A 55-year-old man presented to the Accident and Emergency Department with a 2-month history of dyspnoea (acutely worsening over 2 days preceding admission), cough productive of purulent sputum, fever and weight loss. He was known to be HIV-positive (genotype-2, diagnosed 1991) but had been non-compliant with antiretroviral medication (Truvada, Darunavir and Ritonavir) for 2 years. Additional background included a history of depression, subdural haematoma, recurrent bacterial chest infections and drug abuse (daily heroin smoker).
On examination, he was unkempt, cachectic and dehydrated. He was septic but maintaining normal oxygen saturations on room air. Cardiovascular and neurological examinations were unremarkable. He was tachypnoeic and crepitations were auscultated at the right lung base. His abdomen was non-tender with palpable hepatosplenomegaly. Right-sided anterior cervical and right-sided inguinal lymphadenopathy was palpated.
Blood tests revealed microcytic iron-deficient anaemia, lymphopaenia with white cell count 2.6 x 109/L, C-reactive protein 198 mg/L, normal electrolytes and renal function, raised alkaline phosphatase level (1664 iU/L), hypoalbuminaemia (22 g/L) and deranged clotting. Lactate dehydrogenase was raised at 515 iU/L. Serology demonstrated serum Epstein-Barr Virus (EBV) DNA PCR of 26 900 and positive Hepatitis B core-antigen (e-Antigen negative). HIV-2 viral load was 720 and CD4 count was 28 cells/muL (3%).
A chest radiograph demonstrated right basal opacification. Computerised tomography of the chest abdomen and pelvis (CT-CAP) revealed patchy air space opacification at the left oblique fissure, left lower and right lower lobes, paraseptal and central lobular emphysema and bibasal atelectasis (Figures 1 and 2). Hepatosplenomegaly was confirmed and free fluid was evident throughout the abdomen and pelvis (Figure 3). Multiple enlarged lymph nodes (up to 1.8 cm diameter) were visualised throughout the thorax, abdomen and pelvis (Figures 4 and 5).
Sputum cultures identified Pseudomonas aeruginosa; acid alcohol fast bacilli (AAFB) smears were negative. Tests for respiratory viruses, atypical organisms and Pneumocystis jirovecii were negative. Urine and blood cultures were negative, with no growth on mycobacterial blood cultures up to that point. Optimised antiretroviral therapy was restarted alongside intravenous piperacillin and tazobactam.
On multi-disciplinary team meeting, the clinical case was deemed to be in keeping with a diagnosis of respiratory tuberculosis. Alternative differentials included atypical lower respiratory tract infection (including MAC infection) or lymphoma. The patient subsequently underwent supraclavicular lymph node biopsy, which revealed classical HL. A positron emission tomography CT (PET-CT) scan diagnosed 'Stage 3B' but suggested that some lymphadenopathy may have been secondary to concurrent HIV-related lymphadenopathy or infection. A staging CT head excluded cerebral metastases. He was consequently initiated on a regimen of Adriamycin, Bleomycin, Vinblastine and Dacarbazine (ABVD) chemotherapy.
Notably, one sputum culture subsequently grew Mycobacterium intracellulare; following this, another sputum culture grew Mycobacterium mucogenicum. Neither organism was grown on subsequent sputum samples. Neither of two mycobacterial blood cultures nor a lymph node mycobacterial culture showed any growth on final reporting. At least two sputum cultures positive for the same organism or one positive culture from a 'sterile' site (such as blood, lymph nodes or bone marrow) are required to diagnose atypical mycobacterial infection. The positive sputum cultures were therefore not considered significant.
Axial computerised tomography of the chest demonstrating extensive mediastinal lymph nodes, the blue arrow points to the pre-vascular nodes, the white arrow points to the right hilar node and the red arrow points to the pre-carinal and subcarinal nodes.