Pathogenesis of anemia in Trypanosoma brucei-infected mice

Amole, Babatunde O.; Clarkson, Allen B.; Shear, Hannah L.

doi:10.1128/iai.36.3.1060-1068.1982

Cited by 48 publications

(27 citation statements)

References 43 publications

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“…Results on the PCV showed that mice infected with BSF or CNS derived trypanosomes recorded significant decline confirming previous observations associating anaemia with human infection [34] as well as with experimental human trypanosomiasis using vervet monkeys and mice [35,36]. However, data generated from our study indicated that the decline was more significant in mice infected with CNS than in BSF derived trypanosomes.…”

Section: Discussionsupporting

confidence: 89%

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Phenotypic characteristics distinguishing bloodstream form and central nervous form of Trypanosoma brucei rhodesiense.

Ndung'u¹,

Ga²,

Jk³

et al. 2020

Preprint

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Background: Phenotypic and morphological characteristics distinguishing from bloodstream form (BSF) and central nervous system (CNS) of Trypanosoma brucei rhodesiense (Tbr) are poorly understood. Method: To identify these distinguishing characteristics, we separately infected four donor mice with each of five Tbr isolates (KETRI 2537/3537/2656/3459 and EATRO 2291). At 21 days post infection (DPI), donor mice were euthanized, BSF or CNS derived trypanosomes recovered and used for the following studies: 1) determination of morphological characteristics 2) pathogenicity studies using groups of 10 mice per isolate form. We then assessed differences in their lengths and morphology) and other characteristics including pre-patent period (PP), parasitaemia progression, packed cell volume (PCV), body weight, survival times, gross pathology, and histopathology. All analyses of data were conducted using GenStat, UK where p ⩽ 0.05 were considered statistically significant. Differences between and within the means were analyzed using one-way ANOVA. General Linear Model was used to analyze data on the length of the trypanosome. Survival data analysis was carried out employing the Kaplan–Meier method. Results: Morphologically, the CNS forms were predominantly long slender (LS) while BSF forms consisted of a mixture of short stumpy and intermediate forms. The mean length of CNS trypanosomes was 0.6 micrometer longer than their counterpart BSF derived trypanosomes. The PP was significantly (p<0.05) shorter and progression to peak parasitaemia faster (7 vs 9 days) in CNS than BSF derived trypanosomes. PCV declined by 21.6% and 26.9% in BSF and CNS infected mice respectively whereas non-infected control increased by 3.8% at 14 DPI. Body weight changes in BSF and CNS infected mice were (12.7% and 9.2% respectively) and significantly (p <0.05) lower than in non-infected control (27.6%) at 14 DPI. Gross pathology changes (splenomegaly and hepatomegaly) and histopathology changes were pronounced in mice infected with CNS relative to BSF trypanosome forms. Changes in histopathology included congestion, infiltration with inflammatory cells, hemolysis and necrosis, all indicators of differential virulence of the forms. Conclusion: Our study identified higher pathogenicity in CNS relative to BFS derived trypanosome forms in the mouse model. We also identified KETRI 2656 as a suitable isolate for acute menigo- encephalitic studies.

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Section: Discussionsupporting

confidence: 89%

“…During this period, the decline in PCV recorded stability ( Fig. 6 (vi)) characteristic of chronic phase anaemia [36].…”

Section: Discussionmentioning

confidence: 87%

Phenotypic characteristics distinguishing bloodstream form and central nervous form of Trypanosoma brucei rhodesiense.

Ndung'u¹,

Ga²,

Jk³

et al. 2020

Preprint

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“…Moderate to severe anemia also occurs in mice experimentally infected with Trypanosoma brucei , another blood-borne, extracellular pathogen that features antigenic variation [ 114 ]. This has been attributed to sensitization to IgM-antigen complexes [ 115 ], inflammatory cytokines such as TNF-α [ 116 ], and erythrophagocytosis [ 117 ].…”

Section: Resultsmentioning

confidence: 99%

Pathogen and Host Response Dynamics in a Mouse Model of Borrelia hermsii Relapsing Fever

Crowder

Langeroudi

Estabragh

et al. 2016

Veterinary Sciences

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Most Borrelia species that cause tick-borne relapsing fever utilize rodents as their natural reservoirs, and for decades laboratory-bred rodents have served as informative experimental models for the disease. However, while there has much progress in understanding the pathogenetic mechanisms, including antigenic variation, of the pathogen, the host side of the equation has been neglected. Using different approaches, we studied, in immunocompetent inbred mice, the dynamics of infection with and host responses to North American relapsing fever agent B. hermsii. The spirochete’s generation time in blood of infected mice was between 4–5 h and, after a delay, was matched in rate by the increase of specific agglutinating antibodies in response to the infection. After initiating serotype cells were cleared by antibodies, the surviving spirochetes were a different serotype and, as a population, grew more slowly. The retardation was attributable to the host response and not an inherently slower growth rate. The innate responses at infection peak and immediate aftermath were characterized by elevations of both pro-inflammatory and anti-inflammatory cytokines and chemokines. Immunodeficient mice had higher spirochete burdens and severe anemia, which was accounted for by aggregation of erythrocytes by spirochetes and their partially reversible sequestration in greatly enlarged spleens and elsewhere.

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“…In contrast to the acute phase of infection, dogs infected with T. congolense, T. evansi, T. rangeli, T. cruzi and T. caninum often show a chronic form of the disease with ocular signs such as keratitis, uveitis, coagulopathies in T. evansi and blepharo conjunctivitis (Amole et al, 1982;Mario et al, 1997). T. evansi sometimes produces acute syndrome in dogs manifested as urticarial plaques and ophtalmitis which are transitory and may relapse (Mario et al, 1997).…”

Section: Clinical Signsmentioning

confidence: 99%

A review on trypanosomosis in dogs and cats

Nwoha¹

2013

Afr. J. Biotechnol.

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Trypanosoma brucei brucei, Trypanosoma cruzi and Trypanosoma congolense were initially thought to be the only species of trypanosomes capable of causing diseases in dogs and cats. However, dogs and cats are challenged by diverse species of trypanosomes with varying virulence and pathogenicity. Dogs may develop clinical trypanosomosis by infection with Trypanosoma evansi but are refractory to Trypanosoma rangeli of man. Recently, a new species, Trypanosoma caninum, of unknown pathogenicity and mode of transmission has been reported in dogs. This review describes canine trypanosomosis as an entity of two types, African and American trypanosomosis. It describes the different species involved in each type of the disease condition, the emerging strains, the biological cycle, distribution, clinical symptoms, the pathology and treatment of various species of canine trypanosomes. It also describes different basic diagnostic techniques currently in use and progress towards development of vaccine.

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Pathogenesis of anemia in Trypanosoma brucei-infected mice

Cited by 48 publications

References 43 publications

Phenotypic characteristics distinguishing bloodstream form and central nervous form of Trypanosoma brucei rhodesiense.

Phenotypic characteristics distinguishing bloodstream form and central nervous form of Trypanosoma brucei rhodesiense.

Pathogen and Host Response Dynamics in a Mouse Model of Borrelia hermsii Relapsing Fever

A review on trypanosomosis in dogs and cats

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