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CHaPtEr 37 Infections in the Immunocompromised Host 531

A B C
fIG 37.4 Disseminated Histoplasmosis in a Patient from an Endemic Area 3 Months After
a Heart Transplantation. (A) Chest X-ray with bilateral reticulonodular infiltrates. (B) Computed
tomography (CT) scan of the chest with bilateral patchy and nodular infiltrates. (C) Lung biopsy.
Gomori methenamine silver (GMS) stain shows yeast forms compatible with Histoplasma
capsulatum.

CLINICaL PEarLS
Infections in Bone Marrow Transplant Recipients
• Infections 2–4 weeks posttransplantation are usually caused by profound
neutropenia and damage to mucosal surfaces.
• Between the period of engraftment and posttransplant weeks 15–20,
OIs predominate and are commonly associated with the development
of acute graft-versus-host disease (GvHD) and its treatment.
• Serious infections occurring 4–6 months following transplantation are
seen predominantly in patients with chronic GvHD.

The risk for infection is influenced by several factors and
varies significantly between type of transplantation (autologous
vs allogeneic), stem cell source (bone marrow, PBSC, and cord
blood), degree of human leukocyte antigen (HLA) matching,
+
hematopoietic potential of the graft (number of infused CD34 fIG 37.5 Magnetic resonance imaging (MRI) scan of the brain
cells), T-cell depletion, type of conditioning (myeloablative vs of a patient with human herpesvirus-6 (HHV-6) encephalitis 36
reduced intensity vs nonmyeloablative), underlying disease, days after a matched unrelated donor hematopoietic stem cell
presence of graft rejection or GvHD, donor–recipient serological transplantation (HSCT) for diffuse large B-cell lymphoma. Flair
status to certain infections (e.g., CMV infection), and use of axial image shows bilateral medial temporal lobe edema compat-
antimicrobial prophylaxis. 47 ible with limbic encephalitis.
Autologous HSCT (auto-HSCT) refers to the patient serving
as his or her own donor to allow administration of myeloablative
chemotherapy. Because there is no risk of rejection or GvHD
and because after engraftment there is an early and progressive are associated with faster neutrophil engraftment compared with
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recovery of cell-mediated immunity, the risk for infection is cord blood units and therefore lower rates of infection. Bacterial
much lower than in allo-HSCT. The major compromises in host infections are most common. However, when neutropenia is
defenses occur before engraftment and are usually related to prolonged, the risk of invasive fungal infection increases signifi-
neutropenia and mucosal injury. In contrast, in allo-HSCT, the cantly. Without acyclovir prophylaxis, reactivation of severe HSV
risk for infection can be divided into three periods: preengraft- infection is frequent.
ment, early postengraftment, and late postengraftment periods.
Early Postengraftment Period
Preengraftment Period The resolution of neutropenia marks the beginning of this period
The major impairments in host defenses before engraftment are and usually lasts 2–3 months (Fig. 37.5). This period is character-
neutropenia and mucosal injury. This period varies widely between ized by a progressive but slow recovery of B- and T-lymphocyte
different types of conditioning regimens and stem-cell source. function; thus viral and fungal OIs can occur. The risk of infection
In general, when ablative regimens are used, engraftment occurs is higher in patients who develop acute GvHD and therefore
any time between 15 and 45 days after transplantation and can require high dose steroids. Common bacterial infections can
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be as short as 5–7 days with nonablative regimens. PBSC grafts still occur and are usually related to indwelling catheters or GvHD