Vinchucas are not fast-flying insects like mosquitoes or flies; they only glide by means of poorly developed wings. The wings of triatomines move slowly and arduously and can barely, if at all, lift them upward, unless they are first descending from a perch. Brazilian scientists photographed the flight of these bugs with a low-light-sensitive camera. Triatomines take off from window ledges and ceilings and descend, riding air waves back and forth in large sweeping movements until they alight on their victims. Although they prefer to stay in one house, they can glide up to 1,000 meters, enabling them to travel from house to house in search of blood meals. Radar-like detectors, the two long antennae on their heads, are sensitive to carbon dioxide respiration and guide the triatomines to the exposed and heat-emitting areas of warm-blooded animals.
Compensating for being poor flyers, vinchucas are excellent crawlers, with six long and strong legs. After a blood meal, vinchucas return to their nests, literally like tankers, trailing blood and fecal matter across bedding, tables, floors, walls, and ceilings. Their tracks contaminate food and clothing, as does their fecal matter dropped from the ceiling.
As ugly as these trailing streaks are, they do provide warning signs to wary travelers wishing to spend the night in some unfamiliar room. Wary Bolivians check rooms thoroughly with flashlights and ask if and when the house and rooms have been sprayed for vinchucas. Tiny white eggs and brown blotches on the walls provide evidence that the guest will not spend the night alone. Nor does mosquito netting provide protection against the bugs’ instar stages, which are the size of fleas, from crawling underneath the netting. Vinchucas can live and reproduce for weeks with one blood meal; they remain content until their energy runs low, at which time they begin to look for another blood meal.
Figure 16.
Infected bites from Triatoma infestans (vinchucas). (Photograph by staff of Proyecto Cardenal Maurer)
Figure 17.
Vinchuca and stages of T. cruzi. Vinchucas (Triatoma infestans) deposit metacyclic trypomastigotes in their feces that are infective to humans (as well as other mammals) and temporarily enter the blood. They enter tissues where they become amastigotes, then divide into other amastigotes and short, stumpy trypomastigotes that reenter the blood. These trypomastigotes are ingested by uninfected and infected vinchucas, where they transform into epimastigotes and then metacylic trypomastigotes. (From Franklin Neva and Harold Brown, Basic Clinical Parasitology, p. 66) (See Appendix 1.)
Contamination through the Feces
Contamination through the bugs’ feces is the major mechanism by which T. cruzi passes from vinchucas to humans. T. cruzi transforms from a trypomastigote to an epimastigote to a metacyclic trypomastigote inside vinchucas (see Figure 17). When infected vinchucas take a blood meal, they usually defecate and deposit a metacyclic trypomastigote, which is found in the insect’s intestines, onto the victim’s skin. Metacyclic trypanosomes (tryps) travel from the feces and enter through the bite site, the eye, or other abraded skin. People often scratch the wound and rub parasites into the skin. Metacyclic tryps circulate for a short while in the blood, then enter neuron cells and become encysted as amastigotes. Amastigotes reproduce tryps that enter the blood, where they can be picked up by a vinchuca during its blood meal. (Because T. cruzi is such an infectious parasite, some laboratories in the United States do not experiment with it).
Not all species defecate at the same rate: Rhodniusprolixus and Panstrongylus megistus defecate at a great rate, while Triatoma infestans defecates at only 30 percent of that rate, and Triatoma sordida at only 10 percent (Calvo et al. 1978:70-81). Those species that defecate closest to the injection wound are the most infectious; consequently, T. infestans is most dangerous to humans and most adaptive for T. cruzi, being a very effective vector in transmitting this parasite to hosts. The longer T. cruzi is outside the vector and host, the more vulnerable it is to being lysed, or disintegrating. Children are easily contaminated with the feces of vinchucas. Babies and infants spend considerable time within and around the house, sometimes with little clothing, and they are defenseless victims for vinchucas to feed upon.
Infection through Blood Transfusions
Blood transfusion is the second most important mechanism of transmission of Chagas’ disease. Blood transfusions have enabled T. cruzi to travel beyond tropical and semitropical zones, where it was environmentally limited by the fact that its triatomine vectors needed the warmth and humidity of these areas. This makes Chagas’ disease a worldwide problem, because Latin American countries have been major exporters of blood, as well as organs, through the years (Moraes-Souza et al. 1995; WHO 1990, 1991; Docampo et al 1988). In Brazil alone, 10,000 to 20,000 cases of Chagas’ disease occur yearly because of infections through transfusions (Dias and Brener 1984).[17] Bolivia has a high rate of infected blood. The National Secretariat of Health estimated that in 1988 there were five new cases of Chagas’ disease each day (Bryan and Tonn 1990:15). In seven capital departments of Bolivia, 1,298 sera samples from blood banks were examined for T. cruzi (Carrasco et al. 1990). Percentages of infected blood reached 28 percent, with the following distribution: Santa Cruz (at an elevation of 430 m), 51 percent; Tarija (1,951 m), 45 percent; Sucre (2,750 m), 39 percent; Cochabamba (2,570 m), 28 percent; Potosí (4,060 m), 28 percent; Oruro (3,706 m), 6 percent; and La Paz (3,640 m), 4.9 percent. Other studies for contaminated blood range from 56 percent to 70 percent contamination (Valencia 1990a, Bryan and Tonn 1990) to a less alarming 8 percent (Schmuñis 1991). High percentages of infected blood are found in rural migrants and low-income donors who live in infested dwellings and need money.
Measures to decrease contaminated blood include the screening of donors and the lysing of T. cruzi with gentian violet, a trypanocide (Moraes-Souza et al. 1995; see Appendix 13: Chemotherapy). Blood needs to be stored with gentian violet for twenty-four hours at 4°C for the substance to destroy T. cruzi (Nussenzweig et al. 1953, Schmuñis 1991). Gentian violet gives blood a deep violet coloration, and its side effects are unclear.
Bolivians generally have not adopted these screening measures. Blood is rarely stored in Bolivia, except for export. People receive transfusions directly from someone for about twenty dollars or they purchase a blood bag for five dollars and then have someone fill it for a fee (J. Méndez, interview 5/6/97). Bolivians often refuse transfusions of violet blood, and serological and clinical examinations are expensive.
Fortunately, only 14 to 18 percent of people who receive a transfusion of infected blood develop Chagas’ disease. The following factors are important: the quantity of infected blood received in one or a series of transfusions, the general state of the person’s health, and the immunocompetence of the person (Toro Wayar, interview 6/20/91). Patients receiving multiple transfusions are at high risk, and many patients are immunosuppressed from sickness. People at risk are generally from the poorer classes; wealthy patients usually go to private clinics which have access to blood banks. However, there are not many wealthy people in Bolivia; only 2,000 Bolivians receive annual salaries of more than U.S. $10,000 (Presencia, May 11, 1997).
Chagas’ disease is no longer restricted to Latin America. Immigrants from El Salvador and Nicaragua in Washington, D.C., have tested positive for T. cruzi infection. In 1985, estimates were that 100,000 individuals living in the United States were infected with T. cruzi (Kirchhoff, Gam, and Gillian 1987). I now estimate that number to be more than one million people because of increased immigration from Latin America, increased travel back and forth between countries in Latin America, increased numbers of blood transfusions and organ transplants, and transmission of the disease through birth.[18]
Transmission through Birth
T. cruzi can travel through the placenta, birth canal, and maternal milk. Infected mothers pass Chagas’ disease to their children, but in lesser percentages than might be expected. Some unknown immunologic process often protects the infant (Calvo et al. 1978:80). In general, the incidence of congenital T. cruzi transmission is under 1
0 percent, although this rate is much higher in endemic areas such as Bolivia (Mufioz and Acevedo 1994). In Punata, Bolivia, the mortality rate for children infected congenitally was 47 percent (SOH/CCH 1994). Rates of congenital transmission have increased over the years (Azogue, La Fuente, and Darras 1985:176).[19]
In Bolivia, congenital transmission rates were 7 percent in La Paz and 43 percent in Cochabamba (Brénière et al. 1983). Antibodies were detected in the serum of the mother and in the umbilical cord, with the concentration and quality of the antibodies similar. In Santa Cruz, Bolivia, 329 newborn babies were examined from 1979 to 1980; T. cruzi was found in twenty-five cases (Azogue, La Fuente, and Darras 1985:176-80).[20] Some 51 percent of the mothers and 13 percent of the infants tested positive for Chagas’ disease. Twenty-one (80 percent) of the infected infants weighed less than 2,500 grams (5.5 pounds). It is not clear whether nutrition is an independent or dependent variable; that is, whether the immune system of nutritionally healthy babies resists Chagas’ disease or whether babies infected with Chagas’ disease lose weight. Also, not one case was found before the sixth month of gestation. Although the mother is infected from conception, transmission of T. cruzi from her to the fetus takes time.[21]
The delayed infection of fetuses raises the possibility of treating infected mothers during pregnancy to reduce transmission of the disease to the fetus. The high toxicity levels of nifurtimox and benznidazole used pose serious threats to unborn infants. Moreover, congenitally infected fetuses have been delivered from mothers both positive and negative for parasitemia, and infants have been born uninfected from pregnant women with acute infections and positive parasitemia. Intrauterine T. cruzi infection can cause abortions and premature births (WHO 1991:5).
Mechanisms of transmission of the disease from mother to fetus have not been determined. Possibilities include through the extra-embryonic membranes by diffusion of the parasites, or through progressive migration of the parasite throughout the stroma of the umbilical cord towards the blood vessels, provoking fetal infection by way of the blood (Azogue, La Fuente, and Darras 1985:180).[22]
The chances of getting Chagas’ disease from contaminated blood in Bolivia are higher (14 to 18 percent) than they are of contracting the disease by being born from a Bolivian mother infected with T. cruzi (5 to 10 percent). Even though these percentages vary greatly and are in part guess-estimates, the figures are perplexing in that rates of infected blood and infected mothers are roughly the samefrom 40 to 50 percent. One explanation for the lower rates of congenitally transmitted disease is that it is difficult to diagnose, especially in endemic areas, unless the tests are conducted at birth, since the possibility also exists of infection, or reinfection, by the vector (Mufioz and Acevedo 1994). Secondly, parasites are difficult to detect in the placenta, and, even if they are present, they may not infect the fetus (Thiermann et al. 1985; Muñoz 1990).
Significantly, Chagas’ disease in newborns correlates highly with low weight: in one study, 13 percent of babies weighing less than 2,500 grams (5.5 pounds) were infected with Chagas’ disease in Bolivia (Azogue, La Fuente, and Darras 1985:176-80). Prenatal and postnatal nutrition helps babies resist T. cruzi.
Oral and Organ Transmission
Some less-frequent forms of transmission are by direct ingestion, organ transplant, and skin contact with infected material (Bittencourt 1975; Katz, Despommier, and Gwadz 1989; Schofield, Apt, and Miles 1982). Oral transmission to humans is not well documented, although it is easy to infect animals by this route (Marsden 1967).[23] Because vinchucas defecate in domiciliary and peridomiciliary areas, the possibility of contamination through contact with the insect’s feces and subsequent ingestion of the parasite exists but is not likely.
Three microepidemics in Brazil are attributed to oral transmission (NeryGuimaraes et al. 1968). Schoolchildren became infected with T. cruzi from drinking contaminated milk in Estrella, Rio Grande do Sul, Brazil, an area where triatomines were not found (Calvo et al. 1978:80). The milk had been transported from an endemic area.
In an agricultural school in Rio Grande do Sul, seventeen people were infected and six died from T. cruzi transmitted through food contaminated with opossum urine infected with T. cruzi. The initial misdiagnosis of the illness and the patients’ treatment with steroids aggravated the infection (Di Primio 1971). Trypanosomes can be found in the saliva and urine of animals suffering from acute parasitemia. This constitutes an infective risk for humans working with these animals (Marsden and Hagstrom 1968).
A third instance was in Belem, Para, Brazil, at the mouth of the Amazon, where human Chagas’ disease is rare (Lainson et al. 1979) because only sylvatic species of bugs in this area are known to be infected. It is possible that an infected bug entered the house and fell in a cold soup customarily prepared (Lainson et al. 1980) and infected it with T. cruzi. Because contamination is the major route of transmission, many other possibilities exist for humans coming in contact with T. cruzi through vinchuca feces falling from the ceiling, getting into clothing, and being deposited on tools, among other things. As already mentioned, the periodic washing of the body and clothes is important in combatting the disease, as are good house hygienic practices.
Animals can transmit T. cruzi to humans by licking their skin, and nursing mothers can pass it on to their babies in lactation, possibly through the milk but more likely through sores or inflammations on the breast (Carrasco and Antezana 1991). The parasite’s presence in maternal milk has been confirmed by Medina (1983), but the incidence of transmission by this route has not been reported, probably due to the problem of differentiating it from congenital transmission (Moya 1994).
Transmission by breast-feeding appears to be highly unlikely, and infected mothers need not restrict breast-feeding their infants (WHO 1991:33). This conclusion was based on a systematic parasitological study of 100 milk, or colostrum, samples from seventy-eight mothers with chronic Chagas’ disease in Bahia, Brazil. Even though five mothers had detectable parasitemia, all samples were negative (Bittencourt et al. 1988). In another study in Córdoba, Argentina, and Santa Cruz, Bolivia, ninety-seven children (100 percent of the sample) born free of the infection from infected mothers and subsequently breast-fed tested serologically negative (WHO 1991:33).
Organ transplants from infected donors is an increasing route of T. cruzi transmission for recipients in the United States and Europe. There is an increasing number of organs being sold through the “black market” to patients in the United States from Latin American countries. Americans also travel to clinics in Latin America for organ transplants. Kidney transplants have been shown to be a source of T. cruzi infection, and organ recipients have developed acute episodes of Chagas’ disease (Chocair et al. 1981). In certain transplants, fatality has been attributed to donated organs infected with T. cruzi, because recipients are under immunosuppressive therapy (WHO 1991:34). Conversely, Chagas’ disease patients who receive organ transplants can suffer exacerbation of the infection when given immunosuppressive treatment (Leiguarda et al. 1990).
Laboratories treat T. cruzi with respect. It is the most infectious of the human blood protozoa. By 1976 more than fifty lab technicians had been infected with Chagas’ disease; they suffered meningoencephalitis and megasyndromes (Marsden 1976). Since this time, technicians have learned how to better handle high-risk organisms, but certain research hospitals still refuse to do research on T. cruzi because of its risk factor. Laboratory infections are usually due to punctures with infected needles, contact with contaminated materials, breathing T. cruzi cultures while pipetting, and splashing T. cruzi suspensions on the conjunctivae. Measures for prevention and control are outlined in WHO (1991).
Laboratories in Bolivia present great risks for contracting Chagas’ disease because of their often rudimentary facilities, inadequately trained staff, and insufficient funds to provide protective measures. The exception is the Instituto Boliviano de Biologia de Altura (IBBA), located in La Paz and affiliated with the Pasteur Ins
titute in Paris. Eminent French and Bolivian scientists direct this research laboratory and have done leading work on parasitology. Other, much less developed, laboratories are under control of the Secretaria Nacional de Salud and are funded with minimal budgets. Nonetheless, technicians make do. One technician observed that he was not worried about Chagas’ disease, being already infectedwhich perhaps is the case for many Bolivian researchers.
Epidemiological Reflections
T. cruzi is a silent traveler through vinchucas that has infected 1.5 million people in Bolivia and some 17 million more in other Latin American countries (see Appendix 6). T. cruzi infects people through contamination, blood transfusions, and congenital infection. Vinchucas, T. infestans, have adopted domestic and peridomestic habitats, finding run-down houses crowded with people and animals very suitable for shelter and food. Vinchucas follow migrants and animals to the cities. For the prevention as well as the treatment of Chagas’ disease, the chain of life-stages of the parasite needs to be broken at some point. The possibilities include the elimination of triatomine insects, which is highly unlikely in certain places; prevention of transmission through the bite of the triatomines by means of improved housing, which is presently being done but is very costly; and through vaccinations to block some transformation of epimastigotes to metacyclic trypomastigotes to amastigotes to blood-form trypomastigotes, which is discussed in Appendix 3: Immunization Against T. cruzi.
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