Trypanosoma brucei is an external parasitic protozoan. Class Kinetoplastidae, family Trypanosomatidae belongs to the genus Trypanosoma . There are two subspecies that cause two different forms of African human trypanosomiasis or “sleeping sickness”.
Trypanosoma brucei subsp. gambiense , causes the chronic form and 98% of cases are located in western and central sub-Saharan Africa. Trypanosoma brucei subsp. Rhodesis is the cause of the acute form present in the center and east of sub-Saharan Africa.
Both variants of the disease have been reported in countries in sub-Saharan Africa where the tetus fly, Glossina spp ., is the vector or transmission agent of T. Bruce .
A third subspecies, Trypanosoma brucei subsp. brucea , which causes a similar disease in domestic and wild animals, is called ngana.
“Sleeping sickness” threatens more than 60 million people in 36 countries in sub-Saharan Africa. About 300,000 to 500,000 cases occur per year, of which about 70,000 to 100,000 die. Infiltration by the tsetse fly covers 10 million square kilometres, a third of Africa’s landmass.
The World Health Organization recognizes a significant reduction in the number of new cases of African human trypanosomiasis in recent years. This is due to the persistence of national and international initiatives to control this disease.
This is called “sleep sickness” because it causes a reversal of the patient’s natural sleep cycle. The person sleeps during the day and wakes up at night. It is the product of a series of mental and neurological disturbances that the disease produces in its advanced stage.
Cattle or Nganana trypanosomiasis is an important disease in cattle in Africa. He identified his Trypanosoma brucei as the causal agent in 1899. This was David Bruce while investigating a major outbreak of Nagana in Zooland.
Later, Aldo Castellani identified this species of trypanosomes in the blood and cerebrospinal fluid of human patients with “sleeping sickness”.
Between 1902 and 1910, two forms of the disease and their subspecies were identified in humans. Both animals and humans can act as reservoirs of parasites capable of causing disease in humans.
The genome of the nucleus of Trypanosoma brucei is composed of 11 diploid chromosomes and one hundred microchromosomes. In total it has 9,068 genes. The genome (kinetoplast) of mitochondria is made up of multiple copies of circular DNA.
“Sleeping Sickness” and Global Warming
African human trypanosomiasis is considered one of 12 human infectious diseases that may be exacerbated by global warming.
This is due to the fact that when the ambient temperature increases, the area susceptible to capture by the fly will be enlarged. Glosina sp. When colonizing the fly’s new territories, it will carry it along with the parasite.
Phylogeny and Taxonomy
Trypanosoma brucei P belongs to the kingdom Protista, group Aquatava, phylum Eugelozoa, class Kinetoplastidae, order Trypanosomatida, family Trypanosomatidae, genus Trypanosoma , subgenre Trypanozoon .
There are three subspecies of this species that cause various forms of “sleeping sickness” in humans ( T. B. subsp. gambiense and T. B. subsp. R. hodesiense ) and in domestic and wild animals ( T. B. subsp. Bruce ).
Trypanosoma brucei is an elongated unicellular organism up to 20 µm long and 1–3 µm wide, whose shape, structure and membrane composition vary throughout the life cycle.
It has two basic forms. A tryomastigote form of the basal body lies behind the nucleus and long flagellum. This form acquires subtypes in turn during the life cycle. Of these, the short or stunted subtype ( slumpy in English), is thicker and has a shorter flagellum.
The second basic form is the epimastigote of the basal body anterior to the nucleus and flagellum which is slightly shorter than the previous one.
The cell is covered by a layer of variable surface glycoproteins. This layer replaces its surface glycoproteins and thereby repels the attack of antibodies produced by the host.
The immune system produces new antibodies to attack the new configuration of the layer and the layer changes again. This is called antigenic variation.
An important feature is the presence of kinetosoma. Present in this structure is the condensed mitochondrial DNA located inside the mitochondria. This giant mitochondria is located at the base of the hoof.
The life cycle of Trypanosoma brucei tsetse alternates between fly as a vector and humans as a host. To develop in such a different host, the protozoan undergoes significant metabolic and morphological changes from one to the other.
In the fly, the Trypanosoma brucei resides in the digestive tract, while in humans it is found in the blood.
in the host (human or other mammal)
Trypanosoma brucei comes in three basic forms throughout its cycle. When the fly bites a human or other mammal to extract its blood, it injects a non-proliferative form of the protozoan into the bloodstream from its salivary glands, called a metacyclic.
Once in the bloodstream, it turns into a proliferative form, which is called diluted blood ( diluted in English).
The dilute blood form of Trypanosoma brucei that gets its energy from the glycolysis of glucose present in the blood. This metabolic process is carried out in an organism called glycosoma. These trypanosomes multiply in various body fluids: blood, lymph and cerebrospinal fluid.
As the number of parasites in the blood increases, they again turn into a non-proliferative form. This time it’s a thicker version with a shorter flagellum, called plump blood ( lumpy ).
Tubular blood trypanosomes are adapted to the conditions of the fly’s digestive tract. They activate their mitochondria and enzymes necessary for the cycle of citric acid and the respiratory chain. The source of energy is no longer glucose but proline.
in the fly tse-tsé (vector)
The vector or transmitting agent of Trypanosoma brucei is the tse-tse fly, Glossina spp . This genus is a group of 25 to 30 species of hematophagous flies. They are easy to distinguish from the common fly by their particularly long trunk and usually fully folded wings.
When a disturbed fly bites an infected host mammal and expels blood, these stubby blood forms enter the vector.
Once in the fly’s digestive tract, the stubby blood forms quickly differentiate into pathogenic proliferative trypanosomes.
They multiply by binary fission. They leave the fly’s digestive tract and move to the salivary glands,tThey transform into epimastigotes that reach the walls from the junk.
In the salivary glands, they multiply and turn into metacyclic trypanosomes, ready to be re-inoculated into the blood system of a mammal.
symptoms of infection
The incubation period of this disease is 2 to 3 days after the fly bite. Tea. Neurological symptoms may occur after a few months in the case of B. subsp. gambiense. If it’s about T. B. subsp. Rhodesis can take years to appear.
There are two stages of “sleeping sickness”. The first is called the early stage or hemolymphatic stage, it is characterized by the presence of Trypanosoma brucei only in the blood and lymph.
In this case, the symptoms are fever, headache, muscle pain, vomiting, swollen lymph nodes, weight loss, weakness and irritability.
The disease in this stage may be confused with malaria.
The so-called late stage or neurological stage (encephalitic stage), activated with the arrival of parasites in the central nervous system, is detected in the cerebro-spinal fluid. Here the symptoms are expressed as changes in behavior, confusion, incoordination, changes in sleep cycle and finally coma.
The development of the disease continues with a cycle of up to three years in the case of subspecies gambiense , ending with death. When the subspecies rhodesis is present , death occurs within weeks to months.
Of the cases subject to treatment, 100% die. Of the treated cases, 2-8% also die.
The diagnostic stage is when an infectious form called trypanosome is found in the blood.
The specific form of the parasite is detected through microscopic examination of blood samples. A lumbar puncture is required to analyze the cerebrospinal fluid in the encephalitic stage.
There are several molecular techniques to diagnose the presence of Trypanosoma brucei.
The ability of Trypanosoma brucei to continuously change the configuration of its outer layer of glycoproteins makes it very difficult to develop vaccines against “sleeping sickness”.
There is no prophylactic chemotherapy and no possibility of a vaccine. The four main drugs used for human African trypanosomiasis are toxic.
Melarsoprol is the only drug that is effective for both types of central nervous system disease. However, it is so toxic that it kills 5% of patients receiving it.
Eflornithine, alone or in combination with nifurtimox, is used as the first line of therapy for disease caused by Trypanosoma brucei subsp. gambiense .