Case Presentation: A 58-year-old immunocompetent female with PMHx asthma, obesity and unvaccinated for COVID-19 who presented with 10 days of worsening nonproductive cough, SOB, fatigue, and loss of appetite. Exam was notable for tachypnea with diffusely diminished air movement throughout posterior lung fields. Relevant labs included CRP 15.2 mg/dL, procalcitonin 0.20 ng/mL, blood glucose 343 mg/dL and beta-hydroxybutyrate 4.80 mmol/L. CT Chest revealed peripheral ground glass density and consolidation predominantly involving the lower two thirds of both lungs. Patient was admitted for COVID PNA and new onset diabetes mellitus with DKA. Initially requiring 14L HFNC, was started on 7-day course of Dexamethasone with Remdesivir and Tocilizumab. Amid increasing oxygen requirements and rapid escalation to BiPAP, patient was escalated to ICU for acute respiratory failure intensifying a second round of 14-day course of Dexamethasone. Clinical improvement with decline in oxygen requirements and inflammatory markers soon followed but by the fourth week, hypoxia worsened and a rising CRP with peak elevation at 31.9 mg/dL ensued. Repeat CT Chest showed interval progression of multifocal consolidation with evidence of early cavitation in both apices prompting initiation of Bactrim for Pneumocystis Jiroveci prophylaxis and third round of steroids. Subsequent workup for Cryptococcal Ag, Histoplasma Ag, Quantiferon and Fungitell were all negative. Five days later, Aspergillus Ag was positive bolstering a simultaneous Pulmonary Aspergillosis. Immediately started on Isavuconazole for three-months duration with continued Bactrim prophylaxis and discharged on 6L NC with drastic improvement in CRP 1.7 mg/dL.
Discussion: Given the quandary faced in the treatment of severe COVID-19 infections requiring supplemental oxygen with significantly elevated inflammatory markers, predisposition to secondary infections is imminent. Not only due respiratory viruses cause direct damage to airway epithelium and hamper ciliary clearance thus facilitating aspergillus to invade tissue, but ongoing immunosuppressive therapy further hinders the activity of alveolar macrophages thereby enabling the germination of aspergillus spores. There has been an increasing number of reported CAPA infections in correlation with critically ill patients on mechanical ventilation. While classification of CAPA relies on promising diagnostic modalities to include bronchoalveolar fluid and tracheal aspirate, these are associated with aerosol generation and high risk of viral transmission posing not only a great risk but an added dilemma. Biomarker testing with variable sensitivity and specificity of aspergillus PCR, serum galactomannan and serum (1,3)-β-D-glucan make diagnosis difficult but are still rendered valuable.
Conclusions: CAPA is frequently observed in patients with profound underlying immunosuppression leading to complications with invasive aspergillosis and worsening the disease course of COVID-19. Immunocompetent individuals having received steroid therapy pose a more insidious risk of secondary co-infection with aspergillus species given increased vulnerability of immune dysregulation in the setting of epithelial lung damage. Owing to aggressive workup, our patient was diagnosed swiftly and avoided intubation further depicting the need to assess concomitant risk factors from underlying medical conditions in association with longevity of immunosuppressive therapy.
