Background: Coronavirus disease 2019 , caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), involves multiple organs. Testicular involvement is largely unknown. Objective: To determine the pathological changes and whether SARS-CoV-2 can be detected in the testes of deceased COVID-19 patients. Design, setting, and participants: Postmortem examination of the testes from 12 COVID-19 patients was performed using light and electron microscopy, and immunohistochemistry for lymphocytic and histiocytic markers. Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the virus in testicular tissue. Outcome measurements and statistical analysis: Seminiferous tubular injury was assessed as none, mild, moderate, or severe according to the extent of tubular damage. Leydig cells in the interstitium were counted in ten 400Â microscopy fields. Results and limitations: Microscopically, Sertoli cells showed swelling, vacuolation and cytoplasmic rarefaction, detachment from tubular basement membranes, and loss and sloughing into lumens of the intratubular cell mass. Two, five, and four of 11 cases showed mild, moderate, and severe injury, respectively. The mean number of Leydig cells in COVID-19 testes was significantly lower than in the control group (2.2 vs 7.8, p < 0.001). In the interstitium there was edema and mild inflammatory infiltrates composed of T lymphocytes and histiocytes. Transmission EM did not identify viral particles in three cases. RT-PCR detected the virus in one of 12 cases. Conclusions: Testes from COVID-19 patients exhibited significant seminiferous tubular injury, reduced Leydig cells, and mild lymphocytic inflammation. We found no evidence of SARS-CoV-2 virus in the testes in the majority (90%) of the cases by RT-PCR, and in none by electron microscopy. These findings can provide evidence-based guidance for sperm donation and inform management strategies to mitigate the risk of testicular injury during the COVID-19 disease course.
The lung tissue microbiota features of 20 deceased patients with COVID-19 To the EditorWe read with great interest the article by Yanan Chu and colleagues, accepted for publication in the Journal of Infection. 1 Secondary infection and sepsis are common complications in critically ill patients with COVID-19, 2 , 3 but the underlying pathogen is not clear. We investigated the microbiota characteristics of lung tissue from 20 deceased COVID-19 patients. All cases met the COVID-19 clinical diagnostic criteria provided by the
Aims: Coronavirus Disease 2019 (COVID-19) caused by Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) infection has been deemed as a global pandemic by World Health Organization. While diffuse alveolar damage (DAD) is recognized to be the primary manifestation COVID-19 pneumonia, there has been little emphasis on the progression to the fibrosing phase of DAD. This topic is of great interest due to growing concerns regarding the potential long-term complications in prolonged survivors. Methods: Here we report a detailed histopathologic study of thirty autopsy cases with COVID-19 virus infection, based on minimally invasive autopsies performed between February to March, 2020. Results: The mean age was 69 years, with twenty (67%) males and 10 (33%) females and frequent (70.0%) underlying comorbidities. The duration of illness ranged from 16 to 82 (median=42) days. Histologically, the most common manifestation was diffuse alveolar damage (DAD) in 28 (93.3%) cases which showed predominantly acute (32%), organizing (25%), and/or fibrosing (43%) patterns. Patients with fibrosing DAD were one decade younger (p=0.034) and they had a longer duration of illness (p=0.033), hospitalization (p=0.037) and mechanical ventilation (p=0.014) compared to those with acute DAD. Patients with organizing DAD had a longer duration of illness (p=0.032) and hospitalization (p=0.023) compared to those with acute DAD. Conclusions: COVID-19 pneumonia patients who develop DAD can progress to the fibrosing pattern. While we observed fibrosing DAD in fatal cases, whether surviving patients are at risk for developing pulmonary fibrosis and the frequency of this complication will require further clinical and radiologic follow-up studies.
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