of the colon but includes disturbances of the motility of the large intestines, as Isica first suffered. Usual complaints are abdominal distention caused by gas (meteorism), irregularity of peristalsis, and difficulties in defecation. Similar symptomology is also found in the elderly and is attributed to the physiological diminution of ganglion cells in the colon with the increase of age. In similar fashion, Chagas’ disease diminishes ganglion cells in the colon. If T. cruzi reduce the ganglion cells below a critical limit of 55 percent, dilatation and hypertrophy of the colon begin. The mechanisms of destruction of the nervous intramural plexus are still not clear, but there is strong experimental data indicating that it is related to cell-mediated immunity.[26]

As happened with Isica, this destruction normally leads to the second stage, megacolon, which Andeans usually attribute to entangled colon (volvulo). Its major symptoms are an enlarged colon and the inability to defecate. Peasants sometimes have not defecated for from two to six months before they die (see Figure 9).

In megacolon, amastigote forms of T. cruzi encyst within the muscles of the colon. These amastigotes form psuedocysts which burst within the muscle and cause damage to the nerve ganglia within the myenteric plexus. Another possibility is that ganglia present T. cruzi antigen markers on their surfaces that become targets for attack by the immune systemsort of self attacking selfand are then destroyed. Without proper innervation of the smooth muscles of the gastrointestinal tract, peristalsis diminishes and, in an attempt to compensate, the muscle layers enlarge (hypertrophy). It is not the hypertrophy of the muscles that causes the most dramatic enlargement of the colon, it is the loss of rigidity provided by the muscle layers. The circular and longitudinal muscles give the gastrointestinal tract its shape, a boundary. Once the muscles hypertrophy and begin to lose their functional capability, the intestine begins to lose its form. Food taken in through the mouth can remain in the gut (gastrointestinal tract) for great periods of time, due to lack of peristalsis. As the gut fills up, the intestine expands to hold the contents, having lost its rigidity. Atonic constipation develops and parts of the bowel can become necrous and die. As the disease develops, the entire gastrointestinal tract can be affectedhence, the term megacolon.

Figure 19. Dr. Johnny Mendez is a surgeon at the Instituto de Gastroenterologia Boliviana Japones in Sucre, Department of Chuquisaca. Mendez specializes in operating on patients with megacolon, a common chronic symptom of Chagas’ disease. (Photograph by Joseph W. Bastien)

In the Department of Chuquisaca, Bolivia, approximately 40 percent of patients’ gastrointestinal problems are attributed to Chagas’ disease. Both forms of chagasic colonopathy are found in the Department of Chuquisaca. In contrast, none of the patients in Viacha on the Altiplano, outside of La Paz, suffering from volvulo had Chagas’ disease.[27] This complicates the problem, in that entangled colon (volvulo) caused by altitudinal and genetic factors is found in Andean communities along with chagasic colonopathy. Only recently have biomedical personnel begun to distinguish between entangled colon (volvulo) and chagasic colonopathy. Some Bolivian doctors dispute the high reported percentages of Chagas’ disease and attribute its pathology to altitudinal factors, genetics, and tangled colon (volvulo) caused by improper diets.

Dr. Johnny Mendez Acuna is a surgeon at the Instituto de Gastroenterologia Boliviano Japones in Sucre, Department of Chuquisaca. Mendez attributes toxins produced by T. cruzi as the cause of pathogenesis, a slightly dated theory for which there is less proof than for that of the antigenic mimicry hypothesis theory (Van Voorhis et al. 1991), discussed in Appendix II. Mendez specializes in operating on patients with megacolon, and he presents a surgeon’s view of the situation:

T. cruzi prefers to settle in the large intestines. The problem resulting is dolicomegacolon [large and wide colon]. It starts as retractile mesenteritis, an inflammation and drawing back of the mesentery. The mesentery contains fibers and vessels that support the intestines as well as pass the various nutrients to it. Toxins also affect the muscular walls of the intestines so that they become large and extended. When the intestines become large and wide, they are less able to contract and pass the digested food along, eventually causing aperistalsis. Gases accumulate. There is a problem of impacted bowels and inability to defecate.

Toxins eventually destroy the supporting wall of the mesentery that provides blood to the intestines. When the large intestine becomes too enlarged, it breaks loose from the mesentery and spins around, forming a volvulus, a twisting of the intestine upon itself that causes obstruction. Many Bolivians suffer from volvulus. This is deadly because the stomach becomes extremely enlarged, the person is unable to pass gas and fecal matter, and blood cannot reach the stomach. All patients with volvulus at our hospital have tested positive for Chagas’ disease. These patients have decreased nerve plexus of the colon.

We perform about fifteen operations a year for volvulus. Called the operation of Hartmann, it is a sigmoidectomy where we remove the engorged section of the intestines, disconnecting the intestines from the anus. The patient goes to the bathroom using a tube outside of the body. In six months, we perform an operation of reconversion, to connect the intestines with the rectum. (Mendez Acufia 6/24/91).

As Mendez indicated, for chagasic megacolon surgical repair is needed to remove part of the bowel.[28] Unfortunately, many Bolivians die from severe constipation because they go undiagnosed or are unable to pay for an operation. Others would rather die than undergo an operation and deal with the inconvenience associated with ileostomy, such as Isica illustrated. Ileostomy presents an extremely complicated technological situation for subsistence peasants.

A useful new technique for the treatment of chagasic megacolon is restorative proctocolectomy, practiced in Brazil (MacSweeny, Shankar, and Theodorous 1995:479). A twenty-two-year-old woman was suffering from chronic constipation with overall malaise. Despite regular treatment with laxatives, she became worse. Finally her abdomen was opened and surgically examined. Surgeons found the entire colon grossly dilated, with small perforations of the transverse colon and ischemic caecum. They excised part of the colon (colectomy) and created a surgical passage through the abdominal wall into the ileum so that fecal matter drained into a bag worn on the abdomen (ileostomy). She wished to avoid permanent ileostomy, so they removed the anus and created a J-pouch with a covering-loop ileostomy followed by closure of the ileostomy. Restorative proctocolectomy produced good results in her case in that she subsequently has had four bowel actions per day and full control of continence.

Esophageal Problems

Another gastrointestinal complication found in the Department of Chuquisaca, Bolivia, in chagasic patients is achalasia of the esophagus, or the nonrelaxation of the lower esophageal sphincter (see Marcondes de Rezende and Ostermayer 1994:151-58). Motility of the esophagus is altered in chagasic patients throughout Latin America, and there is no agreement on the prevalence of either megaesophagus or megacolon.[29] The function of the esophagus is to contract and expand so as to push food through the throat to the stomach. A variety of explanations are found for intrinsic denervated esophagus that produces loss of peristalsis, so that the esophagus does not dilate and food cannot pass through it (Marcondes de Rezende and Luquetti 1994). The upper part of the esophagus enlarges, and patients have difficulty swallowing (dysphagia), at times being unable to swallow liquids.[30] Chagasic patients in Santa Cruz often gloss over the fact that they are suffering from dysphagia by a stereotypical answer to the physician’s inquiry. Many respond: “But, Doctor, who doesn’t have difficulty when eating cold rice?”

Very significantly, patients with megaesophagus have lost more than 95 percent of the ganglion cells of the myenteric plexuses (Koberle 1968:91).[31] Temporary stagnation or retention of food stretches the esophagus, causing distention of the muscle fibers, which leads to hypertrophy of the muscle, causing more powerful contractions and making still more difficult the passage of food.

In Sucre, chagasic megaesophagus is commonly found. Resulting serious side effects among patients who are unable to swallow for several days include starvation and malnourishment.

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