General Characteristics. Trypomastigotes (see Table 1 and Figures 1 and 2) are ingested by the reduviid bug (triatomids, kissing bugs, or conenose bugs) as it obtains a blood meal. The trypomastigotes transform into epimastigotes (see Figure 3) that multiply in the posterior portion of the bug’s midgut. After 8 to 10 days, trypomastigotes develop from the epimastigotes. Humans contract Chagas’ disease when the reduviid bug defecates while taking a blood meal and the parasites in the feces are rubbed or scratched into the bite wound or onto mucosal surfaces.

Table1. Characteristics of East and West African  Trypanosomiasis.

Fig1. Trypanosoma cruzi trypomastigote. 

Fig2.  A, Trypanosoma cruzi in blood film (1600×). B, Trypanosoma cruzi parasites in cardiac muscle (2500×). (From Markell  EK, Voge M: Medical parasitology, ed 5, Philadelphia, 1981, WB  Saunders.)

Fig3. Characteristic stages of species of Leishmania and  Trypanosoma in human and insect hosts. (Illustration by Nobuko  Kitamura.)

In humans, T. cruzi is found in two forms: amastigotes and trypomastigotes (see Figure 3). The trypomastigote form is present in the blood and infects the host cells. The amastigote form multiplies within the cell, eventually destroying the cell, and both amastigotes and trypomastigotes are released into the blood.

The trypomastigote (see Figures 1 and 2) is approximately 20 µm long, and it usually assumes a C or U shape in stained blood films. Trypomastigotes occur in the blood in two forms: a long slender form and a short stubby one. The nucleus is situated in the center of the body, with a large oval kinetoplast located at the posterior extremity. A flagellum arises from the kinetoplast and extends along the outer edge of an undulating mem brane until it reaches the anterior end of the body, where it projects as a free flagellum. When the trypomastigotes are stained with any of the blood stains, the cytoplasm stains blue and the nucleus, kinetoplast, and flagellum stain red or violet.

When the trypomastigote penetrates a cell, it loses its flagellum and undulating membrane and divides by binary fission to form an amastigote (see Figure 2). The amastigote continues to divide and eventually fills and destroys the infected cell. Both amastigote and trypomastigote forms are released from the cell. The amastigote is indistinguishable from those found in leishmanial infections. It is 2 to 6 µm in diameter and contains a large nucleus and rod-shaped kinetoplast that stains red or violet with blood stains. The cytoplasm stains blue. Only the trypomastigotes are found free in the peripheral blood.

Pathogenesis and Spectrum of Disease. The clinical stages associated with Chagas’ disease are categorized as acute, indeterminate, and chronic. The acute stage represents the initial encounter of the patient with the parasite, whereas the chronic phase is the result of late sequelae. In children under the age of 5, the disease is seen in its acute form, whereas in older children and adults, the disease is milder and is commonly diagnosed in the subacute or chronic form. The incubation period in humans is about 7 to 14 days but is somewhat longer in some patients.

Acute symptoms occur 2 to 3 weeks after infection and include high fevers, enlarged spleen and liver, myalgia, erythematous rash, acute myocarditis, lymphadenopathy, keratitis, and subcutaneous edema of the face, legs, and feet. There may be symptoms of CNS involvement, which carry a very poor prognosis. Myocarditis is confirmed by electrocardiographic changes, tachycardia, chest pain, and weakness. Amastigotes proliferate within the cardiac muscle cells and destroy the cells, leading to conduction defects and a loss of heart contractility (see Figure 2). Death may occur due to myocardial insufficiency or cardiac arrest. In infants and very young children, swelling of the brain can develop, causing death.

The chronic stage may be initially asymptomatic (indeterminate stage), and even though parasites are rarely seen in blood films, transmission by blood transfusion is a serious problem in endemic areas.

Chronic Chagas’ disease may develop years after undetected infection or after the diagnosis of acute disease. Approximately 30% of patients may develop chronic Chagas’ disease, including cardiac changes and enlargement of the colon and esophagus. Megacolon results in constipation, abdominal pain, and the inability to dis charge feces. There may be acute obstruction leading to perforation, septicemia, and death. However, the most frequent clinical signs of chronic Chagas’ disease involve the heart, where enlargement of the heart and conduction changes are commonly seen.

Laboratory Diagnosis

Routine Methods. Trypomastigotes may be detected in blood by using thick and thin blood films or the buffy coat concentration technique. Any of the blood stains can be used for both amastigote and trypomastigote stages.

Molecular Diagnostics. Referral laboratories have used molecular methods to detect infections with as few as one trypomastigote in 20 mL of blood, but these methods are not routinely used in the field. The PCR based methods have not been standardized and validation studies have not been performed. As with African trypanosomiasis, there have been few studies where the various PCR methods used for diagnostic purposes have been compared. In general, these tests are not available in the routine laboratory.

Xenodiagnosis. In endemic areas where reduviid bugs are readily available, xenodiagnosis can be used to detect light infections; this technique is helpful in the diagnosis of chronic infections when there are few trypomastigotes in the blood. Trypanosome-free bugs are allowed to feed on individuals suspected of having Chagas’ disease. If organisms are ingested in the blood meal, the parasites will multiply and be detected in the bug’s intestinal con tents, which should be examined monthly for flagellated forms over a period of 3 months.

Antigen Detection. Immunoassays have been used to detect antigens in urine and sera in patients with con genital infections and those with chronic Chagas’ disease. Antigen detection can also be valuable for early diagnosis and for diagnosis of chronic cases in patients with conflicting serologic test results.

Antibody Detection. Serologic tests for antibody detection include complement fixation, indirect fluorescent antibody, indirect hemagglutination tests, and ELISA. The use of synthetic peptides and recombinant antigens has improved the sensitivity and specificity of these tests. However, depending on the antigens used, cross reactions have been noted to occur in patients with T. rangeli infection, leishmaniasis, syphilis, toxoplasmosis, hepatitis, leprosy, schistosomiasis, infectious mononucleosis, systemic lupus erythematosus, and rheumatoid arthritis. The sensitivity and specificity of serologic tests for screening blood donors has improved; single-assay screening may be acceptable rather than the two-assay screening method previously recommended.

Histology. In tissue, amastigotes can be differentiated from fungal organisms because they will not stain positive with periodic acid-Schiff, mucicarmine, or silver stains. Although the amastigotes of T. cruzi look like those in leishmaniasis, patient history, including geographic and/ or travel history, and confirmation of organisms in striated muscle rather than reticuloendothelial tissues are very strong evidence for T. cruzi rather than Leishmania donovani as the causative agent.

Therapy. Nifurtimox (Lampit) and benznidazole (Radamil) reduce the severity of acute Chagas’ disease. Other drugs, allopurinol, fluconazole, itraconazole, and ketoconazole, have been used to treat a limited number of patients. However, drug therapy has little effect on reducing the progression of chronic Chagas’ disease. In some cases, surgery has been successfully used to treat cases of chagasic heart disease, megaesophagus, and megacolon.

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