T oxoplasmosis is a widespread parasitic infection that is frequently asymptomatic in immunocompetent patients. However, this obligate intracellular protozoan parasite can evade the immune system (1, 2) and persist for the life of its host in cyst form, predominantly in the brain, retina, and muscles. Reactivation of latent cysts may occur when the immune system fails to maintain cytokine pressure, which mainly relies on gamma interferon (IFN-␥) (3). Cyst reactivation can lead to ocular toxoplasmosis, cerebral toxoplasmosis (CT), or disseminated toxoplasmosis, which involves most frequently the lungs but potentially all organs. Failure of an efficient Th1 immune response mainly results from acquired immunosuppression, through HIV infection or immunosuppressive therapy. Both primary acquired and reactivated infections are life-threatening in immunocompromised patients (ICPs). Definitive diagnosis can be obtained by the detection of parasites in blood, cerebrospinal fluid (CSF), bronchoalveolar lavage (BAL) fluid, or virtually any tissue by using PCR, which is the most sensitive method (4).Prevention of CT in patients with HIV is an object of consensus, and guidelines recommend co-trimoxazole (sulfamethoxazole-trimethoprim) chemoprophylaxis in Toxoplasma-seropositive patients when CD4 ϩ cell counts fall below 200 cells/l (4), a prophylactic regimen which also protects patients from Pneumocystis jirovecii pneumonia. Nevertheless, toxoplasmosis remains Citation Robert-Gangneux F, Sterkers Y, Yera H, Accoceberry I, Menotti J, Cassaing S, Brenier-Pinchart M-P, Hennequin C, Delhaes L, Bonhomme J, Villena I, Scherer E, Dalle F, Touafek F, Filisetti D, Varlet-Marie E, Pelloux H, Bastien P. 2015. Molecular diagnosis of toxoplasmosis in immunocompromised patients: a 3-year multicenter retrospective study.