Mycobacterium avium-intracellulare presenting as an endobronchial tumour due to immune reconstitution inflammatory syndrome

INTRODUCTION

Mycobacterium avium-intracellulare (MAI) infection in HIV AIDS usually presents with low-grade fever, night sweats, cough and non-specific chest and systemic symptoms. Uncommonly, it can present as an endobronchial tumour or a mass lesion. ¹ The infection can also manifest shortly after commencing antiretroviral therapy (ART), due to immune reconstitution inflammatory syndrome (IRIS). We report a rare case of MAI presenting as an endobronchial tumour as a result of IRIS.

CASE REPORT

A 33-year-old woman presented with a history of six weeks of cough, fever, progressive breathlessness and weight loss. On examination, temperature was 39.5°C, heart rate 130/minute and respiratory rate 35/minute. Apart from cervical and axillary lymphadenopathy, systemic examination was normal.

She was slightly anaemic and lymphopaenic with Hb of 10.8 gm/dL and lymphocytes 0.9 × 10⁹/L. Blood culture was negative. Arterial blood gases showed severe hypoxemic respiratory failure with pH 7.58, PaO₂ 4.1 kPa, PaCO₂ 3.06 kPa and bicarbonate 22 mmol/L. Chest X-ray showed bilateral hilar and interstitial infiltrates.

HIV serology was positive with a CD4+ count of 210 cells/μL and viral load >500,000 copies/mL. She was too unwell to withstand bronchoscopy and we were unable to obtain an induced sputum sample. Based on strong clinical and radiological suspicion of Pneumocystis jiroveci infection, she was treated with intravenous co-trimoxazole along with high-dose steroids. She also required continuous positive airway pressure support in the intensive care unit. She responded well to the treatment and was discharged home. Within the next two weeks she was commenced on lamivudine, zidovudine and nevirapine in a twice daily regimen.

Four weeks after commencing ART she developed fever, nights sweats and cough. A repeat chest X-ray showed complete clearance of the interstitial and perihilar shadows but a new mass lesion in the left upper zone. Chest computed tomography scan confirmed a mass occluding the upper division of the left upper lobe encasing the pulmonary artery (Figure 1).

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Figure 1

Computed tomography of the chest showing a mass lesion occluding the left upper lobe bronchus

Bronchoscopy showed a polypoid tumour occluding the apico-posterior segment of the left upper lobe (Figure 2a). Biopsies and bronchial washings were taken. Due to suspected mycobacterial infection she was commenced on standard dosages of antituberculous therapy (rifampicin, isoniazid, ethambutol and pyrazinamide), awaiting results of the investigations. Nevirapine was substituted with efavirenz due to potential drug interactions with the antituberculous medications. Biopsies of the tumour showed a granulomatous lesion with foamy macrophages. Tissue culture after six weeks grew Mycobacterium avium.

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Figure 2

(a) Bronchoscopic images showing a tumour occluding apico-posterior segment of the left upper lobe. (b) Complete clearance of the endobronchial lesion post-treatment

With a diagnosis of MAI confirmed on biopsies and tissue culture, clarithromycin (500 mg BD) was added to rifampicin (10 mg/kg) and ethambutol (15 mg/kg). Pyrazinamide and isoniazid were stopped and ART was continued. The patient showed a good response to treatment and a repeat chest X-ray and bronchoscopy after seven months of treatment showed complete disappearance of the tumour (Figure 2b). CD4+ count improved to 510 cells/μL with viral load less than 50 copies/mL.

DISCUSSION

MAI is a common opportunistic infection in patients with AIDS when the CD4+ count is less than 50/μL. A majority of immunocompromised patients have disseminated infection with bacteraemia and positive sputum cultures. It can also present within a few weeks to months after initiation of ART due to IRIS. This is because of a sudden improvement in immune function as a result of a rise in CD4+ count on ART, resulting in an increased capacity of the immune system to respond to pre-existing antigens, leading either to the appearance of new infections or paradoxical worsening of an existing infection. Predisposing factors for IRIS are low CD4+ count at the initiation of ART, initiation of ART close to the time of diagnosis of opportunistic infection and/or rapid reduction in viral load once ART is commenced. ^2,3

Commonly, MAI manifesting as a result of IRIS presents with focal lymphadenitis (hilar, retro peritoneal or cervical). ⁴ Lung parenchymal involvement is occasionally seen as the presenting feature. Other uncommon manifestations reported in the literature are osteomyelitis, cutaneous lesions, ileitis and focal brain lesions. ⁵ Endobronchial MAI infection presenting as a result of IRIS is rare. ^6,7

Compared with the more common primary MAI infection in HIV patients, which usually presents with disseminated disease, MAI due to IRIS is usually localized with lymph node involvement. Presence of granuloma formation due to significant inflammatory reaction in IRIS also distinguishes the two. Standard treatment for IRIS-associated MAI infection is combination therapy with rifamycins (rifampicin or rifabutin), macrolide (clarithromycin or azithromycin) plus ethambutol. Occasionally, ciprofloxacin or amikacin are added when the infection is very severe. ART is continued unless the infection is life threatening. Anti-MAI therapy can be discontinued once the infection is treated and there is sustained suppression of HIV replication with CD4 counts >100 μL for more than six months.