A 39-year-old woman with systemic lupus erythematosus treated with anti-CD20 monoclonal antibody rituximab was admitted to our hospital with COVID-19 pneumonia. Despite receiving dexamethasone, she developed hypoxaemia and persistent lung opacities. As bronchoalveolar lavage was suggestive of cryptogenic organising pneumonia, high-dose corticosteroid was administered, and she received antimicrobial therapy for opportunistic infections without improvement. Reverse transcription PCR was repeatedly positive for SARS-CoV-2, and virus replication was confirmed in cell cultures. As no anti-SARS-CoV-2 antibodies were detected more than 100 days after symptom onset, she was treated with convalescent plasma with fast clinical improvement, returning home days later. Our case shows that persistent SARS-CoV-2 infection in an immunocompromised patient may be overturned with the appropriate treatment.

Eikenella corrodens is a normal inhabitant of the human oral cavity and gastrointestinal and genitourinary tracts. Pleuropulmonary infections by this microorganism are uncommon. Pulmonary aspiration is a chief predisposing condition. Although the outcome is usually favorable, its distinctive antibiotic sensitivity pattern makes bacterial identification an important feature in dealing with this infection. The authors report a case of pleural empyema caused by co-infection with Eikenella corrodens and Porphyromonas asaccharolytica, in an immunocompetent diabetic patient with obstructive sleep apnea syndrome, followed by a discussion on the role of noninvasive ventilation in the development of this infection.

No abstract

Background: Amyloid fibrils are protein polymers. Functional amyloids play a beneficial role in a variety of physiologic processes. Amyloidosis results from the accumulation of pathogenic amyloids in a variety of tissues. Case Presentation: The authors present a case of a 60-year-old male with a pseudotumoral silicosis, a history of intermittent fever, and renal insufficiency with intermittent proteinuria (maximum of 3 g/dl). The diagnosis of amyloidosis was made from multiple biopsies. During the investigation, it was never possible to characterize the subtype of amyloidosis [the patient had findings either in favor of AL amyloidosis and AA amyloidosis (AA)]. A definite diagnosis was only obtained from an autopsy, and AA was found to be the subtype. Conclusion: At the time of this publication and to the best of authors’ knowledge, AA has never been described to be associated with pseudotumoral form of pulmonary silicosis. We believe that an inflammatory response associated with pulmonary silicosis was the trigger to the development of AA.