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Chagas' Disease (American Trypanosomiais)

Updated 9/2001

Primary Distribution: Chagas' disease is endemic to Central and South America, and is an emerging problem in North America. Based on seroprevalence studies in Hispanic blood donors, between 50,000 and 100,000 people in the United States are infected (Bonomo & Salata, 2000; Ferri, 2001). It is estimated by the World Health Organization that 16-18 million people are infected and up to 45,000 die each year (Kirchhoff, 2000).

Agent and Vector: Trypanosoma cruzi (a protozoan) is transmitted through infected insect feces deposited near the bite of bloodsucking insects, especially reduviid insects ("kissing bugs"); and also perinatally, through transfusion, or through parenteral injection. Vectors are found in the wild or in the nooks and crannies of substandard housing (Kirchhoff, 2000). The most infective strains of T. cruzi are in Brazil and the southern cone of South America, while the northern strains are less infective for humans.

Incubation: Incubation is 5-14 days for the initial lesion (if present). The acute stage lasts two-four months and the chronic stage may be life-long. The mean age of acute infection in endemic areas is 4 years old; and the mean age of chronic infection is 35-45 years old (Ferri, 2001; Kirchhoff, 2000).

Clinical Findings and Treatment

Signs and Symptoms: Signs and symptoms depend on whether the infection is acute or chronic.

Acute stage: The acute stage is often an illness of children but can occur at any age. The clinical severity of acute illness can vary greatly, with 10-20% of patients having a mild undifferentiated febrile syndrome. In the acute stage about 50% of patients develop either a nodular lesion or furuncle (chagoma) at the site of the bite. Conjunctival contamination with the vector's feces results in unilateral painless palpebral and periocular swelling (Romana's sign) and associated lymphadenopathy of nodes draining the lesion. Other symptoms include prolonged fever, tachycardia, fatigue, anemia, weakness, hepatosplenomegaly, lymphadenopathy, and myocarditis. The acute stage lasts 4-8 weeks and in rare cases may include myocarditis or meningoencephalitis. In severe cases temporary electrocardiogram changes are seen, especially first degree A/V block. Most patients experience spontaneous remission of symptoms, followed by a lifelong low-grade parasitemia, which may be exacerbated by HIV infection or other immune compromising conditions.

Chronic stage: In most cases, chronic Chagas' is characterized by lifelong low-grade asymptomatic parasitemia, with only 10-30% of patients developing symptomatic systematic disease - which may occur decades after the acute illness. The parasites have an affinity for smooth, skeletal, and heart muscle; and also the nervous system. The heart is the most commonly effected organ, with manifestations including congestive heart failure (often right sided), rhythm disturbances, thromboembolism, and cardiomyopathy. Megaesophagus may occur, with accompanying dysphagia, odynophagia, chest pain, cough, and regurgitation. Megacolon is also seen. (Chin, 2000; Goldsmith, 2001; Kirchhoff, 2000; Magill & Reed, 2000).

Complications: Chronic Chagas' disease causes denervation of hollow viscus with resulting cardiomyopathy (resembling congestive heart failure with conduction disturbances, potential for sudden cardiac arrest, and thromboemboli); esophageal dilation resulting in dysphagia, regurgitation, or aspiration pneumonia; and/or megacolon resulting in abdominal distension, intractable constipation, obstruction, and perforation and sepsis. Meningoencephalitis or hepatitis may also occur. Megaesophagus and megacolon have not been found north of the equator and are most common in Brazil (Magill & Reed, 2000).

Laboratory Findings: Laboratory finding include anemia, lymphocytosis, thrombocytopenia, and occasional autoimmune abnormalities. Electrocardiograms are abnormal with A/V blocks common.

Diagnosis: Trypanosomes are found in peripheral blood smears. Blood should be obtained in the febrile stage of the acute illness if possible, as this is when parasites can be detected most easily by direct examination of wet preparations of anticoagulated blood or buffy coat. Giemsa stain examination of thick or thin blood slides is also useful. T. cruzi are also detectable in cerebrospinal fluid, pericardial fluid, and organ biopsies. Antibodies appear in the acute stage and then are present for life. There are currently three ELISA based assays (high sensitivity and specificity rate) available that measure human IgG antibodies that bind to the antigen. Indirect florescent antibody testing is also available through the CDC and can be used to distinguish acute from chronic infection. However, it is recommended that at least two independent serologic test be performed as false positives have been reported in patients with malaria, syphilis, or leishmaniasis. Serological screening is not required at this time but is being considered by researchers for high risk populations: pregnancy, organ transplants, and other immune compromised conditions such as HIV (Bonono & Salata, 2000; Magill & Reed, 2000).

Differential Diagnosis: Common differentials include typhoid fever, schistosomiasis, brucellosis, infectious mononucleosis, African trypanosomiasis, toxoplasmosis, malaria, glomerulonephritis as a cause for undifferentiated fever without a Romana's or chagoma sign. The edema associated with the Romana's sign lasts for weeks, which will differentiate it from most causes of unilateral palpebral edema. For the chronic stage, rule out idiopathic cardiomyopathy, achalasis, and congenital or acquired megacolon. Cardiomyopathy in Chagas is typically biventricular without pulmonary edema and often has tricuspid incompetence. Rule out other reasons for cardiomyopathy if serology is negative. Rule out other causes for cardiac, gastrointestinal, neurological diseases, and lymphadenopathies (Ferri, 2001; Magill & Reed, 2000).

Treatment: There is not currently a satisfactory treatment for any stage of Chagas' disease. In the acute stage, medications are effective in reducing the severity and duration of the disease but cure is only achieved in 50% of patients. Treatment in the chronic stage is controversial, as it is not clear whether treatment will alter cardiac complications or progression of the disease (Bonomo & Salata, 2000; Magill & Reed, 2000). Current treatment is with benznidazole or nifurtimox. Nifurtimox is better tolerated in children than adults. The adult dose is 8-10 mg/kg/day po tid after meals for 30-120 days. Children can take up to 15 mg/kg/day tid after meals for 90-120 days. Benznidazole is the drug of choice in Brazil and South America as it is more trypanocidal than nifurtimox. Again children tolerate the drug better than adults so the adult and child recommended dose is 5-10 mg/kg/day in bid dosing for 30-60 days. In the United States, nifurtimox is available only from the Centers for Disease Control and benznidazole is not available (Goldsmith, 2001; Magill & Reed, 2000). Treatment of the heart problems seen in the chronic stage involves treatment of the CHF and arrythmias with diuretics and antiarrhythmics.
Anticoagulants minimize the risk of thromboembolism. Referral to a cardiologist is indicated for Cardiac conditions. A light balanced diet is recommended for megaesophagus. Nitrates and nifedipine have been used to lower esophageal sphincter pressure (Bonomo & Salata, 2000; Goldsmith, 2001; Magill & Reed, 2000; Rosenblatt, 1999).

Authors: Amy Roberts, FNP & Charles Kemp, FNP - Louise Herrington School of Nursing at Baylor University



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