Trypanosoma spp.
Peter M. Lydyard, Michael F. Cole, John Holton, William L. Irving, Nino Porakishvili, Pradhib Venkatesan, Katherine N. Ward in Case Studies in Infectious Disease, 2010
What is the causative agent, how does it enter the body and how does it spread a) within the body and b) from person to person?Trypanosomes are flagellated protozoan parasites.African trypanosomiasis is caused by Trypanosoma brucei rhodesiense or T. brucei gambiense.South American trypanosomiasis is caused by Trypanosoma cruzi.Tsetse flies transmit infection in Africa from other humans or an animal, ungulate reservoir.Triatomine bugs transmit infection in South America from an animal reservoir.After an insect bite trypanosomes spread from local tissue to lymph nodes, then enter the bloodstream, and finally invade tissues.In African trypanosomiasis invasion of the central nervous system occurs after weeks to several months.In South American trypanosomiasis an aflagellate, intracellular life form, the amastigote, forms a pseudocyst within cells.
The Parasite's Way of Life
Eric S. Loker, Bruce V. Hofkin in Parasitology, 2023
The mammalian bloodstream form of Trypanosoma brucei undergoes a change from long and slender to a shorter form known as “stumpy” in preparation for transmission back to the tsetse fly vector. Development into this transmissible form is controlled by the parasites themselves, which monitor their density in the blood. In a process very similar to the quorum sensing observed in many bacteria, the slender forms release a signal called stumpy induction factor (SIF). This soluble protein has only recently been characterized. When slender forms are exposed to enough SIF, indicating that the population of parasites in the blood is sufficiently high, the signal to develop into the stumpy form passes a threshold and development proceeds (Figure 3.26). Metazoans too seem to adjust their life cycle in response to such environmental cues. Filarial worms, for instance, increase their production of microfilariae in response to more aggressive host responses.
African trypanosomiasis
F. Y. Liew in Vaccination Strategies of Tropical Diseases, 2017
As infection with Trypanosoma brucei proceeds, the host mounts strong antibody responses against the highly immunogenic VSG and clears the parasitemia. Within days, however, trypanosomes expressing a different variable antigen type (VAT) appear and proliferate, eliciting a fresh immune response which in turn is ineffectual. Antigenic variation is not infinite; large animals maintained in laboratory conditions can develop immunity to the entire antigenic repertoire of a trypanosome.5 This, however, is unlikely to pertain for susceptible host species under the more arduous conditions of the field, the usual outcome being that the host succumbs before exhaustion of the repertoire, although repeated drug treatment can contribute to survival and concomitant immunization against the repertoire.
Immunotoxins and nanobody-based immunotoxins: review and update
Published in Journal of Drug Targeting, 2021
Mohammad Reza Khirehgesh, Jafar Sharifi, Fatemeh Safari, Bahman Akbari
African protozoan parasite Trypanosoma brucei causes African trypanosomiasis or sleeping sickness. Apolipoprotein L-I (apoL-I) lysis the African trypanosomes except for resistant forms such as Trypanosoma brucei rhodesiense because of expression of a protein known as apoL-I neutralising serum resistance-associated (SRA). Tr-apoL-I, a modified format of apoL-I without the SRA-interacting domain, can overcome this resistance. The cell surface of Trypanosoma brucei rhodesiense is covered by a variant surface glycoprotein (VSG). As a result, many anti-VSG nanobodies are developed. For example, NbAn33, a non-trypanolytic Nb, can access the preserved cryptic epitopes of the VSG. Conjugation of NbAn33 to the Tr-apoL-I led to the generation of recombinant IT (NbAn33–Tr-apoL-I). The IT recognised and lysed the resistant Trypanosoma strains in the in vitro study in a dose-dependent manner. Also, in vivo studies in mouse models showed that the IT leads to complete parasite clearance and did not show any adverse symptoms [155].
Metabolomic profile, anti-trypanosomal potential and molecular docking studies of Thunbergia grandifolia
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2023
Heba A. S. El-Nashar, Ahmed M. Sayed, Hany A. M. El-Sherief, Mostafa E. Rateb, Lina Akil, Ibrahim Khadra, Taghreed A. Majrashi, Sara T. Al-Rashood, Faizah A. Binjubair, Mahmoud A. El Hassab, Wagdy M. Eldehna, Usama Ramadan Abdelmohsen, Nada M. Mostafa
Trypanosomiasis or sleeping sickness is a protozoan disease that infects animals and humans transmitted by the bite of Glossina (tsetse) fly carrying Trypanosoma brucei1. Currently, trypanosomiasis affects more than 50 million cattle and 70 million people in sub-Saharan Africa2. The available current medicines record lack of efficiency, resistance, and toxicity, so there is an urgent need for the development of novel, safe, efficacious, cost-effective drugs with new mechanism of action3,4. In African countries where trypanosomiasis is prevalent, natural products (herbal extracts) have traditionally been utilised for centuries and are still extensively used to cure infections and other parasitic diseases5,6. Interestingly, about 30% of the world population has confidence in traditional therapies due to their wide availability and affordability7. Moreover, various drugs like quinine and artemisinin were established as plant-derived potential antiprotozoal agents8.
Comparative in vitro transportation of pentamidine across the blood-brain barrier using polycaprolactone nanoparticles and phosphatidylcholine liposomes
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Geofrey Omarch, Yunus Kippie, Shireen Mentor, Naushaad Ebrahim, David Fisher, Grace Murilla, Hulda Swai, Admire Dube
Human African Trypanosomiasis (HAT) is a fatal vector borne trypanosomal infection characterized by wasting condition in which there is a slow progressive loss of condition accompanied by increasing anaemia and weakness to the point of extreme emaciation, collapse and death often due to heart failure [1,2]. The disease is endemic in 36 countries of Sub-Saharan Africa and impacts about 70 million people [3–5]. Two distinct subspecies of the Trypanosoma brucei are the causative parasites of the disease [6]. Trypanosoma brucei gambiense which is confined to the Central and West Africa causes a chronic infection and Trypanosoma brucei rhodesience which is found in the East and South of Africa causes an acute form of the disease [3].
Related Knowledge Centers
- African Trypanosomiasis
- Antigenic Variation
- Kinetoplast
- Trypanosoma
- Tsetse Fly
- Animal Trypanosomiasis
- Species Complex
- Disease Vector
- Variant Surface Glycoprotein
- Blood–Brain Barrier