Trypanosoma Brucei Gambiense: Vector, Pathogen And Life Cycle

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Trypanosoma Brucei Gambiense: Vector, Pathogen And Life Cycle
Trypanosoma Brucei Gambiense: Vector, Pathogen And Life Cycle

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Video: Trypanosoma Lifecycle | Trypanosoma gambiense lifecycle | Trypanosoma brucei | Trypanosomiasis 2023, February

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  • Life cycle
  • Trypanosoma brucei in the taxonomy of eukaryotes
  • Trypanosoma brucei - causative agent of diseases of humans and animals
  • Diseases caused by Trypanosoma brucei in ICD-10
  • Sleeping sickness symptoms

    • Early (hemolymphatic) stage
    • Chronic (meningoencephalitic) stage
  • American trypanosomiasis
  • Analyzes and diagnostics
  • You can defeat parasites!

Trypanosoma brucei gambiense is the causative agent of African trypanosomiasis, a fatal disease in Tropical Africa. The main source is man, the carriers are antelopes, pigs, the carrier is the tsetse fly. Trypanosomes are 20-30 microns in size. There is an elongated body, an undulating membrane, and its free end. When the tsetse fly sucks the patient's blood, trypanosomes enter its stomach. They multiply and change in a complex manner - an invasive form for mammals.

When bitten, infected saliva enters and trypanosomes penetrate the human blood. Most often, they settle in the brain, the central nervous system is affected, drowsiness increases, pathological changes occur in the liver, kidneys, lungs and other organs. The disease lasts 5 - 7 years and is fatal without treatment. Diagnosis of the disease by points of the spinal cord, lymph nodes and peripheral blood.

What to do in such a situation? To get started, we recommend reading this article. This article details the methods of dealing with parasites. We also recommend contacting a specialist. Read the article >>>

Trypanosoma brucei gambiense and Tb rhodesiense (flagellate class) are the causative agents of African trypanosomiasis, or sleeping sickness. The parasite has a sinuous, pointed shape on both sides. Its length is 17-28 microns. The stages parasitizing in humans have one flagellum, an undulating membrane from the side, and a well-visible kinetoplast at the base of the flagellum.

Trypanosomes settle in humans in the blood, lymph, cerebrospinal fluid, in the tissues of the brain and spinal cord and in the serous cavities. Tb gambiense is found in West Africa and Tb rhodesiense in East and Southeast Africa.

Trypanosoma Brucei Gambiense
Trypanosoma Brucei Gambiense

Life cycle

The life cycle of Trypanosoma brucei gambiense occurs in humans, domestic and wild mammals, primarily ungulates. Tb gambiense often infects humans, pigs and dogs, Tb rhodesiense - wild animals - antelopes and rhinos. The carrier of the first subspecies is the tsetse fly, Glossina palpalis, living near human dwellings, the second, G. morsitans, which lives in open savannas and savanna forests. In this regard, sleeping sickness, the causative agent of which is Tb gambiense, occurs in anthropogenic foci of cultural landscapes. About 10,000 new infections are registered every year. East African trypanosomiasis is much less common in nature. Basically, hunters, tourists, seasonal workers get sick, every year - about 1500 people.

Sleeping sickness without treatment lasts about 5 years and is expressed in increasing muscle weakness, depression, exhaustion and drowsiness. Cases of self-healing are possible, but usually the disease ends with the death of the patient.

Parasitizing trypanosomes in mammals and humans is characterized by cyclical increases in the intensity of invasion due to their reproduction, accompanied by changes in the structure and antigenic properties of parasites. During the increase in the number of parasites in the blood, elongated trypanosomes predominate. The antigens they form cause antibodies to form in the host.

Under the action of antibodies, many parasites die and the intensity of invasion decreases. The surviving trypanosomes are shortened and begin to produce other antigens. The shortened forms of the parasite, invasive for the tsetse fly, in its body again acquire an elongated shape that is invasive for humans. Changes in body shape and changes in the antigenic properties of the membrane are repeated many times. Thus, the population of the parasite in the host survives and avoids its immune response.

The antigenic properties of the trypanosome surface depend on only one protein - the glycoprotein, which completely covers the entire cell. The glycoprotein is built from 470 amino acid residues. Each new wave of parasite reproduction represents a new population of trypanosomes with a new surface antigen. These variations in antigenic properties help the parasite to overcome the host's immune response and make it impossible to vaccinate the population living in natural foci of trypanosomiasis.

Development cycle
Development cycle

The change in antigenic properties is provided by the replacement of surface glycoproteins encoded by different genes belonging to the same multigenic family. One trypanosome clone can alternately form up to 100 different varying glycoproteins. The genes for these proteins have evolved, probably by duplication and subsequent differentiation, like other gene families.

The trypanosome genome contains an expression site, into which the genes of surface glycoproteins alternately move, approaching the promoter that provides their specific activation. There they are broadcast. It is possible, however, that the site of expression in the genome of trypanosome is not the only one, and it is even possible that different genes of glycoproteins are activated by several mechanisms. In any case, we are talking about a kind of adaptation of the parasite to specific conditions of existence, increasing its survival rate and opening up broad evolutionary prospects for it.

Trypanosoma brucei in the taxonomy of eukaryotes

According to modern views, the species Trypanosoma brucei is included in the subgenus (Latin subgenus) Trypanozoon, which belongs to the genus Trypanosome (Latin Trypanosoma), the Trypanosomatidae family, the order of kinetoplastida (Latin Kinetoplastida), the type of euglenozoa (Latin Eugzarlenozoa),. Eukaryota).

Trypanosoma brucei includes the following subspecies:

  • Trypanosoma brucei brucei
  • Trypanosoma brucei equiperdum
  • Trypanosoma brucei gambiense
  • Trypanosoma brucei rhodesiense

Trypanosoma brucei - causative agent of diseases of humans and animals

  • The subspecies Trypanosoma brucei gambiense causes chronic trypanosomiasis in humans. It develops relatively slowly. Most common in Central and West Africa. Presumably, humans are the main reservoir of infection.
  • The subspecies Trypanosoma brucei rhodesiense causes rapid onset of acute trypanosomiasis in humans. Most common in South and East Africa. There is reason to believe that its main reservoir is game animals and livestock.
  • The subspecies Trypanosoma brucei brucei causes African trypanosomiasis in animals (along with several other trypanosome species). It rarely causes disease in humans.

Diseases caused by Trypanosoma brucei in ICD-10

Diseases caused by Trypanosomabrucei in the International Classification of Diseases ICD-10 in "Class I. Some infectious and parasitic diseases (A00-B99)", in the block "B50-B64 Protozoal diseases" is devoted to the three-character heading "B56 African trypanosomiasis" with the following content:

  • B56.0 Gambian trypanosomiasis Trypanosoma brucei gambiense infection. West African sleeping sickness.
  • B56.1 Rhodesian trypanosomiasis East African sleeping sickness. Trypanosoma brucei rhodesiense infection.
  • B56.9 African trypanosomiasis, unspecified Sleeping sickness without further specification. Trypanosomiasis without additional specification in areas with a predominance of African trypanosomiasis

By order of the Ministry of Health and Social Development of Russia No. 1664n dated December 27, 2011 "On approval of the nomenclature of medical services", the medical service "A26.06.083 Determination of antibodies to trypanosoma brucei in the blood" is included in the nomenclature of medical services, section 26.

Sleeping sickness symptoms

The incubation period for Gambian sleeping sickness is 2-3 weeks, Rhodesian sleeping sickness - 1-2 weeks. The clinical manifestations of African sleeping sickness are characterized by a variety of symptoms and their nonspecificity, since in different endemic foci, they vary significantly in the frequency of occurrence and severity of their manifestations.

For Rhodesian trypanosomiasis, a more acute course is characteristic with the absence of clearly expressed differences between the acute and chronic stages. It is accompanied by fever, early damage to the central nervous system (3-4 weeks after the onset of the disease), severe heart damage, and a fairly rapid onset of death (within several weeks).

For 7-15 days, trypanosomal chancre may develop on the skin (at the site of the tsetse fly bite), predominantly in non-indigenous people of Africa who are infected with Tb rhodesiense: a dark red elastic, painful papule with a diameter of 2 to 5 cm, which disappears spontaneously through 2-3 weeks.

There are 2 stages of the disease:

Early (hemolymphatic) stage

It is manifested by a fever, the duration of which varies from 2 to 7 days. Acute onset is more common with Tb rhodesiense infection in non-native Africans. People living in West Africa usually have a gradual onset of the disease, and it can take several years before the first clinical symptoms appear. In the early stages, attacks of fever often alternate with periods of remission, lasting from 2 to 3 weeks to several months, during which patients feel well. At this stage, neuropsychiatric changes appear - insomnia, headache, irritability, less often drowsiness.

Trypanosoma cruzi
Trypanosoma cruzi

In some cases, an erythematous rash appears on the skin, which has an oval shape with a diameter of 7-10 cm with a predominant localization in the area of ​​the shoulders and hips, and the trunk. Non-indigenous people may experience hyperesthesia (Kerandell's symptom) - soreness of the skin when compressed. With the progression of the disease, an increase in lymph nodes appears, mainly in the posterior cervical region / above the collarbone). At the same time, the lymph nodes are elastic, mobile, painless. In an early stage, there may be pruritus, weight loss, weakness, swelling / pain in the joints of the extremities, tachycardia, hepatosplenomegaly, periorbital edema.

Chronic (meningoencephalitic) stage

Clinical symptoms are due to the development of diffuse meningoencephalitis with damage mainly to the structures of the base of the brain. An increase in neurological symptoms is characteristic - a violation of muscle tone, sleep, motor function, reflexes of oral automatism. Imperceptibly appear and progressively increase neuropsychic changes, manifested by the development of depressive / manic states.

Initially, changes in personality and behavior are noted - fatigue, indifference and indifference to the environment, drowsiness during the day and nighttime insomnia. A number of individuals have extrapyramidal disorders (tremor of the tongue / fingers, stiff neck, fibrillar twitching of the muscles). Speech is slurred, symptoms of cerebellar ataxia appear, leading to gait disturbance. With cerebral edema - edema of the optic nerve head, severe headache. As the disease progresses, euphoria, epileptiform seizures, mania, and severe drowsiness appear. When the hypothalamic-pituitary zone is involved in the pathological process, the feeling of hunger, thirst, libido is disturbed, endocrine disorders appear (impotence, amenorrhea, obesity).

In the terminal stage, patients lie motionless in bed, refusing food. The causes of death are more often the development of cerebral coma, cachexia, the addition of a secondary infection (pneumonia, malaria, dysentery). In African trypanosomiasis, the symptoms of sleeping sickness are accompanied by hemolytic anemia, thrombocytopenia, and blood clotting disorders.

Rhodesian sleeping sickness has a more rapid and severe course. Intoxication / fever is more pronounced, depletion occurs faster, and heart damage is more common. A lethal outcome can occur even before the transition of the disease to the meningoencephalitic stage already in the first year of the disease.

American trypanosomiasis

There are several forms of clinical course.

Acute form is recorded in endemic foci mainly in children under the age of 10 years. The duration of the acute stage varies within 1-1.5 months, while the symptoms of the acute stage may be mild and even go unnoticed. The incubation period for acute clinical manifestations lasts 10-12 days. Acute onset with chills and fever. Pain in the eyes, anorexia, malaise, headache and muscle pain, dyspeptic disorders are characteristic.

In the place where the Cruzi trypanosome is introduced through the skin, in most cases, a primary affect develops - shagoma (local inflammatory reaction), which is an infiltration on the skin of a red-violet color, resembling a moderately painful boil. Shagoma is often accompanied by regional lymphangitis / lymphadenitis. When infected through the conjunctiva of the eye, the primary affect is represented by a sharp periorbital edema, conjunctivitis from the side of the lesion with scant secretions, an increase in regional lymph nodes (Romagna symptom complex).

The disease is accompanied by a remitting fever, with temperature rises in the evening to 39-40 ° C, but with a benign course, the febrile reaction is insignificant. In patients in the acute period of the disease, lymph nodes of almost all groups increase - axillary, cervical, inguinal, hepatosplenomegaly is noted. Changes from the side of the heart are expressed - the boundaries are expanded to the left, systolic murmur, tachycardia, deafness of tones.

Indefinite form - there are no clinically expressed signs of the disease, with the exception of the presence of positive serological reactions. The duration of this phase of the infectious process can last for many years, and in approximately 2/3 of the infected persons, until the end of life. In the remaining 1/3 of persons, after 10-20 years, clinical symptoms of the chronic form of trypanosomiasis, caused by damage to the heart, gastrointestinal tract organs, and the peripheral nervous system, develop.

Chronic form - the leading symptom is myocardiopathy, ventricular dilatation of the heart, cardiomegaly are noted. As the disease progresses, circulatory failure, heart rhythm disturbances, thromboembolism, in particular of the pulmonary arteries, develop. Dysfunction of the endocrine, central / autonomic NS is also characteristic.

On the ECG - violations of conduction and excitability (blockade and extrasystole). Along with myocardiopathy, the important clinical syndromes include "megacolon", which is dilatation (expansion) of internal organs, mainly the esophagus and segments of the large intestine (sigmoid colon), which leads to constipation, impaired swallowing and the development of intestinal obstruction. With a sharp progression of the disease, cachexia develops.


Analyzes and diagnostics

The diagnosis is established on the basis of data from the epidemiological history, clinical symptoms and laboratory tests, including:

  • microscopy of a blood smear, cerebrospinal fluid, punctate / biopsy of the spleen, affected lymph nodes or bone marrow for the detection of trypanosomes in smears stained according to Romanovsky-Giemsa;
  • immunological reactions (detection of IgM antibodies in the blood serum of patients in diagnostic titers);
  • biological method (infection of laboratory rats and mice with intraperitoneal injection of patient's blood).
  • Microbiological examination of cerebrospinal fluid / blood

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