Infected victims pass into early latent Chagas’, which is asymptomatic. Latent Chagas’ offers several possibilities: 1) the infection is arrested at this stage, 2) it develops later to late latent Chagas’ with minor clinical findings, or 3) it develops into classic chronic (tertiary) Chagas’ disease. Those with minor clinical findings progress to either early latent arrested (secondary) Chagas’ or classic chronic (tertiary) Chagas’.
A certain number of patients live out their lives in the early latent arrested phase, with no noticeable symptoms, except perhaps fatigue. As mentioned, one acute patient of Carlos Chagas in 1909, Bernice, lived past the age of seventy and was checked annually, with no symptoms of the disease ever being manifested (Lewinsohn 1979:519). However, in many instances, the disease culminates with classic chronic symptoms of tertiary Chagas’heart disease and enlarged colon and esophaguswhich if untreated result in death. There is no known cure for the chronic phase.
Chagas’ disease is closely related to the immune system. Its progression varies greatly with the immunocompetence of each individual. Bolivians suffer so greatly from it in part because many are malnourished and infected with other diseases (see Appendix II).
At the Brazilian National Academy of Medicine’s session on April 22, 1909, Oswaldo Cruz read Chagas’ work entitled “A New Human Trypanosomiasis.” Cruz referred to the new disease as American trypanosomiasis to distinguish it from African trypanosomiasis, but American trypanosomiasis was soon known as Chagas’ disease (Kean 1977). Shortly after the reading of the paper, Cruz and a group of distinguished physicians traveled to Lassance to visit Chagas at work. Miguel Couto described the visit:
Carlos Chagas was waiting for us with his museum of laboratory items. Examination between cover-glass and slide revealed the raritiesseveral dozen patients of all ages, some idiots, others paralytics, others heart cases, thyroids, myxedemics and asthenics. Microscopes were scattered all over the tables showing trypanosomes in movement, or pathological anatomic lesions. In the cases were animals experimentally infected and jars full of triatomines in all stages of development. Every item of this demonstration was carefully examined by us. The doctors gathered there, undisputable authorities in their fields… had nothing to deny or add to the analysis of the symptoms or their interpretations… On that day it was up to me to give a name to those traditional diseases of the Minas backlands, which were now unified as one disease with cause and development clearly established. To name it after only one of its symptoms would be to limit its description, and to name it for all its symptoms would be impossible… And so, at dinner, while toasting Carlos Chagas, I… chosen because of my age, standing with Oswaldo Cruz on my right and surrounded by the men most representative of Brazilian medicine of that era, with gravity equal to a liturgical act in our religion, such as a baptism, gave the name of Chagas’ Disease to that illness…in the name of the entire delegation (Couto, in Kean 1977).
Figure 8.
Progression of Chagas’ disease. (From Jared Goldstein, “Darwin, Chagas’, Mind, and Body,” Perspectives in Biology and Medicine 32, no. 4 ([1989]:595.)
Carlos Chagas died in 1933 of angina pectoris as he was looking through a microscope into the universe of parasites. A year before his death, he optimistically spoke to a class of graduating physicians: “Gentlemen, the practical applications of hygiene and tropical medicine have destroyed the prejudice of a fatal climate; the scientific methods are prevailing against the sickness of the tropics” (Kean 1977). On a less optimistic occasion, he remarked, “This is a beautiful land, with its tremendous variety of vegetation. Nature made animal and vegetable life stronger and thus created conditions which bring sickness and death to the men who live here” (Chagas Filho 1993).
Since Carlos Chagas’ amazingly rapid discovery of it in 1909, research concerning this disease has been slow. After Chagas discovered Trypanosoma cruzi, the disease was not described until ten years later and was not recognized as a serious health problem in Brazil for another forty years. Other countries of Latin America have been even slower in recognizing the problem, with Bolivia beginning in 1991. The first and only drugsnifurtimox and benznidazolefor treatment did not appear until 1970 and then met with only partial success. Discovering disease is only a short first step toward treating and preventing it.
CHAPTER TWO
Early Andean Disease
The earliest indications of Chagas’ disease in the Andes are found among mummies dated as living at A.D. 400. Anthropologists Rothhammer, Allison, Nufiez, Standen, and Arriaza (1985) recently discovered the ancient mummies of twenty-two Andeans in Quebrada de Tarapacá, Chile. The mummies were 1,500 years old and belonged to an extinct culture, called the Wankari. Eleven of the bodies had greatly enlarged hearts, colons, or esophagi. One forty-five-year-old male had both an enlarged colon and heart. Another twenty-five-year-old male had an enlarged colon and esophagus. Three forty-five-year-old males had enlarged colons, and a three-year-old boy had an enlarged heart and colon. Four women had enlarged colons.
What caused the enlarged organs in half of these bodies? Scientists considered various explanations. Cardiomegaly, enlarged heart, sometimes results from atrophied heart muscles caused by degenerative diseases associated with aging. This could explain the older victims of ages forty to forty-five but not the enlarged heart of the child. The average life span of the people was around thirty-five years at this time.
Megasyndromes appeared in all cases. Enlargement of the colon was explainable by fermentation of food, creating gas and causing intestinal walls to expand, a condition found in unembalmed corpses in warmer climates. The climate of Quebrada de Tarapacá in the northern highlands of Chile is frigid because of its high altitude. The nerves of the intestinal walls were severely atrophied, perhaps resulting from a long-term disease condition.
Another possibility was that the corpses could have suffered severe gastritis and flatulence from spoiled lima beans shortly before death. After the petrified contents (coprolites) of the colons were examined, scientists found carob-tree sheaths (Prosopisjuliflora) but no lima beans (Phaseolus lunatus). It is possible that the victims may have eaten the carob sheaths as medicine. The impacted bowels indicated long-term constipation, usually caused by the inability of the colon’s sphincter muscles to contract, expand, and dispel the feces. Degenerated neuron cells of the sphincter muscles can cause this as well as enlarged hearts and esophagi.
The anthropologists inquired about modern Andeans from this region to see if they suffered from similar symptoms, and, not surprisingly, many peasants suffered these symptoms. Among modern Andeans 90 percent of individuals with megacolon and 100 percent of those with megacolon and megaesophagus are tested seropositive for Chagas’ disease (Atias 1980). Degeneration of neuron tissues of the heart, esophagus, and colon are common to patients with chronic Chagas’ disease. The exhumed Wankari Andeans likely died from Chagas’ disease, which was quite likely as debilitating and as deadly a disease then as it is now, 1,500 years later.
Long-Term Adaptation of T. cruzi
Modern Andeans, however, from this region suffer milder forms of Chagas’ disease than those living in lower regions. This indicates long-term adaptation of early Andeans at Quebrada de Tarapacá. Clinical surveys of chronic Chagas’ patients indicate that in the lower Andean region of northern Chile the infection rate is low and great evidence of cardiac involvement is detected by electrocardiograms (Arribada et al. 1990). In the higher Andean region of Quebrada de Tarapacá a very high infection rate is detected, but cardiac involvement is lower than that of the lower region (Apt et al. 1987). This indicates the importance of altitudinal factors on the T. cruzi infection causing cardiac involvement (Villarroel et al. 1991). The more benign character of Chagas’ disease detected in higher altitudes of Chile is significant because it may relate to the ancient adaptation of the parasite to the human host in the Andean highlands of Quebrada de Tarapacá (González et al. 1995:126; Neghme 1982).
It is possibl
e that the varying severities of Chagas’ disease may be due to different strains of T. cruzi circulating in each area. Such T. cruzi strains display unique characteristics. Individual T. cruzi strains and geographic distribution of different strains and their source (sylvatic or domestic) play a role in the wide variety of clinical signs encountered in Chagas’ disease (Rassi 1977). Nevertheless, early adaptation of T. cruzi to humans in the southern Andean highlands likely explains the more benign character of Chagas’ disease found there today (González et al. 1995: 132-33) (see Appendix 2: Strains of T. cruzi).
Enlarged Colons in Bolivia: A Case of Empacho
In Bolivia in 1992 I observed similar megasyndromes among Quechua peasants in the village of Choromoro, about seventy-five miles east of Sucre, Bolivia. One woman suffered an enormously enlarged heart (five times its normal size) and had died shortly before I arrived. A man named Jacinto had an enlarged intestine about the size of a basketball (see Figure 9). Jacinto hadn’t gone to the toilet for half a year and was dying. Jacinto said that he had empacho, a culturally defined illness that includes constipation. Empacho has accompanying emotions of sadness, lethargy, and embarrassment. Even though his constipation sounded like it could relate to the anthropologists’ fermented-bean theory, Jacinto understood his body better than did physical anthropologists.
Figure 9.
Peasant from the Department of Sucre, Bolivia, with enlarged colon caused by chronic Chagas’ disease. He had not defecated for five months because T. cruzi parasites had destroyed his colon muscles. Surgeons eventually removed the damaged colon and a colestomy was performed. (Photograph by staff of Proyecto Británico Cardenal Maurer)
Curanderos explain that empacho is caused by the accumulation of poisonous fluids excreted by the distillation process of the inner organs. Jacinto’s chuyma (inner organs: from heart to lower bowels) were usu (unable to concentrate and dispel fluids). Andeans such as Jacinto understand the human body as a hydraulic system with a muscular-skeletal framework and conduits through which air, blood, feces, milk, phlegm, semen, sweat, and urine flow in centrifugal and centripetal motion (Bastien 1985). To Jacinto, his body was unable to exchange foods and fluids by means of ingestion and expulsion. He needed to expel toxic substances by increasing the centrifugal motion of his blood, diagnosed as cold and wet.
After many herbal and ritual treatments, Jacinto’s empacho persisted. His stomach grew to the size of that of a pregnant woman. He stopped eating and stayed home. Fearing he would die from empacho, as others have, relatives transported him by truck to the hospital in Sucre, the Instituto de Gastroenterología Boliviano Japonés. Surgeons there removed a large part of his lower colon, stitched him up, and loaded him back on the truck to Choromoro. Jacinto appreciated the “patch up,” as he put it, but believed that the empacho would return, as it had for previous victims in Choromoro. “You always die from it, my uncle and mother did,” he said.
I traveled from Choromoro to Sucre, where I talked with a resident surgeon who had operated on Jacinto, and I explained that Trypanosoma cruziwas the cause of Jacinto’s empacho. After initial infection, metacyclic trypomastigote forms of T. cruzi rapidly travel from the blood to neuron cells of the heart, colon, and esophagus (see Figure 5). There the trypomastigotes encyst, reproduce, and produce amastigotes. These amastigotes change into trypomastigotes and then reenter the blood to be picked up by vinchuca bugs. Encysted amastigotes live within these basically hollow organs, which they eventually destroy. They denervate muscles of the intraneural nervous plexus.
Particular zydomes (strains) of the parasite show a preference for particular organs. T. cruzi zydomes in the geographical Department of Sucre seem to prefer the colon. T. cruzi, although once considered as a single pathogenic factor in Chagas’ disease, is further differentiated into some 100 strains in Bolivia alone, each with its unique genetic structure and destructive capabilities (see Appendix 2: Strains of T. cruzi).
The Spread of Chagas’ Disease in the Andes
The spread of Chagas’ disease throughout the Andes is related to environmental and social factors that bring together T. cruzi, Triatoma infestans, and humans. Vinchucas (Triatoma infestans) probably transmitted T. cruzi to humans as early as 6,000 years ago when early Andeans occupied caves and rock shelters in the central Andes around Pampa de Junin (Wheeler, Pires-Ferreira, and Kailicke 1976).
Another possibility is that early Andeans acquired Chagas’ disease by ingesting raw infected meat of alpacas, llamas, guanacos, guinea pigs, cavy, and deer. These animals probably hosted T. infestans before the Pleistocene epoch and have been found in early Andean archaeological sites (Neghme 1982, Dauelsberg 1983).
The cohabitation of vinchucas, T. cruzi, and humans probably started during the third millennium B.C., a preceramic period, when Andeans began living in settled agricultural communities in permanent dwellings of stone or structures of adobe walls with straw roofs (Nufiez 1983). One such community, at La Galgada, Peru, has recently been excavated (Grieder et al. 1988). These early Andeans cultivated squash, gourds, guava, lúcuma, lima beans, and avocado using irrigation canals. They lived in scattered clusters of small houses, carrying out ceremonies in various chambers which permitted seating only around a circle with a fire in the center. They made cloth with harness looms.
By the second millennium B.C., the people at La Galgada were trading for shells from as far off as Ecuador. They lived in hereditary kin groups. The spread of Chagas’ disease probably was precipitated in such settlements by the proximity of humans and animals (especially guinea pigs) in houses and villages where insect vectors could easily feed, rapidly passing parasites from infected to uninfected mammals. Infected Andeans spread the parasite from village to village in their travels with alpacas and llamas, also carrying parasites and insects in their cargo.
The Wankaris of Tarapacá descended from nomadic hunters and gatherers who had migrated 3,000 years ago from the shores of Lake Poopó in the southern highlands of the Andean mountains across the Atacama desert into the Quebrada de Tarapacá (Nuñez 1982). For thousands of years they foraged and hunted within the southern Andes. They fished and gathered mollusks, berries, nuts, and carrion meat. They lived in caves where they built fires, cooked meat, and told stories. These caves were also inhabited by bears, rats, cavies, viscacha, bats, and triatomine insects.
Around the beginning of the first millennium B.C., Wankaris had changed their nomadic and foraging lifestyle to become semisedentary farmers, herders, and gatherers (Wheeler, Pires-Ferreira, and Kailicke 1976). The Quebrada de Tarapacá provided a more habitable place to settle down, with a warmer climate and lower altitude, 3,737 feet (1,100 m.), than the frigid climate and higher altitudes of the mountains around Lake Poopó at 11,700 feet (3,600 m.).
Also by this time, it is thought that vinchucas inhabited human houses as their primary environment in agroceramic centers of Argentina, southern Peru, and eastern and central Bolivia (notably in Cochabamba, an epicenter from where they evolved from sylvatic, or forest, to domiciliary environments, a fact indicated by the presence of both types there today). Domiciliary preferences of vinchucas enabled them to rapidly reproduce and infect animals and humans, resulting in widespread endemic Chagas’ disease. Vinchucas becoming domiciliary was about as devastating to Andeans’ health as the domestication of alpacas and llamas was to improving their lives. Vinchucas traveled and lived with their herds, spreading T. cruzi up and down the Andes and well into the Amazon.
Certain environmental factors contributed then, as they do now, to triatomines adapting from sylvatic to domestic habitats: the increased size and growth of villages encroached upon their forest habitats and diminished the number of sylvatic mammals from which they could ingest blood meals, while domiciliary environments with humans and animals crowded together provided increased feeding and nesting opportunities for vinchucas.
Human migrants are important vectors of ecological exchange. Humans tend to dominate any environment in which they are a part
, and colonists are a decisive element in any biological conquest. Because the constantly migrating early Andeans were subject to changing environments, they were less able to dominate these environments, in part because diseases spread faster than they could adapt to them. Early Andeans then, and migrating peasants today, transverse a range of microbes, as also was illustrated in the previous chapter when railroad expansion into tropical forests of Brazil brought a disproportionate amount of disease to the workers.
Even though Triatoma infestans inhabited houses in the Andes for thousands of years and symptoms of Chagas’ disease were found among the Wankaris, T. cruzi is first found within an Inca mummy of the central Andes dated around 1400 B.C. (Fornaciari et al. 1992). In 1992, paleopathologists from the University of Pisa examined the mummy of a twenty-year-old woman from Cuzco, ancient capital of the Inca empire from 1275 to 1532, kept at the National Museum of Anthropology and Ethnology in Florence. The mummy sits in a crouched position, wrapped in coils of a basket, with her face protruding through the top. Mummification was customary for Incas until the conquest of Peru in 1532, after which missionaries prohibited it, considering it ancestor worship. The mummified Inca’s heart, esophagus, and colon were abnormally enlarged, suggesting a megavisceral syndrome similar to that of the Wankari mummies.
Paleopathologists examined the mummy’s tissues by means of electronomicroscopy and immunohistochemistry and discovered round nests of amastigotes of Trypanosoma cruzi within the myocardium and esophagus. Their conclusions were written in The Lancet, January 11, 1992: “The macroscopic, historical, immunohistochemical, and ultrastructural findings in this Peruvian mummy constitute an ancient case of chronic Chagas’ disease. This is the first direct demonstration of this disease, and agent causing it in South America during the Inca empire immediately before the Spanish conquest of that continent.”
The Kiss of Death Page 5