has not been identified with a sylvatic source and is the primary source of the domestic transmission cycle; it has been found in domestic situations in acute and chronic cases with cardiac and digestive symptoms being associated with megasyndromes.
Significant research on zymodemes has been done in Bolivia by investigators from a branch of Pasteur Institute in La Paz, Instituto Boliviano de Biologia de Altura (IBBA) (see Breniere et al. 1989, Tibayrenc et al. 1984). In earlier studies, Tibayrenc and colleagues collected 132 Trypanosoma cruzi stocks in southern Boliviain Tupiza and Tarijathat were characterized using enzymes. Five different isoenzymatic strains (IS) were found that are distinguishable from those found in Brazil. The incidence of IS 2 is higher (60 percent) in Tarija (altitude 6,400 feet) than it is in Tupiza (31 percent; altitude 8,528 feet), which suggests that IS 1 seems to be more frequent at high altitude and that IS 2 seems to be more frequent at lower altitudes (Tibayrenc and Desjeux 1983). Genotype frequencies demonstrated the lack of Mendelian sexuality among stocks of T. cruzi from southern Bolivia, which supports a clonal theory of propagation for trypanosomatids (Tibayrenc, Hoffman, et al. 1986, Tibayrenc, Ward, et al. 1986).
All strains were transmitted by Triatoma infestans, in contrast to Brazil, where strains were transmitted by different vectors, perhaps suggesting that different T. cruzi strains were adapting to particular vector species (Miles, Provoa, de Sovza, et al. 1981). Different strains were found in the same suburb and house in Tupiza. Forty-four houses were examined: nine had two different isoenzymic strains, two had three different strains, and one had four different strains. The migration of triatomine bugs from house to house is important; flights of several kilometers are possible (Lehane and Schofield 1981).
In a later Bolivian study (Breniere et al. 1989), researchers at IBBA performed serological and pathological studies on 495 patients with Chagas’ disease from different areas of Bolivia. Eighty-nine Trypanosoma cruzi strains were isolated by xenodiagnosis and characterized by twelve isoenzyme loci; they were related to the presence of cardiac changes and enteric disease with megacolon. There was high heterogeneity of human zymodemes, presenting evidence of two predominant zymodemes genetically dissimilar from each other and ubiquitous in Bolivia. Researchers observed mixtures of different zymodemes within the same patients, and there was no apparent difference of pathogenicity between the two more frequent zymodemes isolated from humans.
In the Andean northern region of Chile, a recent study was completed concerning the biochemical, immunological and biological characterization of T. cruzi (Gonzalez et al. 1995). Within this region (at Quebrada de Tarapaca, discussed in Chapter 2), autopsies performed on mummies dated around A.D. 500 revealed the presence of clinical manifestations of Chagas’ disease (Rothhammer et al. 1985), which indicates a very early adaptation of T. cruzi to human habitats.
Clinical surveys indicated that in the lower Andean region of northern Chile the infection rate was low and great evidence of cardiac involvement was detected by alteration of electrocardiograms (Arribada et al. 1990). In the higher Andean region a very high infection rate was detected, but cardiac involvement was lower than that of the lower region (Apt et al. 1987). This indicates the importance of altitude factors in the T. cruzi infection causing cardiac involvement (Villarroel et al. 1991). The more benign character of Chagas’ disease detected in Chile compared to other endemic areas (Neghme 1982) is significant, either because of the T. cruzi strain circulating in each area and/or because of the ancient adaptation of the parasite to the human host in this country and particularly on the Andean highlands of Quebrada de Tarapaca (Gonzalez et al. 1995:126).
Researchers found more than one type of T. cruzi parasite strain in the Chilean highlands; they also found that the different strains had higher or lower parasitemia levels. Each T. cruzi strain displayed a unique characteristic. Gonzalez and colleagues (1995:131) hypothesize that tissue tropism of individual T. cruzi strains and geographic distribution of different strains and their source (sylvatic or domestic) may play a role in the wide variety of clinical signs encountered in Chagas’ disease (Rassi 1977). Conclusions from the Andean northern of Chile study are as follows:
Finally, the parasite sample studied here from humans resembles the main ones circulating in humans of other endemic areas of Chile as described before (Solari et al. 1992; Hendriksson et al. 1993; Mufioz et al. 1994), in spite of the fact that other T. cruzi populations are also transmitted by the insect vectors and their poor infective capacity in the murine experimental models. This observation probably is explained by a special adaptation of the Zymodeme 30 parasite type in human hosts from the presumably mixed infective T. cruzi populations circulating in nature. This observation and the early adaptation of T. cruzi to humans in the [Andean] highlands and other endemic areas of Chile as well, compared to other countries, could explain the more benign character of Chagas’ disease in this geographic area. The biochemical characterization shows that several T. cruzi subpopulations exist in the endemic area of Chile, but it remains to be demonstrated whether the clinical evolution of this parasitism on humans varies depending upon the infective strain involved (Gonzalez et al. 1995:132-33)
APPENDIX 3
Immunization against T. cruzi
Immunization against trypanosomes needs to be targeted at the surface membrane of the parasite, which presents a number of considerations. American trypanosomes, such as T. cruzi, differ from African trypanosomes and do not employ the dramatic surface modulation seen with African trypanosomes, such as T. bruceigambiense and T. b. rhodesiense, that cause sleeping sickness. T. cruzi’s evasive strategies are to share antigens with host cells and to alter host antigens so that when host antibodies attack the parasites they simultaneously attack host cells (Avila 1994, Brener 1994). This is an evasive function of the surface membrane.
A most vital part of any parasite is its surface, which is the site of nutrient acquisition, the site of dealing with host immunity, and the site where it protects itself from biotic and abiotic components of the environment. The surface membrane of T. cruzi as well as similar protozoa exhibits a wide variety of housekeeping functions. For example, it is responsible for ion balance, nutrient transport, and resisting the physical and chemical perils offered by the vinchuca’s gut. The parasite’s surface is also a key participator in the adherence to and penetration of host cells. Moreover, it is this organelle that deals effectively with the host’s immune response.
The more that is known about T. cruzi’s surface, the more we can learn about how it penetrates cells, what it eats, and how it eats. Consequently, extensive research is being done concerning the biochemistry of T. cruzi’s surface, especially on how it interacts with the host’s immune system.
T. cruzi has a very complex life cycle, which is composed of various stages that pass through a multitude of microenvironments within its mammalian and insect hosts. These microenvironments present many hostile elements which must be overcome since they are essential to the parasite as home or transportation and provide the protozoan with the space and nutrients to survive and reproduce. The capabilities of the organism cannot be assumed to be the same in each environment, since the environments differ so dramatically. If T. cruzi alters its surface to deal with environments, it also consequently alters the basis for attack by the host immune system. T. cruzi’s basic survival strategy is alteration of its surface as it passes through various stages within the vector insectfrom trypomastigotes in the foregut, to epimastigotes in the midgut, and to metacyclic trypomastigotes in the hindgut, which are passed in the feces and deposited on the skin of the animal/human host, and, within the host, from metacyclics in the blood, to amastigote forms in tissues, to trypomastigotes circulating in the blood (see Figure 7).
In comparison, African trypanosomes pass through only two stages, trypomastigote and epimastigote. Within a vertebrate host, African trypanosomes multiply as trypomastigotes in the blood and lymph, whereas
