Regulation of immunity during visceral Leishmania infection

Unicellular eukaryotes of the genus Leishmania are collectively responsible for a heterogeneous group of diseases known as leishmaniasis. The visceral form of leishmaniasis, caused by L. donovani or L. infantum, is a devastating condition, claiming 20,000 to 40,000 lives annually, with particular incidence in some of the poorest regions of the world. Immunity to Leishmania depends on the development of protective type I immune responses capable of activating infected phagocytes to kill intracellular amastigotes. However, despite the induction of protective responses, disease progresses due to a multitude of factors that impede an optimal response. These include the action of suppressive cytokines, exhaustion of specific T cells, loss of lymphoid tissue architecture and a defective humoral response. We will review how these responses are orchestrated during the course of infection, including both early and chronic stages, focusing on the spleen and the liver, which are the main target organs of visceral Leishmania in the host. A comprehensive understanding of the immune events that occur during visceral Leishmania infection is crucial for the implementation of immunotherapeutic approaches that complement the current anti-Leishmania chemotherapy and the development of effective vaccines to prevent disease.The research leading to these results has received funding from the European Community’s Seventh Framework Programme under grant agreement No.602773 (Project KINDRED). VR is supported by a post-doctoral fellowship granted by the KINDReD consortium. RS thanks the Foundation for Science and Technology (FCT) for an Investigator Grant (IF/00021/2014). This work was supported by grants to JE from ANR (LEISH-APO, France), Partenariat Hubert Curien (PHC) (program Volubilis, MA/11/262). JE acknowledges the support of the Canada Research Chair Program

Experimental Infections Of Domestic Rabbits (Oryctolagus cuniculus) With Trypanosoma brucei And Trypanosoma congolense: A Comparative Study

Comparative study of single infections of domestic rabbits (Oryctolagus cuniculus) with Nigerian isolates of Trypanosoma brucei (Gboko strain), and Trypanosoma congolense (Binchi strain) was carried out in the laboratory for clinical and haematological effects. Eighteen rabbits of 10-14 weeks old weighing between 600-1200 grams were used for the study. The rabbits of both sexes were randomly selected and divided into groups. The level of infection was studied by determining total red blood cell (RBC) count, haemoglobin estimation, total and differential white blood cell (WBC) count, changes in body weight, mortality, rectal temperature changes and other clinical signs of trypanosomiasis. There was significant reduction (P<0.001) in the total red blood cell counts and haemoglobin level in the infected rabbits when compared to the control rabbits with the effect of being more pronounced in rabbits infected with T. congolense. Both parasites produced similar clinical symptoms which included weight loss, unthriftiness, anorexia, fever, paleness of mucous membrane, and oedema of the facial region. One death was recorded in each of the infected group. Possible reasons for the significant differences in the total red blood cell count, haemoglobin level, and total white blood cell count are discussed.Keywords: Single infections, T. brucei, T. congolense, rabbits, comparativ