The Kiss of Death

present, perhaps being lysed at an earlier stage. This has led scientists to suspect that the traces or lesions left from the parasite mimic human antigens. The immune system mistakes these human cells as epitopes from T cruzi and attacks them (discussed in Appendix ii). This is similar to rheumatic fever, where people die from the disease long after the pathogen has been removed.

During the acute phase, inflammation, fevers, and cell damage are related to overactivity of the lymphocytes (see Appendix 9). This polyclonal stimulation is triggered by macrophages devouring trypomastigotes. Results include violent onslaughts on the parasites that drive them into central nervous system cells, lysing cells encapsulated with parasites that release toxins into the body, ineffective destruction of antigens, and eventual weakening of immune response. In short, damage from acute Chagas’ disease is more a result of overactivity of the immune system than damage due directly to T. cruzi.

The cardiopathy of chronic Chagas’ disease is an issue of considerable debate, with several lines of evidence to account for, including the inability to consistently find parasites in damaged areas (Torres 1930). The passive transfer of heart lesions by CD4⁺ T cells from T. cruzi-infected mice to uninfected mice indicates that inflammatory heart lesions could be of an autoimmune nature (Andrade 1958, Ribeiro-dos-Santos et al. 1992). (In simpler terms, the T cells from infected mice were encoded with self- destructive tendencies, and when these T cells were placed in uninfected mice, they caused damage as if the sterile mice had the parasites.)

Referred to as the antigenic mimicry hypothesis, lymphocytes in the heart recognize and mount delayed- type hypersensitivity responses toward a tissue-specific heart component bearing structural similarities to a given T. cruzi antigen.[38] A recent study indicates that heart-tissue destruction in chronic Chagas’ disease may be caused by autoimmune recognition of heart tissue by a mononuclear cell infiltrate decades after T. cruzi infection (Cunha-Neto et al. 1995). Indirect evidence suggests that there are antigenic cross-reactions between T. cruzi and heart tissue. Myosin heavy chain (myosin HC) is the most abundant heart protein—50 percent of total protein by weight—and is recognized in heart-specific autoimmunity in rheumatic heart disease (Neu, Beisel, et al. 1987). Research indicates the involvement of cross-reactions between cardiac myosin and a recombinant T. cruzi protein (B13) as targets for attack by the victim’s T cells (Cunha-Neto et al. 1995).[39]

The immune response is also impaired in the chronic stage of Chagas’ disease (see Appendix II: Immune Response). An improper response of the cellular immune system results in tissue damage, which might lead to the autoimmune cardiac and neural damage of chronic T. cruzi infection (Botasso et al. 1994). Trypanosoma cruzi infection impairs immunity to many antigens and mitogens.[40] Chagasic patients have a reduced cellular immune response to common mycobacteria antigens, such as those of tuberculosis and leprosy (Bottasso et al. 1994).[41] T. cruzi causes loss of the TH1 response to mycobacterial antigens.

HIV patients are also unresponsive to mycobacterial antigens (Khoo et al. 1993). The progression from HIV seropositivity to AIDS is accompanied by a shift in T-helper (TH) cells from TH1 to TH2 and selective loss of the response to mycobacterial antigens. Significantly, chagasic patients are predisposed to the establishment of HIV infection and its rapid progression to AIDS (Botasso et al. 1994).

In conclusion, the rapid spread and progression of HIV infection in Latin America is related to the frequency of infection of Chagas’ disease. The rapid spread and progression of tuberculosis and other acute respiratory infections in Bolivia is also related to Chagas’ disease. Bolivian public policy makers often object to the fact that AIDS and tuberculosis take medical priority to Chagas’ disease, when the fact is that Chagas’ disease is also related to the epidemiology of other diseases by the nature of the autoimmune response to it that predisposes its victims to these diseases.

Reflections on the Epidemiology of the Immune System

The following reflections are intuitive considerations of the above findings. AIDS and Chagas’ disease have contributed greatly to our knowledge of the immune system and immunopathology. In Western allopathic medicine, diseases are caused by viruses, bacteria, and parasites; the cure is to rid oneself of the organism. The miracle drugs of the twentieth century have been the antibiotics, which are very successful for lysing bacterial infections but less so for viruses, and they are ineffective for parasites. Trypanicides were developed to lyse trypanosomes of T. cruzi, but they have met with less than satisfactory results.

By the turn of the millennium, super-bacteria, viruses, and parasites have emerged unscathed by antibiotics. Simple principles of natural selection explain this: antibiotics essentially select individuals of the species that are resistant to the drugs; when they reproduce, they pass on these selective features to their offspring. The unwarranted use of antibiotics in Western culture has led to their increasing ineffectiveness and to the evolution of superpathogens. This unwarranted use has also led to humans being less dependent upon their immune systems.

With Chagas’ disease and AIDS, researchers have learned much more about the human immune system and how this system is responsible for illnesses. We are also learning how to live with immune-driven diseasesdiabetes, rheumatism, AIDS, and Chagas’ diseaseand how to build up the immune system by alternative methods of therapy, including dieting, meditation, ritual, and use of herbal medicines. The paradigm of health is changing from that of allopathic medicine, where we lyse the causal agent, to one of immunopathic medicine.

Immunopathic medicine includes figuring out ways to build up our immune system and to help it deal with the realities of our bodies and the organisms within them. Health is learning how to live with what you have. This alternative way of health is not very attractive for those who want the technical quick cure of a drug or vaccine to destroy the pathogen; but, as we have seen, this does not work with Chagas’ disease, among others.

CHAPTER SEVEN Culture and Political Economy of Homes

The condition of houses is a major factor in the spread of Chagas’ disease. Bolivian houses have become habitats for triatomine vectors of Trypanosoma cruzi (see Appendix 5: Housing Infestation in Bolivia). Thatched roofs, cracked walls, and scattered domestic belongings provide nesting sites and hiding places for vinchucas in Bolivian houses. Peasants do not place their clothes in closets but rather beneath beds, in bundles, and in corners. Triatomines nest within mattresses, newspapers, and behind objects hung on walls. Peasants also frequently store wood and crops inside their houses.

House Tour with an Entomologist

Juan Mamani lives with his wife and six children in an adobe house, roughly about the size of a single-car garage in the United States. The adobe walls are unplastered and cracked. Entering the wooden-framed doorway, one sees openings between the frame and the walls. The dirt floor is smoothly packed but covered with stacks of corn, potatoes, rice, and dried beans in one corner. A small earthen stove without a chimney is nestled in another corner with pots and pans surrounding it. The room smells of smoke and cooking. The ceiling is black from the soot of smoke. The building has a thatched roof, which forms the ceiling, and from crossbeams hang clothes, baskets, and several drums. Wooden beds with straw mattresses lie along each wall. Juan and his wife sleep in one bed, their children in the others. Beneath the beds lie shoes, clothes, boxes of valuables, and costumes for