|Year : 2015 | Volume
| Issue : 3 | Page : 295-296
Unusual presentation of pulmonary nocardiosis as pyopneumothorax in HIV
Aswini Kumar1, Aswanth Reddy2, Kumar Satagopan3
1 Department of Internal Medicine, State University of New York Upstate Medical University, New York, USA
2 Department of Internal Medicine, Saint Vincent Hospital, Massachusetts, USA
3 Department of Thoracic Medicine, Government Hospital for Thoracic Medicine, Chennai, Tamil Nadu, India
|Date of Web Publication||5-May-2015|
Department of Internal Medicine, State University of New York Upstate Medical University, New York
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Kumar A, Reddy A, Satagopan K. Unusual presentation of pulmonary nocardiosis as pyopneumothorax in HIV. Lung India 2015;32:295-6
Nocardia are branching, beaded, filamentous bacteria, commonly affecting the lungs, brain and skin in immunocompromised host. It is an uncommon opportunistic pathogen in HIV and is usually associated with advanced immunosuppression and high mortality.  Pulmonary nocardiosis manifests as consolidation with or without cavitation, multiple discrete pulmonary nodules, lung masses and pleural effusion. , Here, we report an unusual presentation of pulmonary nocardiosis as pyopneumothorax. Forty-one-year-old male with no past medical history presented with cough and shortness of breath for 2 weeks. Review of systems was positive for significant loss of weight and appetite for 3 months duration. He was a weaver by occupation with smoking history of 12.5 pack years. He denied history of alcohol or drug use and was sexually active with one female partner. On examination, the patient looked pale, dehydrated and cachectic. He was afebrile; tachycardic with heart rate of 102/min, respiratory rate 30/min, blood pressure 118/72 mmHg and oxygen saturation 91% on room air. Breath sounds were diminished on the left side. Rest of the examination was unremarkable. Laboratory tests revealed hemoglobin 6.2 g/dl, WBC 8600 cells/mm 3 , platelet 150000 cells/mm 3 , blood urea nitrogen 103 mg/dl and creatinine 1.8 mg/dl. Serum electrolytes and hepatic function panel were within normal limits. Chest X-ray showed pyopneumothorax on the left side with no mediastinal shift [Figure 1]. A chest tube was placed which drained 100 ml of purulent material. The patient was evaluated for HIV infection and ELISA was positive. CD4 count was 26 cells/μL and 6%. Pleural fluid showed acid fast filamentous rods by Kinyoun procedure. A presumptive diagnosis of pulmonary nocardiosis was made; treatment was initiated with intravenous trimethoprim-sulfamethoxazole and amikacin. Aerobic culture grew Nocardia after 5 days, confirming the diagnosis. Mycobacterium tuberculosis was ruled out by negative culture. With clinical improvement in 2 weeks, amikacin was stopped and antibiotic therapy was switched to oral trimethoprim-sulfamethoxazole. He received treatment for total of 6 months. Chest X-ray done after completion of treatment showed resolution of disease. Anti-retroviral therapy was subsequently started and CD4 count after 6 months improved to 202 cells/μL. The presentation of pulmonary nocardiosis may be acute, subacute or chronic. It can manifest as fever, night sweats, fatigue, anorexia, weight loss, dyspnea, cough, and hemoptysis or pleuritic chest pain.  The patient in our case had subacute onset with cough and shortness of breath along with loss of weight and appetite. A wide variety of radiographic appearances have been demonstrated in pulmonary nocardiosis like lobar consolidation, single or multiple nodules, lung masses (with or without cavitation), reticulonodular infiltrates, interstitial infiltrates, sub pleural plaques and pleural effusions.  There may be local spread from the lower respiratory tract to the pericardium and mediastinum causing pericarditis and mediastinitis, respectively. Pneumonia caused by nocardial infection may be indistinguishable from other pneumonias, but should be suspected in any prolonged pneumonia that does not respond to empirical treatment and in anyone who is at increased risk due to immunosuppression. Pyopneumothorax as reported in our case is relatively rare and there are only few case reports so far. Nocardia complicating AIDS has a prevalence of approximately 4% in developing world. It usually appears in advanced immunodeficiency with CD4 cell count less than 50 cells/mm 3 in approximately 50% to 85% cases and is more common in patients not on active treatment for HIV. In this population, there is higher incidence of cavitary masses along with more irregular, spiculated nodules. Pulmonary nocardiosis as pyopneumothorax was the initial manifestation in our case which led to the diagnosis of HIV. The most useful diagnostic test is a Gram stain of a clinical specimen. Nocardia may be more readily visualized with the use of the modified acid-fast stain which uses a weaker acid such as 1% sulphuric acid as the decolourizing agent.  Most routine aerobic bacterial culture media can support Nocardia. Colonies of Nocardia require 5-21 days for growth. Trimethoprim-sulfamethoxazole is the commonly used first-line therapy. Most experts recommend combination therapy for severe infection and CNS involvement.  Our patient was started on IV co-trimoxazole as well as amikacin because of severe infection. Duration of treatment of nocardial infection is variable and depends on the burden of infection and the host's immune function, but is usually prescribed for several months. In conclusion, this case highlights the unusual presentation of nocardia as pyopneumothorax. Often there is delay in diagnosis due to its low incidence, nonspecific clinical presentation and relatively difficult culture. Prompt initiation of treatment is life-saving and prevents dissemination.
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