Abstract
Nocardiosis induces a high mortality rate in those infected with HIV. It is now being increasingly described in patients with AIDS. Nocardia infection usually involves the lungs. In immunocompromised individuals it tends to disseminate. It mimics pulmonary TB both clinically and radiologically and many a time is wrongly treated with anti-tubercular drugs. Involvement of the pericardium is uncommon, having only been reported infrequently in the past. We describe a patient who presented with a cardiac tamponade and was confirmed as having pulmonary parenchymal and pleural disease.
Case history
A 35-year-old woman was admitted in our hospital for evaluation of cough with mucopurulent expectoration of one month's duration and two weeks of breathlessness. She also had low grade, intermittent fever for two weeks with a loss of appetite and weight. On examination she had mild pallor with bilateral pitting pedal oedema and no significant lymphadenopathy. Her blood pressure was 90/60 mmHg with pulsus paradoxus. She had tachycardia and tachypnea and a temperature of 100°F. Her jugular venous pressure was significantly raised and the neck veins were engorged. Oral thrush was also noted. A systemic examination revealed muffled heart sounds, features of bilateral pleural effusion and a moderate hepatomegaly. The chest X-ray showed right upper lobe consolidation with bilateral pleural effusion and cardiomegaly (Figure 1A). The echocardiogram confirmed a large pericardial effusion with tamponade. A pericardiocentesis was carried out by the cardiologist and 500 mL of fluid was removed. The initial diagnosis was pulmonary, pericardial and pleural TB. After the laboratory evaluation she was empirically started on isoniazid, rifampicin, pyrazinamide and ethambutol. Laboratory results showed a positive serology for HIV, white blood cell (WBC) count 10300/mm3, haemoglobin 7.8 g/dL, high erythrocyte sedimentation rate (140 mm/hour), urea 35 mg/dL, creatinine 0.8 mg/dL and the remaining blood tests were normal. Blood cultures were negative. Pericardial fluid showed 200 WBCs/mm3 with 90% neutrophils. The pleural fluid revealed 480 WBCs/mm3 with 98% neutrophils. Sputum, pericardial and pleural fluids were negative for acid-fast bacillus (AFB). The odd thing about the patient's fluid reports was that although the cell count was not very high, it was predominantly neutrophilic. A sputum Gram stain showed the presence of Gram-positive branching filaments, which showed up as acid-fast filaments with 1% sulphuric acid suggestive of Nocardia spp (Figure 1B). Two samples of sputum culture grew Nocardia asteroides. However, the pericardial and pleural fluid cultures did not grow any organisms even after four weeks. Antitubercular drugs were stopped at this stage, as the diagnosis of pulmonary nocardiosis and HIV infection was now quite evident. She was initiated on nocardia therapy with a combination of trimethoprim-sulfamethoxazole (TMP-SMX), doxycycline and ceftriaxone. A low dose of steroids were used as the pleural and pericardial collections tended to re-accumulate causing breathlessness. We were able to taper and then stop the steroid within a few weeks. The chest X-ray at discharge showed a significant improvement of the parenchymal shadowing with a marked decrease in both the pleural and pericardial effusions. She was discharged on an oral regime of TMP-SMX and doxycycline. After eight weeks of Nocardia therapy, the CD4 count was 32 cells/mm3. Antiretroviral drugs were initiated at this stage, which she tolerated without incident. Further follow-up showed continued improvement in her chest X-ray and she was asymptomatic.

Chest X-ray showing right upper lobe consolidation with bilateral pleural effusion and cardiomegaly (A). Modified acid-fast staining of sputum showing Gram-positive branching filaments suggestive of Nocardia spp (B)
Discussion
Nocardiosis is an uncommon Gram–positive bacterial infection caused by saprophytic aerobic actinomycetes in the genus Nocardia. Seven species have been associated with human disease. N. asteroides is responsible for approximately 70% of infections caused by these organisms. 1 The incidence of nocardiosis in AIDS is 0.2–1.8%. 2 The lung is the primary site of nocardial infection in more than two-thirds of cases. 3
The onset of pulmonary nocardiosis may be acute, subacute or chronic and is not distinguished by any specific signs or symptoms. Fever, night sweats, fatigue, anorexia, weight loss, dyspnoea, cough, haemoptysis and pleuritic chest pain have all been described. 3,4 The involvement of the pericardium is uncommon and the presence of pericarditis carries a poor prognosis. 5
Radiographic findings are variable and non-specific. Consolidation and large irregular nodules, often cavitary, are common. Interstitial infiltrates, reticulonodular infiltrates and pleural effusion also occurs. 6
Diagnosis of this infection is important and can be achieved by identifying the Nocardia using a variety of methods including Gram stain, modified AFB stain and culture. The Gram stain shows thin filamentous, branching Gram-positive bacilli, which, along with a positive modified AFB stain, supports a preliminary identification of Nocardia spp. A definitive diagnosis of nocardiosis requires the isolation and identification of the organism from a clinical specimen. Nocardia in routine aerobic cultures usually require 5–21 days for growth. 3
N. asteroides is typically susceptible to TMP-SMX, third generation cephalosporins, amikacin and carbapenems. TMP-SMX is considered the standard therapy for nocardiosis and is recommended for at least 12 months in immunocompromised patients. Severe nocardiosis (a life-threatening pulmonary or disseminated disease) in immunocompromised patients should be treated with at least two active agents against Nocardia (TMP-SMX, ceftriaxone, amikacin or others). 4
When there is lung and pericardial involvement, the most common diagnosis entertained, particularly in HIV-infected individuals, is TB. However, as shown in this case other aetiologies such as nocardiosis may need to be considered particularly if atypical features are present. The important clinical indication in our case was of neutrophilic pericardial and pleural fluid without a major elevation in fluid WBC, which should probably make one suspect such organisms particularly when the initial cultures are negative. It is important to ask the microbiologist to incubate the cultures for a longer period.
