A 76-year-old man presented to a quaternary care hospital with a 6-day history of respiratory symptoms, fatigue and a fainting episode. The patient had a resolving postinfectious dry cough from an upper respiratory infection that occurred 3 months before presentation. He had hypertension, gastritis, diabetes, sciatica, a remote 30 pack-year smoking history and no history of recreational drug use. His medications included metformin and rosuvastatin. He worked as a professor and attended language classes.In early March, our patient was informed of a potential classroom exposure to coronavirus disease 2019 (COVID-19). One week after this exposure, he had an outpatient nasopharyngeal swab for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) after 2 days of worsening cough. The results were negative for both the envelope and RNA-dependent RNA polymerase genes, which are common targets for polymerase chain reaction (PCR) amplification of SARS-CoV-2. A worsening dry cough, fatigue, exertional dyspnea, fevers, low appetite and diarrhea developed over the next 4 days. He presented to the emergency department 4 days after his first swab for SARS-CoV-2 (11 d after his potential exposure).The patient was admitted to hospital and placed under droplet and contact precautions. His initial vital signs included a body temperature of 38.6°C, blood pressure of 98/55 mm Hg with an orthostatic drop, pulse 94 beats/min, and a respiratory rate of 18 breaths/ min with an oxygen saturation of 96% on room air. A physical examination showed flat neck veins, and he had mild inspiratory bibasilar crackles. Bloodwork showed lymphopenia, but electrolytes and hepatic and renal function tests were normal. Chest radiography showed ill-defined right basal airspace opacification.We started treatment with crystalloids administered intravenously and ceftriaxone and azithromycin for pneumonia. Blood and stool culture tests performed on admission were negative; influenza A, influenza B and respiratory syncytial virus were not present; and a repeat nasopharyngeal swab for SARS-CoV-2 on admission also returned a negative result.On day 3 after admission, our patient became hypoxemic and he required 2 L/min of oxygen. Repeat radiography of the chest showed new bilateral, ill-defined patchy opacities. Results for an extended viral panel, legionella urinary antigen and a third nasopharyngeal swab for SARS-CoV-2 were negative. Consequently, we stopped droplet and contact precautions on day 3 of admission. A computed tomography (CT) scan of the chest showed bilateral ground glass opacification and septal lines (Figure 1). This was consistent with atypical bacterial or viral infection, and our differential diagnosis included edema, hemorrhage, drug reaction and connective tissue disease.On day 4 of admission, our patient's hypoxemia worsened and he required 5 L/min of oxygen. We consulted our respirology department. Given his history of progressive symptoms, persistent lymphopenia and potential exposure to a student with COVID-19, we were advised to...