Over the course of history, African Sleeping Sickness has only been known since the late 19th century and that was only because of an epidemic. Of course, the actual disease dates back 500 million years ago, a time where there was no way for us to understand or study the parasite. During the millions of years in between the 19th century epidemic the protozoan adapted and was able to live in tsetse flies. Eventually they were able to live in humans, which shortened their already short life spans. The sickness was passed along by the unsuspecting humans through their trading routes.
In the world the disease is most …show more content…
commonly found in Sub-Saharan Africa. Sub-Saharan Africa is a central location that is made up of around 36 countries with the genus Glossina (tsetse fly). At least 55 million people in these countries are at risk of getting African Sleeping Sickness with 50,000 new cases reported annually and about 300,000 to 500,000 actual cases per year. Sadly, it is a disease that kills many, as treatment can often fail or prove unsuccessful.
The parasite is a blood-borne protozoan that primarily targets the extracellular tissue.
Most of the damage inflicted by the Trypanosoma brucei is in the nervous system, which causes the victim to feel a lot of tiredness. As the disease progresses the human body starts to malfunction and die. The nervous system starts to shut down along with the body. Though the sickness is not a toxin it can be just as deadly. Like with most diseases, the immune system fights the sickness until it cannot keep up. After that the human body’s systems simply start to fail. Symptoms of the disease generally begin to show after around one to three weeks, and the second stage could start anywhere from weeks to months after the first stage. Major symptoms include: fever, headache, swollen lymph-nodes, and extreme fatigue. The second stage is slightly different as the signs are confusion, numbness, and little or no sleep. If left untreated this disease will kill its
victim.
Local pain and inflammation is given off in response to the infected bite. If the protozoan does not die, it enters the bloodstream and multiplies rapidly, lowering the chances of the sufferer’s survival. A B-celled mediated antibody response is then generated, which kills the clones of parasite. Unfortunately, some of the creatures are able to change their VSGs, allowing the Trypanosome to escape its own death and create more of itself by dividing and multiplying. The process then repeats over again. There are two medicines currently used to treat African Sleeping Sickness, the first is Suramin, and it is used on patients who are in the early stage. Patients who are in the later stage of the illness receive Melarsoprol. These drugs may stop the protozoan division, and if that works the parasite eventually dies and flushes out, however, both treatments are strong toxins and can have many side effects. Hospitalization for the treatment is very necessary and lasts around two years. At this time there is no present vaccine or prevention aside from: avoiding tsetse flies, using pesticide, and using one’s own common sense.
Because of the increase of trade in the late 19th century, African Sleeping Sickness was spread so much that it became an epidemic. Around 90 to 95 percent of African cattle were killed by the epizootic, and many farmers starved because of this bout of disease. A practice that could possibly help with learning more about this illness is the study of RNA aptamers, though not much has happened with that as of yet. Regrettably, there is not a more successful study or proposal currently.