- General characteristics
- The discovery
- Genetics
- "Sleeping sickness" and global warming
- Phylogeny and taxonomy
- Treatment
- References
Trypanosoma brucei is an extracellular parasitic protozoan. It belongs to the class Kinetoplastidae, family Trypanosomatidae genus Trypanosoma. There are two subspecies that cause two different variants of human African trypanosomiasis or also called “sleeping sickness”.
Trypanosoma brucei subsp. gambiense, causes the chronic form and 98% of cases, located in the west and central sub-Saharan Africa. Trypanosoma brucei subsp. rhodesiense is the cause of the acute form, present in central and eastern sub-Saharan Africa.
Forms of Trypanosoma in blood. Author: Centers for Disease Control and Prevention's Public Health Image Library. Content Providers: CDC / Dr. Myron G. Schultz.
Both variants of this disease have been reported in those sub-Saharan African countries where the tsetse fly, Glossina spp, the vector or transmitting agent of T. brucei is found.
A third subspecies, Trypanosoma brucei subsp. brucei, causes a similar disease in domestic and wild animals, called nagana.
"Sleeping sickness" threatens more than 60 million people in 36 countries in sub-Saharan Africa. There are around 300,000 to 500,000 cases per year, of which about 70,000 to 100,000 die. The tsetse fly infestation covers an area of 10 million square kilometers, one third of the land mass of Africa.
The World Health Organization recognizes a significant decrease in the number of new cases of human African trypanosomiasis in recent years. This is due to the persistence of national and international initiatives to control this disease.
General characteristics
It is called "sleeping sickness" because it causes a reversal of the natural sleep cycle in the patient. The person sleeps during the day and stays awake at night. This is the product of the series of psychic and neurological disturbances that the disease causes in its advanced phase.
The discovery
Animal trypanosomiasis or nagana is a major disease in livestock in Africa. Trypanosoma brucei was identified as the causative agent in 1899. It was David Bruce while investigating a major nagana outbreak in Zululand.
Subsequently, Aldo Castellani identified this species of trypanosome in the blood and cerebrospinal fluid of human patients with “sleeping sickness”.
Between 1902 and 1910, the two variants of the disease in humans and their causative subspecies were identified. Both animals and humans can act as reservoirs for parasites capable of causing disease in humans.
Genetics
The genome of the Trypanosoma brucei nucleus is made up of 11 diploid chromosomes and a hundred microchromosomes. In total it has 9,068 genes. The genome of the mitochondria (the kinetoplast) is made up of numerous copies of circular DNA.
"Sleeping sickness" and global warming
African human trypanosomiasis is considered one of the 12 human infectious diseases that can be aggravated by global warming.
This is because as the ambient temperature increases, the area susceptible to being occupied by the Glossina sp. Fly will expand. As the fly colonizes new territories, it will carry the parasite with it.
Phylogeny and taxonomy
Treatment
The ability of Trypanosoma brucei to constantly vary the configuration of its outer layer of glycoproteins (antigenic variation), makes it very difficult to develop vaccines against "sleeping sickness".
There is no prophylactic chemotherapy and little or no prospect of a vaccine. The four main drugs used for human African trypanosomiasis are toxic.
Melarsoprol is the only drug that is effective for both variants of the central nervous system disease. However, it is so toxic that it kills 5% of patients who receive it.
Eflornithine, alone or in combination with nifurtimox, is increasingly used as the first line of therapy for disease caused by Trypanosoma brucei subsp. gambiense.
References
- Fenn K and KR Matthews (2007) The cell biology of Trypanosoma brucei differentiation. Current Opinion in Microbiology. 10: 539–546.
- Fernández-Moya SM (2013) Functional characterization of RBP33 and DRBD3 RNA-binding proteins as regulators of Trypanosoma brucei gene expression. DOCTORAL THESIS. Institute of Parasitology and Biomedicine "López-Neyra". Editorial University of Granada, Spain. 189 p.
- García-Salcedo JA, D Pérez-Morga, P Gijón, V Dilbeck, E Pays and DP Nolan (2004) A differential role for actin during the life cycle of Trypanosoma brucei. The EMBO Journal 23: 780–789.
- Kennedy PGE (2008) The continuing problem of human African trypanosomiasis (sleeping sickness). Annals of Neurology, 64 (2), 116–126.
- Matthews KR (2005) The developmental cell biology of Trypanosoma brucei. J. Cell Sci. 118: 283-290.
- Welburn SC, EM Fèvre, PG Coleman, M Odiit and I Maudlin (2001) Sleeping sickness: a tale of two diseases. TRENDS in Parasitology. 17 (1): 19-24.