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RESEARCH ARTICLE
Contents Vol 35(1)

Hospital-acquired Pneumocystis pneumonia: a renewed concern?

Sharon Chen A B F , Brian Nankivell C , Carolina Firacative B , Kathy Kable C , Debbie Marriott D , Peter MacDonald E , Wieland Meyer B and Jeremy Chapman C
+ Author Affiliations
- Author Affiliations

A Centre for Infectious Diseases and Microbiology Laboratory Services, ICPMR – Pathology West, Westmead Hospital, NSW 2145, Australia

B Molecular Mycology Research Laboratory, Centre for Infectious Diseases and Microbiology, Sydney Medical School – Western, University of Sydney, NSW 2145, Australia

C Department of Renal Medicine, Westmead Hospital, University of Sydney, NSW 2145, Australia

D Department of Microbiology and Infectious Diseases, St Vincent’s Hospital, NSW 2010, Australia

E Department of Cardiology, St Vincent’s Hospital, NSW 2010, Australia

F Corresponding author. Tel: +61 2 9845 6255, Fax: +61 2 9893 8659, Email: Sharon.chen@health.nsw.gov.au

Microbiology Australia 35(1) 57-59 https://doi.org/10.1071/MA14016
Published: 4 February 2014

Abstract

Pneumocystis pneumonia (PCP), caused by the fungus Pneumocystis jirovecii, is a life-threatening pulmonary infection in immuncompromised hosts. Solid organ transplant (SOT) recipients are among those at increased risk, with infection attributed to reactivation of dormant colonisation1. Prior to the institution of routine antimicrobial prophylaxis, the overall incidence of PCP in SOT recipients was 5–15%, with the lowest incidence in kidney recipients (2–15%) and the highest, in lung and heart/lung recipients (10–40%)2,3. Prophylaxis with trimethoprim-sulfamethoxazole (TMP-SXZ) has reduced the risk of PCP by ≈91% and has largely eliminated PCP within the first year of transplantation. Prophylaxis is important since PCP-related mortality is as high as 60% despite treatment with TMP-SXZ2,4,5. Late infection was considered highly unusual1,6. However, the optimal duration of prophylaxis is uncertain. The occurrence of recent PCP case clusters in kidney transplant units in Europe and Asia (summarised in a review article; see reference 6)6 and in Australia7 has challenged our current appreciation of PCP as an ‘infection of the past’ outside patients with HIV/AIDS. It also gives pause to the likelihood of de novo infection, its mode of transmission and to the validity of current antimicrobial prophylactic regimens used, if any. This article outlines the clusters in Australia, hypothesises why this may have occurred and presents the recent consensus proposal for outbreak containment and prophylaxis against PCP. Details of the outbreaks in other regions are not reviewed.


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