms and chemosensory dysfunction including sensitivity levels, and presence or absence of distortions and phantoms within the 6-week time window surrounding their COVID-19 testing and survey completion.

Results

Three-hundred and sixty-four respondents who reported COVID-19 positive (COVID+; n = 176) or COVID-19 negative (COVID-; n = 188) test results completed the survey. The COVID+ cohort had higher occurrence rates for: (a) chemosensory sensitivity impairments (67.0% vs 30.3%; P < .01), where the rate of complete loss of smell (anosmia) or taste (ageusia) was higher (35.8% vs 4.8%; P < .01), and (b) chemosensory distortions (39.8% vs 19.1%; P < .01), where the rate of anosmia or ageusia with distortions was also higher in the COVID+ cohort (19.9% vs 2.7%; P < .01). Occurrence rates in the two cohorts were similar for chemosensory phantoms (COVID+ 17.0%, COVID- 18.6%; P = .70) and nasal discharge or stuffiness in the presence of sensitivity impairment (COVID+ 63.6%, COVID- 52.6%; P = .17).

Conclusion

Chemosensory dysfunction in COVID-19 is associated with higher rates of smell or taste sensitivity impairments and distortions. Higher rates of anosmia and ageusia drive these key findings. Chemosensory phantoms and nasal symptoms in the presence of sensitivity impairment occur at rates that should demand clinical attention, but they do not appear to be specific to COVID-19 positivity.

Level of evidence

2b.

Objective

Coronavirus disease 2019 (COVID-19) is associated with olfactory dysfunction, but the evolution of the olfactory loss and timeline to recovery are largely unknown. This study examines changes in smell sensitivity in COVID-19-positive (COVID+) and COVID-19-negative (COVID-) viral illness during the initial weeks after infection.

Study design

Cross-sectional cohort comparison.

Setting

National anonymous surveys.

Methods

Survey participants were queried about smell sensitivity and general health status at the time of COVID-19 testing and in the weeks that followed.

Results

In total, 375 (174 COVID+, 201 COVID-) participants completed the survey and 132 (62 COVID+, 70 COVID-) participants completed the 2-week follow-up survey. Normal smell in the COVID+ cohort was less frequent at the time of testing and at follow up (P < .05). Dynamic changes in smell sensitivity in the COVID+ cohort were more frequent in the initial weeks (P < .001). In those with normosmia at the start of infection, 38% of the COVID+ cohort reported worsening smell compared to only 8% in the COVID- cohort (P < .05). Recovery of overall health was associated with normosmia at the time of infection and improvement of smell sensitivity within weeks of infection.

Conclusion

The COVID+ cohort showed greater dynamic change in smell sensitivity and a higher rate of persistent olfactory dysfunction in the weeks after infection. Normal smell at the time of COVID-19 infection may still worsen before recovery. Overall health recovery after viral illness is associated with improvement in smell sensitivity and the absence of initial anosmia or hyposmia.

Background

The coronavirus disease (COVID-19) pandemic has raised concern of transmission of infectious organisms through aerosols formation in endonasal and transoral surgery.

Methods

Retrospective review. We introduce the negative-pressure otolaryngology viral isolation drape (NOVID) system to reduce the risk of aerosol. NOVID consists of a plastic drape suspended above the patient's head and surgical field with a smoke evacuator suction placed inside the chamber.

Results

Four patients underwent endonasal (4) and endo-oral surgery (1). Fluorescein was applied to the surgical field. Black light examination of fluorescein-treated operative fields revealed minimal contamination distant to the surgical field. In two prolonged cases with high-speed drilling, droplets were identified under the barrier and on the tip of the smoke evacuator. Instruments and cottonoids appeared to be a greater contributor to field contamination.

Conclusions

Negative-pressure aspiration of air under a chamber barrier, which appears to successfully keep aerosol and droplet contamination to a minimum.

Background

Epithelial remodeling is a histopathologic feature of chronic inflammatory airway diseases including chronic rhinosinusitis (CRS). Cell-type shifts and their relationship to CRS endotypes and severity are incompletely described.

Objective

We sought to understand the relationship of epithelial cell remodeling to inflammatory endotypes and disease outcomes in CRS.

Methods

Using cell-type transcriptional signatures derived from epithelial single-cell sequencing, we analyzed bulk RNA-sequencing data from sinus epithelial brushings obtained from patients with CRS with and without nasal polyps in comparison to healthy controls.

Results

The airway epithelium in nasal polyposis displayed increased tuft cell transcripts and decreased ciliated cell transcripts along with an IL-13 activation signature. In contrast, CRS without polyps showed an IL-17 activation signature. IL-13 activation scores were associated with increased tuft cell, goblet cell, and mast cell scores and decreased ciliated cell scores. Furthermore, the IL-13 score was strongly associated with a previously reported activated ("polyp") tuft cell score and a prostaglandin E2 activation signature. The Lund-Mackay score, a computed tomographic metric of sinus opacification, correlated positively with activated tuft cell, mast cell, prostaglandin E2, and IL-13 signatures and negatively with ciliated cell transcriptional signatures.

Conclusions

These results demonstrate that cell-type alterations and prostaglandin E2 stimulation are key components of IL-13-induced epithelial remodeling in nasal polyposis, whereas IL-17 signaling is more prominent in CRS without polyps, and that clinical severity correlates with the degree of IL-13-driven epithelial remodeling.

Chronic type 2 (T2) inflammatory diseases of the respiratory tract are characterized by mucus overproduction and disordered mucociliary function, which are largely attributed to the effects of IL-13 on common epithelial cell types (mucus secretory and ciliated cells). The role of rare cells in airway T2 inflammation is less clear, though tuft cells have been shown to be critical in the initiation of T2 immunity in the intestine. Using bulk and single-cell RNA sequencing of airway epithelium and mouse modeling, we found that IL-13 expanded and programmed airway tuft cells toward eicosanoid metabolism and that tuft cell deficiency led to a reduction in airway prostaglandin E2 (PGE2) concentration. Allergic airway epithelia bore a signature of PGE2 activation, and PGE2 activation led to cystic fibrosis transmembrane receptor-dependent ion and fluid secretion and accelerated mucociliary transport. These data reveal a role for tuft cells in regulating epithelial mucociliary function in the allergic airway.