18.5
American Trypanosomiasis
American trypanosomiasis, or Chagas disease, is a zoonotic illness caused by the parasite Trypanosoma cruzi.
A triatomine bug ingests the trypomastigotes of the parasite when it feeds on the blood of an infected human host.
Inside the insect’s midgut, the trypomastigotes transform into epimastigotes and multiply by binary fission.
They then migrate to the hindgut and differentiate into the infective metacyclic trypomastigotes.
When the insect takes another blood meal, it defecates near the bite site, releasing parasites in its feces onto the skin.
Scratching the bite site allows the parasites to enter through the wounded skin.
After entering the host, trypomastigotes invade cells near the site of infection and transform into intracellular amastigotes.
The amastigotes multiply by binary fission and accumulate in the host cell cytoplasm to form clusters known as pseudocysts.
These amastigotes eventually convert back into trypomastigotes, rupture the host cell, and are released into the bloodstream, ready to be taken up by another bug.
Chagas disease, or American trypanosomiasis, is a vector-borne parasitic infection caused by Trypanosoma cruzi, a flagellated protozoan (kinetoplastid) of the family Trypanosomatidae. The disease is endemic in Latin America, although cases are increasingly reported worldwide due to human migration. Transmission most commonly occurs when feces of infected triatomine bugs contaminate bite wounds or mucosal surfaces; additional routes include congenital, transfusional, transplant-related, and oral transmission.
Clinical manifestations are divided into acute and chronic phases. The acute phase is often asymptomatic or mild but may include fever, a localized inflammatory lesion (chagoma), or Romaña sign, characterized by unilateral eyelid swelling. The chronic phase may remain indeterminate or progress to severe complications, including cardiomyopathy, arrhythmias, megacolon, and megaesophagus.
Epidemiology and Pathophysiology
Approximately 6–7 million people are infected globally, with the highest burden in Bolivia, Brazil, and parts of Central America. Triatomine vectors typically inhabit substandard rural housing. Following entry through skin or mucosa, T. cruzi invades host cells, differentiates into intracellular amastigotes, and proliferates, particularly in cardiac muscle and the enteric nervous system. While the acute phase is associated with high parasitemia, chronic infection may lead to progressive tissue damage or remain clinically silent.
Diagnosis and Management
Acute infection is diagnosed via microscopy or polymerase chain reaction, whereas chronic infection requires serological testing. First-line treatment includes benznidazole and nifurtimox, which are most effective in the acute phase. Chronic disease management focuses on complications, including cardiac device implantation or surgical intervention for gastrointestinal involvement.
Interprofessional Care
Effective management requires coordinated care among infectious disease specialists, cardiologists, and other healthcare professionals. Public health measures and early diagnosis are essential to reduce disease burden and improve patient outcomes.
American trypanosomiasis, or Chagas disease, is a zoonotic illness caused by the parasite Trypanosoma cruzi.
A triatomine bug ingests the trypomastigotes of the parasite when it feeds on the blood of an infected human host.
Inside the insect’s midgut, the trypomastigotes transform into epimastigotes and multiply by binary fission.
They then migrate to the hindgut and differentiate into the infective metacyclic trypomastigotes.
When the insect takes another blood meal, it defecates near the bite site, releasing parasites in its feces onto the skin.
Scratching the bite site allows the parasites to enter through the wounded skin.
After entering the host, trypomastigotes invade cells near the site of infection and transform into intracellular amastigotes.
The amastigotes multiply by binary fission and accumulate in the host cell cytoplasm to form clusters known as pseudocysts.
These amastigotes eventually convert back into trypomastigotes, rupture the host cell, and are released into the bloodstream, ready to be taken up by another bug.
From Chapter 18:
Now Playing
18.5 : American Trypanosomiasis
Fungal and Parasitic Infections
43 Views
18.1 : Leishmaniasis
Fungal and Parasitic Infections
60 Views
18.2 : Cryptococcal Meningitis
Fungal and Parasitic Infections
31 Views
18.3 : Malaria
Fungal and Parasitic Infections
34 Views
18.4 : Toxoplasmosis
Fungal and Parasitic Infections
44 Views
18.6 : Giardiasis
Fungal and Parasitic Infections
33 Views
18.7 : Amebiasis
Fungal and Parasitic Infections
36 Views
18.8 : Candidiasis
Fungal and Parasitic Infections
42 Views
18.9 : Trichomoniasis
Fungal and Parasitic Infections
36 Views