Fungal infections in stem cell transplant recipients

Since the first hematopoietic stem cell transplant (HSCT) was performed more than 50 years ago, significant progress has been attained in the field, with changes in conditioning regimens, stem cell sources, and outcomes. The preparative regimen for HSCT may be fully myeloablative or less aggressive (nonmyeloablative). Different sources of stem cells have been used, including bone marrow (BM), peripheral blood stem cells (PBSCs), and cord blood. Stem cells may originate from an identical twin (syngeneic), one's own self (autologous), and another donor (allogeneic). Allogeneic donors may be related (family members) or unrelated to the recipients, with match or mismatch in human leukocyte antigens (HLA). Finally, manipulation of grafts (e.g., T cell depletion, CD34+ selection) may be used to modulate outcomes such as graft-versus-host disease (GVHD) and relapsed malignancy. All these variables impact the risks, timing, and outcomes of opportunistic infections, including invasive fungal infections (IFIs). Historically, infections due to Candida species have been predominately encountered soon after HSCT (prior to engraftment), while invasive mould infections, mainly invasive aspergillosis (IA), occur both early and later (after engraftment). Damage of the gastrointestinal tract mucosa and neutropenia due to conditioning regimens - particularly those designed to be myeloablative - represent the main risks for IFIs prior to engraftment. Neutrophil and T cell impairment associated with delayed engraftment or GVHD and associated therapies are the main risks for IFIs later after a HSCT.