Trypanosoma brucei rhodesiense and Trypanosoma brucei gambiense are protozoan parasites that are the cause of nearly all human African trypanosomiasis (HAT, or African sleeping sickness); the subspecies Trypanosoma brucei brucei infects domestic and wild animals but usually not humans (but see the phylogeographic analysis by Balmer et al. 2011, which concludes that these three "subspecies" are not actually genetically or historically distinct lineages). These extracellular parasites are transmitted by the bite of Glossina tsetse flies. For the most part, at least, Trypanosoma brucei rhodesiense occurs in eastern and southern Africa and Trypanosoma brucei gambiense (which accounts for most cases of HAT) occurs in central and western Africa--although continued expansion of T. brucei rhodesiense to the northwest (e.g., by trade in infected cattle) may eventually result in overlapping ranges (Picozzi et al. 2005). HAT is limited to sub-Saharan Africa by the range of its tsetse fly vector. As of 2010, the best available estimates suggested a total of about 50,000–70,000 cases of HAT in the world. Left untreated, HAT leads to coma and death. Trypanosoma brucei gambiense infection is characterised by a chronic progressive course. The estimated average duration of infection is around 3 years, evenly divided between an initial haemolymphatic stage and a subsequent meningoencephalitic stage, during which the central nervous system is invaded. Abnormal sleep patterns are a leading symptom of the second stage (and account for the disease's colloquial name). Trypanosoma brucei rhodesiense disease is typically acute, with death occurring within weeks or months. (Fevre et al. 2008; Brun et al. 2010)
Three major HAT epidemics are known to have ravaged Africa in modern history. The first, which largely affected equatorial Africa, took place between 1896 and 1906, killing an estimated 800,000 people. The second major epidemic occurred between 1920 and the late 1940s and prompted the colonial powers to invest in vector control and in mobile teams to undertake active surveillance of the population--two strategies that remain the pillars of control today. These control mechanisms were effective, and the disease was almost eradicated in the early 1960s. However, with the advent of political independence across the continent came a collapse of surveillance and control activities in most countries with endemic HAT, often exacerbated by civil conflicts. This collapse led to a progressive re-emergence of the disease, which reached a peak in the late 1990s in the Democratic Republic of the Congo (DRC), Angola, Central African Republic, southern Sudan, and Uganda. Subsequent to this peak of infection in the 1990s, increased control activities have succeeded in rolling back disease related to Trypanosoma brucei gambiense in several countries. (Brun et al. 2010 and references therein)
Human African trypanosomiasis due to T. b. gambiensee is very rare in short-term tourists, but has been reported in immigrants, refugees, and expatriates resident for long periods in rural areas. Because of its long incubation time and chronic nature, the disease should be considered even if a patient’s last stay in an endemic region occurred many years ago. The number of tourists infected in countries that report the most local patients is low, probably because these countries are rarely visited by travellers. In contrast, disease due to T. b. rhodesiense has been reported in short-term tourists travelling to east African game reserves, mainly in Tanzania but also in Botswana, Rwanda, Kenya, and Malawi. (Brun et al. 2010 and references therein)
Using a range of molecular and classical parasitological approaches, Lai et al. (2008) concluded that Trypanosoma equiperdum and Trypanosoma evansi are agents of dourine and surra, diseases of horses, camels, and water buffaloes, are actually forms of T. brucei. They argue that these forms (which they suggest should be treated as subspecies "T. brucei equiperdum" and "T. brucei evansi") are the result of mutations that occurred relatively recently and produced lineages with a fundamentally altered life cycle.
The geographic range of human African trypanosomiasis (sleeping sickness) is restricted to sub-Saharan Africa where there are suitable habitats for its vector, the tsetse fly (Brun et al. 2010). Approximately two-thirds of reported T. b. gambiense cases occur in the Democratic Republic of Congo (DRC) (Simarro et al. 2008).
Trypanosoma brucei rhodesiense and T. b. gambiense are morphologically indistinguishable, but differ in important ways. For example, Trypanosoma brucei rhodesiense has a number of wild and domestic animal species (such as cattle) that act as important disease reservoirs that can lead to human sleeping sickness outbreaks; in contrast, although T. b. gambiense can be detected in non-human animals, these other hosts seem to be of far less importance as reservoirs leading to outbreaks of human sleeping sickness. (Fevre et al. 2008) The course of disease caused by T. b. rhodesiense is typically far more acute and rapidly progressing than that caused by T. b. gambiense (Fevre et al. 2008; Brun et al. 2010).
The trypanosomes causing sleeping sickness are transmitted from one mammalian host to another by blood-feeding Glossina tsetse flies. Both male and female flies are blood-feeders and can thus bring transmit the parasite. There are around 30 species and subspecies of tsetse flies and these are separated into three groups that prefer different habitats and show differing abilities to transmit T. b. gambiense or T. b. rhodesiense sleeping sickness. These flies are viviparous: The female fly deposits a fully developed larva, which burrows into the soil, pupates, and emerges as an adult fly a month later. Newly hatched flies have never been reported to be infected with trypanosomes. To transmit sleeping sickness, the fly must first feed on an infected mammalian host, after which the parasites enter the digestive tract. During the following 3 to 5 weeks the developing parasites undergo several differentiation steps, including migration to the salivary glands, where they develop into the infective form. The complex process of establishment in the midgut and maturation in the salivary glands depends on many factors, some favoring and others inhibiting its completion. Completion of the cycle in the fly is rare in the field: only about 0·1% of flies carry a mature infection that can be transmitted when the fly bites another host. (Brun et al. 2010 and references therein)
Trypanosomes are unicellular organisms (protozoans) in the family Trypanosomatidae and the genus Trypanosoma. The elongated cells are 15 to 30 μm long and move constantly with the help of a flagellum. They have the cellular organisation of eukaryotic cells, with one tubular mitochondrion that contains the kinetoplast, which is a condensation of the circular mitochondrial DNA. In the initial phase of infection, trypanosomes are restricted to the lymph and blood systems. At a later stage they are also seen in brain parenchyma and cerebrospinal fluid, but are generally extracellular. (Brun et al. 2010 and references therein)
