Evidence for the presence of an innate trypanosomicidal factor in the serum of a non-immune African waterbuck (Kobus ellipsiprymnus)

Mulla, A.F.; Rickman, L. R.

doi:10.1016/0035-9203(88)90274-x

Cited by 8 publications

(4 citation statements)

References 4 publications

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“…The mechanisms by which host blood modulate midgut infections in tsetse are still not clearly understood. Blood from certain hosts such as buffalo, eland and waterbuck have trypanolytic molecules in the plasma fraction (Reduth et al, 1992;Mulla & Rickman, 1988). Such molecules may have a direct contribution to the low infection prevalence in tsetse fed on these blood samples.…”

Section: Discussionmentioning

confidence: 99%

“…that act on the trypanosomes directly. For example, fresh buffalo and waterbuck sera cause lysis of the bloodstream trypanosomes (Mulla & Rickman, 1988;Reduth et al, 1992). In addition, the resistance by humans and other ground-dwelling primates to infection by Trypanosoma brucei brucei Plimmer and Bradford has been shown to be due to a cytolytic factor which is a component of the plasma high-density lipoprotein (Seed et al, 1990;Gillet & Owen, 1992).…”

Section: Introductionmentioning

confidence: 99%

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The effect of host blood in the in vitrotransformation of bloodstream trypanosomes by tsetse midgut homogenates

Nguu

Osir

Imbuga

et al. 1996

Medical Vet Entomology

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Midgut homogenates prepared from Glossina morsitans morsitans, that had previously been fed on different host blood samples, were tested for their abilities to transform bloodstream Trypanosoma brucei into procyclic (midgut) forms in vitro. Compared to rat and goat blood samples, eland blood had the least capacity to support trypanosome transformation, whereas buffalo blood showed intermediate capacity. Fractionation of rat blood showed the importance of the cellular portion since both rat and eland red blood cells (RBCs) supported the process. Virtually no transformation was observed in rat and eland plasma or serum fractions. Suspending rat blood cells in eland plasma led to a reduction in parasite transformation rates. Further experiments showed that the RBC membranes were also capable of supporting the process. These results clearly show the important role played by blood, especially the red blood cells, in the transformation of bloodstream trypanosomes. In addition, the low transformation rates observed in eland blood is due to an inhibitory factor(s) present in the plasma fraction.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The effect of host blood in the in vitrotransformation of bloodstream trypanosomes by tsetse midgut homogenates

Nguu

Osir

Imbuga

et al. 1996

Medical Vet Entomology

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“…We are used to the idea that only certain stocks of T. brucei are infective to man but perhaps the same principle could apply to other mammalian hosts. Some hosts are known to display a capacity to resist infection with man-infective T. brucei (Rickman & Kolala, 1982;Mulla & Rickman, 1988) but the role of innate and acquired factors and the strain of T. brucei is not clear. Further sampling of cattle and man from a variety of locations could help to determine if some zymodemes are genuinely unable to survive in cattle or if the result can be explained by a lack of opportunity of zymodemes to infect them.…”

Section: Discussionmentioning

confidence: 99%

Genetic variation in Trypanosoma brucei and the epidemiology of sleeping sickness in the Lambwe Valley, Kenya

Cibulskis

1992

Parasitology

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A contingency table approach was used to explore the influence of location, host species and time on the genetic composition of a Trypanosoma brucei population in Lambwe Valley, Kenya. Significant differences in zymodeme frequencies were noticed over comparatively short geographical distances suggesting that transmission of T. brucei is somewhat localized. A significant association was observed between zymodeme and the mammalian host from which T. brucei was derived. The association was consistent in different localities in Lambwe valley and remained stable for at least 32 months. These observations indicate that zymodemes are adapted to different host species and that genetic exchange has not disrupted host associations over this time-scale. A major change in the composition of the T. brucei population during a sleeping sickness outbreak in 1980 was confirmed. But while new zymodemes emerged, a decline in overall diversity was noted during times of high sleeping sickness incidence. The results can be explained by selection of T. brucei zymodemes for particular transmission cycles. Although it is not necessary to invoke genetic exchange, sex may help T. brucei to adapt to changes in selection pressures. Such a hypothesis helps to explain why T. brucei appears largely clonal in the short term, even though population studies indicate that sex is responsible for much genetic diversity in the long term. It also explains why neighbouring populations of T. brucei are composed of a different range of zymodemes formed from the same alleles. Such a view implies that genetic exchange has an important role in the microevolution of T. brucei populations.

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“…Cattle and wild animals appear to be suitable hosts for both human-and non-human-infective T. brucei, while humans are restricted to the former (23,63). Also some animal hosts can display a resistance to human trypanosomes (92,103). Little is known about these host restrictions, but it has been proposed that trypanosome strains might be adapted for transmission cycles involving specific hosts (23).…”

Section: Genetic Diversity In the Tsetse Flymentioning

confidence: 99%

History of Sleeping Sickness in East Africa

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1999

Clin Microbiol Rev

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SUMMARY The history of human sleeping sickness in East Africa is characterized by the appearance of disease epidemics interspersed by long periods of endemicity. Despite the presence of the tsetse fly in large areas of East Africa, these epidemics tend to occur multiply in specific regions or foci rather than spreading over vast areas. Many theories have been proposed to explain this phenomenon, but recent molecular approaches and detailed analyses of epidemics have highlighted the stability of human-infective trypanosome strains within these foci. The new molecular data, taken alongside the history and biology of human sleeping sickness, are beginning to highlight the important factors involved in the generation of epidemics. Specific, human-infective trypanosome strains may be associated with each focus, which, in the presence of the right conditions, can be responsible for the generation of an epidemic. Changes in agricultural practice, favoring the presence of tsetse flies, and the important contribution of domestic animals as a reservoir for the parasite are key factors in the maintenance of such epidemics. This review examines the contribution of molecular and genetic data to our understanding of the epidemiology and history of human sleeping sickness in East Africa.

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Evidence for the presence of an innate trypanosomicidal factor in the serum of a non-immune African waterbuck (Kobus ellipsiprymnus)

Cited by 8 publications

References 4 publications

The effect of host blood in the in vitrotransformation of bloodstream trypanosomes by tsetse midgut homogenates

The effect of host blood in the in vitrotransformation of bloodstream trypanosomes by tsetse midgut homogenates

Genetic variation in Trypanosoma brucei and the epidemiology of sleeping sickness in the Lambwe Valley, Kenya

History of Sleeping Sickness in East Africa

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