Chagas Disease: Trypanosoma Cruzi Infection and Control

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Chagas Disease and Trypanosoma Cruzi

Chagas disease is an infection of mammals and triatomines caused by the protozoan flagellate Trypanosoma cruzi. It circulates in the form of trypomastigotes in the blood of infected people or animals. It is important to note that birds are refractory and immune to the infection.

Agent and Transmission

The transmitter agents are blood-sucking insects, the most important and widespread being Triatoma infestans, which constitutes the insect vector. The mammalian host can be humans and some domestic or wild animals. In its various hosts and in culture media, T. cruzi has three fundamental morphological aspects: trypomastigote, epimastigote, and amastigote.

The Evolutionary Cycle of Trypanosoma Cruzi

Triatomines become infected by ingesting mammalian blood containing trypomastigotes. In the midgut, the parasites multiply by binary fission as epimastigotes, and after 15 to 30 days, they develop into metacyclic trypomastigotes in the hindgut of the insect. When the insect bites an infected mammal, it deposits feces containing metacyclic trypomastigotes that penetrate the skin through the site of the bite or mucous membranes (for example, in the eye).

The trypomastigotes penetrate cells and transform into amastigotes, which multiply by binary fission, filling up the cell and breaking out into the bloodstream as trypomastigotes, spreading throughout the body. This cycle is repeated many times. Finally, the trypomastigotes are ingested by hematophagous triatomines.

Chagas Disease in Chile

  • Hyperendemic Areas: III and IV Regions.
  • Endemic Areas: I to VI Regions.
  • Kissing Bug Species: Both belong to the genus Triatoma and Mepria.

Comparison of Vectors

  • Triatoma infestans: Domiciliary, nocturnal, zoo-anthropophilic (Domestic Cycle).
  • Mepria spinolai: Wild, diurnal/nocturnal, zoophilic (Wild Cycle).

Clinical Phases of the Infection

  • Acute Phase: Typically symptomatic in 5% of cases, of which 90% are children (2 to 4 months old).
  • Latent Stage: Lasts months or years; generally asymptomatic. The infection may remain so for life. About 25% of cases show subclinical abnormalities.
  • Chronic Phase: Lasts years.
    • Cardiac Form: Rhythm disorders, heart blocks, and cardiomegaly.
    • Digestive Forms: Megacolon and megaesophagus.

Diagnostic Methods

Suspicion: Based on clinical history and epidemiological history.

Confirmation: Direct methods for the research of trypomastigotes.

  • Fresh blood examination: Higher performance.
  • Thick blood smear: Used in the acute phase (high parasitemia).
  • Strout method.
  • Xenodiagnosis: Useful in acute and chronic phases.
  • Nests of amastigotes in tissue: Histopathological examination (biopsy, necropsy).

Control and Prevention Strategies

  • Chemoprophylactic: Current drugs are often ineffective.
  • Vaccine: Remote due to the antigenic complexity of T. cruzi and autoimmune phenomena.
  • Vector Control (The Principal Method):
    • Spraying houses with insecticides.
    • Rural housing improvement.
    • Community health education and participation.
    • Risk of vinchucas presence in housing and collaboration in disinsectization and surveillance actions.
  • Transfusional: Control of donors and treatment of infected blood (e.g., Gentian violet).
  • Transplantation: Control of donors.

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