Acute phase

The acute phase of vector-borne Chagas disease is observed mainly in the first or second decades of life. Clinical manifestations appear around 8—10 days after the penetration of the parasite.7 In transfusion-transmitted Chagas disease this period

Signals of portal of entry. (A and B) Romaha signal. (C and D) Chagoma in the arm (circle)

Figure 28.2 Signals of portal of entry. (A and B) Romaha signal. (C and D) Chagoma in the arm (circle).

may be longer (20—40 days). The acute phase is not clinically recognized in most cases. The experience of those who work in endemic areas is that there is one diagnosed acute case for every 100 chronic patients. When the concentration of the inoculum is small, an atypical clinical picture, not recognized by the patient or the physician, may ensue. Alternatively, the disease may appear as a chronic infection since the beginning.

Romana’s sign is the most typical sign of portal of entry of the parasite. It is characterized by a painless swelling of one or both eyelids of one eye (Fig. 28.2A and B).

The eyelids turn a bluish color, and conjunctival congestion and hypertrophy of satellite lymph nodes (usually preauricular) frequently occur. The edema may spread to half of the face; sometimes dacryoadenitis and diminished conjunctival secretion are observed. Inoculation chagoma is another sign of portal of entry (through the skin), characterized by a maculonodular erythematous lesion, consistent, painless, surrounded by swelling and increased volume of satellite lymph nodes, more often found on open areas and sometimes ulcerated (Fig. 28.2C and D).

Fever is a constant sign, frequently accompanied by malaise, asthenia, anorexia, and headache. Fever is usually higher in children, may be continuous or intermittent, and the temperature may be more elevated during the afternoon.

Lymph node enlargement, hepatomegaly, splenomegaly, and subcutaneous edema are the principal systemic signs, together with cardiac and neurologic alterations. Lymph node enlargement is frequent, of slight or moderate intensity, isolated or contiguous, with a smooth surface, painless, hard and nonadherent, and not fistulous. Hepatomegaly and splenomegaly are also frequent, with characteristics similar to that of lymph nodes.

The edema, whose exact mechanism is unknown, may be generalized or restricted to the face and lower limbs. It is seen most frequently in children. Meningoencephalitis and myocarditis (sometimes with associated pericarditis) are the most severe neurological and cardiological manifestations.7

ECG and radiological alterations are not frequently observed during the acute phase if compared with the histopathological findings, but they may become more evident when these tests are repeated (Fig. 28.3).

A disproportional increase in heart rate may be seen in the recovery phase, when fever is no longer present, a finding well described by Carlos Chagas, who also noticed the rarity of cardiac rhythm disturbances in the acute phase, in contrast with their high prevalence during the chronic phase. Other investigators subsequently confirmed these observations. The most common ECG alterations during the acute phase are: sinus tachycardia, low QRS voltage, primary ST-T changes (Fig. 28.4), prolonged electrical systole, and first-degree atrioventricular block.

Acute phase of Chagas disease. Importance of serial radiography in the detection of cardiac involvement which is observed only in chest radiography of April 06, 1964

Figure 28.3 Acute phase of Chagas disease. Importance of serial radiography in the detection of cardiac involvement which is observed only in chest radiography of April 06, 1964.

Acute phase of Chagas disease. Primary ST-T changes on the 12-lead ECG that start to normalize on the ECG registered on February 13, 1981

Figure 28.4 Acute phase of Chagas disease. Primary ST-T changes on the 12-lead ECG that start to normalize on the ECG registered on February 13, 1981.

The chest radiograph may reveal variable degrees of global cardiomegaly.7 Echocardiography was recently introduced, which explains the lack of information about its performance during the acute phase (since most cases were reported before this method was available). Nevertheless, a recent publication8 described the echocardiographic findings in 108 of 158 patients during the acute phase of the disease. The main abnormalities were variable degrees of pericardial effusion, mitral or tricuspid valve regurgitation, and concentric hypertrophy of the left ventricle, often with more than one abnormality seen in the same patient.

Other less frequent manifestations observed mainly in Argentina are squizotripa- nides (a morbilliform, urticariform, and macular exanthema),9 orchiepididymitis (T. cruzi in the fluid produced by the vaginal tunics), and hematogenic chagomas, described by Mazza and Freire.10 Hematogenic chagomas are flat formations or nodules on the skin and subcutaneous tissues, without color alteration, nonadherent, painless, and of variable size (the size of a coin or larger) that are more palpable than visible.11

The mortality in the acute phase used to be around 5% of all symptomatic cases, often as a consequence of meningoencephalitis or myocarditis. However, nowadays this percentage has decreased as the result of use of specific drugs. Spontaneous cure, although exceptional, may occur as has been described by Zeledon et al.12 and Francolino et al.13

Mild to moderate leukocytosis may occur during the acute phase of the disease, with lymphocytosis (atypical lymphocytes), plasmocytosis, and relative neutropenia. Eosinophilia may be observed during the evolution of the disease. The hemosedi- mentation rate is slightly increased and C-reactive protein is also elevated. Plasma protein electrophoresis usually shows hypoalbuminemia and increased levels of alpha-2 and gamma-globulins. When meningoencephalitis is present, the spinal fluid shows hypercellularity with lymphocytosis (>100 cells/mL), low glucose level, and a slight increase in protein level. It is possible to find trypomastigote forms of T. cruzi after centrifugation and specific staining.7

The natural evolution of the acute phase in about 90—95% of infected individuals is to pseudocure, when all clinical symptoms and signs disappear spontaneously in approximately 2 months. A direct progression from the acute phase to a clinical form of Chagas disease has been recorded in a few patients (5—10%).

Diagnosis in the acute phase is based on the demonstration of the parasite in peripheral blood, via a wet smear, or after staining (thick smear) or via concentration methods (Strout, microhematocrit).

Identification by these methods is generally possible only during the initial weeks of the disease. Other methods used for diagnosis are skin biopsy of a suspected chagoma, lymph node, and skeletal muscle. Xenodiagnosis with an early examination of the parasites (5—10 days after the blood meal), the search for specific IgM class antibodies by indirect immunofluorescence and the polymerase chain reaction (PCR) are alternative methods. PCR assays may also be used to monitor for acute T. cruzi infection in the recipient of an infected organ or after accidental exposure.

 
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