scholarly journals History of Sleeping Sickness in East Africa

1999 ◽  
Vol 12 (1) ◽  
pp. 112-125 ◽  
Author(s):  
Geoff Hide

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.

2019 ◽  
Vol 9 ◽  
pp. 59-64
Author(s):  
Ramesh Agrawal ◽  
Dolly P. Patel ◽  
Bhagyashree B. Desai

The current paper depicts the challenges faced during the treatment of a complicated case of mandibular condylar head fracture, facial asymmetry, and centric relation-centric occlusion (CR-CO) discrepancy along with Class III malocclusion. A 20-year-old female reported with the chief complaint of difficulty in chewing and concern with her appearance due to deviated jaw and had a history of trauma over chin region. The clinical and radiographic examination revealed significant facial asymmetry with long face, right-sided deviation of the mandible, fractured condyle, CR-CO discrepancy, cross- bite with Class III malocclusion, and a missing mandibular single incisor along with non-vital 21 and 22. She was treated with 0.022 MBT appliance along with guiding plane for CR-CO correction followed by asymmetric bilateral sagittal split osteotomy and differential set back on the right and left sides and finally rigid fixation. A good facial profile and functional occlusion were achieved and non-vital 21 and 22 were esthetically rehabilitated with PFM crowns. The stability of surgical as well as orthodontic corrections was excellent and appreciable in the records obtained 2-year post-treatment. When faced with mutilated malocclusion, with multiple problems, sequential correction of functional malocclusion with dental decompensation followed by skeletal correction with surgical approach has yielded a appreciable facial correction with good stability showing 2-year post-treatment follow-up.


Author(s):  
August Stich

Human African trypanosomiasis (HAT, sleeping sickness) is caused by two subspecies of the protozoan parasite Trypanosoma brucei: T. b. rhodesiense is prevalent in East Africa among many wild and domestic mammals; T. b. gambiense causes an anthroponosis in Central and West Africa. The disease is restricted to tropical Africa where it is transmitted by the bite of infected tsetse flies (...


In order to gain a general idea of this important species of trypanosome, it will be necessary to study as many individual strains as possible. It may be thought unnecessary to describe each strain so much in detail, but without this it will be impossible to get any order out of the chaos which rules at present in the classification of the African species of trypanosomes pathogenic to man and the domestic animals. Up to the present the Commission have only had an opportunity of working with five human strains. Four of these are from natives infected in the Sleeping-Sickness Area, Nyasaland, the fifth from an European who contracted the disease in Portuguese East Africa. It is intended, in later papers, to describe five strains from wild game and the same number from the tsetse fly, Glossina morsitans .


1996 ◽  
Vol 04 (04) ◽  
pp. 459-477 ◽  
Author(s):  
MARC ARTZROUNI ◽  
JEAN-PAUL GOUTEUX

We present a five-variable compartmental model for the spread of Trypanosoma brucei gambiense, the parasite responsible for the transmission (through tsetse flies) of sleeping sickness in Central Africa. The model’s equilibrium points depend on two “summary parameters”: gr, the proportion removed among human infectives, and R0, the basic reproduction rate. Stability results are obtained for the origin but not for other equilibrium points. A two-variable simplified version of the model is presented and the stability of all its equilibrium points can be investigated analytically. Both models are applied to the Niari focus of Central Africa and used to test the impact of a vector control strategy. The models’ results are in agreement with the extinction of the epidemic that was brought about by a fifty percent decrease in vector density.


2004 ◽  
Vol 199 (10) ◽  
pp. 1445-1450 ◽  
Author(s):  
Kisaburo Nagamune ◽  
Alvaro Acosta-Serrano ◽  
Haruki Uemura ◽  
Reto Brun ◽  
Christina Kunz-Renggli ◽  
...  

The African trypanosome Trypanosoma brucei, which causes sleeping sickness in humans and Nagana disease in livestock, is spread via blood-sucking Tsetse flies. In the fly's intestine, the trypanosomes survive digestive and trypanocidal environments, proliferate, and translocate into the salivary gland, where they become infectious to the next mammalian host. Here, we show that for successful survival in Tsetse flies, the trypanosomes use trans-sialidase to transfer sialic acids that they cannot synthesize from host's glycoconjugates to the glycosylphosphatidylinositols (GPIs), which are abundantly expressed on their surface. Trypanosomes lacking sialic acids due to a defective generation of GPI-anchored trans-sialidase could not survive in the intestine, but regained the ability to survive when sialylated by means of soluble trans-sialidase. Thus, surface sialic acids appear to protect the parasites from the digestive and trypanocidal environments in the midgut of Tsetse flies.


1912 ◽  
Vol 3 (4) ◽  
pp. 355-360 ◽  
Author(s):  
R. Newstead

In pursuing my studies of the genital armature of the tsetse-flies, I have been fortunate in securing some valuable and interesting material from various parts of the African continent which has enabled me to offer a further contribution on the specific characters of the recently discovered Glossina austeni, Newst., from British East Africa; to present a detailed account of the armature of the apparently rare G. fuscipleuris, Aust., and to clear up some doubtful points in regard to the structural details of the male genital armature in G. longipennis, Corti. Later I hope to be able to offer some further remarks on G. palpalis, R.D., especially in regard to the colour and structural variations existing in this species. Meanwhile I may here state, for the guidance of the student, that G. fuscipes, Newst., which was described by me as a distinct species, must sink as a well-marked race of G. palpalis.


2021 ◽  
Author(s):  
Caroline E Dewar ◽  
Aitor Casas-Sánchez ◽  
Constentin Dieme ◽  
Aline Crouzols ◽  
Lee Haines ◽  
...  

The single-celled parasite Trypanosoma brucei causes sleeping sickness in humans and nagana in livestock and is transmitted by hematophagous tsetse flies. Lifecycle progression from mammalian bloodstream form to tsetse midgut form and, subsequently, infective salivary gland form depends on complex developmental steps and migration within different fly tissues. As the parasite colonises the glucose-poor insect midgut, its ATP production is thought to depend on activation of mitochondrial amino acid catabolism via oxidative phosphorylation. This process involves respiratory chain complexes and the F1FO-ATP synthase, and it requires protein subunits of these complexes that are encoded in the parasite's mitochondrial DNA (kinetoplast or kDNA). Here we show that a progressive loss of kDNA-encoded functions correlates with an increasingly impaired ability of T. brucei to initiate and complete its development in the tsetse. First, parasites with a mutated F1FO-ATP synthase with a reduced capacity for oxidative phosphorylation can initiate differentiation from bloodstream to insect form, but they are unable to proliferate in vitro. Unexpectedly, these cells can still colonise the tsetse midgut. However, these parasites exhibit a motility defect and are severely impaired in colonising or migrating to subsequent tsetse tissues. Second, parasites with a fully disrupted F1FO-ATP synthase complex that is completely unable to produce ATP by oxidative phosphorylation can still differentiate to the first insect stage in vitro but die within a few days and cannot establish a midgut infection in vivo. Third, mutant parasites lacking kDNA entirely can initiate differentiation but die within 24 h. Together, these three scenarios show that efficient ATP production via oxidative phosphorylation is not essential for initial colonisation of the tsetse vector, but it is required to power trypanosome migration within the fly.


mBio ◽  
2022 ◽  
Author(s):  
Caroline E. Dewar ◽  
Aitor Casas-Sanchez ◽  
Constentin Dieme ◽  
Aline Crouzols ◽  
Lee R. Haines ◽  
...  

African trypanosomes cause disease in humans and their livestock and are transmitted by tsetse flies. The insect ingests these parasites with its blood meal, but to be transmitted to another mammal, the trypanosome must undergo complex development within the tsetse fly and migrate from the insect's gut to its salivary glands.


2021 ◽  
Vol 27 ◽  
Author(s):  
Samuel Dean

: Trypanosoma brucei are protozoan parasites that causes the lethal human disease African sleeping sickness, and the economically devastating disease of cattle, Nagana. African sleeping sickness, or Human African Trypanosomiasis (HAT) threatens 65 million people, and animal trypanosomiasis makes large areas of farmland unusable. There is no vaccine and licenced therapies against the most severe, late-stage disease are toxic, impractical and ineffective. Trypanosomes are transmitted by tsetse flies and HAT is therefore predominantly confined to the tsetse fly belt in subSaharan African. They are exclusively extracellular, and they differentiate between at least seven developmental forms that are highly adapted to host and vector niches. In the mammalian (human) host they inhabit the blood, cerebrospinal fluid (late stage disease), skin and adipose fat. In the tsetse fly vector, they travel from the tsetse midgut to the salivary glands via the ectoperitrophic space and proventriculus. Trypanosomes are evolutionarily divergent compared with most branches of eukaryotic life. Perhaps most famous for their extraordinary mechanisms of monoallelic gene expression and antigenic variation, they have also been investigated because much of their biology is either highly unconventional or extreme. Moreover, in addition to their importance as pathogens, many researchers have been attracted to the field because trypanosomes have some of the most advanced molecular genetic tools and database resources of any model system. The following will cover just some aspects of trypanosome biology and how its divergent biochemistry has been leveraged to develop drugs to treat African Sleeping sickness. It is by no means intended to be a comprehensive survey of trypanosome features. Rather, it is hoped that it will present trypanosomes as one of the most fascinating and tractable systems in which to do discovery biology.


1964 ◽  
Vol 5 (1) ◽  
pp. 1-24 ◽  
Author(s):  
Frank L. Lambrecht

Exposure to and invasion by parasitic organisms may play an important part among many other intrinsic factors that guide the evolution of animal forms. Trypanosomes, two species of which cause African sleeping sickness today, are blood parasites of great antiquity. Their presence in Africa at the time of the first stages of human evolution may have been of great consequence, at first acting as a discriminating agent between resistant and non-resistant types of hominids, and later also in shaping migration routes and settlement patterns. As a possible clue as to why man arose in Africa, the author postulates that trypanosomes may have precluded the development of certain ground-dwelling faunas, allowing certain more resistant primates to fill the empty ecological niches. Some of these primates, thus becoming ground-dwellers, became the precursors of the hominid branch. The evolution of T. gambiense and T. rhodestense, the two human parasites, and their development in the tsetse fly, are debated. The epidemiological aspects and patterns of the disease are examined under the changing climatic conditions of the Pleistocene and during later times, when Africa was opened up by Western exploration.


Sign in / Sign up

Export Citation Format

Share Document