Pneumocystis Pneumonia in Solid Organ Transplant Recipients

Abstract

Pneumocystis spp. are thought to be ubiquitous in nature with serologic studies suggesting that exposure occurs commonly in childhood (2). Symptomatic Pneumocystis pneumonia (PCP) is generally limited to individuals with immune deficits. Animal models demonstrate both de novo infection via airborne transmission and by reactivation of previously established latent infections (3). Clusters of infection have been described in medical facilities among renal transplant recipients (4–6). Based on studies before routine implementation of prophylaxis, the overall incidence of infection among solid organ transplant recipients varied mostly in the range of 5–15% depending on organ type, transplant center and immunosuppressive regimens (7). In older reports before implementation of extensive prophylaxis, the attack rate appeared highest in lung and combined heart–lung transplant recipients with an overall incidence ranging from less than 10% to just over 40%. Among liver and kidney transplant recipients, the incidence appeared to be less at anywhere from close to 2% to 10–15% (1). The incidence overall may be decreasing with reduction in the routine use of corticosteroids in organ transplantation and the adoption of effective prophylactic measures. Table 1 outlines some risk factors for PCP among non-HIV-infected individuals.