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Despite widespread use of effective antimicrobial prophylaxis in susceptible immunocompromised patient populations, Pneumocystis jiroveci remains an important opportunistic pathogen. The incidence of Pneumocystis pneumonia (PCP) has decreased with the appropriate deployment of antimicrobial prophylaxis in susceptible hosts and with the advent of highly effective antiretroviral therapy (HAART) in HIV-infected individuals. PCP remains, however, an important syndrome in HIV infection in the developing world with high mortality. Pneumocystis also impacts the growing population of immunocompromised individuals following organ and hematopoietic stem cell and bone marrow transplantation, and with the broader use of immunosuppressive therapies in connective tissue, cancer, and immune disorders. The change in nomenclature this past decade, renaming of Pneumocystis carinii as P. jiroveci, reflects knowledge about the organisms responsible for this syndrome in different host species. This change has generated significant controversy among scientists, clinicians, and journal editors. Advocates and detractors alike agree that no matter the species name, Pneumocystis pneumonia or PCP should continue to be used to describe disease caused by this organism in humans.

History and Background

The cyst form of Pneumocystis was first described in 1909 by the famous parasitologist, Chagas and in 1910 by his colleague Carinii, and was described as a parasite and part of the life cycle of Trypanosoma cruzi.1 The organism was first associated with pulmonary infection in rats by Delanoe and Delanoe but was not recognized in humans until 1942 (Van der Meer and Brug) and was not associated with human disease until 1952 (Vanek and Jírovec) when it was found in association with “plasma cell interstitial pneumonitis” among malnourished children and neonates.2 Small epidemics of plasma cell interstitial pneumonitis had been noted in children in orphanages in Europe in the 1930s and following World War II and the Vietnam War. In the 1950s, recognition of congenital immune deficiencies and the development of immunosuppressive therapies identified new hosts for PCP. At that time, PCP was recognized in patients receiving corticosteroids and chemotherapeutic drugs and in immunosuppressed rats receiving corticosteroids.

The increasing incidence of PCP led to epidemiologic and therapeutic studies of the disease by the Centers for Disease Control (CDC) in the 1970s, based on the provision of the sole therapeutic agent available at that time (pentamidine). Clusters of P. carinii were reported at a variety of clinical oncology and transplant centers. However, the development of pyrimethamine, sulfadoxine, and of trimethoprim (TMP) and sulfamethoxazole (SMX) for the treatment and prevention of Pneumocystis infection greatly reduced the occurrence and the morbidity of the infection. These agents are now generally used in a fixed combination (TMP-SMX, or cotrimoxazole). P. carinii became known the world over as being the first disease-defining illness associated with AIDS in the 1980s, causing over one-fourth of community-acquired pneumonias in HIV-infected persons and more than 200,000 cases of PCP since 1979. What was once an obscure, poorly understood opportunistic disease, became a common clinical ...

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