Abstract
Pneumocystis jiroveci remains an important fungal pathogen in a broad range of immunocompromised hosts.
The natural reservoir of infection remains unknown. Pneumocystis jiroveci Pneumonia (PJP) develops via airborne transmission or reactivation of inadequately
treated infection. Nosocomial clusters of infection have been described among immunocompromised
hosts. Subclinical infection or colonization may occur. Pneumocystis pneumonia occurs
most often within 6 months of organ transplantation and with intensified or prolonged
immunosuppression, notably with corticosteroids. Infection is also common during neutropenia
and low-lymphocyte counts, with hypogammaglobulinemia, and following cytomegalovirus
(CMV) infection. The clinical presentation generally includes fever, dyspnea with
hypoxemia, and nonproductive cough. Chest radiographic patterns are best visualized
by computed tomography (CT) scan with diffuse interstitial processes. Laboratory examination
reveals hypoxemia, elevated serum lactic dehydrogenase levels, and elevated serum
(1→3) β-D-glucan assays. Specific diagnosis is achieved using respiratory specimens
with direct immunofluorescent staining; invasive procedures may be required and are
important to avoid unnecessary therapies. Quantitative nucleic acid amplification
is a useful adjunct to diagnosis but may be overly sensitive. Trimethoprim-sulfamethoxazole
(TMP-SMX) remains the drug of choice for therapy; drug allergy should be documented
before resorting to alternative therapies. Adjunctive corticosteroids may be useful
early in the clinical course; aggressive reductions in immunosuppression may provoke
immune reconstitution syndromes. Pneumocystis pneumonia (PJP) prophylaxis is recommended
and effective for immunocompromised individuals in the most commonly affected risk
groups.
Keywords
Pneumocystis jiroveci - Pneumocystis pneumonia - fungal infection - cytomegalovirus
- HIV - AIDS - Corticosteroids - organ transplantation - hematopoietic stem cell transplantation
