7. There is hope that a novel compound code-named D0870, which has been shown to cure both long-term and short-term Chagas’ disease in mice (Urbina et al. 1996), will do the same in humans; however, it is in the early phases of clinical development for other infections. (See Appendix 13.)
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1. Meningoencephalitis due to T. cruzi has been reported in pharmacologically immunodepressed patients and in patients with AIDS (Jost et al. 1977; Corona et al. 1988; Del Castillo et al. 1990). (See Appendix II.)
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2. In addition to these practical considerations, T. cruzi have unique properties that make them evasive targets for potential chemotherapeutic agents and therefore present formidable challenges to pharmacologists and medical chemists. T. cruzi are intracellular parasites, found in a variety of tissues. The effectiveness of a chemical compound depends on its capacity to cross the vascular endothelium and cell membranes into the cytoplasmic compartment of the parasite. T. cruzi is not a homogenous speciesthere are geographic strains which vary in tissue tropism and response to chemotherapy and biochemical parameters such as electrophoretic profiles of isoenzymes and peptides. The value of a particular drug depends on its effectiveness against both the amastigote and trypomastigote stages of all geographic strains (McGreevy and Marsden 1986:115-27). (See Appendix 13.)
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3. In another study, Bryan and Tonn (1990:14) report higher rates of T. cruzi infection in captured (domestic) triatomines, with averages from 40 to 50 percent and infection rates of 70 to 90 percent in rural areas of the Cochabamba and Chuquisaca departments of Bolivia. (See Appendix 5.)
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4. A recent study analyzed hemotherapy and the problem of transfusional Chagas’ disease in 850 Brazilian municipalities from 1988 to 1989. It found that some type of hemotherapy was practiced in 68.8 percent of these municipalities (Moraes-Souza et al. 1995). Prior screening of donors was carried out by 75.2 percent of the services for syphilis, 65.4 percent for hepatitis, 53.8 percent for AIDS, and 66.8 percent for Chagas’ disease. In the case of Chagas’ disease, only 10.3 percent of services used the chemoprophylaxis of gentian violet. Most services used only one serologic technique to screen donors, and the proportion of potential donors with positive serology for anti-T. cruzi was around 1 percent. (See Appendix 13.)
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5. Although the potential problem of the blood supply in the United States has been recognized for some time (Schmuñis 1985), the recent diagnosis of Chagas’ disease acquired through blood transfusion in the United States (Grant et al. 1989) and Canada (Nickerson et al. 1989) has significantly highlighted the seriousness of this problem (Skolnick 1989, Kirchhoff 1989).
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6. In Brazil in 1911 Carlos Chagas considered the possibility of congenital transmission of T. cruzi when he found trypomastigotes in the blood-smear of a two-month-old child whose mother was also infected (quoted in Howard and Rubio 1968). In Venezuela in 1949 Dao reported other cases of congenital Chagas’ disease in Latin America (quoted in Bittencourt 1976). In Chile, Howard (1962) observed that 0.5 percent of premature babies weighing less than 2,000 grams (4.4 pounds) suffered from congenital Chagas’ disease. In Salvador, Bahia, and Brazil, Bittencourt and colleagues (Bittencourt and Barbosa 1972, Bittencourt, Barbosa, et al. 1972) found that 2 percent of stillborn babies were infected with T. cruzi; and, in Argentina, Salem and colleagues found slightly higher rates, 2.35 percent among stillborn infants (quoted in Bittencourt 1975). By 1979 the number of described cases had reached 100, giving the impression that congenital transmission of Chagas’ disease is infrequent. However, this impression is misleading, because the registered cases are only of fetuses and premature stillborns and do not include congenital Chagas’ disease in newborns delivered at term (Bittencourt et al. 1974). The varying degrees of fetal and neonatal pathology in such countries as Argentina, Brazil, and Chile may be related to inherent characteristics of the parasite (Moya 1994). The fact that the incidence of infection remains the same in each of these countries and geographic regions suggests that population-related factors are not involved. Various factors having to do with the mother, the fetus, and the parasite are more likely implicated in transplacental transmission.
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7. The newborns were delivered at the Percy Boland Maternity Hospital in the city of Santa Cruz and observed from August 1979 until July 1980. Blood samples from newborns and mothers were used to investigate the presence of T. cruzi by means of the modified Strout concentration, which has the highest sensitivity (95.2 percent; but only for acute cases) when compared to other direct parasitological testing methods (Flores et al. 1966; Cerisola 1972:97-100). (See Appendix 12.)
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8. Fetal infection can occur when the mother is in acute, indeterminate, and chronic phases of infection. Most infected pregnant women experience the chronic, or inapparent, form of the disease during their pregnancy, although cases of acute infection have been reported (Moya 1994). The fetus of an infected pregnant woman is usually unaffected, with no observed alterations in the growth or viability of the fetus, nor is the newborn predisposed to exhibit specific disorders. Chagas’ disease in the mother poses little risk to the baby during the perinatal period, which is after the twenty-eighth week of pregnancy through twenty-eight days following birth (Moya 1977, 1994; Moya and Barousse 1984; Castilho and Da Silva 1976).
If the fetus is infected, the outcome of pregnancy may be spontaneous abortion, fetal death, premature birth, low birth weight for gestational age, and even full-term delivery (Moya 1994). Congenitally infected infants present a broad spectrum of clinical manifestationsfrom grave illness with multisystem compromise (usually in premature neonates) to a total absence of symptoms at birth. Some infants remain asymptomatic; others present manifestations of the disease several weeks or months later. Clinical manifestations are encephalitis, meningoencephalitis, lesions in the retina or choroid, and elevated protein levels and cell counts in cerebrospinal fluid (Mufioz and Acevedo 1994).
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9. Another route for T. cruzi is through the blood, by hematogenous spread, and through crossing of the placenta, with multiplication of the parasite in the Hofbauer cells (Bittencourt 1975). The amniotic fluid may provide another vehicle for T. cruzi to travel to fetuses as well as to obstetricians and gynecologists (Apt, Tejada, and Atrozz 1968; Bittencourt et al. 1981; Nattan-Larrier 1921). Contact of the skin with infected amniotic fluid could allow penetration of the skin, and T. cruzi has been found in the skin (Bittencourt 1976). Research is needed to evaluate the exact mechanisms of congenital transmission.
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10. In laboratory experiments, animals have been infected by eating infected triatomines or mammals, but this has not been documented in experiments with humans (WHO 1991:34).
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1. Volvulus is found among Andeans at high altitudes (13,500 feet) and its predisposing cause is a prolapsed mesentery intestine, which may be caused by T. cruzi within this organ.
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2. This doctor’s behavior represents an elitist attitude that some Bolivian doctors exhibit in their treatment of peasants. There has been a considerable change within the 1990s with other Bolivian doctors who are able to communicate cross-culturally with the peasants (see Bastien 1992: 173-91).
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3. See Marcondes de Rezende and Ostermayer 1994; Teixeira et al. 1980; Ribeiro dos Santos and L. Hudson 1980; Petry and Eisen 1989.
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4. Dr. Mario Barragan Vargas conducted a five-year study of megacolon in Viacha, elevation 13,123 feet, located twenty miles from La Paz on the Altiplano. He found many cases of megacolon,
which he attributed to altitudinal and genetic dispositions, not to Chagas’ disease.
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5. See MacSweeney, Shankar, and Theodorous 1995; Cutait and Cutait 1991; and Da Silveira 1976 for a discussion of current procedures.
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6. See Rezende and Rassi 1958; Godoy and Haddad 1961; Vieira and Godoy 1963; Morales Rojas et al. 1961; and Ifiiguez-Montenegro 1961.
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7. In Brazil, chagasic esophageal problems are well known to the people, who refer to it in Portuguese as Mal de Engasgo (“Sickness of Choking”), Entalo (“Stuck”), and Embuchamento (“Engorgement”). The most frequent symptoms expressed are difficulty in swallowing, 99 percent; regurgitation, 57 percent; painful swallowing, 52 percent; belching, 41 percent; hiccups, 38 percent; sensation of plenitude, 32 percent; and coughing, 26 percent (Köberle 1968:90-91). Loss of weight, heartburn, and sour eructations are also very frequent, occurring in 70 percent of the cases. Advanced cases show elongation of esophagus muscles that can reach twenty-six times their normal weight. Advanced cases also have a predisposition to carcinoma, which may occur in 10 percent of the cases (Camara-Lopes 1962).
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8. Nerve cells are decreased along the whole extension of the esophagus, resulting in loss of the coordinated peristalsis and sensitivity of the denervated musculature. This phenomenon, which occurs in the denervated hollow muscular organ, is called “aperistalsis” and describes the absence of esophageal motility (Brasil 1956). The denervated structure becomes supersensitive to any stimulus, inducing diffuse and severe spasms of the esophagus, which occasionally needs an urgent application of atropine.
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9. The consistency of what is ingested is very important, because the transport of solids requires a more coordinated peristalsis than does the movement of liquids; also, excessive solid transport can cause a high overload to the damaged organ. In addition, increased consistency (reduced liquidity) of the contents of the esophagus favors the development of megaesophagus. Patients often drink large quantities of liquids to aid the passage of solids through the organ. Generally either very hot or very cold food intensifies difficulties in swallowing, and perhaps the associated abundant salivation constitutes a type of auxiliary mechanism for the deficient deglutition.
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1. This center began in 1984 with assistance from Banco InterAmericano Desarrollo (BID) and a contract with the Universidad El Salvador de Buenos Aires, Ministerio de Previsión Social y Salud Pública, and La Universidad de Sucre.
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2. Figures have been adjusted to the 1992 census.
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3. Such pathologies include cardiac enlargement, mitral and tricuspid valve insufficiency, and pulmonary embolization. An abnormal left ventricular impulse may reflect the frequent apical aneurysm formation. Right-bundle-branch block is frequent. Complete heart block, high-grade ventricular ectopy, and atrial fibrillation have a grave prognostic significance, both aggravating the congestive heart failure and enhancing predisposition for sudden cardiac death (see Iosa 1994). (See Appendix 10.)
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4. Ventricular arrhythmias are a prominent feature of chronic Chagas’ disease. Ventricular premature depolarization, often with multiple morphologies, is seen frequently. Bouts of ventricular tachycardia and arterial hypertension may occur as well as bradycardia and arterial hypotension (Braunwald 1988:1447; Iosa 1994).
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5. See Brener (1994) and Appendix II for an overview of current theories on pathogenesis.
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6. Investigators have found autoantibody and self-reactive T-cell formation in human and experimental T. cruzi infections (Teixeira, Teixeira, and Santos-Buch 1975; Cossio et al. 1974). Cross-reactive autoantibodies were mainly directed toward ubiquitous and evolutionary conservative molecules (Levin et al. 1989, Kerner et al. 1991, Van Voorhis et al. 1991) which lack clinical and biological significance for the different clinical forms of chronic Chagas’ disease.
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7. The presence of an antibody against cardiac myosin is correlated with the development of chronic inflammatory cardiopathy in T. cruzi-infected mice (Tibbetts et al. 1994). Immunization with cardiac myosin HC induces aggressive myocarditis (Neu et al. 1987b). Cunha-Neto and colleagues (1995) have recognized a heart-specific T. cruzi cross-reactive epitope, with chronic heart lesions further indicating the involvement of cross-reactions of myosin and B13 in the pathogenesis of chronic Chagas’ disease.
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8. See Voltarelli, Donadi, and Falcao 1987; Cunningham, Grogl, and Kuhn 1980; Mosca, Briceño, and Hernández 1991.
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9. These antigens include many stress proteins with sequence homology to those of living organisms (Young, Lathigra, and Hendrix 1988).
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1. An appropriate technology for chagasic control is to teach peasants how to prevent vinchuca infestation by means of readily available materials, such as the use of cow dung in plastering and the use of bottle caps with nails through them to secure roofing and sheeting. For an excellent study on housing in La Paz, see Köster 1995.
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2. Bolivia has traditionally had authoritarian governments, a carryover from colonial times. Presidents enjoyed power akin to the concept of the “divine right of kings.” By 1985, Bolivians had suffered a series of military dictators, the most brutal being Luis Garcia Meza, presently serving thirty years in prison for his crimes. In 1997, Bolivians voted for another “old time” military leader, General Hugo Banzer.
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1. Another acronym for the organization is PSBB, which refers to Proyecto Social Boliviano-Británico “Cardenal Maurer.” By 1994, the British government no longer partially financed this project, so it was shortened to the Cardenal Maurer Project (CM).
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2. The Proyecto Británico Cardenal Maurer project in Chuquisaca was included in 1991 as one of three pilot projects sponsored by the Bolivian Secretariat of Health (SOH) and Community and Child Health (CCH), with assistance from the United States Agency for International Development (USAID) and the Centers for Disease Control (CDC). The SOH/CCH Chagas Control Program ended on December 31, 1994.
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3. Other successful health projects in Bolivia support this conclusion. Enthusiastic leaders include Gregory Rake with the CHW program in Oruro, Oscar Velasco with Project Concern in Potosí, Evaristo Mayda with ethnomedicinal practitioners in Cochabamba, Irene Vance with Pro-Habitat in La Paz, and José Beltrán with Plan International in Tarija.
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4. These nongovernmental organizations (NGOs) include Pro-Habitat (Tarija), Plan-International (Tarija), and Proyecto Chagas (Cochabamba).
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5. As authorities on the control of Chagas’ disease in Bolivia, Bryan and Tonn (1990) wrote: “PBCM in Sucre is the best project of Chagas’ disease control. It is a small project but well organized, with emphasis on community participation, health education, fumigation, and improvement of housing. It serves as a model for other chagasic control projects.”
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The Kiss of Death Page 42
