Chagas Disease

By I. Motkovsky · Infectious Diseases, Parasitology, Pathology

Also known as: American Trypanosomiasis, South American Trypanosomiasis

Historical document, translated for reference. It reflects medical knowledge of the 1920s–30s and is not medical advice.

Summary

Chagas disease is a parasitic infection caused by Trypanosoma cruzi, transmitted by triatomine bugs in Central and South America. It presents with acute or chronic symptoms affecting the heart, thyroid gland, nervous system, and other organs.

Encyclopedia article (1928–1936)

Chagas Disease (Chagas), American trypanosomiasis, a widespread disease in Central and South America (Brazil, Venezuela, Peru, Argentina, Panama, San Salvador) caused by Schizotrypanum cruzi, occurring acutely or chronically, primarily affecting children and manifesting as changes in the heart, thyroid gland, nervous system, and other organs. The vector is bugs of the family Reduviidae, belonging to the genera Triatoma (Conorrhinus), Rhodnius, and others. The main vector is the flying bug Triatoma megista, which lives in large numbers in human dwellings, where it bites sleeping people at night, most often on the face or lips; hence the local names for this bug are "tsirulnik" and "kissing bug." The causative agent is Trypanosoma (Schizotrypanum) cruzi, Chagas, 1909 (synonyms Trypanosoma escomeli Yorke, 1920). In the peripheral blood, it appears as a short, broad trypanosome with a poorly expressed undulating membrane and a large blepharoplast located almost at the very posterior end of the body. Length 15-20 microns. Parasites that penetrate muscle cells, particularly cardiac muscle cells, glial cells, and others, and multiply in them, take on a leishmaniform shape without a flagellum. In the vector's intestinal canal, trypanosomes absorbed from the patient's blood undergo a complex developmental cycle. They first transform into crithidia, partly into leishmanias, and then again take on the form of trypanosomes (metacyclic trypanosomes), located in the hindgut of the bug. From here, the parasites, getting on the mucous membrane of a vertebrate with the insect's excretions, penetrate through it and cause infection. In experimental animals, infection was obtained by applying metacyclic trypanosomes to intact skin. The work of Chagas and other authors, who proved that the trypanosome undergoes a sexual cycle in the bug's body and that infection occurs through bites, was refuted by Brumpt, who proved the transmission path described above. The latest works by Dias, conducted in the same institute where Chagas worked, fully confirmed Brumpt's point of view. - Reservoir of the virus. Armadillos Tatus novemcinctus, opossums Didelphys aurita and many other animal species are heavily affected under natural conditions. Monkeys, dogs, cats and other domestic and laboratory animals also become infected. The area of virus distribution in animals extends further north in America than the area where human diseases have been recorded. Recently, the causative agent of Chagas disease has been found in monkeys from the Dutch East Indies. Clinical cases of Chagas disease in the Old World have not yet been described. Incubation 8-10 days. The bite is painless and leaves no traces. The insect's secretions easily get on the mucous membranes, as the bite often occurs on the lips. The acute form is accompanied by constant-type fever, facial swelling, enlargement of the thyroid gland, and swelling of the lymph glands. Temperature can reach 40° and last from 10 days to 1 month. Sometimes abundant and extensive effusions from all serous membranes are observed. The liver and spleen are enlarged. The acute period can either lead to death with symptoms of encephalitis or meningitis, or end in complete recovery or transition to a chronic form. Acute forms are observed only in children. - The chronic stage, according to Chagas, can be divided into pseudomyxedematous, myxedematous, cardiac, and nervous forms. The pseudomyxedematous form is most often observed in children under 15 years. Low-grade fever, tachycardia, infiltration of subcutaneous tissue, especially on the face. The skin often shows a bronze color due to adrenal damage. The thyroid gland, spleen, and lymph glands are enlarged. In the myxedematous type, there is an even more pronounced damage to the thyroid gland. The question of the relationship of this form to endemic goiter has not yet been clarified. The cardiac form is characterized by arrhythmia, sometimes with severe bradycardia. A frequent complication is pericarditis. The nervous form gives very diverse phenomena: bilateral motor lesions, paralysis, contractures, athetosis, speech disorders, cerebral diplegias, intellectual damage. The disease leads to developmental delay and infantilism. The chronic period is accompanied by periodic exacerbations that can lead to death. Diagnosis due to difficulties in clinical diagnosis of Chagas disease is based mainly on the detection of parasites. Parasites circulate in the peripheral blood during the febrile period. For their detection, it is preferable to use the thick drop method. One can also inoculate a young guinea pig with 5-10 cm3 of the patient's blood. Brugsh recommends the xenodiagnosis method: fresh Triatoma or Rhodnius bugs, raised in the laboratory, are fed on the patient; even with a small number of parasites in the blood, the bugs can become infected. - Pathological anatomy. Infiltration of subcutaneous connective tissue, abundant serous effusions; hypertrophy of the heart, ecchymoses in the pericardium; enlarged spleen, fatty degeneration of the liver; inflammatory condition of the intestinal mucosa and enlargement of the mesenteric glands; enlargement of the thyroid gland; adhesions on the meninges; pinpoint hemorrhages in the brain substance. In microscopic preparations, the characteristic feature is the accumulation of leishmanialike stages of the trypanosome in the muscle fibers of the heart and skeletal muscles. Treatment. Ordinary trypanocidal drugs do not help. A good result from the intravenous use of tartar emetic has been described. In experimental animals, it is possible to prevent the disease if, along with the introduction of infectious material, bismuth preparations, quinoline derivatives in pyridine, are administered. Prevention requires a radical overhaul of houses, replacement of roofs usually made of palm leaves with roofs of other material, careful sealing of cracks in the floor and walls (in which bugs live) and the use of bed nets. In rural conditions of Central and South America, the fight against Chagas disease under modern social conditions presents practically an insoluble problem.

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“Chagas Disease.” Soviet Medical Encyclopedia. English translation of Bolshaya Meditsinskaya Entsiklopediya, 1st ed. (Moscow, 1928–1936), ed. N. A. Semashko. https://sovietmedicalencyclopedia.pages.dev/article/chagas-disease/