ABSTRACT
Pneumocystis jiroveci, the etiologic agent of Pneumocystis infection in humans, was first described in 1909 by Carlos Chagas, who, in his study of guinea pigs, mistook the cysts for the sexual state of Trypanosoma cruzi. With the development of more sophisticated laboratory techniques, the diagnosis of Pneumocystis pneumonia (PCP) can be definitively established by rapid, noninvasive methods. Human disease has been attributed to reactivation of latent disease acquired in childhood. There is a growing body of evidence to suggest that re-infection also takes place. Multiple reports in the literature describe patients with recurrent episodes of PCP who were found to have strains that were genotypically different from prior episodes. Patients with PCP have a wide variety of underlying diseases, both congenital and acquired. While most of these involve disorders in T-cell function, pure B-cell defects can also predispose to infection. In Human Immunodeficiency Virus-infected patients, the risk of developing PCP closely correlates with the CD4 + lymphocyte count.
