RESUMEN
Introduction: Human African trypanosomiasis (HAT) and schistosomiasis are neglected parasitic diseases found in the African continent. This study was conducted to determine how primary infection with Schistosoma mansoni affects HAT disease progression with a secondary infection with Trypanosoma brucei rhodesiense (T.b.r) in a mouse model. Methods: Female BALB-c mice (6-8 weeks old) were randomly divided into four groups of 12 mice each. The different groups were infected with Schistosoma mansoni (100 cercariae) and Trypanosoma brucei rhodesiense (5.0 × 104) separately or together. Twenty-one days after infection with T.b.r, mice were sacrificed and samples were collected for analysis. Results: The primary infection with S. mansoni significantly enhanced successive infection by the T.b.r; consequently, promoting HAT disease severity and curtailing host survival time. T.b.r-induced impairment of the neurological integrity and breach of the blood-brain barrier were markedly pronounced on coinfection with S. mansoni. Coinfection with S. mansoni and T.b.r resulted in microcytic hypochromic anemia characterized by the suppression of RBCs, hematocrit, hemoglobin, and red cell indices. Moreover, coinfection of the mice with the two parasites resulted in leukocytosis which was accompanied by the elevation of basophils, neutrophils, lymphocytes, monocytes, and eosinophils. More importantly, coinfection resulted in a significant elevation of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total bilirubin, creatinine, urea, and uric acid, which are the markers of liver and kidney damage. Meanwhile, S. mansoni-driven dyslipidemia was significantly enhanced by the coinfection of mice with T.b.r. Moreover, coinfection with S. mansoni and T.b.r led to a strong immune response characterized by a significant increase in serum TNF-α and IFN-γ. T.b.r infection enhanced S. mansoni-induced depletion of cellular-reduced glutathione (GSH) in the brain and liver tissues, indicative of lethal oxidative damage. Similarly, coinfection resulted in a significant rise in nitric oxide (NO) and malondialdehyde (MDA) levels. Conclusion: Primary infection with S. mansoni exacerbates disease severity of secondary infection with T.b.r in a mouse model that is associated with harmful inflammatory response, oxidative stress, and organ injury.
RESUMEN
Animal models for the toxoplasmosis are scarce and have limitations. In this study, a neurological mouse model was developed in BALB/c mice infected intraperitoneally with 15 cysts of a Toxoplasma gondii isolate. The mice were monitored for 42 days and euthanized at different time points. Another group of mice were orally treated with dexamethasone (DXM: 2.66 mg/kg daily, 5.32 mg/kg daily) at 42 days after infection and monitored for a further 42 days. A mortality rate of 15% and 28.6% was observed in mice given 2.66 mg/kg/day and 5.32 mg/kg/day of DXM, respectively. The mean cyst numbers in the brain of DXM treated mice increased up to twofold compared with chronically infected untreated mice. Infections up to 42 days were associated with an increase in both IgM and IgG levels but following dexamethasone treatment, IgM levels declined but IgG levels continued on rising. The brain of toxoplasmosis infected mice showed mononuclear cellular infiltrations, neuronal necrosis, and cuffing. The severity of pathology was higher in mice treated with dexamethasone compared to the positive control groups. The findings of this study demonstrate that DXM-induced reactivation of chronic toxoplasmosis may be a useful development of laboratory animal model in outbred mice used for in vivo studies.
