Editing African trypanosomiasis (section)

===''Trypanosoma brucei (T. brucei)''===
{{Main|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 [[Africa]], whereas ''[[Trypanosoma brucei rhodesiense]]'' has a limited geographical range and is responsible for causing the disease in east and southern Africa. In addition, a third subspecies of the parasite known as ''[[Trypanosoma brucei brucei]]'' is responsible for affecting animals but not humans.<ref name=Brun10/>

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 Africa 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 (medicine)|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.<ref name=Brun10/>

''T. b. rhodesiense'' is the [[acute (medicine)|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 glycoprotein]]s (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).<ref name=Brun10/>

These antibodies will then act to destroy the parasites that circulate in 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.<ref name=Brun10/>