AMERICAN TRYPANOSOMIASIS ( CHAGAS’ DISEASE) :CLINICAL ASPECTS
Serologic studies suggest that only one third of newly infected individuals develop clinical illness. Acute manifestations, when they occur, are seen primarily in children. They begin with the appearance of the nodular, erythematous chagoma 1 to 3 weeks after the bite of the reduviid. If the eye served as a portal of entry, the patient will present with Romaña’s sign: reddened eye, swollen lid, and enlarged preauricular lymph node. The on-set of parasitemia is signaled by the development of a sustained fever; enlargement of the liver, spleen, and lymph nodes; signs of meningeal irritation; and the appearance of pe-ripheral edema or a transient skin rash. In a small percentage of symptomatic patients, heart involvement results in tachycardia, electrocardiographic changes, and occasionally arrhythmia, enlargement, and congestive heart failure. Newborns may experience acute meningoencephalitis. Clinical manifestations persist for weeks to months. In 5 to 10% of untreated patients, severe myocardial involvement or meningoencephalitis leads to death.
Chronic disease, the result of end-stage organ damage, is usually seen only in adult-hood. Ironically, the majority of patients with late manifestations deny a history of acute illness. The most serious of the late manifestations is heart disease. Studies of asympto-matic, seropositive patients in endemic areas have shown that a significant proportion have cardiac abnormalities demonstrated by electrocardiographic, echocardiographic, or cineangiographic techniques, suggesting that Chagas’ cardiomyopathy is a progressive, focal disease of the myocardium and conduction system, leading eventually to clinical disease. This may present as arrhythmia, thromboembolic events, heart block, enlarge-ment with congestive heart failure, and cardiac arrest. In some areas of rural Latin Amer-ica, as much as 10% of the adult population may show cardiac manifestations. In the United States, chagasic heart disease in immigrants is usually initially misdiagnosed as coronary artery disease or idiopathic dilated cardiomyopathy. Megaesophagus and mega-colon, which are less devastating than the heart disease, are typically seen in more southern latitudes. This geographic variation in clinical manifestations is thought to be attributable to a difference in tissue tropism between individual strains of T. cruzi. Megaesophagus leads to difficulty in swallowing and regurgitation, particularly at night. Megacolon produces severe constipation with irregular passage of voluminous stools. T. cruzi brain abscess has been de-scribed in a small number of AIDS patients.
The diagnosis of acute Chagas’ disease rests on finding the trypomastigotes in the periph-eral blood or buffy coat, and their morphologic identification as T. cruzi. The methods are similar to those described for diagnosis of African trypanosomiasis. If the results are negative, a laboratory-raised reduviid can be fed on the patient, then dissected and exam-ined for the presence of parasites, a procedure known as xenodiagnosis. Alternatively, the blood may be cultured in a variety of artificial media or experimental animals. In the di- agnosis of chronic disease, recovery of the organisms is the exception rather than the rule, and diagnosis depends on the clinical, epidemiologic, and immunodiagnostic findings.
A variety of serologic tests are available; small numbers of false-positive results limit their usefulness, particularly when used as screening procedures in non-endemic areas. The recent production of specific recombinant proteins and synthetic peptides for use as antibody targets may improve the reliability of these procedures. PCR techniques for the amplification of trypomastigote DNA are available in a small number of research laboratories.
The role of treatment in Chagas’ disease remains unsettled. Two agents, nifurtimox and benznidazole, effectively reduce the severity of acute disease but appear to be ineffective in chronic infections. Both drugs must be taken for prolonged periods of time, may cause serious side effects and do not always result in parasitologic cure. Allopurinol, a hypo-xanthine oxidase inhibitor devoid of serious side effects, has recently been shown to be capable of suppressing parasitemia and reversing the serostatus of patients with acute dis-ease. Additional studies to confirm these encouraging results are necessary.
The reduviid vector can be controlled by applying residual insecticides to rural buildings at 2- or 3-month intervals. The addition of latex to the insecticide creates a colorless paint that prolongs activity. Fumigants can be used to prevent reinfection. Patching wall cracks, cementing floors, and moving debris and woodpiles away from human dwellings reduces the number of reduviids within the home. Transfusion-induced disease, a major problem in endemic areas, has been partially controlled by the addition of gentian violet to all blood packs before use or by screening potential donors serologically for Chagas’ disease. The large number of infected immigrants now entering nonendemic countries presents an increasing risk of transfusion-mediated parasite transmission in these areas as well. Cases of acute Chagas’ disease have been reported in the United States in immunosuppressed patients who received blood from donors unaware of their infection status; the resulting diseases were particularly fulminant. Immunodiagnostic tests for Chagas’ disease are nei-ther readily available nor sufficiently specific for use in nonendemic areas; prevention will probably require deferral of blood donations from persons who have recently immi-grated from endemic areas. Immunoprophylaxis is not available at present.
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