The Kiss of Death

unsuccessful treatments for ridding patients of trypanosomes. (Toro Wayar, interview 6/20/91.)

Dr. Wayar questioned the fact that trypanicides were able to rid chagasic patients of trypanosomes, and there is considerable debate concerning this. Even if the patient can be rid of T. cruzi, that would not eliminate the immunological consequences of the original infection (see Appendix II: Immune Response).

An important conclusion of Toro Wayar is that electrocardiographic abnormalities were found in lower percentages than was commonly thought. He attributed this to strains of T. cruzi infecting the colons of patients rather than their hearts. Wayar’s conclusion supports the adaptive ability of T. cruzi strains to select intracellular locations that promote their reproductive process. As in La Paz, heart disease is especially lethal in Sucre because of hypoxia, and it is only natural that strains of parasites that reside in the colon have a longer time to reproduce than those in the heart, which die off with their hosts.

Apparently this reasoning runs counter to the findings of Jauregui and Casanovas (1987:30-33), who reported a higher incidence of heart disease in mesothermic regions than was typically found in tropic zones. It does suggest that many chronic chagasic patients with heart problems in La Paz were infected at lower altitudes and later moved to La Paz. The resulting hypoxic stress then interacted with chagasic heart disease to produce ECG abnormalities.

As already mentioned, natives of higher altitudes have developed physiologically to hypoxia and have well- adapted cardiovascular systems to deal with the resulting low-oxygen stress. Conversely, peasants migrating from the lowlands to higher altitudes lack these adaptive features and, if they become infected with Chagas’ disease, they are at greater risk for heart problems because they are unaccustomed to hypoxic stress, which interacts synergistically with chronic myocarditis. One advantage these migrant lowlanders have in living in La Paz is the decreased possibility of reinfection with additional parasites or new strains brought about by vinchuca bites. Thus, verticality, or people living at different altitudes in Bolivia, adds additional complexity to chronic Chagas’ disease in this country.

Although cardiopathy is frequently associated with chronic Chagas’ disease in Bolivia, this disease also manifests itself in other organs of the body, possibly as a function of strain diversity within T. cruzi the organisms adapting to host physiology and hypoxic stress. As living organisms, T. cruzi and humans establish parasitic relationships that dynamically vary with environmental stresses. By the time the patient is chronically ill, these parasites have become established in human organs, where they have had ample time to reproduce. It is often environmental stresses, such as moving to higher altitudes, or compromised immune systems that eventually destroy the host.

Chronic heart disease is treated symptomatically, with emphasis placed on the cardiovascular aspects. Bolivian doctors also recommend benznidazole or nifurtimox to prevent the spread of parasites from tissue to tissue, but these trypanocides are questionable with regard to their effectiveness against intracellular parasites in the amastigote form (Gutteridge 1982, 1985; Brener 1975, 1979; see also Appendix 13: Chemotherapy).

The Burden of a Weakened Heart in the Andes

Very few Bolivians with chagasic heart disease (.01 percent) are as fortunate as Bertha in being able to have pacemakers installed and to be treated by an expert doctor. Acquired in her infancy, Chagas’ disease has left Bertha with irreversible heart damage: arrhythmia (irregular heartbeats) and bradycardia (slow heartbeats), which could lead to heart failure or sudden death without the help of a pacemaker. Many Bolivians have no medical insurance. Pacemaker implantation costs about U.S. $3,000 per person in Bolivia, prohibitively expensive where the average income is U.S. $580 per person per year. No drug exists to reverse these patients’ chronic condition, because of the immunological consequences of the original infection. Many victims are farm or mine workers who are unqualified to find lighter jobs. They have little alternative but to continue work and face the daily prospect of their hearts failing to pump enough blood through their bodies to keep them alive. Chagas’ disease can seem especially cruel to these workers: when they are supposed to be at the strongest phase of their lives and most able to support young children, they are debilitated and unable to work as hard.

The socioeconomic impact of the disease during the chronic stage is high, as data from Bolivia show: about 25 percent of the infected population (1,500,000 people) will develop severe cardiac and digestive lesions such as cardiac arrhythmia (215,000) and megaesophagus and megacolon (150,000; see Valencia, Jemio, and Aguilar 1989).[34] In 1992, the indirect costs of lost production in Bolivia due to Chagas’ disease morbidity and mortality amounted to $100 million, and the direct cost for Chagas’ disease treatment reached $20 million (SOH/CCH 1994). The collective biomedical cost for pacemakers and corrective surgery at $3,000 per person would run about $1 billionastronomically unfeasible in Bolivia as well as in other Andean countries. Put another way, this is enough for the improvement or construction of a million rural dwellings at a minimum estimated cost for each of U.S. $1,000. Data from Brazil are equally grim, with 45,000 cases of cardiac arrhythmia and 30,000 cases of megaesophagus and megacolon estimated annually, with the collective cost at about U.S. $225 million per year (Special Programmes 1991 Report).

In the Andes, chronic Chagas’ disease debilitates Andeans who have evolved with strong hearts adapted to the low oxygen of higher altitudes. Highland Andeans have an extra pint of blood in their bodies and larger lungs to accommodate the 20 to 30 percent less oxygen at levels between 9,000 and 16,000 feet. Climbing up and down hills and mountains, Andeans have enjoyed the aerobic effect that daily exercise provides runners. Chagas’ disease has not been particularly prevalent at higher altitudes because vinchucas prefer warmer and more humid climates. However, this has drastically changed with the massive migration of infected Bolivians and vinchucas to practically every site in the Andes. Because of layoffs in the mines, droughts, floods, and increased cocaine production, peasants seasonally travel to endemic areas, where some become infected with T. cruzi and bring it and vinchucas to other regions. Lowland peoples have also spread this disease to highland Andeans through blood transfusions.

Pathology of Chronic Disease

Chronic manifestations usually take three formsin order of prevalence: cardiac, colonic, and esophagealand more than half of the patients with Chagas’ disease reveal abnormal electrocardiograms. Up to 30 percent of people with the indeterminate or inapparent form of the infection suffer from cardiac, digestive, or neurological damage ten to twenty years after having contracted the disease, while the remainder never exhibit any manifest organ involvement (WHO 1991; see Figure 8). Symptoms of chagasic heart disease progress from barely decipherable indicators, such as fever, anemia, and hypertension, to serious pathologies.[35] Cardiomegaly results in the heart enlarging five or six times its normal size; but it is not found in all chronic patients, such as Bertha, whose symptoms of Chagas’ disease were expressed by ventricular arrhythmias, which frequently cause death sooner than does cardiomegaly.[36] Heart disease illustrates how widespread the damage of Chagas’s disease can be and how difficult it is to diagnose this disease by means of only a specific set of symptoms.

The pathology of the chronic stage of Chagas’ disease is related to denervation within the nervous system of the colonized organ (Brener 1994). Degeneration of neurons in the heart’s parasympathetic ganglia is common in chagasic patients with heart ailments. With megacolon and megaesophagus, lesions of the colon and esophagus are caused by destruction of nerve cells. These lesions are jointly caused by the parasite (intracellular invasion of the trypomastigotes, encystation of amastigotes, and bursting of cells) and by the autoimmune response of the host. Increasing evidence indicates that the pathogenesis of Chagas’ disease is related to the parasite’s ability to manipulate the host’s immune system.[37] It has been found that people die from chronic manifestations in which lesions are left from T. cruzi but the parasite is not