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 possible 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 ).

 








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