Our patient’s hospital admission chest CT scan revealed bullous emphysematous changes of the bilateral apices and the right middle and lower lung fields; extensive consolidation and bleb formation of the right middle and lower lobes with bronchiectatic changes; and right pleural thickening. There was also a left pleural effusion with compressive atelectasis and early infiltrates in the left lower lobe, and extensive mediastinal lymphadenopathy. Therapy with ceftriaxone and levofloxacin was started for the treatment of suspected community-acquired pneumonia. Thoracentesis was not performed, as the left pleural effusion was small and the risk of pneumothorax was thought to be high due to underlying bullous emphysema. Therapy with ceftriaxone was switched to piperacillin-tazobactam as the patient became febrile and leukocytosis developed. Cultures of blood, sputum, BAL fluid, and transbronchial biopsy specimens did not grow any organisms. Markedly elevated serum IgE levels suggested the diagnosis of Job syndrome, and therapy with vancomycin was started on hospital day 4 after discontinuing therapy with other antibiotics. The patient’s clinical status improved by day 8, and he was discharged from the hospital receiving therapy with trimethoprim-sulfamethoxazole. He presented 2 months later with new-onset cervical lymphadenopathy. A chest CT scan showed near-complete resolution of the right lung infiltrates and disappearance of the left pleural effusion; however, the mediastinal lymphadenopathy had worsened. A lymph node biopsy revealed Hodgkin lymphoma (mixed cellular type), for which he is receiving chemotherapy (stage III). In retrospect, our patient had possible staphylococcal pneumonia and mediastinal lymphadenopathy from Hodgkin disease. Plausible explanations for the left pleural effusion could be uncomplicated parapneumonic effusion secondary to a subtle pneumonic process in the left lower lobe and hypoalbuminemia.