Impact of latent toxoplasmosis on the fertility indices of male rats.

Infertility is a prevalent condition affecting approximately 70 million people worldwide and male factor contributes to about fifty percent of the issues. Studies on infectious agents as a possible cause of infertility has become prominent in the past decade. Toxoplasma gondii has emerged as a prime candidate as it has been found in the reproductive organs and semen of males of many animal species and humans. The aim of this study is to assess the effect of latent toxoplasmosis on experimental rat fertility. Ninety Toxoplasma infected rat were used as the experimental group besides, thirty control naïve ones. Both groups were observed clinically. Weekly assessment of fertility indices starting from the 7th week post infection till the 12th week were done by recording rat body weight, weight of testes, semen analysis and histo-morphometric analysis of the testes. Toxoplasma infected rats exhibited significant gradual loss of body weight and the absolute weight of the testes. The sperm characteristic parameters including percentage of motile sperm, percentage of viable sperm and sperm concentration in Toxoplasma infected rats showed highly significant decrease throughout the observation period in comparison to the control group with recording highly significant increase in the percentage of abnormal sperm forms. Pathological insults in tests of the infected rat group were denoted. Our findings demonstrated that Toxoplasma gondii is accused for affecting male rat main reproductive parameters and is implicated in the male reproductive disorders.

Immunological, histopathological, and ultrastructural evidence of steroid-induced reactivation of chronic murine toxoplasmosis.

We developed a model of steroid-induced reactivation of chronic murine toxoplasmosis to mirror similar effects of steroids or other immunosuppressants in infected humans. Immunological, histopathological, and ultrastructural parameters were reported. Prior to steroid administration, mice were infected with 10 cysts of the Me49 strain of Toxoplasma gondii. Mice were treated with dexamethasone (DXM, 2.5 mg/kg/day in drinking water), alone or combined with Solu-Cortef (SOLU, 50 mg/kg by subcutaneous injection 3 times a week) for 7 weeks or left untreated as control. Histopathological changes and ultrastructural effects of steroids on the course of chronic toxoplasmosis were recorded. By electron microscopy, the brains of infected combined treated mice showed an increase in number of tachyzoites and bradyzoites, degeneration, and necrosis of neural cells and hydropic degeneration besides the observed rupture of toxoplasma cysts releasing free tachyzoites in brain tissue. DXM+SOLU-combined treatment also significantly increased mortality, mean brain cyst count as compared to infected untreated mice (P = .01 and). Moreover, 3/12 (25%) treated animals developed clinical signs of toxoplasmic encephalitis. This simple model of drug-induced reactivation of chronic toxoplasmosis permits investigation of host-parasite interaction and may be used for the evaluation of chemotherapeutics in immunocompromised infected patients.

Histopathological, Immunohistochemical and Biochemical Studies of Murine Hepatosplenic Tissues Affected by Chronic Toxoplasmosis.

Toxoplasmosis is a serious health problem in humans and animals resulting from obligatory intracellular invasion of reticuloendothelial tissue by Toxoplasma gondii. The profound pathologic effect of toxoplasmosis is confined to nervous tissue, but many other organs, including the liver and spleen, are insulted. Many molecules like caspase-3, CD3, and CD138 are implicated in the tissue immune response in a trial to alleviate hazardous toxoplasmosis impact. This study aimed to investigate the effect of chronic toxoplasmosis on the liver and spleen tissues of mice using biochemical and histopathological techniques and to detect the activity and level of expression of caspase-3, CD3, and CD138 in these tissues using immunohistochemical labeling. Compared with normal control, altered normal histological features accompanied by inflammatory reaction were recorded in hepatosplenic reticuloendothelial tissues in chronically infected mice. The biochemical profile of the liver has been changed in the form of increased liver enzymes, and oxidative stress has been evidenced by elevated nitric oxide (NO) concentration in liver homogenate. The levels of caspase3, CD3, and CD138 were markedly expressed in the liver and spleen of infected mice. Our findings revealed the persistent effect of latent toxoplasmosis on the host's histological architecture, metabolic, and immunological profile, creating a continued challenging host-parasite relationship.

Simvastatin exerts antifibrotic effect and potentiates the antischistosomal effects of praziquantel in a murine model: Role of IL10.

Previous studies on simvastatin use in experimental schistosomiasis in mice did not provide a full explanation of its mechanism as antischisome. In this study, we tried to find out the role of IL-10 in the mechanism of action of simvastatin. We used 50 clear mice. Ten were used as normal not treated while 40 were infected with shistosome mansoni then divided into 4 groups; 3 treated groups by praziquantel, simvastatin and combined (praziquantel plus simvastatin) respectively and one group non-treated. The simvastatin treated group showed shortening and loss of the tubercles and disappearance of the spines with swelling and twisted shape of the worms. In addition, it also showed mitigation of ovideposition activity of the worms in the liver and reduction of the fibrous component of the liver granuloma producing a protective effect on the liver. This effect was associated with lowering of IL-10. This may explain the role of IL-10 in the protective effect of simvastatin. Combination of treatment with simvastatin plus praziquantel produced more significant effects in different parameters compared with praziquantel treated group. We recommend using simvastatin as add on therapy to standard antischistosomal therapy, praziquantel. Both drugs affect the worm motility and sucker activity and the ova deposition. Simvastatin has an additional pleiotropic effect halting inflammation and decreasing fibrosis due to increasing IL-10 leading to a hepatoprotective effect. Further clinical studies are needed to further validate these findings.