Coinfection with Schistosoma mansoni Enhances Disease Severity in Human African Trypanosomiasis

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 bruc...

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Main Authors: Nancy S. Mitalo, Naomi N. Waiganjo, John Mokua Mose, David O. Bosire, James O. Oula, Alfred Orina Isaac, James Nyabuga Nyariki
Format: Article
Language:English
Published: Wiley 2023-01-01
Series:Journal of Tropical Medicine
Online Access:http://dx.doi.org/10.1155/2023/1063169
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author Nancy S. Mitalo
Naomi N. Waiganjo
John Mokua Mose
David O. Bosire
James O. Oula
Alfred Orina Isaac
James Nyabuga Nyariki
author_facet Nancy S. Mitalo
Naomi N. Waiganjo
John Mokua Mose
David O. Bosire
James O. Oula
Alfred Orina Isaac
James Nyabuga Nyariki
author_sort Nancy S. Mitalo
collection DOAJ
description 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.
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spelling doaj-art-1ba85cc7763344e9b87c43c0f33dcfb22025-08-20T02:01:50ZengWileyJournal of Tropical Medicine1687-96942023-01-01202310.1155/2023/1063169Coinfection with Schistosoma mansoni Enhances Disease Severity in Human African TrypanosomiasisNancy S. Mitalo0Naomi N. Waiganjo1John Mokua Mose2David O. Bosire3James O. Oula4Alfred Orina Isaac5James Nyabuga Nyariki6Department of Biomedical Science & TechnologyDepartment of Biomedical Science & TechnologyDepartment of Biomedical Science & TechnologyDepartment of Biochemistry and BiotechnologyDepartment of Biomedical Science & TechnologyDepartment of Pharmaceutical Sciences and TechnologyDepartment of Biochemistry and BiotechnologyIntroduction. 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.http://dx.doi.org/10.1155/2023/1063169
spellingShingle Nancy S. Mitalo
Naomi N. Waiganjo
John Mokua Mose
David O. Bosire
James O. Oula
Alfred Orina Isaac
James Nyabuga Nyariki
Coinfection with Schistosoma mansoni Enhances Disease Severity in Human African Trypanosomiasis
Journal of Tropical Medicine
title Coinfection with Schistosoma mansoni Enhances Disease Severity in Human African Trypanosomiasis
title_full Coinfection with Schistosoma mansoni Enhances Disease Severity in Human African Trypanosomiasis
title_fullStr Coinfection with Schistosoma mansoni Enhances Disease Severity in Human African Trypanosomiasis
title_full_unstemmed Coinfection with Schistosoma mansoni Enhances Disease Severity in Human African Trypanosomiasis
title_short Coinfection with Schistosoma mansoni Enhances Disease Severity in Human African Trypanosomiasis
title_sort coinfection with schistosoma mansoni enhances disease severity in human african trypanosomiasis
url http://dx.doi.org/10.1155/2023/1063169
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