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Review
. 2022 Nov 5;8(11):1167.
doi: 10.3390/jof8111167.

The Pathogenesis and Diagnosis of Pneumocystis jiroveci Pneumonia

Affiliations
Review

The Pathogenesis and Diagnosis of Pneumocystis jiroveci Pneumonia

Anna Apostolopoulou et al. J Fungi (Basel). .

Abstract

Pneumocystis jiroveci remains an important fungal pathogen in immunocompromised hosts. The environmental reservoir remains unknown. Pneumonia (PJP) results from airborne transmission, including in nosocomial clusters, or with reactivation after an inadequately treated infection. Pneumocystis pneumonia most often occurs within 6 months of organ transplantation, with intensified or prolonged immunosuppression, notably with corticosteroids and following cytomegalovirus (CMV) infections. Infection may be recognized during recovery from neutropenia and lymphopenia. Invasive procedures may be required for early diagnosis and therapy. Despite being a well-established entity, aspects of the pathogenesis of PJP remain poorly understood. The goal of this review is to summarize the data on the pathogenesis of PJP, review the strengths and weaknesses of the pertinent diagnostic modalities, and discuss areas for future research.

Keywords: AIDS; HIV; Pneumocystis jiroveci; Pneumocystis pneumonia; corticosteroids; cytomegalovirus; fungal infection; hematopoietic stem cell transplantation; organ transplantation.

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Conflict of interest statement

The authors declare no conflict of interest related to this manuscript and its contents.

Figures

Figure 2
Figure 2
Approach to the diagnosis of Pneumocystis pneumonia. In immunocompromised patients at risk for Pneumocystis jirovecii pneumonia (PJP), early antimicrobial therapy is initiated based on clinical signs and symptoms, radiology, and available laboratory data [118,119]. Microbiological demonstration of organisms on bronchoalveolar lavage (BAL) or induced sputum specimens should not delay treatment. Other processes, including co-infections, may alter the radiologic picture or mimic PJP clinically.
Figure 1
Figure 1
A 65-year-old woman 18 months after deceased donor kidney transplantation presents to emergency room with increasing dyspnea over the past three weeks and new fevers. She completed trimethoprim-sulfamethoxazole prophylaxis one year prior to admission. She is hypoxic with decreased breath sounds bilaterally and fine diffuse crackles, LDH is 416, β-1,3-glucan assay positive (>500), and induced sputum sample positive of Pneumocystis jiroveci by immunofluorescence. (A). Baseline chest radiograph. (B). Admission chest radiograph with slightly increased upper lobe ground glass markings. (C). Chest CT scan without intravenous contrast reveals a mixed pattern of patchy ground-glass opacities and scattered dense pulmonary infiltrates with associated septal thickening.

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