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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 rats.

  • In contrast to most fungi, Pneumocystis lacks ergosterol and thus is not susceptible to antifungal drugs that inhibit ergosterol synthesis.

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

EPIDEMIOLOGY

  • Pneumocystis is found worldwide, and most healthy children have been exposed to the organism by 3–4 years of age.

  • Both airborne transmission and person-to-person transmission have been demonstrated; the cyst is the transmissible form.

  • Defects in cellular and humoral immunity (including immunosuppressive medications) predispose to Pneumocystis pneumonia. The risk in HIV-infected pts rises dramatically when CD4+ T cell counts fall below 200/μL.

PATHOGENESIS

  • The organisms are inhaled and attach tightly to type I cells in alveoli, although they remain extracellular.

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

  • Severe disease may cause interstitial edema, fibrosis, and hyaline membrane formation.

CLINICAL MANIFESTATIONS

  • Pts develop dyspnea, fever, and nonproductive cough.

    • – HIV-infected pts are usually ill for several weeks or longer with subtle manifestations.

    • – Pts without HIV infection often become symptomatic after their glucocorticoid dose has been tapered, and their symptoms are of shorter duration.

  • Physical exam reveals tachypnea, tachycardia, and cyanosis out of proportion to the few abnormalities present on chest auscultation.

  • Nonspecific laboratory findings include elevated serum concentrations of lactate dehydrogenase and β-D-glucan, a component of the fungal cell wall.

  • CXR classically reveals bilateral diffuse infiltrates beginning in the perihilar regions. Other findings (e.g., nodular densities, cavitary lesions) have been described.

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

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.

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

  • Proper specimens are key.

    • – Fiberoptic bronchoscopy with bronchoalveolar lavage remains the mainstay of diagnosis.

    • – Sputum induction and oral washes are noninvasive options that are gaining popularity.

    • – Transbronchial biopsy and open lung biopsy are used only when a diagnosis cannot be made by bronchoalveolar lavage.

TREATMENT Pneumocystis Infections

  • Trimethoprim-sulfamethoxazole (TMP-SMX) is the drug of choice for all pts. For doses and adverse effects of TMP-SMX and alternative regimens, see Table 116-1.

  • For mild to moderate cases (a Pao2 >70 mmHg or a PAo2 – Pao2 gradient <35 mmHg on room air), alternatives include TMP plus dapsone and clindamycin plus primaquine. Atovaquone is less effective than TMP-SMX but is better tolerated.

  • For moderate to severe cases (a Pao2 >70 mmHg or a PAo2 – Pao2 gradient <35 mmHg), alternatives include IV pentamidine, IV clindamycin plus primaquine (potentially more effective than pentamidine), and trimetrexate plus leucovorin.

  • Adjunctive ...

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