CT, computed tomography; GGO, ground glass opacities; HIV, human immunodeficiency virus; PCR, polymerase chain reaction; PJP, Pneumocystis jiroveci pneumonia.
Non-human immunodeficiency virus Pneumocystis jiroveci pneumonia
Article first published online: 26 DEC 2012
© 2012 The Authors. Respirology © 2012 Asian Pacific Society of Respirology
Volume 18, Issue 1, pages 191–192, January 2013
How to Cite
Chang, C.-H., Ruan, S.-Y., Li, C.-C. and Yu, C.-J. (2013), Non-human immunodeficiency virus Pneumocystis jiroveci pneumonia. Respirology, 18: 191–192. doi: 10.1111/resp.12004
- Issue published online: 26 DEC 2012
- Article first published online: 26 DEC 2012
- Accepted manuscript online: 2 NOV 2012 08:41AM EST
We read with great interest the recent two studies by Hardak et al. and Enomoto et al. about the diagnosis of Pneumocystis jiroveci pneumonia (PJP) in non-human immunodeficiency virus (HIV)-infected patients.1,2 Here, we would like to describe a case of PJP and highlight several important issues regarding the diagnosis of this disease in non-HIV-infected patients.
A 32-year-old lady, who underwent allogeneic peripheral blood stem cell transplantation for leukaemia 6 months earlier, was admitted to the hospital for high fever, dry cough and progressive dyspnoea for 5 days. Chest radiography showed alveolar opacities in the bilateral lower lungs (Fig. 1a), while thin-section chest computed tomography showed major findings of subpleural consolidation, with peripheral distribution and focal ground glass opacities (GGO) in the bilateral lower lungs (Fig. 1b,c). The results of the microbiology study were inconclusive. To achieve a definitive diagnosis, surgical lung biopsies by thoracoscopy were obtained. Thoracoscopic biopsy of the right middle and lower lungs showed PJP. After a 2-week treatment, there was evolutional change from consolidation to GGO with crazy-paving pattern (Fig. 1d). The lower lung opacities resolved after 4 weeks of sulfamethoxazole-trimethoprim treatment, and she was discharged.
The clinical course of PJP in non-HIV-infected patients is substantially different from those of HIV-infected patients.2,3 The disease usually presents with a more acute and fulminant course in non-HIV-infected patients. In contrast, the presentation is usually indolent in HIV-infected patients. In addition, the mortality rate is higher among non-HIV-infected patients.2,3 Table 1 summarizes the differences of PJP between HIV-infected and non-HIV-infected patients.
|PJP in HIV-infected patients||PJP in non-HIV-infected patients|
|Clinical course||Fever, cough, dyspnoea and hypoxaemia||Similar symptoms but usually more severe and in rapid progression; higher mortality|
|Pathology||More Pneumocystis organisms with fewer neutrophils; alveolar exudate, marked interstitial lymphocyte infiltrate with early honey combing||Fewer Pneumocystis organisms and more neutrophils, indicating more severe inflammation response|
|CT pattern||Predominant GGO and less consolidation; crazy-paving appearance (GGO plus septal line thickening) in some cases; architectural distortions and cyst formation in subacute and chronic infection||Presented with consolidation more frequently than HIV-infected patients; rare cystic lesions|
|CT distribution||Bilateral GGO in a mosaic pattern, distributed mostly in the central and upper lungs||Similar to HIV-infected patients but atypical presentation not unusual|
|Diagnosis by PCR||High sensitivity and specificity but with limitation to differentiate true infection and colonization||Less sensitive among non-HIV-infected patients, especially those with leukaemia and lymphoma|
Typical computed tomography findings of PJP include diffuse GGO in a mosaic pattern, distributed mostly at the central and upper lungs, with peripheral sparing. However, atypical imaging presentation, such as dense consolidation and atypical distribution of the involved lungs, is not unusual in non-HIV-infected patients. The greater consolidation and less GGO in chest computed tomography of non-HIV-infected patients may reflect more extensive lung inflammation due to more inflammatory cells and fewer Pneumocystis organisms. Therefore, a consolidation-predominant pattern should not preclude a suspicion of PJP. Early diagnosis of PJP usually relies on a high index of suspicion. In non-HIV-infected patients, transplantation and corticosteroid use are two important risk factors. A susceptible host with risk factors presenting with atypical pneumonia should elicit a suspicion of this disease regardless of typical chest imaging presented.
Furthermore, the imaging pattern of PJP varies with HIV-infected status and disease stage. Evolutionary changes may occur after treatment. In this presented case, the subpleural lesions changed from consolidation to GGO with crazy-paving pattern after 2 weeks of treatment (Fig. 1d). Nevertheless, initial GGO lesions may progress to alveolar consolidation in few days, if no definite treatment is provided.
In conclusion, PJP in non-HIV-infected patients has different clinical and radiographical presentations from that in HIV-infected patients. The clinical and radiographical features from HIV-infected patients cannot be totally applied to diagnose PJP in non-HIV-infected patients.