Pneumocystosis

Abstract

Pneumocystis is the classic opportunistic pathogen in that it does not produce any recognizable disease in an immunologically intact host, yet infection of the at-risk immunocompromised host results in a pneumonitis that is universally fatal if untreated. The organism was first identified in the early 1900s but was not appreciated to be a significant human pathogen until after World War II when outbreaks of Pneumocystis pneumonia (PCP) occurred in orphanages in Europe. These young infants who developed what was termed “interstitial plasma cell pneumonitis” were suspected to be immunosuppressed secondary to severe malnutrition. Two subsequent events firmly established Pneumocystis as a major opportunistic pathogen: the development of successful cancer chemotherapy in the late 1950s and 1960s and the start of the AIDS epidemic in the early 1980s. In fact, it was the recognition of a cluster of this “rare” pneumonia, PCP, in apparently healthy young gay men over a short period of time that led to the recognition that a new syndrome (AIDS) and infection (HIV) had emerged.

Presently, the population of patients at risk to develop PCP is growing steadily as we develop new modalities of therapy and potent immunosuppressive drugs to treat malignancies, organ failure, autoimmune, and inflammatory diseases. For example, in solid organ transplant recipients, as survival improves so does the recognition that these patients are at risk of developing PCP if not on specific prophylaxis. Most recently, the addition of antitumor necrosis factor (TNF) therapy to the management of patients with Crohn’s disease, rheumatoid arthritis, and other inflammatory conditions has resulted in the occurrence of PCP in populations that previously had not been considered to be at risk for the development of PCP. The importance of PCP as an opportunistic pneumonia is likely to increase as the use of immunosuppressive biologic response modifiers increases.