“…16,17 Whatever the reason for the presence of inapparent infections in the population of endemic areas for Chagas disease, what is important is to know that people with these inapparent infections will eventually develop the disease in a severe form, as previously suggested. 18 This fact has been demonstrated in the present work by the conversion or reactivation of a patient with inapparent infection into symptomatic infection 1-3 months after being diagnosed (see Table 1). Our results also support Garnham's assumption that ''inapparent infections are at least as numerous as and probably much in excess of the clinical disease.''…”
Section: Discussionsupporting
confidence: 69%
“…Our results also support Garnham's assumption that ''inapparent infections are at least as numerous as and probably much in excess of the clinical disease.'' 18 The fact of finding 61% T. cruzi inapparent infections appears to corroborate this statement.…”
Abstract. Inapparent infections of Trypanosoma cruzi were detected in symptomless seropositive people living in close proximity, and under the same conditions of risk, to patients with acute Chagas disease. Similar infections were also detected in sera samples of people from 25 villages of western Venezuela where Chagas disease is endemic. Seropositivity in all the 1,251 studied samples was established by use of 3 serological methods (direct agglutination test, indirect immunofluorescence antibody test, and enzyme-linked immunosorbent assay). Each seropositive sample was tested for detection of anti-T. cruzi-specific immunoglobulin (Ig) M and IgG levels and specific T. cruzi infection by molecular methodology (polymerase chain reaction assay). The combined analysis of the serologic (IgM and IgG levels), molecular (specific T. cruzi DNA), and statistical findings demonstrated the existence of a different stage of T. cruzi infection in asymptomatic patients, which is suggested to be recognized as inapparent infection. Its definition, significance, and comparison with typical Chagas disease phases are presented, and its potential epidemiological importance is discussed.
“…16,17 Whatever the reason for the presence of inapparent infections in the population of endemic areas for Chagas disease, what is important is to know that people with these inapparent infections will eventually develop the disease in a severe form, as previously suggested. 18 This fact has been demonstrated in the present work by the conversion or reactivation of a patient with inapparent infection into symptomatic infection 1-3 months after being diagnosed (see Table 1). Our results also support Garnham's assumption that ''inapparent infections are at least as numerous as and probably much in excess of the clinical disease.''…”
Section: Discussionsupporting
confidence: 69%
“…Our results also support Garnham's assumption that ''inapparent infections are at least as numerous as and probably much in excess of the clinical disease.'' 18 The fact of finding 61% T. cruzi inapparent infections appears to corroborate this statement.…”
Abstract. Inapparent infections of Trypanosoma cruzi were detected in symptomless seropositive people living in close proximity, and under the same conditions of risk, to patients with acute Chagas disease. Similar infections were also detected in sera samples of people from 25 villages of western Venezuela where Chagas disease is endemic. Seropositivity in all the 1,251 studied samples was established by use of 3 serological methods (direct agglutination test, indirect immunofluorescence antibody test, and enzyme-linked immunosorbent assay). Each seropositive sample was tested for detection of anti-T. cruzi-specific immunoglobulin (Ig) M and IgG levels and specific T. cruzi infection by molecular methodology (polymerase chain reaction assay). The combined analysis of the serologic (IgM and IgG levels), molecular (specific T. cruzi DNA), and statistical findings demonstrated the existence of a different stage of T. cruzi infection in asymptomatic patients, which is suggested to be recognized as inapparent infection. Its definition, significance, and comparison with typical Chagas disease phases are presented, and its potential epidemiological importance is discussed.
“…Mixed infections with T. rangeli and Trypanosoma cruzi (the causative agent of Chagas' disease) may occur in both vertebrate and invertebrate hosts (Schaub and Wunderlich 1985;D'Alessandro and Saravia 1999;Grisard et al 1999). The presence of both parasites in the mammalian host can be detected by xenodiagnosis or immunological tests (Garnham 1980;Acosta et al 1991;Guhl et al 2002). In opposition to T. cruzi, T. rangeli causes a harmless infection in mammals, including man (Hoare 1972;D'Alessandro 1976), but induces pathological effects in the triatomine bugs, such as death of nymphs during the molting due to morphological abnormalities (Grewal 1957;Tobie 1965;An˜ez 1984).…”
Penetration of the heteroxenous protozoan Trypanosoma rangeli into the salivary glands of its invertebrate host Rhodnius domesticus has been investigated here using different approaches. Electron microscopy showed that epimastigotes coming from the insect hemocoel cross the basal lamina that surrounds the salivary glands and penetrate through the gland cells cytoplasm. After reaching the gland lumen, epimastigote forms remain adhered to the gland cell microvilli by their flagella, while metacyclic trypomastigotes are found swimming free in the saliva. Analysis by flow cytometry, western blotting and hemolytic activity allowed to demonstrate the presence in T. rangeli of a hemolytic molecule with antigenic cross-reactivity with murine perforin, which could be used by the parasites to reach the salivary gland lumen. This molecule, which we named as rangelysin, has 120 kDa molecular weight, is able to induce hemolysis only in acidic pH, and is produced by both trypomastigote and epimastigote forms.
“…She died at the age of 73 years, apparently due to causes other than Chagas' disease (Rocha 1992). Berenice exhibited a balanced human host-T. cruzi relationship and constitutes the best example of the indeterminate form of Chagas' disease (Garnham 1980). The isolate obtained by Salgado et al (1962) has been characterized and studied in many aspects by different authors (Brener 1965;Brener et al 1974;Melo and Brener 1978) and has been further compared with the isolate obtained in 1978 (Lana 1981;Lana and Chiari 1986).…”
Two isolates of Trypanosoma cruzi were obtained from the patient Berenice, the first human case of Chagas' disease (Chagas 1909), when she was 55 and 71 years old, respectively. The isolates were characterized on the basis of their epimastigote-trypomastigote differentiation in liquid media and of the electrophoretic pattern of EcoR1 digestion products of kinetoplast DNA (k-DNA) minicircles (schizodeme) and isoenzyme patterns (zymodeme). Clear differences were found between the isolates, suggesting the occurrence of a heterogeneous population of T. cruzi in the infection of this patient.
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