ABSTRACT
The fungus now known as Pneumocystis jirovecii that infects humans entered modern medicine as a trypanosomal infection of guinea pigs reported by Carlos Chagas in 1909.1 The eminent parasitologist’s misclassi–cation was soon corrected, and it was rechristened in deference both to its distinct parasitic morphology and to early investigator Dr. Antonio Carini as Pneumocystis carinii.2 It retained this name through the balance of the twentieth century but assumed varied medical guises, –rst as a rare cause of sporadic respiratory infection, then as a signi–cant cause of pneumonia (Pneumocystis carinii-pneumonia [PcP]) in undernourished children in Europe in the wake of World War II.3 Subsequently, severely immunosuppressed children and adults receiving cytotoxic chemotherapy became the main victims of this persistent yet uncommon pathogen.4 In 1981, clusters of PcP in injectiondrug users and men who have sex with men in the United States presaged the recognition of the acquired immunode–- ciency syndrome (AIDS),5 and in the early years of the AIDS epidemic PcP was thrust center stage as a common and devastating AIDS-de–ning opportunistic infection.6 With aggressive chemoprophylaxis in high-risk patients and the effective treatment of human immunode–ciency virus (HIV) infection in the developed world, the overall incidence of PcP has declined signi–cantly, though it remains an important cause of opportunistic pneumonia in patients with immunode–ciency due to therapeutic immunosuppression, congenital disorders, or inadequately treated or undiagnosed HIV infection.7
