Hematopoietic Stem Cell Transplantation (HSCT)

Pathogenesis: The myeloablative processes involved in HSCT result in the complete absence of innate and adaptive immune cells. This transient state of complete immunologic incompetence and the reconstitution that follows make the host extremely susceptible to infections.
Etiology: Most infections occur in a predictable time frame after HSCT (Table 79-2).
- - Bacterial infections: Neutropenia-related infectious complications are most common during the first month. Some centers give prophylactic antibiotics (e.g., quinolones) that may decrease the risk of gram-negative bacteremia but increase the risk of Clostridium difficile colitis.
  - Skin and bowel flora (e.g., S. aureus, coagulase-negative staphylococci, E. coli) are responsible for most infections in the first few days following HSCT, after which nosocomial pathogens and filamentous bacteria (e.g., vancomycin-resistant enterococci, Acinetobacter, antibiotic-resistant gram-negative bacteria, and Nocardia species) become more common.
  - In the late posttransplantation period (>6 months after reconstitution), bacteremia due to encapsulated organisms is most common, particularly among pts who are asplenic or hypogammaglobulinemic.
- - Fungal infections: Fungal infections are increasingly common beyond the first week after HSCT, particularly among pts who receive broad-spectrum antibiotics. Infections with Candida species are most common, although resistant fungi (e.g., Aspergillus, Fusarium) are becoming more common because of the increased use of prophylactic fluconazole.
  - Prolonged treatment with glucocorticoids or other immunosuppressive agents increases the risk of infection with Candida or Aspergillus and of reactivation of endemic fungi even after resolution of neutropenia.
  - Maintenance prophylaxis with trimethoprim-sulfamethoxazole (TMP-SMX; 160/800 mg/d starting 1 month after engraftment and continuing for at least 1 year) is recommended to prevent Pneumocystis jirovecii pneumonia.
- - Parasitic infections: Prophylaxis with TMP-SMX is also protective against disease caused by Toxoplasma as well as against late infections caused by certain bacteria, including Nocardia, Listeria monocytogenes, S. pneumoniae, and H. influenzae.
  - Given increasing international travel, parasitic diseases (e.g., caused by Strongyloides, Leishmania, Giardia, Cryptosporidium) that are typically restricted to particular environments may be more likely to be reactivated in pts after HSCT.
- - Viral infections: Prophylactic acyclovir or valacyclovir for HSV-seropositive pts reduces rates of mucositis and prevents pneumonia and other HSV manifestations.
  - Zoster generally occurs several months after HSCT and usually is managed readily with acyclovir.
  - Human herpesvirus type 6 delays monocyte and platelet engraftment and may be linked to encephalitis or pneumonitis; the efficacy of antiviral treatment has not been well studied.
  - CMV disease (e.g., interstitial pneumonia, bone marrow suppression, colitis, and graft failure) usually occurs 30-90 days after HSCT. Severe disease is more common among allogeneic transplant recipients and is often associated with graft-versus-host disease, with pneumonia as the foremost cause of death. Preemptive therapy (initiation of antiviral therapy only after CMV is detected in blood) has supplanted prophylactic therapy (treatment of all transplant recipients when either the recipient or the donor is seropositive) because of the toxic side effects associated with ganciclovir.
  - EBV lymphoproliferative disease as well as infections caused by respiratory viruses (e.g., respiratory syncytial virus, parainfluenza virus, metapneumovirus, influenza virus, adenovirus) can occur. BK virus (a polyomavirus) has been found in the urine of pts after HSCT and may be associated with hemorrhagic cystitis.

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