Trypanosoma Cruzi: Vector, Invasive Stage, Spread

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Trypanosoma Cruzi: Vector, Invasive Stage, Spread
Trypanosoma Cruzi: Vector, Invasive Stage, Spread

Video: Trypanosoma Cruzi: Vector, Invasive Stage, Spread

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Video: trypanosoma cruzi development and life cycle in vector || Chagas disease 2023, February
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  • The structure of Trypanosoma cruzi
  • Development cycle
  • Pathogenesis of American trypanosomiasis
  • Trypanosoma cruzi symptoms
  • Diagnostics
  • Treatment, prevention
  • You can defeat parasites!

American trypanosomiasis, or Chagas disease, is caused by Trypanosoma cruzi, which differs from the causative agents of African trypanosomiasis by a shorter body length (13-20 microns) and a larger kinetoplast of the tripomastigous forms. In fixed blood preparations Tr. cruzi often has a curved shape, like the letters C or S (C- and S-shaped).

The causative agent of American trypanosomiasis belongs to the category of Stercoraria (Latin stercus - feces, oralis - oral), and the disease American trypanosomiasis (Chagas disease) belongs to stercorarium trypanosomiasis, thus the pathogen is transmitted through the feces of the carrier bug. Also, for Tr. cruzi are characterized by persistence (Latin persistere - to remain, to persist) - the ability of the parasite to persist in the host's body throughout its life with the development of resistance (resistance) to reinvasion (re-infection). At the same time, trypanosomes continue to multiply slowly throughout the life of the host in the cells of some tissues.

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 cruzi
Trypanosoma cruzi
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The structure of Trypanosoma cruzi

The microorganism is a single-celled mitochondria that can take on various forms. The body of trypanosomes is elongated and so small that it is impossible to see the causative agent of a dangerous disease with the naked eye. Parasitic microorganisms are divided into classes and subclasses. Trypanosome is at the very bottom of the hierarchical division (a subclass of unicellular organisms).

The internal structure of the trypanosome is quite simple. The cell of the parasite is covered with a dense thick membrane, consisting of a glycoprotein. The protective shell contains:

  • cytoplasmic nucleus;
  • kinetoplast and kinetosome;
  • flagella;
  • membrane, which may be absent altogether.

While developing, the microorganism transforms, mutates and becomes more resistant to external negative factors. The forms that all microorganisms pass through, subsequently causing undesirable consequences in a person in the form of dangerous diseases. Trypanosome transformation includes:

Flagellates and amastigous form of the parasite. Trypanosome may have special flagella, which are attached to the surface of blood vessels or the mucous membrane of human internal organs, or not have flagella at all. There are also forms of a parasitic microorganism: promastigous and epimastigous.

The structure of Trypanosoma cruzi
The structure of Trypanosoma cruzi
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Development cycle

The development cycle of Trypanosoma cruzi takes place with a change of owners: a) vertebrates (more than 100 species) and humans; b) a carrier of the pathogen (bugs of the Triatominae subfamily).

The developmental cycle in the vector takes place in the triatomaceous bug.

The invasive stage for the vector, as well as for the vertebrate animal and man, is the trypomastigotes. Since the piercing mouth apparatus, unlike the tsetse fly, is very weak in bedbugs and is not able to pierce even human skin, they find abrasions or mucous membranes, conjunctiva, nasal membranes, lips (for which they got the name - kissing bug).

Infection of bedbugs occurs when they feed on the blood of humans or animals containing trypomastigotes.

Once in the organism of triatomaceous bugs (carriers of American trypanosomiasis), trypanosomes of T. cruzi also reach the stomach of the insect, turn into epimastigotes here and multiply within several days. Then they pass into the posterior and rectum, where they return to the trypomastigous form. From this point on, bedbugs become infectious. After or during the suction of blood, bugs empty the rectum, and pathogens enter the human skin or mucous membranes (conjunctiva, lips, nose). In this regard, the causative agent of American trypanosomiasis is referred to as stercorarium trypanosomiasis. The duration of the development cycle of parasites in the vector is from 5 to 15 days, depending on the air temperature. Once infested, the bug retains parasites until the end of its life (about 2 years). There is no transovarian transmission.

The invasive stage for the vertebrate host is the trypomastigous form. The transmission of the invasion to humans and other warm-blooded animals does not occur directly through the bug bite, but by contamination with bug excrement containing trypanosomes, bite wounds or mucous membranes. At the site of the bite, "chagoma" is formed - the primary symptom of tryponasomosis.

As a rule, bugs defecate directly during bloodsucking. Bedbug bites cause severe itching and inflammation, as a result of which the parasites can be carried into the wound during scratching. Cases of congenital trypanosomiasis have also been reported in humans.

Development cycle
Development cycle
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Then they penetrate into muscle cells and endothelial cells of the lungs, liver, lymph nodes and other organs. However, mainly parasites accumulate in the cells of the heart muscle. Inside the cells, trypomastigotes are transformed into epimastigous and promastigous forms, and, finally, at the end of the transformation, they turn into a round, flagellate form - amastigote, 2.5-6.5 microns in size, containing a round nucleus and a small oval kinetogast. Inside the cell, amastigotes reproduce by binary division.

A human or animal cell filled with amastigotes increases in size and turns into a pseudocyst, the shell of which is the host cell wall. Before rupture and immediately after rupture of such a pseudocyst, the amastigote (bypassing the promastigous epimastigous stage) turns into a trypomastigote. The latter invade neighboring cells, multiply at the amastigote stage with the formation of new pseudocysts. Thus, amastigotes are purely intracellular parasites. Some of the trypomastigotes that have been released from the pseudocyst and have not entered the neighboring cells enter the bloodstream, where it circulates, and from there they can enter the carrier's body.

Pathogenesis of American trypanosomiasis

Trypanosoma cruzi parasitize and multiply in humans and vertebrates, first in the macrophages of the skin and subcutaneous tissue, then in the regional lymph nodes, then in all organs. Thus, with the introduction of trypanosomes, a local tissue reaction develops in the form of cell destruction, infiltration and tissue edema, then regional lymph nodes increase. The next stage of pathogenesis is parasitemia and hematogenous dissemination of trypanosomes, followed by localization in tissues of various organs, where pathogens multiply.

The most often and severely affected are the heart, skeletal and smooth muscles, and the nervous system. In the acute stage of the disease in the early stages, parasitemia is quite massive, but over time its intensity decreases, it is detected only periodically, and in the later stages of the chronic stage - in rare episodes. There is, however, an opinion that if untreated, parasitemia persists for life.

Gradually, the next most important stage in the pathogenesis of American trypanosomiasis comes to the fore - allergic and autoimmune processes, as well as the formation of immune complexes. As a result of the pathogenic action of trypanosomes and their decay products, specific sensitization and autoallergies, inflammatory, infiltrative and degenerative changes in the cells of internal organs, central and peripheral nervous systems occur.

Trypanosoma cruzi
Trypanosoma cruzi
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The most affected organ in Chagas disease is the heart. In the acute stage of infection, a widespread interstitial inflammatory process develops in the myocardium with edema and destruction of myofibrils and infiltration with neutrophilic leukocytes, monocytes and lymphoid cells.

The muscle cells adjacent to the infiltration can degenerate. In the chronic stage of Chagas disease, steady myocytolysis, fibrosis occur in the heart muscle, and cellular infiltration persists or increases.

In some patients infected with T. cruzi (more often in younger children), acute specific meningoencephalitis with mononuclear infiltration of the pia mater, perivascular inflammatory reactions, sometimes simultaneously with hemorrhage and glial proliferation, develops in the brain.

The structures of the ganglia of the autonomic nervous system are seriously affected, which leads to disorders of the innervation of internal organs. The defeat of the peripheral elements of the autonomic nervous system aggravates the violation of cardiac activity and is the cause of the occurrence of mega organs in the gastrointestinal tract (megaesophagus, megagastrium, megacolon), urinary system, etc.

Trypanosoma cruzi symptoms

It is believed that the incubation period for American trypanosomiasis (Chagas disease) ranges from 1 to 2 weeks. At the site of inoculation of parasites, an inflammatory reaction occurs - "chagoma". In the case of the penetration of parasites through the skin, the primary local inflammation resembles a non-suppurative boil. When penetrating the mucous membrane of the eyes, edema, conjunctivitis, puffiness of the face occur - a symptom of Romagna. In the future, local lymphangitis and lymphadenitis develop.

Common symptoms of American trypanosomiasis (Chagas disease): fever of a persistent or remitting type with fever up to 39-40 ° C, general adenopathy, hepatosplenomegaly, edema, and sometimes macular rash. These clinical symptoms occur against the background of acute myocarditis and irritation of the meningeal membrane. These symptoms of American trypanosomiasis (Chagas disease) are typically seen in endemic areas in children. In this case, the severity of the course is the more pronounced, the younger the patient's age.

After the acute period, American trypanosomiasis disease (Chagas disease) becomes chronic. The symptoms of this stage are vague. The disease is often asymptomatic for many years. Depending on the severity of the lesions of the autonomic system and the heart, the symptoms of heart failure come to the fore, as well as the development of megaesophagus, megaduodenum, megacolon or megasigma with corresponding symptoms.

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Diagnostics

In the acute stage, parasites are easily detected by microscopy of peripheral blood preparations. Along with stained fixed preparations, it is possible to examine a crushed drop of blood, while motile parasites are clearly visible under a microscope. In the chronic stage, microscopy is ineffective.

Diagnosis of American trypanosomiasis (Chagas disease) uses serological tests, more often CSCs with an antigen from the heart affected by trypanosomes. Xenodiagnostics has become widespread in endemic areas - feeding uninfected triatomaceous bugs on a patient with subsequent examination of insect excrement in order to detect parasites. Also used is an isodiagnostic test - inoculation of the patient's blood with laboratory animals, and an intradermal test with "crucin" (inactivated culture of Trypanosoma cruzi)

Treatment, prevention

Trypanosomiasis can be cured without severe and even fatal consequences only if the disease is diagnosed at an early stage of development.

  • examination of the skin, taking anamnesis;
  • biopsy of lymph nodes and chancre;
  • microscopic examination of cerebrospinal fluid, blood, samples of infected tissue;
  • RSK, testMashad-Guerreiro - methods allow detecting antibodies to trypanosome;
  • cultivation of parasites on a nutrient medium to determine their type;
  • intradermal allergic test - if blisters and redness appear after the introduction of an allergen, this indicates infection with trypanosomes;
  • xenodiagnostics - healthy bugs bite a person, after 14 days the intestines of bloodsuckers are examined for trypanosomes in it.

Illustratively about trypanosomes and trypanosomiasis:

  • For the treatment of trypanosomiasis, potent antiparasitic drugs are used - Nifurtimox, Benznidazole. The therapy lasts at least two months.
  • In severe cases of the disease, glucocorticosteroids are additionally used to eliminate the inflammatory process and other manifestations of trypanosomiasis.
  • At a late stage of development of trypanosomiasis, drugs do not help, therapy is aimed at eliminating complications of the pathology.
Benzylpenicillin
Benzylpenicillin
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Methods for the prevention of trypanosomiasis in endemic regions - avoidance of places of possible accumulation of bloodsuckers, adherence to the rules of preparation, storage of food, and hygiene standards. Tourists need to put protective nets at night, use repellents.

American trypanosomiasis is not common in the Russian Federation. But, since the number of tourists to exotic countries increases every year, the area of ​​spread of the disease may increase. Only timely diagnosis and proper treatment will help to avoid complications or death from infection with trypanosomes.

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