Post by Nadica (She/Her) on Jul 28, 2024 2:42:08 GMT
A Case of COVID-19 and Pneumocystis jirovecii Coinfection - Published July 1, 2020
To the Editor:
Lymphocytopenia has been identified as a common laboratory finding in patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, particularly among those with more severe presentations (1); however, there are limited data on which specific lymphocyte populations may be affected or the clinical sequelae. In this report, we describe the case of a woman with hypoxemic respiratory failure found to have coinfection with SARS-CoV-2 and Pneumocystis jirovecii, a pathogen commonly seen in patients with defects in T-cell immunity.
An 83-year-old female nonsmoker presented to our hospital on March 12, 2020, with fevers, malaise, headache, dry cough, and dyspnea. She had a history of mild intermittent asthma, managed with an albuterol inhaler as needed, mitral valve prolapse with moderate to severe mitral regurgitation, and mild to moderate ulcerative colitis, which was well controlled on oral budesonide (3 mg daily and being tapered) as well as maintenance-dose sulfasalazine (1,500 mg twice daily). Her symptoms had started approximately 2 weeks prior to presentation, shortly after travel from Florida to Massachusetts, and had failed to improve with courses of azithromycin and amoxicillin-clavulanate. In the emergency department, she had a fever of 39.3°C and oxygen saturation of 86% on room air, which improved to 95% on 5 L/min of supplemental oxygen by nasal cannula. Initial laboratory evaluation revealed leukocytosis and relative lymphocytopenia (absolute lymphocyte count, 1,090 cells/μl) (Table 1). Chest computed tomography was notable for diffuse bilateral ground-glass opacities with patchy bands of atelectasis and small nodular foci of consolidation with a distribution suggestive of a viral pneumonia. Subtle cystic changes were also seen in the affected regions (Figure 1). She was admitted to the medical intensive care unit and placed on strict isolation precautions given concern for community-acquired SARS-CoV-2. She developed worsening tachypnea with a respiratory rate of 40 breaths/min and hypoxia with an oxygen saturation of 80% requiring supplemental oxygen through a nonrebreather mask at a rate of 15 L/min. An arterial blood gas measurement showed a PaO2 of 63 mm Hg on 15 L/min of supplemental oxygen. She was intubated for hypoxemic respiratory failure and supported on low Vt ventilation according to the Acute Respiratory Distress Syndrome Network lower Vt protocol. Her PaO2/FiO2 was consistent with moderate acute respiratory distress syndrome.
To the Editor:
Lymphocytopenia has been identified as a common laboratory finding in patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, particularly among those with more severe presentations (1); however, there are limited data on which specific lymphocyte populations may be affected or the clinical sequelae. In this report, we describe the case of a woman with hypoxemic respiratory failure found to have coinfection with SARS-CoV-2 and Pneumocystis jirovecii, a pathogen commonly seen in patients with defects in T-cell immunity.
An 83-year-old female nonsmoker presented to our hospital on March 12, 2020, with fevers, malaise, headache, dry cough, and dyspnea. She had a history of mild intermittent asthma, managed with an albuterol inhaler as needed, mitral valve prolapse with moderate to severe mitral regurgitation, and mild to moderate ulcerative colitis, which was well controlled on oral budesonide (3 mg daily and being tapered) as well as maintenance-dose sulfasalazine (1,500 mg twice daily). Her symptoms had started approximately 2 weeks prior to presentation, shortly after travel from Florida to Massachusetts, and had failed to improve with courses of azithromycin and amoxicillin-clavulanate. In the emergency department, she had a fever of 39.3°C and oxygen saturation of 86% on room air, which improved to 95% on 5 L/min of supplemental oxygen by nasal cannula. Initial laboratory evaluation revealed leukocytosis and relative lymphocytopenia (absolute lymphocyte count, 1,090 cells/μl) (Table 1). Chest computed tomography was notable for diffuse bilateral ground-glass opacities with patchy bands of atelectasis and small nodular foci of consolidation with a distribution suggestive of a viral pneumonia. Subtle cystic changes were also seen in the affected regions (Figure 1). She was admitted to the medical intensive care unit and placed on strict isolation precautions given concern for community-acquired SARS-CoV-2. She developed worsening tachypnea with a respiratory rate of 40 breaths/min and hypoxia with an oxygen saturation of 80% requiring supplemental oxygen through a nonrebreather mask at a rate of 15 L/min. An arterial blood gas measurement showed a PaO2 of 63 mm Hg on 15 L/min of supplemental oxygen. She was intubated for hypoxemic respiratory failure and supported on low Vt ventilation according to the Acute Respiratory Distress Syndrome Network lower Vt protocol. Her PaO2/FiO2 was consistent with moderate acute respiratory distress syndrome.