Skip to main content
NCBI home page
NIHPA Author Manuscripts logoLink to NIHPA Author Manuscripts
. Author manuscript; available in PMC: 2021 Jun 1.
Published in final edited form as: Trends Parasitol. 2019 Nov 20;36(6):571–572. doi: 10.1016/j.pt.2019.10.007

Trypanosoma brucei

Gabriela Romero-Meza 1, Monica R Mugnier 1,*
PMCID: PMC7375462  NIHMSID: NIHMS1606728  PMID: 31757771

Graphical Abstract

graphic file with name nihms-1606728-f0001.jpg

TAXONOMY AND CLASSIFICATION: PHYLUM: Euglenozoa, CLASS: Kinetoplastida, ORDER: Kinetoplastida, FAMILY: Trypanosomatidae, GENUS: Trypanosoma, SPECIES: T. brucei

Trypanosoma brucei causes African trypanosomiasis in humans and nagana in domestic animals. This vector-borne parasite, transmitted by the tsetse fly, affects rural areas in sub-Saharan Africa. When injected by the fly, metacyclic-form parasites are introduced into the host dermis and then disseminate into the bloodstream as replicative long slender forms. Throughout its life cycle, T. brucei is entirely extracellular. To evade host antibody recognition, the parasite uses antigenic variation: it periodically changes a dense coat of only one kind of variant surface glycoprotein (VSG), drawing from a genomic repertoire of about 2000 VSG-encoding genes. Using quorum sensing mechanisms, slender forms develop into stumpy forms that are preadapted to the insect environment. Once taken up by the fly, the parasite replaces its VSG coat with procyclins and progresses through procyclic and epimastigote stages. Finally, the parasites become VSG-expressing metacyclic trypomastigotes.

graphic file with name nihms-1606728-f0002.jpg

KEY FACTS:

T. brucei possesses a unique organelle, the kinetoplast: a network of circular DNA inside a single mitochondrion.

The 35 Mb diploid genome contains three types of chromosome: megabase, intermediate, and minichromosomes.

The 11 megabase chromosomes contain the majority of transcriptionally active genes arranged in polycistronic units, as well as subtelomeric arrays of silent VSG genes.

Minichromosomes and intermediate chromosomes contain VSG genes and DNA repeats.

T. brucei typically invades tissues, including blood, lymph, bone marrow, skin, brain, eye, and heart.

DISEASE FACTS:

T. brucei is lysed by a primate serum component called trypanosome lytic factor (TLF), rendering it noninfectious to humans. Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense are resistant to TLF and can infect humans.

Symptoms in the early stage of infection: fever, joint pain, and swollen lymph nodes. In the late stage the central nervous system is affected.

Detection of parasites in body fluids by microscopy is required for diagnosis.

After treatment, patients are monitored for relapse by a periodic check for parasites and leukocyte counts in the cerebrospinal fluid.

Affected populations live in areas with limited access to diagnosis and treatment, but human African trypanosomiasis is on its way to elimination in most endemic countries.

Acknowledgments

M.R.M. is supported by the Office of the Director, National Institutes of Health (DP5OD023065). VSG figure adapted from Engstler, 2007. We thank Jay Bangs, School of Medicine, University at Buffalo, and Peter Bush, School of Dental Medicine, University at Buffalo, for the T. brucei scanning electron microscope (SEM) image.

Footnotes

Literature

  • 1.Shapiro TA et al. (1995) The structure and replication of kinetoplast DNA. Annu. Rev. Microbiol 49, 117–143 [DOI] [PubMed] [Google Scholar]
  • 2.Berriman M et al. (2005) The genome of the African trypanosome Trypanosoma brucei. Science 309, 416–422 [DOI] [PubMed] [Google Scholar]
  • 3.Engstler M et al. (2007) Hydrodynamic flow-mediated protein sorting on the cell surface of trypanosomes. Cell 131, 505–515 [DOI] [PubMed] [Google Scholar]
  • 4.Hendriks E et al. (2000) Life-cycle differentiation in Trypanosoma brucei: molecules and mutants. Biochem. Soc. Trans 28, 531–536 [DOI] [PubMed] [Google Scholar]
  • 5.Jackson AP et al. (2013) A cell-surface phylome for African Trypanosomes. PLoS Negl. Trop. Dis 7, e2121–17 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 6.Matthews KR (2013) Bloodstream form pre-adaptation to the tsetse fly in Trypanosoma brucei. Front. Cell Infect. Microbiol 3, 78. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 7.Büscher P et al. (2017) Human African trypanosomiasis. Lancet 390, 2397–2409 [DOI] [PubMed] [Google Scholar]
  • 8.Mugnier MR et al. (2016) Masters of disguise: antigenic variation and the VSG coat in Trypanosoma brucei. PLoS Pathog 12 e1005784–6 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 9.Bangs JD (2018) Evolution of antigenic variation in African Trypanosomes: variant surface glycoprotein expression, structure, and function. Bioessays 40 e1800181–8 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 10.Silva Pereira S et al. (2019) Tissue tropism in parasitic diseases. Open Biol 9, 190036. [DOI] [PMC free article] [PubMed] [Google Scholar]

RESOURCES