Chagas’ disease
South American trypanosomiasis, or Chagas’ disease, is caused by the protozoa Trypanosoma cruzi. It is excreted in the faeces of the triatomine bugs and gains entry to the individual via the site of the triatomine bite. An iatrogenic spread has also been reported via organ and blood transfusions. As with African trypanosomiasis, there is an acute phase and a late phase. However, the acute early phase is often asymptomatic and there is a latency period of years between acute infection and chronic manifestations. Acute infection may cause fever, lymphadenopathy, and splenomegaly. A chagoma is a swelling of the skin related to parasite entry. Romaña’s sign involves periorbital swelling and conjunctivitis after ophthalmic parasite entry. Rarely, the acute phase can cause pericarditis and meningoencephalitis. This is more common in young children and immunosuppressed patients. Chronic disease leads to gastrointestinal tract pathology – megaoeseophagus and megacolon – and cardiac pathology – cardiomegaly and associated conduction abnormalities. The acute phase can generally be diagnosed using a blood film or serology. Early treatment with nifurtimox and benznidazole can prevent acute complications and reduce the risk of chronic infection. Chronic infection is more difficult to diagnose due to low level parasitaemia. The mainstay of treatment for chronic chagas disease involves managing complications. For example, the insertion of a pacemaker for a complete heart block. Xenodiagnosis is a valid method of establishing the diagnosis with low-level parasitaemia. Uninfected triatomine bugs are fed blood from suspected patients and then examined for evidence of parasites. This is not commonly used due to several factors, such as the incubation time needed for low-level parasite replication and the need for a supply of uninfected triatomine bugs.
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