American trypanosomiasis (Chagas disease)

American trypanosomiasis (Chagas disease, or Chagas) is a transmissible natural focal protozoal disease characterized by the presence of acute and chronic phases during the process.

In 1907, the Brazilian doctor Chagas discovered in triatholic (kiss) bugs of the pathogen, and in 1909 isolated it from the patient's blood and described the disease caused by him, named after him by the disease of Chagas.

[1], [2], [3], [4], [5], [6], [7], [8]

The development cycle of trypanosomes

The cycle of development of TC cruzi occurs with a change of hosts: a) vertebrates (more than 100 species) and man; b) carrier of the pathogen (bedbugs of the subfamily Triatominae).

The cycle of development in the carrier takes place in a triatomic bug.

Invasive stage for the carrier, as well as for the vertebrate and human, are tripomastigots. Since the stitching device, in contrast to the tsetse fly, is very weak in bedbugs and is unable to pierce even the skin of a person, they find abrasions or mucous membranes, conjunctiva, nasal membranes, lips (for which they call it a kiss bug).

Infection of bedbugs occurs when feeding on human blood or animals containing tripomastigots.

Getting into the body of triatomic bugs (carriers of American trypanosomiasis), trypanosomes T. Cruzi also reach the stomach of an insect, they turn into epimastigotes and multiply for several days. Then they pass into the back and rectum, where they return to the tripomastigot form. From this point on bugs become contagious. After or during a blood suction, the bugs empty the rectum, and the pathogens fall on the human skin or mucous membranes (conjunctiva, membranes of the lips, nose). The causative agent of American trypanosomiasis relates in this connection to steric triganosomiasis. The duration of the parasite development cycle in the carrier is 5 to 15 days, depending on the air temperature. A once invaded bug retains parasites until the end of life (about 2 years). Transovarial transmission is absent.

The invasive stage for the vertebral host is the tripomastigot form. Transmission of invasion to humans and other warm-blooded animals does not take place directly through the bug's bite, but through contamination by excrement of bugs containing trypanosomes, wounds from the bite or mucous membranes. At the site of the bite, "chagoma" is formed - the primary symptom of trypanosomiasis.

As a rule, defecation in bedbugs occurs directly during bloodsucking. Bites bugs cause severe itching and inflammation, as a result of which parasites can be brought into the wound during combing. In humans, there are also cases of congenital trypanosomiasis.

After entering the body of a vertebrate (natural reservoir) or human, trypomastigot remain in the peripheral blood for some time, but do not reproduce.

Then they penetrate into the 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, the tripomastigots are transformed into epimastigotic and promastigot forms, and finally, at the end of the transformation, they are converted into a round, bezzhgutikovu form - amastigot, 2.5-6.5 microns in size, containing a round nucleus and a small oval-shaped kinetogiast. Inside the cells, the amastigots multiply by binary division.

The amastigot-filled cell of a human or animal grows in size and turns into a pseudocyst, the shell of which is the wall of the host cell. Before the rupture and immediately after the rupture of such pseudocysts, amastigot (bypassing the promastigot epimastigotic stage) becomes a tripomastigot. The latter invade neighboring cells, multiply in the amastigot stage with the formation of new pseudocysts. Thus, amastigots are purely intracellular parasites. Part of the tripomastigot, released from pseudocysts and not in neighboring cells, enter the blood, where it circulates, and from there they can enter the body of the vector.

Epidemiology of American trypanosomiasis (Chagas disease)

The main carriers of the causative agent of American trypanosomiasis are flying bugs: Triatoma megistis, Triatoma infestens, etc. These insects are distinguished by their bright coloration and relatively large size - 15-35 mm in length, attacking humans and animals at night. Transovarial transmission of trypanosomes from generation to generation in triatomic bugs does not occur.

Transmission of the causative agent of Chagas disease occurs as a type of specific contamination. Trypanosomes isolated with feces of bedbugs during bloodsucking penetrate into the human body or animals through damaged skin or mucous membranes of the eyes, nose, mouth cavity near the site of the bite. Infection with trypanosomiasis is also possible by alimentary route (including, with mother's milk) and with blood transfusions.

At present, it has been established that transplacental transmission of T. Cruzi is possible, but its level is relatively small: on average, 2-4% of infected children are born in sick mothers. The mechanism of protective action of the placenta has not been fully studied.

Synanthropic and natural foci of Chagas disease are known. In the foci of the first type, bedbugs live in adobe houses, crusts, poultry houses, burrows of brown rodents. Especially a lot, up to several thousand bedbugs (whose infection reaches 60% and higher) is found in adobe huts. In the synanthropic foci, except for man, the reservoirs of the pathogen are dogs, cats, pigs and other domestic animals. According to available data, the infection of dogs in synanthropic foci in certain regions of Brazil is 28.2%, in Chile - 9%, cats - in Brazil 19.7%, in Chile - 12%.

In natural foci, the reservoirs of the pathogen are battleships (they themselves do not get sick), opossums (the most important because they have a high parasitemia index), anteaters, foxes, monkeys, etc. In Bolivia and some areas of Peru, certain marine reservoirs of T. Cruzi mumps, which the population keeps houses for consumption. Their natural infection reaches 25-60%.

Infection of people occurs when visiting such foci in the warm season, when the vectors are active. In natural foci, men are more often infected. In general, Chagas disease is registered throughout the year in all age groups, but more often in children. Sporadic cases are more typical, but with a massive attack of infected triathom bugs on humans, epidemic outbreaks are possible.

Chagas disease is widespread, it is found in almost all countries of the American continent from 42 ° N. W. Up to 43 ° S. W. Particularly active and persistent natural foci of the disease are found in Latin American countries south of Mexico, with the exception of the islands of the Caribbean Sea, Belize, Guyana and Suriname. Single cases of American trypanosomiasis in the United States (Texas) are described. Most often, the infection is registered in Brazil, Argentina, Venezuela; It also appears in Bolivia, Guatemala, Honduras, Colombia, Costa Rica, Panama, Paraguay, Peru, El Salvador, Uruguay, Chile, Ecuador. In other parts of the world, infection does not occur. Perhaps Chagas disease is more common than commonly believed. Under the risk of infection T. Cruzi live more than 35 million people. According to preliminary estimates, at least 7 million

[9], [10], [11],

What causes American trypanosomiasis (Chagas disease)?

American trypanosomiasis, or Chagas disease, is caused by Trypanosoma cruzi, which differs from the pathogens of African trypanosomiasis with a shorter body length (13-20 microns) and a larger kinetoplastic of tripomastigotic forms. In the fixed blood Tr. Cruzi often has a curved shape, similar to the letters C or S (C- and S-forms).

The causative agent of the American trypanosomiasis belongs to the category Stercoraria (Latin stercus - feces, oralis - oral), and the disease American trypanosomiasis (Chagas disease) - to the steric triganosomiasis, thus the causative agent is transmitted through the feces of the bug-carrier. In addition, for Tr. Cruzi is characterized by persistence (persistente persisting) - the ability of the parasite to persist in the host throughout life with the development of resistance (resistance) to reinfusion (re-infection). In this case trypanosomes continue to multiply slowly throughout the life of the host in the cells of some tissues.

Pathogenesis of American trypanosomiasis (Chagas disease)

Parasitize and propagate T. Cruzi in the human body and vertebrate host first in macrophages of the skin and subcutaneous tissue, then in 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 edema of tissues, then regional lymph nodes increase. The next stage of pathogenesis is parasitemia and hematogenous dissemination of trypanosomes with subsequent localization in the tissues of various organs, where the propagation of pathogens occurs. The heart and skeletal and smooth musculature, the nervous system are most often affected. In the acute stage of the disease in the early stages of parasitemia is massive enough, but with time its intensity decreases, it is only occasionally detected, and in the late stages of the chronic stage - in rare episodes. There is, however, the opinion that in the absence of treatment parasitemia persists for life.

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

The most affected organ in Chagas disease is the heart. In the acute stage of infection in the myocardium, a widespread interstitial inflammatory process develops with edema and destruction of myofibrils and infiltration by neutrophilic leukocytes, monocytes and lymphoid cells. The muscle cells adjacent to the infiltrate can degenerate regenerate. In the chronic stage of Chagas disease in the heart muscle there is a steady myocytolysis, fibrosis, cell infiltration persists or grows.

In some patients, invaded by T. Cruzi (more often in younger children), acute specific meningoencephalitis develops with the mononuclear infiltration of the soft meninges, perivascular inflammatory reactions, sometimes simultaneously with hemorrhage and proliferation of glia.

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

Symptoms of American trypanosomiasis (Chagas disease)

It is believed that the incubation period of American trypanosomiasis (Chagas disease) ranges from 1 to 2 weeks. On the site of inoculation of parasites, an inflammatory reaction occurs - "chagoma". In case of penetration of parasites through the skin, the primary local inflammation resembles an unpronounced furuncle. When penetrating through the mucous eyes, there are swelling, conjunctivitis, puffiness of the face - a symptom of Romagna. Later on, local lymphangitis and lymphadenitis develop.

Common symptoms of American trypanosomiasis (Chagas disease): persistent or remitting fever with fever up to 39-40 ° C, general adenopathy, hepatosplenomegaly, edema, sometimes macular eruptions. These clinical symptoms occur against the background of acute myocarditis and irritation of the meningeal membrane. Such symptoms of American trypanosomiasis (Chagas disease), as a rule, are observed in endemic areas in children. In this case, the severity of the course is more pronounced, the smaller the age of the patient. Approximately 10% of cases terminate lethal as a result of progressive meningoencephalitis or severe myocarditis with heart failure.

After an acute period of illness, American trypanosomiasis (Chagas disease) goes into a chronic stage. Symptoms of this stage are uncertain. Often over many years the disease is asymptomatic. Depending on the severity of the lesions of the vegetative system and the heart, the symptoms of heart failure, as well as the development of mega-esophagus, megaduodenum, megacolon or megasigma with the corresponding symptomatic

Diagnosis of American trypanosomiasis (Chagas disease)

In acute stage, parasites are easily detected by microscopy of peripheral blood preparations. Along with colored fixed preparations, a crushed blood drop can be examined, while mobile parasites are clearly visible under a microscope. In a chronic stage, microscopy is ineffective.

Diagnosis of American trypanosomiasis (Chagas disease) uses serological reactions, more often - RSK with an antigen from the affected trypanosomes of the heart. Widespread in endemic areas received xenodiagnosis - feeding uninfected triatomic bedbugs on the patient with the subsequent study of excrement of insects in order to detect parasites. An isodiagnostic test is also used - inoculation of the patient's blood to laboratory animals, and an intradermal test with "krucin" (inactivated culture of T cruzi)

[12], [13], [14], [15], [16],

Treatment of American trypanosomiasis (Chagas disease)

Specific treatment of American trypanosomiasis (Chagas disease) is not sufficiently developed. Some of the efficacy in the acute stage, especially during the "chagoma" period, are derivatives of nitrofuran. Sometimes in cases of megacolon, surgical treatment is indicated.

How to prevent American trypanosomiasis (Chagas disease)?

American trypanosomiasis (Chagas disease) can be avoided by using persistent contact insecticides for the destruction of bedbug-carriers. In connection with the presence of asymptomatic carriers in endemic areas, a donor survey should be conducted serologically and with the help of xenodiagnostics.