Case Presentation:
A 55 year old male with past medical history significant for congestive heart failure, severe persistent asthma and eosinophilic pneumonia on chronic prednisone and status post bronchial thermoplasty presented with fever, cough, shortness of breath and chest pain of 2 weeks and hemoptysis of 3 days duration. He also had two recent hospitalizations for pneumonia. At presentation, he had respiratory rate of 28 per min with SPO2 in mid 80s. He was afebrile with normal blood pressure. He had bilateral diffuse crackles and bipedal edema. Complete blood count had leukocytosis of 17,000/mm3. Comprehensive metabolic panel was unremarkable except for albumin of 2.8 gm/dl. Arterial blood gas(ABG) showed respiratory alkalosis and SPO2-86% on 40% FiO2. Chest X-ray(CXR) and computed tomography(CT) thorax suggested multifocal pneumonia. He underwent bronchoscopy after elective intubation. He then started spiking fever. He was on piperacillin/tazobactam, vancomycin, levofloxacin and atovaquone. ABG and CXR suggested severe ARDS. Vent was changed to Duo positive airway pressure (DuoPap). He was proned intermittently. Cultures of bronchial aspirate grew Nocardia Otitidiscaviarum after 6 days. His antibiotics were switched to amikacin and imipenum. His respiratory status continued to worsen. Inhaled Nitric oxide was used but there was no improvement. Family mentioned that he would not have wanted to continue in his current state for long. He passed away on comfort care measures.
Discussion:
Nocardia can cause pulmonary, cutaneous and disseminated infections. Pulmonary nocardiosis can be acute, subacute or chronic. Most of the patients with pulmonary nocardiosis have underlying lung pathology like COPD, TB or malignancy and 2/3rd of them are immunosuppressed. Our patient had severe persistent asthma, he was on chronic steroid therapy and had recurrent pneumonia. Given it’s low pathogenecity, N. Otitidiscaviarum infection is much less common than other Nocardia. The mortality rate from ARDS from any cause can range from 26% to 58%. The data on mortality from pulmonary nocardiosis is sparse but can be as high as 41%.
Conclusions:
Clinical suspicion for Nocardia should be established when risk factors are present and there is no clinical improvement on treating conventional organisms; laboratory should be notified of suspicion. Given the difficulty in isolating and Nocardiosis not being a mandatory reportable infection, the true morbidity and mortality from it might be higher than currently reported.
