Acute Chagas’ Disease

In 1909 Carlos Chagas diagnosed a child named Rita as having an acute attack of parasitemia caused by T. cruzi, and accurately described its symptoms:

Among the chief clinical symptoms of this child, whose fever had come on some eight or ten days before examination, were the following: axillary temperature 40°C (105°F) spleen enlarged and to be felt under the edge of the ribs; liver also enlarged; groups of peripheral lymph nodes swollen etc. Most noticeable was a generalized infiltration, more pronounced in the face, and which did not show the characteristics of renal oedema but rather of myxoedema. This last symptom, which I later found to be one of the most characteristic of the acute form of the disease, already then revealed some functional alternation of the thyroid gland, perhaps affected by the pathogenic action of the parasite (Chagas 1922).

Rita died three days later. The pathology of acute Chagas’ disease varies from a mild to a virulent infection. Some symptoms of acute Chagas’ are related to inflammation, which is one of the body’s defenses against T. cruzi and tissue damage, facilitating repair of the damage. Inflammation often includes fever, general malaise, and swelling and soreness of the lymph nodes and spleen, which contain large numbers of macrophages and T and B lymphocytes activated to combat antigens peculiar to T. cruzi. Inflammation’s redness and warmth result from the increased amount of blood in the area. Swelling results from more proteins and fluids escaping into the tissue (Schmidt and Roberts 1989:27).

Definite symptoms of acute Chagas’ are the ophthalmo‑ganglial complex (Romafia’s sign) and chagoma of cutaneous inoculation, which occurs near the bite site in 90 percent of the people recently infected (WHO 1991; see Figure 4). However, Borda (1981) claims lesser percentages of from 1 to 3 percent. Romafia’s sign is not frequently found in Bolivia; if found, it is usually confused with an eye irritation. Appearing suddenly, Romafia’s sign is the swelling of the upper and lower eyelids in one eye. An infection occurs through the skin of the eyelid, developing into inflammation around the eye with edema and inflammation of the local lymph nodes. The swollen eyelids are firm to the touch, purple, and not painful. There can be an inflammation of the conjunctiva or the mucous membrane that lines the eyelids (Katz, Despommier, and Gwadz 1989:174). Moderate swelling extends to the same side of the face, which, if touched, is found to be hard. This swelling gradually disappears after a month. The duration and durability of Romafia’s sign set it apart from the swelling of other minor eye irritations.

Chagomas also appear at the infected bite sites of other parts of the body, especially on uncovered areashands, forearms, feet, calves, and legs. Nodule‑like protrusions, chagomas are cutaneous tumors beneath the skin, resulting from the hardening of skin and subcutaneous cells. Chagomas are painful, firm, feverish, and abnormally red, which is due to capillary congestion in inflammations. When chagomas slowly disappear after a month, they leave a depigmentation, like a burn wound.

Acute infections also alter the cardiovascular system, with tachycardia (without correspondence to the intensity of fever), cardiac enlargement, hypotension, and heart failure (Andrade 1994, Köberle 1968:80). Heart alterations vary from slight to severe, as registered by electrocardiogram, but disappear after the acute phase (Borda 1981). Seventy percent of acute cases show no electrocardiographic or radiological abnormalities due to acute myocarditis of different stages (Laranja et al. 1956, WHO 1991:3). The remaining 30 percent indicate such electrocardiographic irregularities as sinus tachycardia, low QRS voltage, prolonged P‑R interval, and primary T‑wave changes. Chest x‑rays can reveal cardiomegaly of varying degrees of severity.

About 2‑3 percent of the acute cases with myocarditis die. Infants under two years constitute the greater number in this group. Also common to children of this age group is meningoencephalitis, another severe complication of the acute stage. Patients suffer convulsions, with or without fever, and lose consciousness to varying degrees (WHO 1991:3). The death rate for acute Chagas’ with meningoencephalitis can be as high as 50 percent (WHO 1991).

For the remaining cases, the symptoms subside spontaneously within one to two months, without clinical symptoms in the short or medium term. Sometimes the frequency of tachycardia is extremely high and continues to increase after the remission of the temperature during the recovery process (Köberle 1968:80).

For those who survive the acute phase or who do not experience it, death from subsequent acute phases is frequently prevented by the presence of the parasite and the complement immune system. This is referred to as partial immunity, and it is important to consider in attempts to destroy the parasite during initial attacks within the acute stagewhich may not be a good idea if the patient is to be subjected to new infections and subsequent violent acute phases. However, even with partial immunity over time, there is molecular mimicry between T. cruzi and the host’s nervous tissue (Avila 1994), rendering Chagas’ an autoimmune disease in that its antibodies destroy nerve cells. As one bonus, research concerning Chagas’ disease adds to the scientific understanding of autoimmune diseases.