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Multisystem febrile illness in a cord-blood transplant recipient.

Diagnosis: Acute disseminated toxoplasmosis in a cord-blood transplant recipient. Figure 1 shows Toxoplasma gondii tachyzoites, whereas Figure 2 portrays a cystic form within a macrophage. T. gondii was confirmed by polymerase chain reaction detection in bone marrow and blood specimens. T. gondii is an intracellular parasite with a worldwide distribution. Seroprevalence is usually reported to be ∼15% in the United States but 150% in southern Europe. Recipients of allogeneic hematopoietic stem cell transplants (HCTs) are profoundly immunocompromised and represent a patient population at risk for severe infection. However, toxoplasmosis following HCT is infrequently reported and is usually caused by reactivation of latent infection in seropositive patients. The overall incidence of reactivation in allogeneic HCT is 1% [1–3]. Reactivation toxoplasmosis typically occurs in the second to third month after receipt of the transplant, and patients usually have an AIDS-like presentation with central nervous system lesions [2]. In contrast, seronegative recipients usually develop acute primary infection. Acute infection in this population generally results from the allograft itself (from a seropositive donor) or the direct infusion of contaminated blood or blood products (survival of organisms in stored citrated blood has been documented for up to 2 months). Acute toxoplasmosis presents in the immediate period after engraftment (3 weeks to 3 months) and is of greater severity than reactivation disease. The clinical picture is often one of disseminated disease, as demonstrated by multisystem organ failure, isolation of the organism from numerous body sites (brain, liver, lungs, bone marrow, heart, spleen, omentum, and intestines), and widespread involvement at autopsy [3, 4]. Definite diagnosis is made by pathologic examination of an infected organ; however, molecular diagnosis by detection of T. gondii DNA in blood is possible, because parasitemia is common in the compromised host [5, 6]. Effective therapy consists of the combination of pyrimethamine plus sulfadiazine or pyrimethamine plus clindamycin [7]. In HCT, trimethoprim-sulfamethoxazole is usually used for Pneumocystis carinii pneumonia prophylaxis, and this combination also offers protection against T. gondii. However, in cord-blood HCT, myelosuppressive drugs, such as trimetho-