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Infection in the solid organ transplant recipient

Jay A Fishman, MD
Section Editor
Carol A Kauffman, MD
Deputy Editor
Sheila Bond, MD


Solid organ transplantation has increased worldwide since the first successful human kidney transplant was performed in 1954. As immunosuppressive agents and graft survival have improved, infection and malignancy have become the main barriers to disease-free survival after organ transplantation. As a result of the growing population of immunosuppressed patients with prolonged survival, an increased incidence and spectrum of opportunistic infections is observed [1-3]. Guidelines for the diagnosis and treatment of infection in transplant recipients have been developed [4].

The risks of infection and an overview of specific infections in the solid organ transplant recipient will be reviewed here. The pretransplant evaluation for solid organ and hematopoietic cell transplant (HCT) recipients, prophylaxis of infections in solid organ transplant and HCT recipients, and an overview of infections following HCT are discussed separately. (See "Evaluation for infection before solid organ transplantation" and "Evaluation for infection before hematopoietic cell transplantation" and "Prophylaxis of infections in solid organ transplantation" and "Prevention of infections in hematopoietic cell transplant recipients" and "Overview of infections following hematopoietic cell transplantation".)


When infection occurs, early and specific diagnosis and rapid and aggressive treatment are essential to good clinical outcomes.

Potential etiologies of infection in these patients are diverse, including common, community-acquired bacterial and viral diseases and uncommon opportunistic infections of clinical significance only in immunocompromised hosts [1-3]. Pulmonary processes can progress rapidly and may constitute medical emergencies [1]. These include infections due to Pneumocystis jirovecii (formerly P. carinii), Nocardia asteroides, Aspergillus spp, Cryptococcus neoformans, cytomegalovirus (CMV), varicella-zoster virus (VZV), influenza, respiratory syncytial virus (RSV), and Legionella spp.

Inflammatory responses associated with microbial invasion are impaired by immunosuppressive therapy, which results in diminished symptoms and muted clinical and radiologic findings. Fever is neither a sensitive nor a specific predictor of infection; up to 40 percent of infections cause no fever (especially with fungal infections) and up to 22 percent of fevers are noninfectious in origin [5]. Infections are often advanced (ie, disseminated) at the time of clinical presentation.

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Literature review current through: Nov 2017. | This topic last updated: Sep 25, 2017.
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