Federal Bacterium Investigators

Staphylococcus aureus

Mycobacterium tuberculosis

Trypanosoma brucei

Yersinia pestis

Lethal Fugitive: Trypanosoma brucei

Charged with: Inflicting Africans with African sleeping sickness through the vector of the tsetse fly

 

 

Trypanosoma brucei

The Trypanosoma brucei is a curious villain. Having a structure similar to many eukaryotes, it differs in its single large mitochondria that contains the DNA structure known as kinetoplast. This is associated with the basal body of the flagellum.

In the bloodstream form, the cell surface of T. brucei has a dense coat of variable surface glycoproteins, later replaced by a dense coat of procyclins as the parasite transforms.

The coat of variable surface glycoproteins enables evasion of the human host's immune system due to it's two properties: uniformly shielding the microbe from the immune system, which doesn't recognize the trypanosome as a threat; and antigenitic variation, during which the coat genetically modifies itself to escape the immune attack that may have risen up against the previous coat. While the human body is capable of killing much of this disease, through this trickery it still manages to evade the immune system and cause chronic disease. (Source 1)

Trypanosoma brucei is a trypomastigote, meaning it has a long flagellum that is attached to the cell body. It also contains a basal body posterior of the nucleus. This microbe is slender and should be approached with extreme caution.

Once attacked, the body will experience a large sore at the scene of the crime (tsetse bite).

False color SEM micrograph of procyclic T. brucei, found in the midgut of the tsetse fly. Cell body=orange Flagellum=red

 

 

Pathophysiology of Trypanosoma brucei

Trypanosoma brucei (blue) among red blood cells

Trpanosoma brucei usually finds its vector by an uninfected Glossina insect, commonly known as a tsetse fly, biting an infected individual. The fly will take a blood meal and ingests bloodstream trypomastigotes. These early-stage form of the parasite develop into procyclic trypomastigotes in the midgut of the fly, multiplying through binary fission. After leaving the midgut of the fly, the microbes will transform into epimastigotes, and then multiply in the salivary gland. These then transform into metacyclic trypomastigotes, and wait patiently for the tsetse fly to bite an uninfected human.

Once inside the human host, Trypanosoma brucei becomes bloodstream trypomastigotes and are carried throughout the body, reaching bodily fluids such as the lymph and spinal fluids. These microbes continue to replicate throughout the body through binary fission. The natural defenses of the body generally destroys many of the parasites. However, a few of the trypanosomes are capable of infiltrating the immune system through antigenic variation - modifying their surface membrane. There are over 1,000 different variants that can multiply and get passed the immune system. (Source 2)

As Trypanosoma brucei crosses the blood-brain barrier, it may infiltrate the nervous system and enters its second stage. After a sore develops at the site of the bite, fever, headache, muscle and joint aches, enlarged lymph nodes and rash may develop. This all occurs within the span of 1-2 weeks. After a few weeks of T. brucei enraging the immune system, the central nervous system is invaded and mental deterioration and neurological problems occur. (Source 4) Victims typically develop a weary shuffling walk, tremors, spastic or flaccid paralysis, chorea, and extreme sleepiness while eating or standing or walking. In fact, exerting effort at all is made an almost impossible task when one's nervous system has been attacked by Trypanosoma brucei. (Source 5) Without treatment, victims quickly fall into a coma and die.

 

 

Threat Level:

The World Health Organization found that in 1995, there were an estimated 60 million people who were at risk for developing Human African trypanosomiasis, with an increasing rate of 300,000 new cases per year. Fewer than 30,000 people, it was estimated, were actually properly diagnosed and treated

Luckily, due to the knowledgeable efforts of such aforementioned organizations and the FBI itself, in a 2004 report, the number of new reported cases for the year came to 17,616. This drop is assumed due to increased prevention and control, and the cumulative rate was estimated to fall between 50,000 and 70,000. (Source 3)

Therea re 36 countries in which trypanosomiasis is endemic, or constantly present. Social and economic factors seem apparent regarding who is treated (note - not cured) and who is not. African countries affected with the disease are impacted by political disorder and instability. This allows for poorer, less stable nations to have increased number of infected citizens that go untreated, due to systematic medical surveillance being interrupted by the government, changes to the environment, and the displacement of populations as Africa continues to represent an unstable continent.

Regarding diagnosis, the presence of T. brucei can be confirmed with body fluid analyzation, most commonly blood or lymph fluid.

Four drugs are registered to treat T. brucei: pentamidine, suramin, melarsoprol and eflornithine. All of these have a certain level of toxicity, and are employed at different stages of the disease, for at certain stages they may be found completely ineffective against the microbe.

Side view of a tsetse fly

 

 

Protect Yourself and Your Loved Ones

Ablation of flagellar proteins of T. brucei, "monstrous cells arise (main picture) and rapidly die as parasites fail to divide." The inserted picture is a normal trypanosome to compare, it is not to scale.

Throughout the history of the disease, there have been many instances during which scientists have reported eradicating the tsetse fly or curing T. brucei. Often, the treatments for this disease have proven just as dangerous as leaving the disease untreated. For example, in 1932, 700 patients received the wrong dose of Atoxyl, which is quite toxic, and became blind. The response to this was the development of the drug melarsoprol, which contained a highly toxic arsenic based molecule.

Unfortunately, this disease is so volatile that curing seems difficult, though treating is possible in all nations, so long as government and environment allow for it.

Currently, efforts have been made to control the disease, which leaves some regions of sub-Saharan Africa uninhabitable due to tsetse fly excessiveness. Isolation and appropriate treatment to all those infected or possible carriers and protection from tsetse fly bites using insecticides have both been employed to prevent the spread of this nasty villain. Also, once every 60 to 90 days, people who must enter the jungle can be given prophylactic doses of suramin or diamidine compounds in order to stave off infection from fly bites. Finally, there have been efforts to remove severely affected villages to disease-free zones.

 

In order to protect yourself and those you love from the sleeping sickness, and granted you are in sub-Saharan Africa, one may wear protective, neutral colored clothing, inspect vehicles for tsetse flies before entering, avoid bushes and implement insect repellant (though this has not been proven effective in preventing tsetse fly bites).

If you believe you have been infected with T. brucei, seek professional healthcare in order to take a blood test or spinal tap to investigate for infection. Be alert - T. brucei is fatal if not treated.

Giemsa-stained light photomicrograph, revealing T. brucei in a thin film blood smear. Magnification: 1000x

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