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Chaga's disease also known as South American trypanosomiasis is a parasitic disease of the tropics caused by a protozoan known as Trypanosoma cruzi. It is spread by triatomine bugs, known as 'kissing bugs

Life-cycle and pathogenesis Of Chaga's disease

South American trypanosomiasis is a disease that affects humans and a large number of wild and domestic animals and is more common in Central and South America.

Chaga’s disease is caused by an organism known as Trypanosoma cruzi, Trypanosoma cruzi differs from trypomastigotes of the T. brucei group by having a large kinetoplast.

They usually bite an exposed area of the skin hence its common name ‘kissing bug’, and the bug defecates close to the area of the bite.

Trypanosomes in the bloodstream of the host are taken up by triatomine bugs (reduviid, assassin bug, kissing bugs), which usually bite mostly at night.

All stages of T cruzi feed on blood but only adult bugs can fly.

Organisms then multiply in the hindgut of the triatomine bug as epimastigotes and develop into metacyclic trypanosomes which are then excreted into the faeces of the bug when it is feeding.

Modes of infection

These bugs, vectors that carry the parasites, typically live in the wall or roof cracks of poorly-constructed homes in rural or suburban areas. They feed on human blood and hide during day time.

  • Chaga’s infection is acquired by rubbing faeces of the bug into a wound or conjunctiva.
  • Acquired by transfusion or
  • Congenital infection,
  • Ingesting fruit juices contaminated by triatomine bugs.
  • Laboratory accident.

In the host, trypomastigotes multiply at the site of the bite and enter the bloodstream and to a variety of tissue cells, particularly neuroglia and muscle cells. These parasites develop as intracellular amastigotes and form pseudocysts that rupture causing inflammation, tissue damage and further dissemination to other tissues.

Most pathological effects of Chaga’s disease are chronic, probably related to a combination of tissue damage, neuronal loss and an autoimmune response.

Signs and symptoms of Chaga's disease

Chaga's disease develops in 2 phases.  The initial acute phase and later chronic phase. The initial phase lasts for about 2 months after infection.

Acute Chagas’ disease

Acute Chaga’s disease occurs more commonly in children but may occur at any age: only one-third of individuals develop symptoms.

During this phase, there is a high number of parasites circulating in the bloodstream but in most cases, it is asymptomatic or mild and unspecific symptoms may be present.

Penetration and local multiplication of the parasite at the site of entry may cause an area of cutaneous oedema known as chagoma.

If the route of entry is via the conjunctiva then orbital oedema develops. This is referred to as Romaña’s sign.

A febrile reaction may occur after 1–2 weeks with the development of lymphadenopathy, hepatomegaly and splenomegaly.

Death may occur sometimes at this stage due to cardiac damage or meningoencephalitis, especially in children.

If the individual becomes symptomatic, then the acute phase lasts between one to three months and resolves spontaneously.

Asymptomatic low-level parasitaemia may continue for many years if these patients are untreated. This is known as an indeterminate phase. 15–40% of these patients will then develop chronic Chagas’ disease.

Clinical features of Chronic Chagas’ disease

During the chronic phase of this disease, the parasites are hidden mainly in the heart and digestive muscles.

Chronic Chaga’s disease normally occurs 10–20 years after initial infection and the classical manifestations are;

  • Cardiac/heart disease. Biventricular cardiomyopathy, heart block (cardiac rhythm disturbance) or progressive heart failure.
  • Bowen motility disorders such as megacolon or mega-oesophagus that develops as a result of the destruction of the intramural parasympathetic nerve plexus. This will present as aspiration pneumonia or intractable constipation and abdominal distension.
  • Small bowel and ureter mega disorders may also occur resulting from nerve damage.

Reactivation of latent infection may occur due to HIV infection or the use of immunosuppressive drugs causing severe myocarditis or neurological problems.

Diagnosis of Chaga's disease

The major diagnostic tests are parasitological tests although some tests have also been developed.

Parasitological techniques

1 Microscopic tests. In the acute phase of the disease, parasites can be easily found on thick or thin films; centrifugation techniques usually increases the sensitivity of the test.

2 Culture. Parasites can be cultured but require specific media and expertise to perform it.

3 Xenodiagnostic test. This is used to detect low-level parasitaemias by allowing uninfected bugs to feed on patients. Then three to four weeks later, the bugs are dissected to look for a gut infection.

4 A biopsy can demonstrate amastigotes in pathological specimens.

Other techniques used

Immunoglobulin M and life-long Immunoglobulin G responses can be detected by complement fixation test and ELISA tests.

When there is cross-reactivity with other parasitic infections and autoimmune disorders there is poor specificity. Therefore in these cases diagnosis should be based upon at least two positive techniques.

Serological tests mostly come out to be positive after a parasitological cure.

Polymerase chain infection (PCR) is an effective test in acute infection but ineffective in chronic disease.

Treatment of Chaga's disease

Treatment and eradication of Chaga’s disease are usually difficult. Some drugs have shown to be partially effective but of uncertain effect on chronic Chaga’s disease.

These drugs are effective if given soon after infection at the onset of the acute phase including the cases of congenital transmission. There efficacy of diminishes as thereafter.

Acute stage of the disease

Drugs used in the treatment of Chaga’s disease include Nifurtimox and benznidazole. They work by suppressing parasitaemia, shortening the course of the acute illness and have the ability to prevent acute neurological and myocardial complications. Benznidazole is better tolerated compared to Nifurtimox.

However, complete eradication of the parasites and prevention of chronic disease only occurs in 50–80% of patients.

In indeterminate and chronic phase of Chaga’s disease, evaluation of the efficacy of treatment is difficult because of the limited reliability of tests for a cure.

Benznidazole is thought to be of benefit in clearing parasitaemia and may prevent progression to chronic disease in some patients.

These medications should not be taken by pregnant women or by people with kidney failure or liver failure

Cardiac complications require symptomatic treatment.

Blood donations should be screened for evidence of infection.

Control can be achieved by the use of seroprevalence surveys to determine areas at risk and spraying of pyrethroid insecticides.

Improvement in the standard of housing is also important.

Elimination of cracks in mud walls or replacement of natural material roofing with iron sheets reduces available habitats for the bugs.


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