Arifa Parker, Jane Shaw, Sumanth Karamchand, Sa’ad Lahri, Neshaad Schrueder, Mogamat-Yazied Chothia, Abdurasiet Mowlana, Usha Lalla, Brian Allwood, Coenraad Koegelenberg, Jantjie Taljaard
Department of Medicine, Faculty of Medicine and Health Sciences, Stellenbosch University and Tygerberg Hospital, Cape Town, South Africa
Date of presentation: 26 March 2020
Case presentation: A 41-year-old man, known with HIV, presented to our centre with acute hypoxaemic respiratory failure. He complained of a 12-day history of fever, a non-productive cough, myalgia, diarrhoea, and gradually worsening dyspnoea. He was employed as a taxi driver, and provided transport to international travellers for up to one day prior to symptom onset. He was unable to recall if any of the passengers had flu-like symptoms. Three days prior to admission, he presented to his local community health centre specifically requesting a test for COVID-19; however, he did not meet the case definition at the time and was treated symptomatically. He was receiving a fixed drug combination of antiretroviral therapy (tenofovir, emtricitabine and efavirenz) since 2016. No recent CD4 count was available but he had an undetectable viral load 6-months prior to this presentation. He was initially admitted to an isolation ward but required intubation due to rapid clinical deterioration and was transferred to the intensive care unit (ICU).
Physical examination: He had evidence of acute hypoxaemic respiratory failure with peripheral oxygen saturation of 73% while breathing ambient air, and a respiratory rate of 28 breaths per minute. Chest examination revealed symmetrical crackles.
Laboratory findings: Initial biochemistry revealed lymphopaenia of 0.56 x 10^9/L (normal range: 1.4 - 4.2 x 10^9/L), mild thrombocytopenia of 166 x 10^9/L (normal range: 171 - 388 x 10^9/L), a CD4 count of 78 cells/µL, CRP was 225 mg/L (normal: < 10 mg/L), and procalcitonin was 0.97 µg/L (normal: < 0.1 µg/L). Mild hepatic transaminitis was also present with normal kidney function.
Pertinent imaging: Chest radiograph (Figure 1) demonstrated diffuse, bilateral, ground glass opacification and patchy areas of consolidation.
Treatment: Due to the HIV co-infection, our differential diagnosis included Pneumocystis jirovecii pneumonia (PCP), influenza, pulmonary tuberculosis and bacterial pneumonia. Due to his clinical picture of acute severe respiratory illness, COVID-19 pneumonitis was included in the differential diagnosis. He was started empirically on intravenous amoxicillin-clavulanic acid and azithromycin for severe community acquired pneumonia, as well as trimethoprim-sulfamethoxazole for presumed PCP. Empiric oseltamivir was withheld as his symptoms had been present for more than 72-hours. Subsequent testing of endotracheal aspirates confirmed a positive polymerase chain reaction (PCR) for SARS-CoV-2, with a negative multiplex respiratory virus panel, negative Xpert MTB/RIF Ultra for tuberculosis, negative bacterial staining and culture and negative immunofluorescence for Pneumocystis jirovecii. Due to the low sensitivity of the latter, a serum (1,3)-β-D-glucan assay was requested which was negative. After 3-weeks, he continues to require mechanical ventilation.
Lessons learned: This case highlights the diagnostic and therapeutic challenges of HIV patients presenting with acute hypoxaemic respiratory failure during the COVID-19 pandemic. The differential diagnosis remains broad. PCP shares many clinical and radiographic features with COVID-19 pneumonitis and therefore it is important to maintain a high index of clinical suspicion for both infections. In our setting, the diagnosis of PCP in HIV patients is usually made on clinical grounds together with characteristic chest radiographic features. During the COVID-19 pandemic we recommend further diagnostic testing when PCP is considered including an expectorated sputum sample, or tracheal aspirate if the patient is intubated, for Pneumocystis jirovecii PCR or immunofluorescence and serum for (1,3)-β-D-glucan. Due to the potential for generating aerosols, obtaining an induced sputum sample for PCP testing is currently not advised. A negative sputum sample in conjunction with a negative serum (1,3)-β-D-glucan assay has been shown to have a high negative predictive value for excluding PCP. Accurate distinction between COVID-19 and PCP is also important because current treatment guidelines for PCP in HIV patients include the addition of oral steroids, while the latter may be contraindicated for COVID-19 pneumonitis.
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