A Novel Calcium-Dependent Protein Kinase 1 Inhibitor Potently Prevents Transmission to Foetuses in Mouse.

Treatments currently used to prevent congenital toxoplasmosis are non-specific of and have grievous side effects. To develop a more specific and less toxic drug, we have designed SP230, an imidazo[1,2-]pyridazine salt targeting the calcium-dependent protein kinase 1 (CDPK1) and active against acute toxoplasmosis in mice. Efficiency of SP230 to inhibit foetal transmission of the parasite was evaluated in a mouse model of congenital toxoplasmosis.

Engineering and Functional Evaluation of Neutralizing Antibody Fragments Against Congenital Toxoplasmosis.

Maternal-fetal transmission of Toxoplasma gondii tachyzoites acquired during pregnancy has potentially dramatic consequences for the fetus. Current reference-standard treatments are not specific to the parasite and can induce severe side effects. In order to provide treatments with a higher specificity against toxoplasmosis, we developed antibody fragments-single-chain fragment variable (scFv) and scFv fused with mouse immunoglobulin G2a crystallizable fragment (scFv-Fc)-directed against the major surface protein SAG1.

[Tricks and misuses of rapid diagnostic testing for malaria diagnosis].

Molecular biology or immunochromatographic tests are conventionally offered as aids in the routine diagnosis of malaria. However, the interpretation of their results requires a precise knowledge of their limits, both by the biologist and the physician. It is in particular conditioned by thorough interview of the patient in order to seek a history of recent or even older malaria disease.

Imidazo[1,2-b]pyridazines targeting Toxoplasma gondii calcium-dependent protein kinase 1 decrease the parasite burden in mice with acute toxoplasmosis.

The current therapeutic arsenal for toxoplasmosis is restricted to drugs non-specific to the parasite which cause important side effects. Development of more efficient and specific anti-Toxoplasma compounds is urgently needed. Imidazo[1,2-b]pyridazines designed to inhibit the calcium-dependent protein kinase 1 of Toxoplasma gondii (TgCDPK1) and effective against tachyzoite growth in vitro at submicromolar ranges were modified into hydrochloride salts to be administered in vivo in a mouse model of acute toxoplasmosis.

Synthetic parasites: a successful mucosal nanoparticle vaccine against Toxoplasma congenital infection in mice.

Aim: Development of protein vaccine to prevent congenital infection is a major public health priority. Our goal is the design of mucosal synthetic pathogen inducing protective immune responses against congenital toxoplasmosis.

Materials & Methods: Mice were immunized intranasally, establishing pregnancy and challenging orally.

Pulmonary toxoplasmosis in immunocompromised patients with interstitial pneumonia: a single-centre prospective study assessing PCR-based diagnosis.

Aims: Pulmonary toxoplasmosis has become a very rare parasitic infection since the advent of highly active antiretroviral therapies. It is generally diagnosed by the direct microscopic observation of Toxoplasma gondii tachyzoites in bronchoalveolar lavage fluid (BALF). The aim of this study was to assess possible improvements in diagnostic performance associated with the use of real-time PCR.

[Toxoplasmic cyst and heart transplant: a case report of serological reactivation in an acute graft rejection context].

We describe the case of a serological reactivation in a Toxoplasma-seropositive subject, following a cardiac transplantation transmitting cysts contained in the myocardial tissue. In a context of acute graft rejection, primary chemoprophylaxis enables to avoid onset of opportunistic toxoplasmosis, emerging with immunodepletion performed by high-dose steroids. Then, we draw up a brief review of the bibliographical literature about pathophysiological mechanisms of toxoplasmic reactivation in heart transplants.

Interleukin 17 receptor signaling is deleterious during Toxoplasma gondii infection in susceptible BL6 mice.

Th17 cells are involved in host defense against several pathogens. Using interleukin (IL) 17RA-deficient mice, we demonstrated reduced ileitis with diminished neutrophil recruitment and inflammatory lesions in the ileum, in the regional lymph node, in the spleen, and in the liver at day 7 and prolonged survival after Toxoplasma gondii infection. In addition, IL-17A antibody neutralization reduced inflammation and enhanced survival in BL6 mice.