Abdominal pain and bacterial meningitis in a previously healthy young adult.

Figure 1. Peripheral blood smear showing flower or floret cell (arrow) with characteristic cerebriform nucleus associated with human T cell lymphotropic virus infection. Diagnosis: human T cell lymphotropic virus type 1 (HTLV-1) infection with associated Strongyloides stercoralis hyperin-fection and bacterial (i.e., vancomycin-resistant Enterococcus faecium) meningitis. HTLV-1 is a single-stranded RNA retrovirus endemic to focal areas of the world (Japan, Israel, Iran, and Melanesia), as well as larger geographic regions (West Africa, South America, and the Caribbean) [1]. Transmission is thought to be primarily cell associated, occurring peripartum, intravenously, or sexually [1]. Our patient likely acquired HTLV-1 via mother-to-child transmission at birth or during breast-feeding while still an infant in Sierra Leone. The flowe cell (also known as a flo et or cleaved cell) is characteristic of HTLV-1 infection. HTLV-1 infects CD4 + cells and induces clonal proliferation [2]. Several studies suggest that the nuclear abnormalities of flowe cells are a consequence of viral expression of the oncoprotein Tax [3, 4]. Tax causes cell-cycle dysregulation by targeting key regulators of the cell cycle and interfering with tumor-suppressor proteins [4]. This interference may then contribute to the induction of genomic instability and defective cell division that results in the formation of multinucleated giant cells with the characteristic cer-ebriform or convoluted nuclear structure [3, 5]. Flower cells can be found in asymptomatic carriers of HTLV-1 [6, 7], but they are also the characteristic morphologic feature of both acute and chronic adult T cell leukemia and/or lym-phoma, which is a severe complication of HTLV-1 infection. Flower cells can also be seen in mycosis fungoides (Sézary cells) [8, 9]; other malignant disorders, including acute T cell lym-phoblastic leukemia; and chronic B cell lymphoproliferative diseases [10]. HTLV-1 infection is associated with immunodeficienc and a predisposition to opportunistic infections, such as Pneumo-cystis carinii pneumonia, Cryptococcus neoformans meningitis, disseminated fungal infections, and S. stercoralis hyperinfection [11, 12]. The relationship between HTLV-1 and strongyloidiasis has been well documented in Japan [13] and Peru [14]. HTLV-1 decreases the Th2 immune response that is necessary for control of strongyloidiasis [15]. This decreased immune response to infection with S. stercoralis leads to more-severe strongyloidiasis, as well as decreased efficac of anthelminthic treatment [12, 16]. The strongyloidiasis hyperinfection syndrome is characterized by disseminated infection and an association with enteric bacteremia and meningitis [12, 17–19]. Strongyloidiasis hy-perinfection syndrome has been classically described in association with corticosteroid therapy but is also associated with other immunosuppressive …