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American trypanosomiasis (Chagas disease) is a protozoal disease caused by certain species of Trypanosoma parasites restricted to the Americas. It is different from African trypanosomiasis (also known as sleeping sickness) – which is caused by different species of Trypanosoma parasites. Chagas disease occurs in the Southern and Central parts of America including the United States of America (USA), Brazil and Mexico. The name “Chagas” is from the name of the Brazilian physician (Carlos Chagas) who discovered American trypanosomiasis in the early nineteenth century. Chagas disease is caused by a species of Trypanosome called Trypanosoma cruzi. There is also another species of Trypanosome which causes an asymptomatic trypanosomiasis in some parts of South and Central America. The name of this Trypanosome species that causes asymptomatic trypanosomiasis is called Trypanosoma rangeli. T. cruzi is very different from T. rangeli, and it is the main causative agent of Chagas disease in the Americas.


Type and morphology of Trypanosoma cruzi

T. cruzi just like other species of protozoan’s in the genus Trypanosome is a haemoflagellate (i.e., the parasite lives in the blood and lymph nodes of its host). T. cruzi is flagellated and they exist in three morphological forms which are: the epimastigotes, trypomastigotes and the amastigotes.

Vector, reservoir and habitat of Trypanosoma cruzi

T. cruzi is transmitted to humans through the faeces of an insect vector. The vector that transmits T. cruzi to human beings is called triatomine (kissing) bugs in the genus Triatoma (e.g., T. infestans, T. braziliensis, and T. dimidiata), Panstrongylus (e.g., P. megistus) and Rhodnius (e.g., R. prolixus which harbours T. rangeli). The kissing bug can also be called assassin bug. Triatomine bugs discharge T. cruzi through their faeces on the skin of susceptible human host during a blood meal. The insect vectors become infected with T. cruzi after taking a blood meal from an infected individual or mammals that have infective stage of the parasite (trypomastigotes) in them. Upon ingestion, the trypomastigotes undergo differentiation in the midgut of the insect vector to form epimastigotes which later divide to form metacyclic trypomastigotes that are released in large amount in the faeces of triatomine bugs during a blood meal.

Metacyclic trypomastigotes from the insect vector’s faeces gains entry into the body of the host through wounds, abrasions or cuts on the skin. Contact of the faeces with the conjunctiva of the host’s eye can also give T. cruzi entrance into the body. Trypanosoma cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally (from mother to an unborn child in endemic regions), and in laboratory accidents when suspected specimens are not handled with care. Inside the body of the host, T. cruzi go on to attack vital organs such as the spleen, liver and lymph nodes. The reservoir hosts for T. cruzi include rats, dogs, mice, armadillos, bats, sheep, goats, pigs and rabbits. Other mammals can also serve as reservoirs for the parasite. Human contacts with any of these reservoirs and a bite from a triatomine or kissing bug help to increase the spread and transmission of Chagas disease in a given population.

Clinical signs and symptoms of Chagas disease

The appearance of a skin tumour (chagoma) on the skin of an infected individual is usually the first sign of acute Chagas disease. Chagoma is an undulating inflammatory lesion that appears on the site of entry of T. cruzi on the body of an individual after the bite of a triatomine bug. Other clinical signs and symptoms of American trypanosomiasis include fever, myocarditis, malaise, and swelling of the face. Occasionally, there can be swelling of the spleen and liver in episodes of Chagas disease. The heart muscles and the central nervous system (CNS) are amongst the seriously affected organs of the body. In some scenario, Chagas disease is more common in children and infants than it does in adults, and it has been reported in all countries of the Americas especially in the rural areas of Latin America where hygiene and sanitation are poor. The clinical manifestation of Chagas disease shows a discrepancy and is dependent on whether the disease is acute or at a chronic stage.   

Pathogenesis of Chagas disease

American trypanosomiasis (Chagas disease) is caused by T. cruzi, and the disease is restricted solely to countries in the Americas including the USA, Brazil, Mexico. Another species of Trypanosome called T. rangeli is responsible for causing asymptomatic trypanosomiasis in Central America. T. rangeli is transmitted through the bite of bugs in the genus Rhodnius. T. cruzi is transmitted to humans through direct body contact with the faeces of infected blood-sucking triatomine bugs (Figure 1). The T. cruzi parasites are released in the faeces of the insect vector (kissing bugs) as it takes a blood meal from a human host.

Figure 1. Life cycle of American Trypanosomiasis. 1. An infected Triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its faeces near the site of the bite wound. Trypomastigotes enter the host through the wound or through intact mucosal membranes, such as the conjunctiva. 2. Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes. 3. The amastigotes multiply by binary fission. 4. Amastigotes differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes. 5. Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle. The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. The “kissing” bug becomes infected by feeding on human or animal blood that contains circulating parasites. 6. The ingested trypomastigotes transform into epimastigotes in the vector’s midgut. 7. The parasites multiply and differentiate in the midgut of Triatomine bug. 8. Parasites differentiate into infective metacyclic trypomastigotes in the hindgut of the insect vector. CDC

After the deposition of the faeces (containing infective trypomastigotes of T. cruzi) on the skin of the human host during the triatomine bug blood meal, the infective trypomastigotes enters the body when the faeces are scrubbed or rubbed into the bite site of the insect vector on the skin or via wounds, abrasions or cuts on the skin. Infective trypomastigotes can also be rubbed into the eye of the host where an oedema or swelling called Romaña’s sign occur. But for T. rangeli, infective forms of the parasite are introduced into the body of humans via the bite of an infected triatomine or Rhodnius bug unlike in T. cruzi infection where the parasite gains entry via the faeces of the kissing bug released on the skin of the host during a blood meal. This is a distinguishing feature between T. cruzi and T. rangeli (which is a non-pathogenic form of Trypanosome). T. cruzi exhibits three morphological/clinical forms, and they are: trypomastigotes (infective blood form of the parasite), amastigotes (tissue form of the parasite) and epimastigotes (which occur in the insect vector).

In the course of a blood meal, triatomine bugs picks up trypomastigotes from an infected human host. Inside the midgut of the insect vector, the trypomastigotes become transformed to epimastigotes which after differentiation develops into metacyclic infective trypomastigotes. The infective trypomastigotes are released in large amounts in faeces as the insect vector takes a blood meal, after entry into the skin, the trypomastigotes changes to amastigotes and are later released as Trypanosomes into the circulation of blood. The Trypanosomes go on to invade other cells and tissues including the heart, spleen, lymph nodes, CNS and the liver. Inflammatory reactions at the sites of entry of T. cruzi into the hosts are responsible for the formation of lesions (Chagoma and Romaña’s sign) which are characteristic of American trypanosomiasis.          

Laboratory diagnosis of Chagas disease

Chagas disease can be diagnosed in the laboratory by detecting T. cruzi parasites in fresh blood specimens of infected populations or patients. A record of previous exposure to the disease as well as stay in endemic areas is among the factors considered in diagnosing American trypanosomiasis. Microscopical examination of blood samples and serological tests including ELISA, indirect fluorescent antibody (IFA) test and indirect haemagglutination antibody (IHA) tests are used in detecting motile forms of the parasites and antigens or antibodies produced as a result of T. cruzi infection in infected human population. The trypomastigotes of T. cruzi can be detected in both thick blood smear (Figure 2) and thin blood smear (Figure 3).

Figure 2. Trypomastigotes of T. cruzi in a thick blood smear stained with Giemsa stain. CDC
Figure 3. Trypomastigote of T. cruzi in a thin blood smear stained with Giemsa stain. Kinetoplast of T. cruzi is shown by arrow. CDC

CSF and lymph node aspirates are barely required for the laboratory diagnosis of the diseases, but trypomastigote of T. cruzi can still be found in CSF samples via Giemsa stain microscopy (Figure 4). Clinical specimens can also be cultured in vitro in liquid medium including NNN media, Wenyon’s semisolid media or Tobies media incorporated with antibiotics (to prevent bacterial contamination) to demonstrate T. cruzi and the non-pathogenic T. rangeli forms. Fluids from such cultures are usually examined microscopically to detect motile forms of the parasite. Xenodiagnosis is another diagnostic tool for the laboratory diagnosis of American trypanosomiasis. In xenodiagnosis, susceptible laboratory-reared insect vectors of the disease (triatomine bugs) are starved for about two weeks, and they are later fed with blood from patients suspected to have acute American trypanosomiasis. The faeces of the triatomine bug is examined after 10 days in order to detect the epimastigote and trypomastigote forms of the parasite if actually the blood they were fed contained infective trypomastigotes.  Both culture and xenodiagnosis are cumbersome and time consuming to perform; and test results takes weeks before they are released. Thus, these methods are scarcely used for the laboratory diagnosis of Chagas disease because they delay treatment options. 

Figure 4. Trypomastigote of T. cruzi in cerebrospinal fluid (CSF) stained with Giemsa stain. CDC

Treatment of Chagas disease Chagas disease has no effective therapy like African trypanosomiasis. However, some of the anti-parasitic drugs used for treating American trypanosomiasis include benznidazole (a nitroimidazole) and nifurtimox (nitrofuran). Interferon gamma (IFN-γ) is also included as a supplementary therapy in addition to the anti-parasitic drugs in treating Chagas disease. Antigenic variation and mutation of American forms of Trypanosomes has made it difficult to develop effective vaccine for the disease.

Control and prevention of Chagas disease

Chagas disease has no effective treatment and thus, the insect vectors that transmit the parasite must be controlled using insecticides and fumigants. Houses with cracks in rural areas where the disease is endemic should be plastered and properly covered to prevent and reduce breeding sites and habitation for the triatomine bugs that harbours the parasite. Human contact with known animal reservoirs of the disease should be reduced as much as possible, and donor blood should be properly screened for possible T. cruzi infection. Re-infestation of new homes with triatomine bugs should be prevented by spraying clothing’s, furniture’s and other materials moved from kissing bug infested homes or areas with insecticides. Tourists and travelers to endemic areas of the disease should sleep under bed-nets to avoid bite from the insect vectors.    


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