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Team:Aberdeen Scotland/Project/Disease
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<p>2% of reported cases are due to <i>T.b. rhodesiense</i>, which is an acute infection, however this figure may be skewed by the fact this develops rapidly, invading the central nervous system with symptoms appearing after only a few weeks or months. If it persists, infected have a similar prognosis of almost unanimous mortality.</p> | <p>2% of reported cases are due to <i>T.b. rhodesiense</i>, which is an acute infection, however this figure may be skewed by the fact this develops rapidly, invading the central nervous system with symptoms appearing after only a few weeks or months. If it persists, infected have a similar prognosis of almost unanimous mortality.</p> | ||
<p>Chagas disease of South America is of a different subgenus, <i>Trypanosoma cruzi</i>, and utilises a different vector, Triatominae (‘assassin bugs’).</p> | <p>Chagas disease of South America is of a different subgenus, <i>Trypanosoma cruzi</i>, and utilises a different vector, Triatominae (‘assassin bugs’).</p> | ||
| - | <h3>Disease Progression</h3> | + | <h3>Disease Progression</h3><p></p> |
| + | <img src="https://static.igem.org/mediawiki/2014/c/cb/Trypanosoma-evansi-rat-blood-Giemsa-stain.jpg"> | ||
| + | Giemsa-stained trypanasoma parasites in blood | ||
<p><i>T. b. gambiense</i> stage 1 exists free in blood serum or lymph, usually pathogens like this will be quickly destroyed by an active immune response, however it exhibits antigenic variation of its LiTat1.3/1.5 coat that changes every 20 minutes with over 100 possible phenotypes encoded in its chromosome; this negates an active immunity from being effectively generated.</p> | <p><i>T. b. gambiense</i> stage 1 exists free in blood serum or lymph, usually pathogens like this will be quickly destroyed by an active immune response, however it exhibits antigenic variation of its LiTat1.3/1.5 coat that changes every 20 minutes with over 100 possible phenotypes encoded in its chromosome; this negates an active immunity from being effectively generated.</p> | ||
<p>After a period of approximately 6 months it progresses to stage 2 where the parasite enters the central nervous system, here it is protected from an immune response and may proliferate at will. Clearer symptoms emerge at this point including muscle weakness, sleep disturbance, partial paralysis, parkinsonism, psychosis and other psychiatric symptoms, and coma. If untreated, <i>T. b. gambiense</i> almost always results in death.</p> | <p>After a period of approximately 6 months it progresses to stage 2 where the parasite enters the central nervous system, here it is protected from an immune response and may proliferate at will. Clearer symptoms emerge at this point including muscle weakness, sleep disturbance, partial paralysis, parkinsonism, psychosis and other psychiatric symptoms, and coma. If untreated, <i>T. b. gambiense</i> almost always results in death.</p> | ||
Latest revision as of 02:58, 18 October 2014
Trypanosomiasis
Human African Trypanosomiasis (Sleeping Sickness) Epidemiology
Over 98% of reported cases of Human African Trypanosomiasis (HAT) are caused by a chronic infection of parasite Trypanosoma brucei gambiense. Its vector is through the bite of an infected Tsetse fly in sub-saharan Africa.
WHO estimates as of 2014, 30,000 people are currently infected, with more than 80% of new cases occurring in Democratic Republic of the Congo.
T.b. gambiense sufferers may be infected for months or even years without major signs or symptoms of the disease. When more evident symptoms emerge, the patient is often already in an advanced disease stage where the central nervous system is affected.
During epidemic periods prevalence reached 50% in several villages in the Angola, Democratic Republic of Congo, and South Sudan. Sleeping sickness was the first or second greatest cause of mortality in those communities, ahead of even HIV/AIDS.
The World Health Organisation included HAT in its roadmap for elimination and control of neglected tropical diseases in 2012, setting a date of 2020 to eliminate the disease as a public health problem.
2% of reported cases are due to T.b. rhodesiense, which is an acute infection, however this figure may be skewed by the fact this develops rapidly, invading the central nervous system with symptoms appearing after only a few weeks or months. If it persists, infected have a similar prognosis of almost unanimous mortality.
Chagas disease of South America is of a different subgenus, Trypanosoma cruzi, and utilises a different vector, Triatominae (‘assassin bugs’).
Disease Progression
Giemsa-stained trypanasoma parasites in blood
T. b. gambiense stage 1 exists free in blood serum or lymph, usually pathogens like this will be quickly destroyed by an active immune response, however it exhibits antigenic variation of its LiTat1.3/1.5 coat that changes every 20 minutes with over 100 possible phenotypes encoded in its chromosome; this negates an active immunity from being effectively generated.
After a period of approximately 6 months it progresses to stage 2 where the parasite enters the central nervous system, here it is protected from an immune response and may proliferate at will. Clearer symptoms emerge at this point including muscle weakness, sleep disturbance, partial paralysis, parkinsonism, psychosis and other psychiatric symptoms, and coma. If untreated, T. b. gambiense almost always results in death.
