Hhv6

Community acquired respiratory

Fungi

Zygomycetes Candida species

Fusaria species

Pseudallescheria boydii

Parasites

Pneumocystis Pneumonia carinii

Toxoplasma gondii CNS, pneumonia, disseminated disease;

reactivation of latent infection Strongyloides Enterocolitis, pneumonia, bowel stercoralis perforation, Gram-negative bacteremia;

accelerated autoinfection cycle

Several pathogens require special comment. Legionellosis is uncommon but has been reported in the setting of HSCT.43 The disease may occur in the pretransplant or preengraftment periods, but is most common in the early engraftment period.43 A sentinel

Intravascular devices Mouth and bowel with GVHD Mouth and bowel with GVHD Intravascular devices, GI tract with GVHD

Pneumonia, nephritis, hemorrhagic cystitis, hemorrhagic colitis, hepatitis Fever, rash, interstitial pneumonia, encephalitis

Upper respiratory tract infections, pneumonia viruses

Pneumonia, sinusitis

Fungemia, hepatosplenic candidiasis, disseminated infection; intravascular devices and gut with GVHD

Fungemia, cutaneous disease, pneumonia

Pneumonia case occurring beyond day 10 of hospitalization should raise the possibility of nosocomial transmission, and an appropriate epidemiologic and environmental investigation is mandatory.2 Unrecognized nosocomial transmission of legionellosis for over a decade in the transplant setting has been described.44 HSCT patients with legionellosis present with fever and lobar, patchy, or nodular pulmonary infiltrates. In those with nodular infiltrates, the disease may mimic invasive pulmonary aspergillosis, the most common cause of such infiltrates in this setting. HSCT recipients with legionellosis are at increased risk for mortality and may require more prolonged courses of therapy than immunocompetent individuals.44 Legionella pneu-mophila infections are more often fatal than those due to non-pneumophila Legionella strains.

Listeriosis in HSCT recipients is rare, but occurs most often in the early postengraftment period.45 Meningoencephalitis and bacteremia are the most common clinical presentations. A history of high-risk food ingestion associated with listeriosis is typically absent.

Parasitic infections are uncommon following HSCT, but are most likely to occur in the early postengraft-ment period. The incidence of Pneumocystis carinii pneumonia has declined dramatically with the widespread use of chemoprophylaxis. The median time to onset is 9 weeks following HSCT. Patients typically present with fever, worsening dyspnea, dry cough, and interstitial pulmonary infiltrates.46 One hundred and ten cases of toxoplasmosis have been described following HSCT47; 64% have occurred between days 31 and 100, likely representing reactivation of latent infection in the face of immunosuppression. Forty-eight percent of cases have been confined to the brain. Disseminated infection occurred in 48%. Fever was the most common sign, but was only present in 43%. Focal neurologic symptoms, headache, altered mentation, and respiratory complaints were present in a minority of patients. Meningitis occasionally accompanies cerebral toxoplasmosis, and the organism can been identified on cytologic examination of cerebrospinal fluid. Hyperinfection strongyloidiasis is rare following HSCT and has not been reported in autologous recipients.2 Immunosuppression in allogeneic recipients leads to acceleration of the autoinfection cycle of S. stercoralis in those with unrecognized asymptomatic infection. Patients typically develop symptoms 4-6 weeks from the initiation of immunosuppressive therapy consisting of fever, diarrhea, respiratory symptoms, and occasionally intestinal perforation owing to widespread migration of larval parasites through the bowel wall and the lungs.48 Specimens of stool, sputum, and bronchoalveolar lavage fluid typically demonstrate larvae of S. stercoralis on parasitologic examination.

CMV is the most important and common viral pathogen encountered in the early postengraftment period. In the era prior to prophylactic or preemptive therapy, morbidity and mortality from CMV were substantial. Among seropositive allogeneic HSCT recipients, the group at greatest risk, the incidence of CMV infection varied from 42% to 69%; symptomatic disease developed in 16-25%, with pneumonia in up to 5%.49 The incidence in autologous HSCT recipients was lower but still substantial. Prior to the availability of antiviral therapy, mortality from CMV pneumonia following HSCT approached 50%.50 The widespread used of targeted prophylaxis or preemptive therapy from engraftment to day 100 in allogeneic HSCT recipients has led to a significant decline in the incidence of symptomatic disease during the early engraftment period, but late disease beyond day 100 is increasingly recognized.551 Risk factors for symptomatic CMV disease include advanced age, conditioning with total body irradiation, seropositive recipient status, HSCT from a matched unrelated donor, CD34+ allogeneic HSCT, acute GVHD, and high titers of circulating CMV. Symptomatic disease is uncommon in autologous HSCT recipients; patients at higher risk include seropositive recipients with underlying hematologic malignancies, those receiving intensive conditioning regimens, and recent recipients of fludarabine or 2-chlorodeoxyadeno-sine.2 CMV appears to be immunomodulatory and seronegative allogeneic HSCT recipients with seropositive donors have a higher risk of death from bacterial and fungal infections.49

The common clinical syndromes produced by CMV include fever without localizing findings, interstitial pneumonia, enterocolitis, and bone marrow suppression. Hepatitis, retinitis, and CNS disease are less common.

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