Dexamethasone provides benefits in patients with coronavirus disease 2019 (COVID-19), although data regarding immunological profiles and viral clearance are limited. This study aimed to evaluate for differences in biomarkers among patients with severe COVID-19 who did and did not receive dexamethasone. We measured plasma biomarkers of lung epithelial/endothelial injury and inflammation in 31 patients with severe COVID-19 and in 13 controls. Changes in biomarkers and clinical parameters were compared during the 7-day period among COVID-19 patients, and also according to dexamethasone use. Thirty-two patients with severe COVID-19 who received mechanical ventilation (n = 6), high-flow nasal cannula (n = 11), and supplemental oxygen (n = 15) were analyzed. Relative to controls, patients with severe COVID-19 had significantly higher concentrations of biomarkers related to glycocalyx shedding (endocan and syndecan-1), endothelial injury (von Willebrand factor), and inflammation (soluble receptor for advanced glycation end-products [sRAGE] and interleukin-6). The 7-day decreases in biomarkers of endothelial injury (angiopoietin-2 [Ang-2] and intercellular adhesion molecule-1 [ICAM-1]) and sRAGE, but not in the biomarker of lung epithelial injury (surfactant protein D), were correlated with decreases in C-reactive protein and radiologic score at day 7. Twenty patients (63%) received dexamethasone, and the dexamethasone and non-dexamethasone groups differed in terms of disease severity. However, dexamethasone was associated marginally with increased SpO2/FiO2 and significantly with decreases in C-reactive protein and radiologic score after adjusting for baseline imbalances. Furthermore, the dexamethasone group exhibited a significant decrease in the concentrations of Ang-2, ICAM-1, soluble form of the Tie2 receptor (a biomarker of glycocalyx shedding), and sRAGE. Both groups exhibited a clinically insignificant increase in the cycle threshold value. Severe COVID-19 may be characterized by more severe endothelial injury and inflammation, and less severe lung epithelial injury. There is a possibility that dexamethasone improved severe COVID-19 and related endothelial injury without delaying viral clearance.
Recently, several studies have revealed that commercial microbial identification systems do not accurately identify the uncommon causative species of candidiasis, including ,, and . We investigated the accuracy of species-level identification in a collection of clinical isolates previously identified as ( = 38), ( = 1 2), and ( = 5) by the Vitek 2 system. All 55 isolates were re-analyzed by the Phoenix system (Becton Dickinson Diagnostics), two matrix-assisted laser desorption ionization-time of flight mass spectrometry analyzers (a Vitek MS and a Bruker Biotyper), and by sequencing of internal transcribed spacer (ITS) regions or 26S rRNA gene D1/D2 domains. Among 38 isolates previously identified as by the Vitek 2 system, the majority (27/38 isolates, 71.1%) were identified as (20 isolates) or C. albicans (7 isolates) by ITS sequencing, and none was identified as . Among 20 isolates that were identified as, 17 (85%) were isolated from urine. The two isolates that were identified as by ITS sequencing originated from ear discharge. The Phoenix system did not accurately identify, , or. The correct identification rate for 55 isolates was 92.7% (51/55 isolates) for the Vitek MS and 94.6% (52/55 isolates) for the Bruker Biotyper, as compared with results from ITS sequencing. These results suggest that is very rare in Korea, and that the possibility of misidentification should be noted when an uncommon species is identified.
a b s t r a c tBacterial and viral coinfected community-acquired pneumonia (CAP) is poorly characterized in adults. The aim of this study was to investigate the influence of bacterial and viral coinfection in patients with CAP. A total of 235 adults who requested molecular tests of pneumonia and were diagnosed with CAP were enrolled in this study. Microbiological tests included blood and sputum cultures, PCR for bacterial and viral pathogens, antigen test for Streptococcus pneumoniae and the influenza virus, and antibody detection of Mycoplasma pneumonia. Of the 235 patients, 32 (13.6%) patients were coinfected with bacteria and virus. Among 64 severe CAP patients, the concurrent infections were confirmed in 14 patients (21.9%). The proportion of severe pneumonia was significantly higher in patients with coinfection, and they showed a significantly higher mortality rate. In conclusion, bacterial and viral coinfection in CAP is not a rare occurrence in adults. Viral and bacterial coinfections have an adverse impact on the severity of the pneumonia, and increase morbidity and mortality in patients with CAP.
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