A 45-year old male presented to the ED with mild fever, sneezing, rhinorrhea, cough, right-sided dull chest pain and shortness of breath. He was recently exposed to a co-worker suffering from 'flu' and started experiencing upper respiratory tract infection symptoms two days ago. He was nauseous, vomited several times and suffered from diarrhea. The persistent dull chest pain and worsening exertional shortness of breath for a day prompted the ED visit. His past medical history was significant for Crohn s disease for which he was not on any medication. The patient was a smoker of about half a pack per day and denied any history of alcohol or recreational drug abuse. He traveled to South Africa twenty-three years ago and didn t have any pet at home. No personal history of tuberculosis (TB) or known exposure to anyone with TB. He worked at a fast-food restaurant and did not have any family history of vasculitis or lung cancer. Vital signs on admission were, a blood pressure of 135/89 mmHg, a pulse of 124 beats per minutes, a temperature of 37.8 C, a respiratory rate of 23 breaths per minute and oxygen saturation of 94% on 5L oxygen via nasal cannula. Physical examination showed a young man in mild distress from tachypnea.
He appeared dehydrated. Chest auscultation revealed bronchial breath sound and coarse crackles in the right mid and lower lung zone, both anteriorly and posteriorly. The rest of the examination was normal. Blood work was significant for leukocytosis, 27.1 x103/micro L with neutrophilia of 88% and bandemia of 3%. The rest of the complete blood count and comprehensive metabolic panel were normal. His lactic acid was 1.5mmol/L, and procalcitonin level was elevated at 0.69ng/ml. The chest X-ray is shown in Figure 1. A computed tomography (CT) of the chest was performed and representative slices are shown in Figure 1. The respiratory viral panel was positive for coronavirus. Sputum gram stain and culture showed normal respiratory flora. Urinary antigen testing for legionella and pneumococcus were negative. A workup for vasculitic disorders was negative. HIV antibody test was also negative. A diagnosis of necrotizing pneumonia due to secondary bacterial infection in the setting of coronavirus infection was made. Staphylococcus aureus (SA) was strongly suspected to be the etiologic agent. However, the patient was less toxic appearing than what would be expected with SA necrotizing pneumonia and a subacute vasculitic disorder, like granulomatosis with polyangiitis, was also considered.
Cavitary pneumonia with a fungal pathogen and lung malignancy were other possibilities, but no significant risk factors, such as prolonged neutropenia, chronic steroid use or prior structural lung disease were present. The patient was started on linezolid and meropenem. High-flow oxygen was used to achieve acceptable oxygen saturation level. Repeat chest X-rays on day one, two and three are shown in Figure 2. A repeat CT scan was obtained on day three to identify the structural lung damage better (Figure 3). He developed progressive respiratory failure requiring intubation and mechanical ventilation. An ultrasound revealed complex pleural effusion (Figure 4). A chest tube was inserted and 1.4L of frank pus was drained. A large air leak was noted from bronchopleural fistula (BPF) due to rupture of the abscess cavity in the pleural space. Pleural fluid analysis showed 457,000 leukocyte per cubic milliliter with 99% neutrophil, pH 6.9, glucose < 10mg/dL, protein 4.3gm/dL and lactate dehydrogenase > 10,000 IU/L. The culture was positive for SAG, species S constellatus. The patient was treated with ceftriaxone with subsequent improvement. He got liberated from mechanical ventilation. The BPF resolved, and the chest tube was successfully removed (Figure 5). He was completely functional during his outpatient visit a month later.