Description

A person living with HIV (PLHIV) in his 40s was admitted to the emergency department with low-grade fever, progressive dyspnoea, and cough with scanty sputum for 2 months. He was recently diagnosed with PLHIV and did not receive antiretroviral therapy. On vital examination, the pulse was 116 beats/min, the blood pressure was 108/66 mm Hg, the respiratory rate was 30 breaths/min and the oxygen saturation was 90% with high-flow oxygen supplementation through a non-rebreathing mask. The ratio of arterial oxygen partial pressure to fractional inspired oxygen was 94. A high-resolution CT (HRCT) showed variable-sized pneumatoceles, ground-glass opacities (GGOs) with peripheral sparing and interstitial infiltrates in both lungs (figure 1). The pneumatoceles had a predilection for the upper lobes and subpleural location. Sputum examination for bacterial culture, fungal organisms and cartridge-based nucleic acid amplification and culture for Mycobacterium tuberculosis were negative. Serum (1-3)-beta-d-glucan level was 417 pg/mL (normal, <60).

• Download figure
• Open in new tab
• Download powerpoint

Figure 1

A high-resolution CT showing variable-sized pneumatoceles (arrows), ground-glass opacities with peripheral sparing (arrowheads) and interstitial infiltrates in both lungs.

A markedly elevated serum (1-3)-beta-d-glucan level in PLHIV with characteristic radioimaging features has a high predictive value for Pneumocystis pneumonia (PCP). The patient received oral cotrimoxazole and prednisolone for 3 weeks for severe PCP. However, the diagnosis could not be confirmed by PCR or staining of the cyst because of the inability to perform broncho-alveolar lavage due to a high oxygen requirement. The CD4 count was 16/µL. He was started on antiretroviral therapy with tenofovir, dolutegravir and lamivudine. A spontaneous pneumothorax occurred in the left lung, which required drainage. He improved gradually and was discharged after 1 month of hospital stay.

Thoracic CT remains the cornerstone of diagnosing respiratory infections in PLHIV, especially in the absence of sputum or broncho-alveolar lavage examination. An HRCT has about 90% positive predictive value and about 100% negative predictive value for the diagnosis of PCP in PLHIV.^1,2 Diffuse symmetrical GGOs and interstitial infiltrates are seen in almost all patients, yet not specific.1 Pneumatoceles or lung cysts are less common, seen in 10%–34% of cases, but are specific for the diagnosis of PCP.2 Their presence, along with GGOs, is highly suggestive of PCP in PLHIV. A small proportion of cases cause nodules; however, tree-in-bud nodules, mediastinal lymphadenopathy and pleural effusions are rare and suggest an alternate aetiology.

The lung cysts in PCP are usually thin-walled, though they may vary in size and shape. They typically have a predilection for the upper lobes and a subpleural location and may occur bilaterally. Large and subpleural cysts are associated with an increased risk of rupture and spontaneous pneumothorax.1 2 The exact pathogenesis of cyst formation in PCP is not fully understood; however, the possible mechanisms include bronchiolar obstruction, alveolar damage by macrophage activation or direct cytotoxic effect by the infection.3 Cystic lung disease represents a longstanding or advanced Pneumocystis infection. Prompt adequate treatment of PCP often (but not invariably) resolves the cysts.