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 affects HAT disease progression with a secondary infection with () 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 (100 cercariae) and (5.0 × 104) separately or together. Twenty-one days after infection with , mice were sacrificed and samples were collected for analysis.

RESULTS

The primary infection with significantly enhanced successive infection by the ; consequently, promoting HAT disease severity and curtailing host survival time. -induced impairment of the neurological integrity and breach of the blood-brain barrier were markedly pronounced on coinfection with Coinfection with and 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, -driven dyslipidemia was significantly enhanced by the coinfection of mice with Moreover, coinfection with and led to a strong immune response characterized by a significant increase in serum TNF- and IFN-. infection enhanced -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 exacerbates disease severity of secondary infection with in a mouse model that is associated with harmful inflammatory response, oxidative stress, and organ injury.