Background. The incidence and epidemiology of invasive fungal infections (IFIs), a leading cause of death among hematopoeitic stem cell transplant (HSCT) recipients, are derived mainly from single-institution retrospective studies. Methods. The Transplant Associated Infections Surveillance Network, a network of 23 US transplant centers, prospectively enrolled HSCT recipients with proven and probable IFIs occurring between March 2001 and March 2006. We collected denominator data on all HSCTs preformed at each site and clinical, diagnostic, and outcome information for each IFI case. To estimate trends in IFI, we calculated the 12-month cumulative incidence among 9 sequential subcohorts. Results. We identified 983 IFIs among 875 HSCT recipients. The median age of the patients was 49 years; 60% were male. Invasive aspergillosis (43%), invasive candidiasis (28%), and zygomycosis (8%) were the most common IFIs. Fifty-nine percent and 61% of IFIs were recognized within 60 days of neutropenia and graft-versushost disease, respectively. Median onset of candidiasis and aspergillosis after HSCT was 61 days and 99 days, respectively. Within a cohort of 16,200 HSCT recipients who received their first transplants between March 2001 and September 2005 and were followed up through March 2006, we identified 718 IFIs in 639 persons. Twelvemonth cumulative incidences, based on the first IFI, were 7.7 cases per 100 transplants for matched unrelated allogeneic, 8.1 cases per 100 transplants for mismatched-related allogeneic, 5.8 cases per 100 transplants for matchedrelated allogeneic, and 1.2 cases per 100 transplants for autologous HSCT. Conclusions. In this national prospective surveillance study of IFIs in HSCT recipients, the cumulative incidence was highest for aspergillosis, followed by candidiasis. Understanding the epidemiologic trends and burden of IFIs may lead to improved management strategies and study design.
|Original language||English (US)|
|Number of pages||10|
|Journal||Clinical Infectious Diseases|
|State||Published - Apr 15 2010|
Bibliographical noteFunding Information:
Potential conflicts of interest. D.P.K. has received research support and honoraria from Schering-Plough, Pfizer, Astellas Pharma, Enzon Pharmaceuticals, and Merck. P.G.P. has received grant support from Merck, Pfizer, Schereing-Plough, and Astellas and serves as an adhoc advisor for Novartis, Basilea, Merck, Pfizer, and Astellas. D.R.A. has received grant support and serves as an ad hoc advisor for Merck, Pfizer, and Schering-Plough. T.F.P. has received esearch support and honoraria from Merck, Pfizer, Schering-Plough, and Nektar Therapeutics and has served as a consultant for Basilea, Merck, Nektar, and Pfizer. K.A.M. has received grant support from Merck and Enzon and serves as an ad hoc advisor and consultant for Astellas, Basilea, Enzon, Merck, Pfizer, and Schering-Plough. J.I.I. has received honoraria from Astellas, Enzon, Pfizer, and Schering-Plough. V.A.M. is on the speakers’ bureau for Amgen, Merck, Pfizer, Scher-ing-Plough, and Celgene. J.R.W. has received honoraria from Pfizer, As-tellas, Basilea, and Merck. All other authors: no conflicts.
Financial support. Centers for Disease Control and Prevention (grant 5U01CI000286-05) and grants from Merck, Astellas, Pfizer, Schering-Plough Research Institute, and Enzon Pharmaceuticals.