Effect of strains of mice and challenge dose on the infectivity and virulence of Trypanosoma vivax

Joshua, R.A.

doi:10.1016/0304-4017(86)90030-0

Cited by 4 publications

(3 citation statements)

References 13 publications

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“…Death seemed to correlate with parasite load since average time to death was also dependent on the number of parasites in the inoculum (not shown). Thus, the more elevated the parasite inoculum, the lower the survival rate, corroborating published data based on the original parasite isolate [43].…”

Section: Resultssupporting

confidence: 87%

Trypanosoma vivax Infections: Pushing Ahead with Mouse Models for the Study of Nagana. I. Parasitological, Hematological and Pathological Parameters

et al. 2010

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African trypanosomiasis is a severe parasitic disease that affects both humans and livestock. Several different species may cause animal trypanosomosis and although Trypanosoma vivax (sub-genus Duttonella) is currently responsible for the vast majority of debilitating cases causing great economic hardship in West Africa and South America, little is known about its biology and interaction with its hosts. Relatively speaking, T. vivax has been more than neglected despite an urgent need to develop efficient control strategies. Some pioneering rodent models were developed to circumvent the difficulties of working with livestock, but disappointedly were for the most part discontinued decades ago. To gain more insight into the biology of T. vivax, its interactions with the host and consequently its pathogenesis, we have developed a number of reproducible murine models using a parasite isolate that is infectious for rodents. Firstly, we analyzed the parasitical characteristics of the infection using inbred and outbred mouse strains to compare the impact of host genetic background on the infection and on survival rates. Hematological studies showed that the infection gave rise to severe anemia, and histopathological investigations in various organs showed multifocal inflammatory infiltrates associated with extramedullary hematopoiesis in the liver, and cerebral edema. The models developed are consistent with field observations and pave the way for subsequent in-depth studies into the pathogenesis of T. vivax - trypanosomosis.

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Section: Resultssupporting

confidence: 87%

Trypanosoma vivax Infections: Pushing Ahead with Mouse Models for the Study of Nagana. I. Parasitological, Hematological and Pathological Parameters

et al. 2010

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“…They include T. brucei species which infect both humans and ruminants, but also T. congolense and particularly T. vivax which are responsible for the vast majority of animal trypanosomosis in sub-Saharan Africa, South America and South Asia [1]–[3]. Due mainly to technical constraints such as a lack of reproducible in vitro culture conditions and relatively poor accessibility to natural hosts, our understanding of the biology and fate of T. vivax in its vertebrate hosts largely stems from the extrapolation of data obtained from the experimental murine infection with T. brucei , T. congolense and T. ewansi , but just a few studies using T. vivax infected mice [4]–[8]. Recently, in a move to gain further insight into the host - T. vivax interaction, we further developed reproducible and reliable in vivo models of T. vivax infection using three different mouse strains and the IL 1392 West African isolate ( see accompanying paper ).…”

Section: Introductionmentioning

confidence: 99%

Trypanosoma vivax Infections: Pushing Ahead with Mouse Models for the Study of Nagana. II. Immunobiological Dysfunctions

et al. 2010

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Trypanosoma vivax is the main species involved in trypanosomosis, but very little is known about the immunobiology of the infective process caused by this parasite. Recently we undertook to further characterize the main parasitological, haematological and pathological characteristics of mouse models of T. vivax infection and noted severe anemia and thrombocytopenia coincident with rising parasitemia. To gain more insight into the organism's immunobiology, we studied lymphocyte populations in central (bone marrow) and peripherical (spleen and blood) tissues following mouse infection with T. vivax and showed that the immune system apparatus is affected both quantitatively and qualitatively. More precisely, after an initial increase that primarily involves CD4+ T cells and macrophages, the number of splenic B cells decreases in a step-wise manner. Our results show that while infection triggers the activation and proliferation of Hematopoietic Stem Cells, Granulocyte-Monocyte, Common Myeloid and Megacaryocyte Erythrocyte progenitors decrease in number in the course of the infection. An in-depth analysis of B-cell progenitors also indicated that maturation of pro-B into pre-B precursors seems to be compromised. This interferes with the mature B cell dynamics and renewal in the periphery. Altogether, our results show that T. vivax induces profound immunological alterations in myeloid and lymphoid progenitors which may prevent adequate control of T. vivax trypanosomosis.

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“…R Africa are pleomorphic [6,7,161, and vary in their ability to initiate infections in naive rodents when collected at different times after infection [7,9,161. During infection, the West African T. viva [lo] transforms from a population with many members in S, G2 and M stages of the cell cycle to a population with few members in these cell cycle stages [16].…”

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Differentiation, Multiplication and Control of Bloodstream Form Trypanosoma (Duttonella) vivax in Mice

Mahan¹,

Black²

1989

The Journal of Protozoology

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The growth and differentiation of Trypanosoma vivax was studied in intact and irradiated C3H/He and C57Bl/6 mice. In irradiated (800 R) or intact C3H/He and irradiated (800 R) C57Bl/6 mice, T. vivax parasitaemia increased rapidly then entered a plateau phase and thereafter declined in an antibody-independent remission phase. Throughout the infection, variations were observed in parasite morphology, density, DNA content, number of organisms with 2 nuclei and 2 kinetoplasts and infectivity of parasites for mice. Parasites in exponential phase had the highest number of members in the S, G2 and M phases of the cell cycle as determined by staining with the interchalating dye Chromomycin A3 and analysis on a flow cytometer. During this phase there were numerous parasites with 2 nuclei and 2 kinetoplasts and infectivity was high for mice. As the parasitaemia approached and entered the plateau phase, the proportion of organisms in the S, G2 and M phases of the cell cycle as well as the number of those with 2 kinetoplasts decreased slightly; the number of organisms with 2 nuclei decreased rapidly; and parasites had a considerably reduced capacity to infect mice. Organisms from the remission phase contained only 1 nucleus and 1 kinetoplast and were not infective for mice. The study suggests that T. vivax organisms transit from dividing to committed non-dividing forms and that some non-diving, non-infective T. vivax organisms remain trapped in the S, G2 and M stages of the cell cycle and die without completing binary fission.(ABSTRACT TRUNCATED AT 250 WORDS)

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Effect of strains of mice and challenge dose on the infectivity and virulence of Trypanosoma vivax

Cited by 4 publications

References 13 publications

Trypanosoma vivax Infections: Pushing Ahead with Mouse Models for the Study of Nagana. I. Parasitological, Hematological and Pathological Parameters

Trypanosoma vivax Infections: Pushing Ahead with Mouse Models for the Study of Nagana. I. Parasitological, Hematological and Pathological Parameters

Trypanosoma vivax Infections: Pushing Ahead with Mouse Models for the Study of Nagana. II. Immunobiological Dysfunctions

Differentiation, Multiplication and Control of Bloodstream Form Trypanosoma (Duttonella) vivax in Mice

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