Nosocomial Trichosporon asahii Fungemia in a Patient with Secondary Hemochromatosis: A Rare Case Report

Trichosporon asahii (formerly known as T. beigelii) is an emerging, life-threatening opportunistic pathogen, especially in severely granulocytopenic patients with underlying hematological malignancies. Other reported predisposing factors for infection with this pathogen include organ transplantation, extensive burns, human immunodeficiency virus infection, corticosteroid therapy, prosthetic valve surgery, and peritoneal dialysis. We report a 53-year-old nongranulocytopenic female with secondary hemochromatosis, who developed nosocomial fungemia caused by T. asahii. This case suggests that clinicians should be aware that T. asahii fungemia can develop in nongranulocytopenic patients with secondary hemochromatosis

Analysis of Erythrocyte C4d to Complement Receptor 1 Ratio: Use in Distinguishing between Infection and Flare-Up in Febrile Patients with Systemic Lupus Erythematosus

Objective. Fever in systemic lupus erythematosus (SLE) can be caused by infection or flare-up of the disease. This study aimed to determine whether the ratio of the level of erythrocyte-bound C4d to that of complement receptor 1 (C4d/CR1) can serve as a useful biomarker in the differentiation between infection and flare-up in febrile SLE patients. Methods. We enrolled febrile SLE patients and determined the ratio on the day of admission. The patients were divided into 2 groups according to the subsequent clinical course. Results. Among the febrile SLE patients, those with flare-up had higher ratios and lower C-reactive protein (CRP) levels than those with infection. Cut-off values of <1.2447 and >4.67 for C4d/CR1 ratio and CRP, respectively, were 40.91% sensitive and 100.0% specific for the presence of infection in febrile SLE patients; similarly, cut-off values of >1.2447 and <2.2, respectively, were 80% sensitive and 100% specific for the absence of infection in febrile SLE patients. Conclusion. The C4d/CR1 ratio is a simple and quickly determinable biomarker that enables the differentiation between infection and flare-up in febrile SLE patients at initial evaluation. Further, when combined with the CRP level, it is useful to evaluate disease activity in SLE patients with infection

Clinical Application of Ultraviolet C Inactivation of Severe Acute Respiratory Syndrome Coronavirus 2 in Contaminated Hospital Environments

To overcome the ongoing coronavirus disease 2019 (COVID-19) pandemic, transmission routes, such as healthcare worker infection, must be effectively prevented. Ultraviolet C (UVC) (254 nm) has recently been demonstrated to prevent environmental contamination by infected patients; however, studies on its application in contaminated hospital settings are limited. Herein, we explored the clinical application of UVC and determined its optimal dose. Environmental samples (n = 267) collected in 2021 were analyzed by a reverse transcription-polymerase chain reaction and subjected to UVC irradiation for different durations (minutes). We found that washbasins had a high contamination rate (45.5%). SARS-CoV-2 was inactivated after 15 min (estimated dose: 126 mJ/cm2) of UVC irradiation, and the contamination decreased from 41.7% before irradiation to 16.7%, 8.3%, and 0% after 5, 10, and 15 min of irradiation, respectively (p = 0.005). However, SARS-CoV-2 was still detected in washbasins after irradiation for 20 min but not after 30 min (252 mJ/cm2). Thus, 15 min of 254-nm UVC irradiation was effective in cleaning plastic, steel, and wood surfaces in the isolation ward. For silicon items, such as washbasins, 30 min was suggested; however, further studies using hospital environmental samples are needed to confirm the effective UVC inactivation of SARS-CoV-2

Immunological Aspects of SARS-CoV-2 Infection and the Putative Beneficial Role of Vitamin-D

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is still an ongoing global health crisis. Immediately after the inhalation of SARS-CoV-2 viral particles, alveolar type II epithelial cells harbor and initiate local innate immunity. These particles can infect circulating macrophages, which then present the coronavirus antigens to T cells. Subsequently, the activation and differentiation of various types of T cells, as well as uncontrollable cytokine release (also known as cytokine storms), result in tissue destruction and amplification of the immune response. Vitamin D enhances the innate immunity required for combating COVID-19 by activating toll-like receptor 2. It also enhances antimicrobial peptide synthesis, such as through the promotion of the expression and secretion of cathelicidin and β-defensin; promotes autophagy through autophagosome formation; and increases the synthesis of lysosomal degradation enzymes within macrophages. Regarding adaptive immunity, vitamin D enhances CD4+ T cells, suppresses T helper 17 cells, and promotes the production of virus-specific antibodies by activating T cell-dependent B cells. Moreover, vitamin D attenuates the release of pro-inflammatory cytokines by CD4+ T cells through nuclear factor κB signaling, thereby inhibiting the development of a cytokine storm. SARS-CoV-2 enters cells after its spike proteins are bound to angiotensin-converting enzyme 2 (ACE2) receptors. Vitamin D increases the bioavailability and expression of ACE2, which may be responsible for trapping and inactivating the virus. Activation of the renin–angiotensin–aldosterone system (RAS) is responsible for tissue destruction, inflammation, and organ failure related to SARS-CoV-2. Vitamin D inhibits renin expression and serves as a negative RAS regulator. In conclusion, vitamin D defends the body against SARS-CoV-2 through a novel complex mechanism that operates through interactions between the activation of both innate and adaptive immunity, ACE2 expression, and inhibition of the RAS system. Multiple observation studies have shown that serum concentrations of 25 hydroxyvitamin D are inversely correlated with the incidence or severity of COVID-19. The evidence gathered thus far, generally meets Hill’s causality criteria in a biological system, although experimental verification is not sufficient. We speculated that adequate vitamin D supplementation may be essential for mitigating the progression and severity of COVID-19. Future studies are warranted to determine the dosage and effectiveness of vitamin D supplementation among different populations of individuals with COVID-19