T oxoplasma gondii is a protozoan parasite distributed worldwide and infecting one-third of the global population. Infection is acquired by ingestion of parasites via consumption of undercooked meat containing tissue cysts or of water, fruits, or vegetables contaminated with oocysts. In immunocompetent individuals, primary infection results in the formation of tissue cysts and in serological evidence of infection. However, in immunocompromized patients, such as hematopoietic stem cell transplant (HSCT) recipients, toxoplasmosis is often a life-threatening opportunistic infection arising either from transmission of the parasites via a graft from a seropositive donor to a seronegative recipient or, far more frequently, from reactivation of a preexisting latent infection in a seropositive recipient, regardless of the donor's serological status (1). After allogeneic HSCT, studies have shown an incidence of invasive toxoplasmosis among seropositive recipients of 4% to 6%, with an estimated mortality rate of 60% to 90% (2, 3).Nijmegen breakage syndrome (NBS) is a rare, autosome-recessive DNA repair disorder characterized by microcephaly with normal intelligence, facial dysmorphia (bird-like facial features), primary immunodeficiency, and a predisposition to lymphoid malignancies at a young age (4, 5). Treatment of NBS-related malignancies is challenging due to the chromosomal instability and immunodeficiency which make the patients more susceptible to the toxic effects of standard chemotherapy and radiation. Although lymphoid malignancies occurring in NBS patients can be successfully brought into remission using standard chemotherapy regimens with minor dose modifications (6, 7), a high rate of treatment failure and relapse has been observed (8). An alternative treatment option for malignancies in NBS is HSCT from HLAidentical donors, which has been shown not only to correct humoral and cellular immunodeficiency but also to lower the secondary malignancy rate (9).We here present a case of an early and fulminant post-HSCT reactivation of toxoplasmosis caused by an atypical T. gondii strain in a young patient with NBS that contributed to a subsequent fatal outcome within 40 days after transplantation. This case is the first report of increased clinical severity of toxoplasmosis caused by an atypical strain in the setting of immunosuppression. It also stresses the value and necessity of the use of quantitative molecular methods to monitor T. gondii reactivation in cases of reactivation risk.(The results of this study have been presented in part at the 11th European Multicolloquium of Parasitology [EMOP XI],