A 52‐year‐old man presented with 4 weeks of dry cough, dyspnea, weight loss, chills, subcutaneous nodules, fatigue, and generalized weakness. His past medical history was significant for myasthenia gravis, metastatic thymoma to lungs, and pure red cell aplasia. Medications included cyclosporine, prednisone, and pyridostigmine. Exam revealed a chronically‐ill appearing man with decreased breath sounds at the left lung base and golf ball sized nodules on his extremities (see image). Laboratory analysis was significant for leukocytosis (15.7 K/uL). Chest radiograph revealed a new left‐sided pleural effusion and upper lobe infiltrates. Empiric broad spectrum antibiotics were initiated and cyclosporine was held. Preliminary pleural fluid gram stain was reported as gram positive cocci in chains. Ultimately surgical deep tissue biopsy was required as skin biopsy was non‐diagnostic. His hospital course was complicated by headache and delirium. Lumbar puncture was unremarkable. Brain MRI revealed two cerebellar lesions. Discordant results from the pleural fluid culture and the deep tissue biopsy prompted a re‐evaluation of the initial laboratory data and a unifying diagnosis of disseminated Nocardia farcinica was made. Directed therapy with meropenem and trimethoprim/sulfamethoxazole (TMP‐SMX) commenced. Given his history of thymoma, immunoglobulin levels were checked and found to be low. IVIG was administered. Serial MRIs revealed resolution of cerebellar foci of infection and serial chest imaging revealed resolution of the pleural effusion and infiltrates.
Nocardia is a delicate filamentous gram‐positive branching rod and typically requires a high degree of suspicion and invasive testing to diagnose. Roughly one‐third of cases are systemic with pulmonary cases having the highest incidence followed by CNS and then cutaneous. TMP‐SMX is the classic treatment agent but resistance is reported. Severe systemic infections are typically treated with two or three intravenous agents while awaiting susceptibility results (TMP‐SMX+imipenem+/‐amikacin+/‐ceftriaxone). The optimal duration of therapy depends on extent of infection and immune status of the patient. Good’s syndrome is diagnosed, when a patient has thymoma and immunodeficiency. The patient typically presents in the 4th‐5thdecade of life and has increased susceptibility to bacterial and opportunistic infections resulting in increased mortality. All patients with thymoma should have immunoglobulins and B and T cell subsets measured. Treatment includes resection of thymoma and immoglobulin replacement to maintain adequate IgG trough levels.
A high degree of suspicion and clinical persistence is required when making a diagnosis of Nocardiosis. It is important to avoid premature closure and pursue additional diagnostic studies if the preliminary data remains inconclusive. Any immunocompromised patient presenting with subcutaneous nodules merits dermatologic consultation for skin biopsies, histopathology, and deep tissue culture for bacterial, fungal, and mycobacterial organisms. Nocardia may even require a surgical biopsy to diagnose. Furthermore, hospitalists should recognize that thymoma can be associated with immunodeficiency in 6‐11% of cases (Good’s syndrome). Consider giving adjunctive therapy with IVIG in the setting of severe systemic infection
To cite this abstract:Wargo J, Hart A, Kim A, Waldinger J, Berg A. The Tale of a Diagnostically Bumpy Ride. Abstract published at Hospital Medicine 2014, March 24-27, Las Vegas, Nev. Abstract 671. Journal of Hospital Medicine. 2014; 9 (suppl 2). https://www.shmabstracts.com/abstract/the-tale-of-a-diagnostically-bumpy-ride/. Accessed July 22, 2019.