Pneumocystis

Abstract

Pneumocystis is a host-specific, opportunistic fungal pathogen found in humans and many mammals. In immunocompromised humans Pneumocystis jirovecii causes Pneumocystis pneumonia (PCP). Infection is acquired by inhalation of the cystic form of the organism and primary infection occurs in the first few years of life in most people. In patients infected with human immunodeficiency virus (HIV), Pneumocystis pneumonia has a slower onset, a milder disease phenotype associated with a mortality of 10–12%. By contrast, in patients with other causes of immunocompromise, Pneumocystis pneumonia usually has a more rapid onset and is more severe with a mortality between 30% and 50%. The “gold standard” for diagnosis is by demonstrating the organism in respiratory tract specimens [induced sputum, bronchoalveolar lavage (BAL) fluid] by staining or by immunofluorescence (IF). Other methods, including polymerase chain reaction (PCR) to detect P. jirovecii DNA in BAL fluid, and measurement of serum β-1,3-d-glucan (BDG) levels are increasingly being used for diagnosis. Trimethoprim-sulfamethoxazole (TMP-SMX) for 14–21days is the treatment of choice for Pneumocystis pneumonia irrespective of the severity of infection. Alternative regimens may be suitable, but some are not indicated in severe disease. Adjunctive corticosteroids are given for moderate-to-severe HIV-associated Pneumocystis pneumonia [PaO2≤9.3kPa (≤70mmHg), or alveolar-arterial O2 gradient >6.0kPa (>35mmHg)], and should be started immediately or within the first 3days of starting anti-Pneumocystis therapy. There is less evidence for use of adjunctive corticosteroids in patients with Pneumocystis pneumonia due to other causes of immune compromise. Current evidence does not support isolation of patients with Pneumocystis pneumonia from other immunocompromised (susceptible) hosts.