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Background: Toxoplasma gondii, a common opportunistic protozoan, is a leading cause of illness and mortality among immunosuppressed individuals and during congenital infections. Current therapeutic strategies for toxoplasmosis are not fully effective at curtailing disease progression in these cases. Given the parasite ability to influence host immunity and metabolism, understanding of the metabolic alterations in the host's immune organs during T. gondii infection may enhance the understanding of the molecular mechanisms that define the pathophysiology of T. gondii infection. Methods: We investigated the global metabolic changes in the spleen of BALB/c mice at early and late stage of infection with T. gondii using LC-MS/MS-based metabolomics. Multivariate data analysis methods, principal components analysis (PCA) and partial least squares discriminant analysis (PLS-DA), were used to identify metabolites that are influenced by T. gondii infection. Results: Multivariate analyses clearly separated the metabolites of spleen of infected and control mice. A total of 132 differential metabolites were identified, 23 metabolites from acutely infected versus control mice and 109 metabolites from chronically infected versus control mice. Lipids, hormones, lactones, acids, peptides, antibiotics, alkaloids and natural toxins were the most influenced chemical groups. There were 12 shared differential metabolites between acutely infected versus control mice and chronically infected versus control mice, of which 4,4-Dimethyl-5alpha-cholesta-8,14,24-trien-3beta-ol was significantly upregulated and ubiquinone-8 was significantly downregulated. Major perturbed metabolic pathways included primary bile acid biosynthesis, steroid hormone biosynthesis, biotin metabolism, and steroid biosynthesis, with arachidonic acid metabolism being the most significantly impacted pathway. These metabolic changes suggest a multifactorial nature of the immunometabolic responses of mouse spleen to T. gondii infection. Conclusions: This study demonstrated that T. gondii infection can cause significant metabolomic alterations in the spleen of infected mice. These findings provide new insights into the molecular mechanisms that underpin the pathogenesis of T. gondii infection. [ABSTRACT FROM AUTHOR]

Paratubercolosis (PTB) is an important bacterial disease in ruminants caused by Mycobacterium avium subspecies paratuberculosis (MAP). However, no information is available about MAP infection in yaks (Bos mutus) in China. Blood samples were collected from 1584 yaks, which consist of 610 black yaks and 974 white yaks from April 2013 through March 2014 from Gansu province, northwest China, and were tested for the antibodies against MAP using an indirect ELISA kit commercially available. The seroprevalence of MAP in yaks was 20.52% (325/1584), 22.13% (135/610) for black yaks and 19.51% (190/974) for white yaks. The MAP seroprevalences of yaks were detected in all three regions, 19.51, 19.86 and 22.84%, respectively. Logistic regression analysis suggested that abortion history was the risk factor concerning MAP infection in yaks (P<0.05), breed, gender, age, geographic origin, and season were not considered as risk factors in this study. As far as we know, this is the first report of MAP infection in yaks in China, which provides information for controlling MAP infection in yaks. [ABSTRACT FROM AUTHOR]