Invasive aspergillosis in Stem Cell Transplant Recipients during the 1990's: Increased Post-Engraftment aspergillosis Is Associated with GVHD and Viral Infections.

Kieren A. Marr, Rachel A. Carter, Michael Boeckh, Lawrence Corey.

Author address: 

Fred Hutchinson Cancer Research Center, Seattle, WA; University of Washington, Seattle, WA, USA


Background: Invasive mould infections, particularly those due to aspergillus species, have become a leading cause of infection-related death in recipients of allogeneic hematopoietic stem cell transplantation (HSCT). Multiple changes in transplant practices, which could potentially alter the epidemiology of infection, have occurred during the last decade. Methods: To review the incidence and risks for invasive aspergillosis (IA), we examined the records of 5589 patients at our center (1985-1999). Cases were identified by review of microbiology, pathology and hospital epidemiology records. Timing after HSCT were compared in the cohorts of patients who developed IA between 1988-1992 (n=158) and 1993-1998 (n=187). Risks and outcomes were determined using Cox regression modeling and Kaplan Meier curves. Results: The 1-year cumulative incidence of IA increased in allograft recipients (matched-related and mismatched or unrelated graft recipients), from 4.5% in 1990 to 12% in 1998, with the largest increase occurring after 1992. More allograft recipients in the latter years (1993-1998) developed IA greater than 6 months after HSCT (31/187 vs. 7/158, p2, HR12, 95%CI 3.0-49.6), receipt of a mismatched or unrelated PBSC transplant (HR 5.2, 95%CI 1.5-18.1), CMV disease (HR 11, 95%CI 6.1-20.9), and infection with respiratory viruses (HR 2.1, 95%CI 1.1-3.8). Risks associated with IA very late (>6 months) after allogeneic HSCT include secondary neutropenia (HR 5.7, 95%CI 2.3-13), chronic GVHD (HR 7.3, 95%CI 2.2-24), and CMV disease (HR 6.1, 95%CI 2.1-17.8). One-year survival after IA early, late, and very late after allogeneic HSCT was equivalent, approximating 20%. In autograft recipients, the 1-year cumulative incidence of IA remained low, but increased from 2.1% in 1997 to 5.3% in 1998. This increase appeared to be associated with receipt of CD34-selected grafts. Conclusion: The incidence of IA after allogeneic HSCT has tripled during the 1990's, now predominantly occurring in non-neutropenic hosts, late after engraftment. The development of non-neutropenic IA is associated with severe GVHD and viral infections.

abstract No: 


Full conference title: 

43rd American Society of Hematology (ASH) Annual Meeting
    • ASH 43rd (2001)