The life cycle of the Trypanosoma brucei parasites Trypanosoma brucei gambiense accounts for the majority of<unk>  cases, with humans as the main reservoir needed for the transmission, while Trypanosoma brucei rhodesiense is mainly zoonotic, with the occasional human infection.<unk>  is dependent on the interaction of the parasite (trypanosome) with the tsetse flies (vector), as well as the host (human for Trypanosoma brucei gambiense, and animals for Trypanosoma brucei rhodesiense). The risk of contracting<unk>  is dependent on coming in contact with an infected tsetse fly. Trypanosoma brucei There are two subspecies of the parasite that are responsible for starting the disease in humans. Trypanosoma brucei gambiense causes the diseases in west and central<unk>  whereas Trypanosoma brucei rhodesiense has a limited geographical range and is responsible for causing the disease in east and southern<unk>  In addition, a third subspecies of the parasite known as Trypanosoma brucei brucei is responsible for affecting animals but not humans. Humans are the main reservoir for T. b. gambiense but this species can also be found in pigs and other animals. Wild game animals and cattle are the main reservoir of T. b. rhodesiense. These parasites primarily infect individuals in sub-Saharan<unk> because that is where the vector (tsetse fly) is located. The two human forms of the disease also vary greatly in intensity. T. b. gambiense causes a chronic condition that can remain in a passive phase for months or years before symptoms emerge and the infection can last about three years before death occurs. T. b. rhodesiense is the acute form of the disease, and death can occur within months since the symptoms emerge within weeks and it is more virulent and faster developing than T. b. gambiense. Furthermore, trypanosomes are surrounded by a coat that is composed of variant surface glycoproteins (VSG). These proteins act to protect the parasite from any lytic factors that are present in human plasma. The host's immune system recognizes the glycoproteins present on the coat of the parasite leading to the production of different antibodies (IgM and IgG). These antibodies will then act to destroy the parasites that circulate around the blood. However, from the several parasites present in the plasma, a small number of them will experience changes in their surface coats resulting in the formation of new VSGs. Thus, the antibodies produced by the immune system will no longer recognize the parasite leading to proliferation until new antibodies are created to combat the novel VSGs. Eventually, the immune system will no longer be able to fight off the parasite due to the constant changes in VSGs and infection will arise. Vector Type Trypanosoma Distribution Vector Chronic T. brucei gambiense Western<unk> G. palpalis G. tachinoides G. fuscipes G. morsitans Acute T. brucei rhodesiense Eastern<unk> G. morsitans G. swynnertoni G. pallidipes G. fuscipes Drawing of a tsetse fly from 1880 The tsetse fly (genus Glossina) is a large, brown, biting fly that serves as both a host and vector for the trypanosome parasites. While taking blood from a mammalian host, an infected tsetse fly injects metacyclic trypomastigotes into skin tissue. From the bite, parasites first enter the lymphatic system and then pass into the bloodstream. Inside the mammalian host, they transform into bloodstream trypomastigotes, and are carried to other sites throughout the body, reach other body fluids (e.g., lymph, spinal fluid), and continue to replicate by binary fission. The entire life cycle of<unk>  trypanosomes is represented by extracellular stages. A tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host. In the fly's midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission, leave the midgut, and transform into epimastigotes. The epimastigotes reach the fly's salivary glands and continue multiplication by binary fission. The entire life cycle of the fly takes about three weeks. In addition to the bite of the tsetse fly, the disease can be transmitted by: * Mother-to-child infection: the trypanosome can sometimes cross the placenta and infect the fetus. * Laboratories: accidental infections, for example, through the handling of blood of an infected person and organ transplantation, although this is uncommon. * Blood transfusion * Sexual contact (This may be possible) Horse-flies (Tabanidae) and stable flies (Muscidae) possibly play a role in transmission of nagana (the animal form of sleeping sickness) and the human disease form. Pathophysiology Tryptophol is a chemical compound produced by the trypanosomal parasite in sleeping sickness which induces sleep in humans.
African trypanosomiasis
Leishmaniasis
Trypanosomiasis
Psittacosis
Visceral leishmaniasis
Human trypanosomiasis
Babesiosis
Mansonelliasis