African Trypanosomiasis: a parasitic disease of the CNS
Introduction
By Maeve McLaughlin
Human African Trypanosomiasis (HAT) informally known as African Sleeping Sickness is an infection directly linked to a microscopic parasitic species known as Trypanosoma brucei. T. brucei are members of the Trypanosoma genus as well as the Trypanosomatidae family of unicellular parasites [3]. HAT is an extremely rare disease in the United States with fewer than 1,000 cases per year, but has a history of epidemics in Sub-Saharan regions of Africa [1]. There are a number of species of trypanosomes but only 2 have been known to infect humans, those being T.b gambiense and T.b rhodesiense [1].
Its transmission occurs through the tsetse fly, a member of the Glossina genus, only found in regions of Sub-Saharan Africa [1]. A bite from the infected species enters the human bloodstream, allowing the parasite to colonize areas up through the lymph nodes. Once infected, the spread of the disease easily develops into the central nervous system working its way to the brain. There are two main stages early and late, the late stage results in neurological defects. Early symptoms commonly consist of headache, fever, rash, or drowsiness [1].
Infected hosts may experience differences in circadian rhythm, insomnia, drowsiness throughout the day, and eventually potential death if left untreated [1]. Those in late stages of the disease experience disturbances in their circadian rhythm, insomnia, or other psychological symptoms such as dementia, depression, mania, irritability, or memory loss [1]. If left untreated, almost all patients are left in a coma, often resulting in death.
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Trypanosoma Brucei
Trypanosoma brucei is an extracellular protozoan flagellate parasitic species belonging to the Trypanosoma genus, residing mainly in Sub-Saharan regions of Africa. T. brucei are frequently located extracellularly in blood and tissue regions of the mammalian host, transmitting via leech or arthropod vectors [3]. There are 3 subspecies of T. brucei, yet only 2 species, T. b. gambiense (Tbg), T. b. rhodesiense (Tbr) cause infection in humans [2]. In general, T.brucei has a larger genome than most bacteria, and is a motile bacteria.
The genome of T.brucei is 26 Mb, contains roughly 1700 variant surface glycoproteins along with around 900 pseudogenes [11]. Genome analysis has shown horizontal gene transfer allows for increased metabolic properties for trypanosome parasites [11]. T.b. gambiense is the strain mainly responsible for human infection, accounting for 98% of all diagnosed cases of african trypanosomiasis [3]. This strain is also responsible for retaining the majority of the genetic information with a smaller genome.
Epidemiology
African Sleeping Sickness, or HAT infection is limited to regions of Sub-Saharan Africa specifically. There are two strains of Trypanosoma that infect humans, each infecting separate regions of Africa. T.b. gambiense, is centered in Central and West Africa while T.b. rhodiense is found in the southern and eastern portions of Africa [3]. Poor and rural communities face an increased risk due to frequent interaction with the land and water which are breeding grounds for bacteria.
Previous epidemics of Human African Trypanosomiasis have been documented in Uganda, Congo, and Cameroon, all of which are located in Central Africa [3]. As of late, most reported cases of T.b gambiense are found in the Democratic Republic of Congo and continue to decrease at a steady rate, hovering in the low thousands [8]. Popular tourist destinations such as Kenya, Malawi, Uganda, and Zambia may also notice an increase in T.b. rhodesiense cases due to constant visitation [3]. Travelers still face an increased risk of possible infection, especially those staying in areas of wildlife and nature preserves.
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Symptoms
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Pathogenesis
Path of Infection
Impact on the Central Nervous System
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Diagnosis & Treatment
Diagnosis
Treatment
Prevention
Immune Response
Next Steps
Conclusion
References
Authored for BIOL 238 Microbiology, taught by Joan Slonczewski,at Kenyon College,2024
