Trypanosoma brucei it is an extracellular parasitic protozoan. It belongs to the class Kinetoplastidae, family Trypanosomatidae genus Trypanosoma. There are two subspecies that cause two different variants of human African trypanosomiasis or also called "sleeping sickness".
Trypanosoma brucei subsp. gambiense, causes the chronic form and 98% of cases, located in western and central sub-Saharan Africa. Trypanosoma brucei subsp. rhodesian is the cause of the acute form, present in central and eastern sub-Saharan Africa.
Both variants of this disease have been reported in those sub-Saharan African countries where the tsetse fly is found., Glossina spp, the vector or transmitting agent of T. brucei.
A third subspecies, Trypanosoma brucei subsp. brucei, causes a similar disease in domestic and wild animals, called nagana.
"Sleeping sickness" threatens more than 60 million people in 36 countries in sub-Saharan Africa. There are around 300,000 to 500,000 cases per year, of which about 70,000 to 100,000 die. Tsetse fly infestation covers an area of 10 million square kilometers, one-third of the land mass of Africa.
The World Health Organization recognizes a significant decrease in the number of new cases of human African trypanosomiasis in recent years. This is due to the persistence of national and international initiatives to control this disease..
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It is called "sleeping sickness" because it causes a reversal of the natural sleep cycle in the patient. The person sleeps during the day and stays awake at night. This is the product of the series of psychic and neurological disturbances that the disease causes in its advanced phase..
Animal trypanosomiasis or nagana is a major disease in livestock in Africa. Was identified Trypanosoma brucei as the causative agent in 1899. It was David Bruce while investigating a major nagana outbreak in Zululand.
Subsequently, Aldo Castellani identified this species of trypanosome in the blood and cerebrospinal fluid of human patients with "sleeping sickness".
Between 1902 and 1910, the two variants of the disease in humans and their causative subspecies were identified. Both animals and humans can act as reservoirs for parasites capable of causing disease in humans..
The nucleus genome of Trypanosoma brucei It is made up of 11 diploid chromosomes and a hundred microchromosomes. In total it has 9,068 genes. The mitochondrial genome (the kinetoplast) is made up of numerous copies of circular DNA.
African human trypanosomiasis is considered one of the 12 human infectious diseases that can be aggravated by global warming.
This is because as the ambient temperature increases, the area susceptible to being occupied by the fly will expand. Glossina sp. As the fly colonizes new territories, it will carry the parasite with it.
Trypanosoma brucei pIt belongs to the Protista kingdom, Excavata group, Euglenozoa phylum, Kinetoplastidae class, Trypanosomatida order, Trypanosomatidae family, genus Trypanosoma, subgenre Trypanozoon.
This species has three subspecies that cause different variants of "sleeping sickness" in humans (T. b. subsp. gambiense Y T. b. subsp. rhodesian) and in domestic and wild animals (T. b. subsp. brucei).
Trypanosoma brucei is an elongated unicellular organism 20 μm long and 1-3 μm wide, whose shape, structure and membrane composition vary throughout its life cycle.
It has two basic shapes. A trypomastigotic form with a basal body posterior to the nucleus and a long flagellum. This form in turn assumes subtypes during the life cycle. Of these, the short or stocky subtype (slumpy in English), it is thicker and its flagellum is short.
The second basic form is the epimastigote of the basal body anterior to the nucleus and flagellum somewhat shorter than the previous one..
The cell is covered by a layer of variable surface glycoprotein. This layer changes the glycoproteins on its surface and thus avoids the attack of the antibodies generated by the host..
The immune system produces new antibodies to attack the new configuration of the coat and the coat changes again. This is what is called antigenic variation.
An important feature is the presence of the kinetosoma. This structure consists of condensed mitochondrial DNA located inside the only mitochondrion present. This large mitochondrion is located at the base of the flagellum.
The life cycle of Trypanosoma brucei alternates between the tsetse fly as a vector and the human as a host. In order to develop in such different hosts, the protozoan undergoes important metabolic and morphological changes from one to the other..
In the fly, the Trypanosoma brucei inhabits the digestive tract, while in humans it is found in the blood.
Trypanosoma brucei It comes in three basic forms throughout its cycle. When the fly bites a human or other mammal to extract its blood, it injects from its salivary glands into the bloodstream a non-proliferative form of the protozoan, called metacyclic..
Once in the bloodstream, it transforms into the proliferative form, called slender blood (slender in English).
The slender sanguine form of Trypanosoma brucei It gets its energy from the glycolysis of glucose present in the blood. This metabolic process takes place in an organelle called a glycosome. These trypanosomes multiply in different body fluids: blood, lymph, and cerebrospinal fluid..
As the number of parasites in the blood increases, they begin to change back to a non-proliferative form. This time it is a thicker and shorter flagellum variant, called sanguine chubby (stumpy).
Chubby blood trypanosomes are adapted to the conditions of the fly's digestive system. They activate your mitochondria and the enzymes necessary for the citric acid cycle and respiratory chain. The source of energy is no longer glucose but proline.
The vector or transmitting agent of Trypanosoma brucei it's the tsetse fly, Glossina spp. This genus groups 25 to 30 species of blood-sucking flies. They are easy to differentiate from the housefly by their particularly long proboscis and fully folded wings at rest..
When a tsetse fly again bites the infected host mammal and draws its blood, these chubby blood forms enter the vector.
Once in the digestive tract of the fly the chubby blood forms rapidly differentiate into proliferative procyclic trypanosomes.
They multiply by binary fission. They leave the fly's digestive tract and head for the salivary glands. They transform into epimastigotes that are anchored to the walls by the flagellum.
In the salivary glands, they multiply and transform into metacyclic trypanosomes, ready to be inoculated again into the blood system of a mammal..
The incubation period for this disease is 2 to 3 days after the fly bite. Neurological symptoms may appear after a few months in the case of T. b. subsp. gambiense. If it's about T. b. subsp. rhodesian, can take years to manifest.
"Sleeping sickness" has two stages. The first is called the early stage or hemolymphatic phase, it is characterized by the presence of Trypanosoma brucei only in blood and lymph.
In this case, the symptoms are fever, headaches, muscle aches, vomiting, swollen lymph nodes, weight loss, weakness and irritability..
In this phase the disease can be confused with malaria.
The so-called late stage or neurological phase (encephalitic state), is activated with the arrival of the parasite to the central nervous system, being detected in the cerebrospinal fluid. Here the symptoms are expressed as behavioral changes, confusion, incoordination, alteration of the sleep cycle and finally coma..
The development of the disease continues with a cycle of up to three years in the case of the subspecies gambiense, ending with death. When the subspecies is present rhodesian, death comes from weeks to months.
Of the cases not submitted to treatment, 100% died. 2-8% of cases treated equally die.
The diagnostic stage is when the infective form, that is, the blood trypanosome, is found in the blood..
Microscopic examination of blood samples detects the specific form of the parasite. In the encephalitic phase, a lumbar puncture is required to analyze the cerebrospinal fluid.
There are various molecular techniques to diagnose the presence of Trypanosoma brucei.
The capacity it has Trypanosoma brucei constantly varying the configuration of its outer layer of glycoproteins (antigenic variation), makes it very difficult to develop vaccines against "sleeping sickness".
There is no prophylactic chemotherapy and little or no prospect of a vaccine. The four main drugs used for human African trypanosomiasis are toxic.
Melarsoprol is the only drug that is effective for both variants of the central nervous system disease. However, it is so toxic that it kills 5% of patients who receive it..
Eflornithine, alone or in combination with nifurtimox, is increasingly used as the first line of therapy for disease caused by Trypanosoma brucei subsp. gambiense.
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