Chagas disease in the state of Jalisco, Mexico was described for the first time in 1967; however, knowledge on the disease remains in a slow process. Between 1967 and 2006, the disease was described in its acute and chronic forms. The vector species have been identified, and the parasite Trypanosoma cruzi has been isolated and genetically characterized. Also, the magnitude of the infection in humans has been determined through serological studies of different populations as well as of blood donors. The up-to-dateness of knowledge of the disease in the state of Jalisco, unveils a necessity of increased research on the epidemiology of Chagas disease as well as on clinical studies to assess the health of individuals and the populations.

La enfermedad de Chagas en el estado de Jalisco, México, apareció por primera vez en 1967, aunque su conocimiento ha seguido un proceso lento. Entre los años de 1967 y 2006 se describió la enfermedad en sus formas agudas y crónicas; se identificaron las especies de vectores y se aisló el parásito Trypanosoma cruzi, que luego se caracterizó en el plano genético. La magnitud de la infección en el hombre se determinó con estudios serológicos en diversas poblaciones, así como en donadores de sangre. En la actualización presente del conocimiento de la enfermedad en el estado de Jalisco se mostró la necesidad de incrementar las investigaciones sobre la epidemiología de la enfermedad de Chagas, así como los estudios clínicos para determinar la salud de los individuos y las poblaciones.

Chagas disease in the state of Jalisco, Mexico was described for the first time in 1967; however, knowledge on the disease remains in a slow process. Between 1967 and 2006, the disease was described in its acute and chronic forms. The vector species have been identified, and the parasite Trypanosoma cruzi has been isolated and genetically characterized. Also, the magnitude of the infection in humans has been determined through serological studies of different populations as well as of blood donors. The up-to-dateness of knowledge of the disease in the state of Jalisco, unveils a necessity of increased research on the epidemiology of Chagas disease as well as on clinical studies to assess the health of individuals and the populations.

La enfermedad de Chagas en el estado de Jalisco, México, apareció por primera vez en 1967, aunque su conocimiento ha seguido un proceso lento. Entre los años de 1967 y 2006 se describió la enfermedad en sus formas agudas y crónicas; se identificaron las especies de vectores y se aisló el parásito Trypanosoma cruzi, que luego se caracterizó en el plano genético. La magnitud de la infección en el hombre se determinó con estudios serológicos en diversas poblaciones, así como en donadores de sangre. En la actualización presente del conocimiento de la enfermedad en el estado de Jalisco se mostró la necesidad de incrementar las investigaciones sobre la epidemiología de la enfermedad de Chagas, así como los estudios clínicos para determinar la salud de los individuos y las poblaciones.

Previous studies showed that two groups of Trypanosoma cruzi clonal genotypes named clonet 20 and clonet 39 were predominant in Triatoma infestans, the unique vector of Chagas disease in Bolivia. These groups of clones correspond to distinct genetic clusters. These clonets were detected in T. infestans and Rhodnius pictipes fecal samples before isolation and after culture by kDNA PCR (polymerase chain rreaction) and hybridization of the amplified products with clonet specific kDNA probes named 20 and 39 as previously reported. Forty eight T. infestans and three R. pictipes infected insects captured at random in different Bolivian departments were proceeded. As previously reported the direct identification of the two major clonets in fecal samples allowed the detection of abundant mixed infections: 41% in the original sample, however after culture, only 6% of mixed infections were detected. Among the 21 parasite stocks isolated from digestive tracts where mixed infections were initially detected (clonet 20 + 39) clonet 20 alone was detected in 81% of them. This result clearly showed that the culture step selected clonet 20 parasites over those belonging to clonet 39. The taxonomic status of the isolated stocks was also confirmed by isoenzyme typing, and correlation was observed between clustering topology and hybridization patterns with the probes 20 and 39.

Homologies of minicircle kDNA of 27 Mexican stocks were studied by cross-hybridization with four kDNA probes derived from three reference stocks belonging to groups Trypanosoma cruzi I (SO34 cl4 and Silvio) and T. cruzi II (MN) and one Mexican stock. High homologies were only observed with Silvio (six stocks) and Mexican probes (11 stocks). After 30 min exposure (low homology) additional stocks were recognized with SO34 cl4 (three stocks) and Silvio (six stocks) probes; with the Mexican probe only five stocks remained non-reactive. All the stocks were typed by isoenzyme (16 loci) and Mexican stocks belonged to T. cruzi I. Hybridization patterns were not strictly correlated with the observed clustering and cross-hybridization of kDNA minicircles is not available to distinct Mexican stocks.

A field study of the immune response to the shed acute phase antigen (SAPA) of Trypanosoma cruzi was carried out in the locality of Mizque, Cochabamba department, Bolivia. Schoolchildren (266), with an average of 8.6 ± 3.6 years, were surveyed for parasitological and serological diagnosis, as well as antibodies directed against SAPA using the corresponding recombinant protein in ELISA. The antibodies against SAPA were shown in 82% of patients presenting positive serological diagnosis (IgG specific antibodies). The positive and negative predictive values were 0.88. Antibodies anti-SAPA were shown in 80.8% of the chagasic patients in the initial stage of the infection (positive IgM serology and/or positive buffy coat (BC) test) and in 81.4% of the patients in the indeterminate stage of the infection (positive IgG serology with negative BC and IgM tests). These results show that the anti-SAPA response is not only present during the initial stage of the infection (few months) but extends some years after infection