Tuesday, February 1, 2011

Trypanosoma brucei--Not Your Average Sleeping Beauty


Introduction
Trypanosoma brucei is a microscopic parasite that causes African Trypanosomiasis, also known as "African sleeping sickness." [1] It is transmitted by the tsetse fly (Glossina species), and can affect both humans and animals. T. brucei will be transmitted through the salivary glands of the tsetse fly, enter the hosts bloodstream, infect the blood-brain barrier, and if not treated, cause the host’s death. [2]. Both forms of T. brucei—T.b. gambiense and T.b.rhodesiense—can affect humans and animals, and are found in western and eastern Africa respectively, [2] Currently, about 10,000 new cases each year are reported to the World Health organization, although there may be many cases that go unreported and untreated. [1]



Symbiont Description
Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense develop into a trypomastigote once it is deposited into the host by the tsetse fly. Typically, a trypomastigote has a small kinetoplast located at the posterior end, a centrally located nucleus, an undulating membrane, and a flagellum running along the undulating membrane, leaving the body at the anterior end. There are two subspecies of Trypanosoma brucei that cause African Sleeping Sickness, T. b. gambiense and T. b. rhodesiense, and they are unable to be distinguished morphologically. Trypomastigotes are the only stage found in patients and they range in length from 14 to 33 ┬Ám. [3]





Host Description
Both forms of sleeping sickness, T.b. gambiense and T.b.rhodesiense, are transmitted by the bite of the tsetse fly (Glossina species). Tsetse flies inhabit rural areas, living in the woodlands and thickets of the East African savannah, or in the forests and vegetation along streams of central and West Africa. Both male and female flies can transmit the infection, and they usually bite during daylight hours. Although the vast majority of infections are transmitted by the tsetse fly, other modes of transmission are possible such as a pregnant woman passing the parasite to her child. [1] Animals can also host these two forms of the parasite. T.b.rhodesiense is most commonly found in domestic animals such as cows, and has become a major problem in rural areas. [2] Humans are the important reservoir of infection of T.b. gambiense, although the parasite can sometimes be found in domestic animals. [1]

Life Cycle
The tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host such as a cow or human. 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 and mature into metacyclic trypomastigotes. The cycle in the fly takes approximately 3 weeks. The tsetse fly (genus Glossina) then transfers the parasite by injecting metacyclic trypomastigotes into skin tissue of another host. The parasites enter the lymphatic system and pass into the bloodstream. They are carried to other sites throughout the body, reach other blood fluids (e.g., lymph, spinal fluid), and continue the replication by binary fission.[1]



In this hemolymphatic phase, the trypansomoses multiply in the subcutaneous tissue, blood and lymph. [2] While there, the parasite has an amazing ability to trick the immune system! When the immune system attacks, the parasite is able to create a glycoprotein shell that protects it from white blood cells. In the time it takes for the immune system to create antibodies, the parasite sheds the original variable surface glycoprotein (VSG) shell and creates a new one, always staying one step ahead of the host’s immune response. [4] In this first stage, the parasite causes bouts of fever, headaches, joint pains and itching. In the second stage, or the neurological phase, the parasites cross the blood-brain barrier to infect the central nervous system. In general this is when more obvious signs and symptoms of the disease appear including changes of behaviour, confusion, sensory disturbances and poor coordination. Along with many other neurological signs, the feature that gives the disease its name is disturbance of the sleep cycle. [2]The parasite will then cross the blood-brain barrier and affect the central nervous system. The tsetse fly will then take another blood meal from the human or animal host to continue the life cycle. [1]

Ecology
African Sleeping Sickness threatens millions of people in 36 countries in sub-Saharan Africa. Many of the affected populations live in remote areas with limited access to adequate health services, war-tone societies, and displaced people groups, which hampers the surveillance of cases. In 1998, there were an estimated 300,000 reported and unreported cases. Through careful surveillance, in 2009 the number dropped significantly to 30,000. [2]The two subspecies are found in different regions of Africa. Presently, there is no overlap in their geographic distribution. T. b. rhodesiense (East African sleeping sickness) is found in certain areas eastern and southeastern Africa.[1] Each year T.b. rhodensiense causes approximately 5% of African sleeping sickness cases that are reported to the World Health Organization and causes an acute infection. Those infected show signs within a few weeks, where the parasite rapidly invades the nervous system. [2] Over 95% of the cases of human infection occur in Tanzania, Uganda, Malawi, and Zambia. [1]

T. b. gambiense (West African sleeping sickness) is found primarily in central Africa and in limited areas of West Africa. [1] Approximately 95% of reported cases of the sleeping sickness in Africa is caused by this form of the parasite and causes a chronic infection. Those infected may not show signs for years, and when shown, the central nervous system is already diseased. [2] Epidemics of sleeping sickness have been a significant public health problem in the past, but the disease is reasonably well-controlled at present, with about 10,000 cases reported annually in recent years. Over 95% of the cases of human infection are found in Democratic Republic of Congo, Angola, Sudan, Central African Republic, Chad, and northern Uganda. [1]

Check out this video!
Monsters Inside Me : Sleeping Sickness, Trypanosomiasis: Animal Planet

An example of…
African Sleeping Sickness, is a vector-borne parasitic disease. A vector-borne disease is one in which the pathogenic microorganism is transmitted from an infected individual to another individual by an agent, sometimes with other animals serving as intermediary hosts. The transmission depends upon the attributes and requirements of at least three different living organisms: the parasite (Trypanosoma brucei), the vector (tsetse fly), and the human host. In addition, intermediary hosts such as domesticated (in this case cattle) and/or wild animals often serve as a reservoir for the pathogen until susceptible human populations are exposed.[5]


References
[1] http://www.cdc.gov/parasites/sleepingsickness/
[2] http://www.who.int/mediacentre/factsheets/fs259/en/
[3] http://www.dpd.cdc.gov/dpdx/html/frames/s-z/trypanosomiasisafrican/body_trypanosomiasisafrican_mic1.htm
[4] http://pathmicro.med.sc.edu/lecture/trypanosomiasis.htm
[5] http://www.ciesin.columbia.edu/TG/HH/veclev2.html

4 comments:

  1. Amongst your research, what did you find out about the treatment of ridding this parasite? Also, if this is so wide spread in the rural countries, what are these countries doing to stop these attacks?

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  2. Somewhat in relationship to the comment above, the WHO link that was sited in this blog said that the most recent epidemic of the sleeping sickness was in 1970; that was 41 years ago. If the WHO was successful in riding most of the infected countries with the disease, what is preventing total eradication? Maybe it is the microscopic relationship between the fly and the parasite which cannot be controlled, but where has this relationship gone in the countries in which humans are no longer hosts? Are there perhaps noticeable infections of other mammals?
    And would it not be a scary thing if this parasite pulled a move like the Ebola virus did during the 1970's and unnoticeably infected another host, and appeared to be gone for years, only to return and continue to infect?

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  3. I don't know if I missed this in the reading or what but how does the parasite continue to be transmitted if it kills its host? I see how it would be transmitted from mother to baby but if most hosts die from the parasite how does the parasite continue?

    Since the parasite tricks the immune system, do you think it will be able to "trick" medication as well?

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  4. Thank you for all of your comments!
    Stephanie...here is a link to see the available drugs for treating this parasite. The key is catching this parasite before it hits the brain. Also see the prologue of Parasite Rex.

    http://emedicine.medscape.com/article/228613-treatment

    Amanda and Nicole...your answers are found under "life cycle". This parasite is so hard to control because the tsetse fly can infect a human host, then come back and take another parasite from the same human host, to another host. People in developing countries do not have the funds or access to medications to take care of individual cases. If every single host is not cured, the fly can continue to infect the population.

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