The best way to combat the infection is to seek medical treatment were specific drugs can be used to remove the protozoan from the body. When in the first stage the most effective drug for T. brucei rhodesiense is Suramin. The most effective way for the drug to be administered is intravenously because it is not absorbed well by the intestines. It’s most effective against trypomastigotes that are in the bloodstream. The drug acts upon T. b. rhodesiense by inhibiting the glycosomal enzymes involved in glycolysis, the bloodstream form's only source of energy. This inhibition happens at a slow and gradual rate and it is even possible that suramin might affect newly-synthesized glycolytic enzymes within the cytosol before they are imported into
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When a foreign microbe enters the body a natural immune response is initiated to protect the body from harm. However, when the body cannot detect when it has been invaded the appropriated self-preservation responses cannot be enacted to fend off invaders. Without identification of the invading microbe the immune system resorts to innate responses, or non-specific responses, such as fever, inflammation, pain in the joints, and occasionally irritation of the skin at the infection site. In the case of the Trypanosoma family the first stage consist of continuous waves of parasites in the blood also known as parasotaema. The immune system begins to target the protozoans and is able to remove some of them however, they begin evading the immune system through a process called antigenic variation. During this process, the trypanosome switches its variable surface glycoprotein (VSG) coat, which the antibodies of the immune system use to recognize invading cells, to a new VSG coat that is not recognized by the host immune system. This continuous action exhausts the host immune defenses leading to weaker response. The process of evasion also includes endocytosis of VSG-antibody complexes, allowing them to escape detection by the antibodies responsible for complement-mediated killing.2 Antigenic variation prolongs the time that trypanosomes spend within the host, thus allowing for further proliferation and transmission to other hosts via the tsetse vector. This process also allows trypanosomes to infect hosts that already recognize VSGs from prior
When a foreign microbe enters the body a natural immune response is initiated to protect the body from harm. However, when the body cannot detect when it has been invaded the appropriated self-preservation responses cannot be enacted to fend off invaders. Without identification of the invading microbe the immune system resorts to innate responses, or non-specific responses, such as fever, inflammation, pain in the joints, and occasionally irritation of the skin at the infection site. In the case of the Trypanosoma family the first stage consist of continuous waves of parasites in the blood also known as parasotaema. The immune system begins to target the protozoans and is able to remove some of them however, they begin evading the immune system through a process called antigenic variation. During this process, the trypanosome switches its variable surface glycoprotein (VSG) coat, which the antibodies of the immune system use to recognize invading cells, to a new VSG coat that is not recognized by the host immune system. This continuous action exhausts the host immune defenses leading to weaker response. The process of evasion also includes endocytosis of VSG-antibody complexes, allowing them to escape detection by the antibodies responsible for complement-mediated killing.2 Antigenic variation prolongs the time that trypanosomes spend within the host, thus allowing for further proliferation and transmission to other hosts via the tsetse vector. This process also allows trypanosomes to infect hosts that already recognize VSGs from prior