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INTRODUCTION

Pneumocystis, an opportunistic fungal pulmonary pathogen, is an important cause of pneumonia in immunocompromised hosts.

MICROBIOLOGY

  • P. jirovecii infects humans, whereas P. carinii—the original species described—infects rodents.

  • Developmental stages include the small trophic form, the cyst, and the intermediate precyst stage.

EPIDEMIOLOGY

  • Pneumocystis is found worldwide, and most people are exposed to the organism early in life.

  • Infections resulting from environmental sources and person-to-person transmission have been demonstrated; the role of airborne transmission is unclear.

  • Defects in cellular and humoral immunity (e.g., due to HIV infection, malignancy, transplantation, immunosuppressive medications) predispose to Pneumocystis pneumonia (PCP). The incidence among HIV-infected pts is inversely related to the CD4+ T-cell count: ≥80% of cases occur at counts <200 cells/μL, and most cases develop at counts <100/μL.

PATHOGENESIS

  • The organisms are inhaled into the alveolar space, where they proliferate, provoking a mononuclear cell response. Alveoli become filled with and are damaged by proteinaceous material, with consequently increased alveolar–capillary injury and surfactant abnormalities.

  • On histology, alveoli are seen to be filled with foamy, vacuolated exudates.

CLINICAL MANIFESTATIONS

  • Pts develop dyspnea, fever, and nonproductive cough.

    • – HIV-infected pts often have an indolent course that presents as mild exercise intolerance or chest tightness without fever or cough. Over days to months, these pts develop the more typical symptoms of PCP.

    • – Some pts with HIV infection and most pts with other types of immunosuppression have more acute disease that progresses over a few days to respiratory failure.

  • Physical examination findings are nonspecific and invariably include hypoxemia. Pts may initially have a normal chest examination but later, without treatment, develop diffuse rales and signs of consolidation.

  • Serum levels of LDH may be elevated because of pulmonary damage, but this finding is neither sensitive nor specific.

  • CXR classically reveals bilateral diffuse interstitial infiltrates that are perihilar and symmetrical, although this finding is not specific for PCP. Cysts and pneumothoraces are common CXR findings. Chest CT shows diffuse ground-glass opacities in virtually all pts with PCP, and a normal chest CT essentially rules out the diagnosis.

  • Rare cases of disseminated infection have been described, generally involving lymph nodes, spleen, and liver.

DIAGNOSIS

  • Histopathologic staining makes the definitive diagnosis.

    • – Cell-wall stains (e.g., methenamine silver) are used for Pneumocystis cysts and Wright-Giemsa stains for the nuclei of all developmental stages.

    • – Immunofluorescence with monoclonal antibodies increases diagnostic sensitivity.

  • The demonstration of organisms in bronchoalveolar lavage fluid is almost 100% sensitive and specific for PCP in immunocompromised pts.

  • While detection of organisms in expectorated sputum or throat swabs has very low sensitivity, detection in an induced sputum sample can be—depending on the experience of the center conducting the test—highly sensitive (up to 90%) and specific.

  • DNA amplification by PCR is most sensitive but may not distinguish ...

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