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Biomedical subjects

S G Andrade

Publications and source records attributed to S G Andrade.

At least 19 recordsLinked to original sources
PubMed1991

Experimental chemotherapy of Trypanosoma cruzi infection: persistence of parasite antigens and positive serology in parasitologically cured mice.

Mice infected with Trypanosoma cruzi, but parasitologically cured after specific chemotherapy, continued to exhibit positive indirect immunofluorescence serological tests 3-6 months after the therapy. Treatment of trypanosome antigens with monospecific antisera produced in rabbits, and examination by immunoelectron-microscopy following peroxidase labelling disclosed the presence of membrane deposits in cell processes in the spleens of the mice. Similar deposits were observed in the external membranes of T. cruzi amastigotes in the spleens of acutely infected mice, but not in normal control mice. No reaction occurred in tissues not previously treated with the monospecific anti-T. cruzi serum. Positive cells in treated and cured mice, as well as in the not cured or untreated control mice, were located in germinal centres of the splenic white pulp and presented long and branching cytoplasmic processes, which are indicative of dendritic cells of the lymphoid follicles of the spleen.

Animals↗
PubMed1989

Sequential changes of the connective matrix components of the myocardium (fibronectin and laminin) and evolution of cardiac fibrosis in mice infected with Trypanosoma cruzi.

Interstitial matrix alterations due to chronic Trypanosoma cruzi myocarditis were studied in mice by immunofluorescent microscopy with specific purified antibodies against the main different collagen isotypes, laminin and fibronectin. During the early subacute stage (26-30 days postinfection), sarcolemmal and perivascular deposits of laminin and fibronectin were prominent. The presence of fibronectin appeared to correlate with the presence of inflammatory cells. By the late subacute phase and early chronic phase (50-90 and 80-90 days postinfection, respectively), laminin and Type IV collagen were present. These were the principal features, although fibronectin continued to be found among inflammatory cells, and pro-III and III collagens formed irregular bands and periarteriolar deposits. During the late chronic phase (150-200 days postinoculation) the interstitium was enlarged and irregular, with positive staining for laminin, Types III, pro-III, and IV collagens; fibronectin appeared as focal, subendocardial, interstitial, and perivascular deposits. The relative absence of Type I collagen and the apparent positive correlation between interstitial matrix amplification and the presence of mononuclear inflammatory cells suggest that fibrotic changes in chronic T. cruzi myocarditis can be reversed if the inflammatory changes subside.

Animals↗
PubMed1989

Treatment of chronic experimental Trypanosoma cruzi infections in mice with MK-436, a 2-substituted 5-nitroimidazole.

The antiprotozoal drug 3-(1-methyl-5-nitroimidazol-2-yl)-3a, 4,5,6,7,7a-hexahydro-1,2-benzisoxazole (MK-436) is highly efficacious for treating mice chronically infected with different strains of Trypanosoma cruzi. The compound was administered by gavage in two daily doses of 250 mg per kg body weight to 130 mice that had been infected for 90 to 400 days with either type II or III strains of T. cruzi. The following parasitological cure tests were carried out: xenodiagnosis, haemoculture, and inoculation of blood into newborn mice. Indirect immunofluorescence tests and histopathological studies were also performed. The results indicate that the drug is highly efficacious against chronic infection caused by both type II (cure rate, 90%) and type III strains (cure rate, 95.7%). Histopathological examinations showed complete clearance of the cardiac and muscular lesions in 36% of the mice infected with type II strains and a decrease in the intensity and extension of the lesions in mice infected with type III strains. Indirect immunofluorescence tests were persistently positive for all the mice 3-6 months after the treatment.

Animals↗
PubMed1987

Trypanosoma cruzi strain-specific monoclonal antibodies: identification of Colombian strain flagellates in the insect vector.

Spleen cells from mice immunized with insect-derived Trypanosoma cruzi metacyclic trypomastigotes were used to obtain Colombian strain-specific monoclonal antibodies. At least 4 different strain-specific antigens were recognized by the monoclonal antibodies on epimastigotes or metacyclic trypomastigotes. There was no reactivity with other stages of Colombian strain T. cruzi, nor with any stage of 15 other T. cruzi strains or isolates, nor with 22 other Trypanosomatidae. One of the monoclonal antibodies was used to identify, by indirect immunofluorescence, Colombian strain flagellates in cryostat sections or glass-slide smears of the insect vector's intestine.

Animals↗
PubMed1987

Therapeutic action of MK-436 (2,5-nitroimidazole) on Trypanosoma cruzi infections in mice: a parasitological, serological, histopathological, and ultrastructural study.

The anti-protozoal drug MK-436 (3-(1-methyl-5-nitroimidazol-2-yl)-3a,4,5,6,7,7a-hexahydro-1,2-benzisoxazole) was found to be effective against Trypanosoma cruzi infections in mice (2 daily doses of 250 mg per kg body weight). Parasitaemia disappeared within 24 hours of treatment which was commenced during the early or late stages of acute infection. Intracellular T. cruzi parasites were also affected by the drug, ultrastructural findings showing severe cytoplasmic vacuolization and membrane alterations. Positive serological responses persisted in the majority of treated and parasitologically cured mice in the study. Cure rates varied from 72% to 100% and were similar regardless of the T. cruzi strain used (Y strain, type I; 12 SF strain, type II; or Colombian strain, type III). However, the proportion of positive serological tests and the frequency of inflammatory lesions were greatest for mice that were infected with the Colombian strain of the parasite.

Animals↗
PubMed1987

Enhancement of chronic Trypanosoma cruzi myocarditis in dogs treated with low doses of cyclophosphamide.

An enhancement of chronic myocarditis was obtained in dogs chronically infected with Trypanosoma cruzi protozoa soon after they were submitted to treatment with low doses of cyclophosphamide (50 mg/sq m bs three times a week for 3 weeks). Such treatment did not cause immunodepression. Myocarditis varied in intensity, but was quite severe and diffuse in some animals, with focal fibrinoid, coagulative, and lytic necrosis and invasion of disintegrating myocardial fibers by the mononuclear inflammatory cells. Untreated infected controls exhibited mild focal myocarditis, usually represented by accumulation of lymphocytes in the interstitial connective tissue. It is suggested that the administration of low doses of cyclophosphamide interfered with the immunologic suppressor network that is thought to maintain the chronic indeterminate (or latent) phase of T cruzi infection.

Animals↗
PubMed1986

Electrocardiographic changes in experimental chronic murine Chagas' disease.

An electrocardiographic study was performed on 26 AKR and 32 A/J inbred mice and on 100 Swiss outbred mice, chronically infected with different strains of T. cruzi, characterized as Types I, II and III. The incidence of electrocardiographic alterations in AKR mice was of 87.0%, 80.0% and 83.3% respectively for infection with the Type I, Type II and Type III strains of T. cruzi. In A/J mice the incidence of electrocardiographic alterations was 100% in the infection with the Type I and Type III strains and 26.1% with the Type II strain of T. cruzi. In Swiss mice the electrocardiographic alterations occurred in 53.5% of the mice infected with the Type II strain and in 71.4% of those infected with the Type III strain of T. cruzi. The most frequent electrocardiographic alterations in chronically infected mice, independently of mouse or T. cruzi strain, were first degree AV block, intraventricular conduction abnormalities, sinus tachycardia and bradycardia. The predominant alterations caused by each of the T. cruzi strains varied according to mouse strain. In A/J mice, the electrocardiographic alterations were more frequent in those animals infected with Type I and III strains of T. cruzi and in Swiss mice the alterations were more frequent in those infected with the Type III strain. The results presented in this study demonstrate that the murine model is suitable for electrocardiographic studies related to the heart lesions that occur in Chagas' disease.

Animals↗
PubMed1985

Immunological response of Swiss mice to infection with three different strains of Trypanosoma cruzi.

The immunological response of Swiss mice to infection with three strains of Trypanosoma cruzi which differ in their morphobiological, antigenic and isoenzymic characters [Peruvian, 12 SF (São Felipe) and Colombian strains] was investigated. The three strains stimulated an elevation of the immunoglobulin fractions IgG2a, IgG2b and IgM during acute infection, as measured by radial immunodiffusion, and an early drop of IgG1 levels. There were low levels of specific antibodies and a negative cutaneous delayed hypersensitivity test to T. cruzi antigens. Cellular reaction of the spleen was evident, with proliferation of lymphocytes and the presence of blastic lymphoid cells in the red and white pulp, and hyperplasia of germinal centres of the lymphoid follicles. Those aspects were consistent with a depletion of the T-cell zone (periarteriolar lymphocyte sheath). Despite these common features, there were clear differences in the onset, intensity and evolution of the splenic cellular reaction and IgG serum levels and in the relationship between these levels and parasitaemia in the mice infected with the three strains of T. cruzi. A positive correlation was seen between high IgG levels and mortality, corresponding to intense exudative tissue lesions, showing that a raised immunoglobulin level was not associated with protection. It is worth observing that the 12 SF strain, which showed the lowest parasitaemic profile and mortality rate, stimulated the greatest elevation of IgG2b during acute infection; and also that IgG2a and IgG2b were the immunoglobulins which showed the greatest increases following infection by all three strains of T. cruzi.

Animals↗
PubMed1985

Evaluation of chemotherapy with benznidazole and nifurtimox in mice infected with Trypanosoma cruzi strains of different types.

A test was made of the susceptibility of 30 strains of Trypanosoma cruzi to chemotherapy with nifurtimox (Bay 2502) and benznidazole (Ro 7-1051). The strains had previously been classified as type I, II, or III according to their morphobiological and isoenzymic characteristics. Three type I strains, 14 type II strains, and 13 type III strains were studied. Mice were infected with 2 x 10(5) blood forms of these parasites and treated for 90 days with benznidazole or nifurtimox. All the surviving mice were submitted to parasitological tests (direct parasitaemia, xenodiagnosis, inoculation in new-born mice, and haemoculture) and serological tests (indirect immunofluorescence). As the latter remained positive in about 80% of the parasitologically negative animals, the cure rates were based on the more reliable parasitological tests. Type I strains displayed high susceptibility, type II strains showed medium to high susceptibility, and type III strains were highly resistant to both drugs. The fact that a particular strain type, with its own level of susceptibility, usually predominates in a given geographical area may explain the contradictory results after chemotherapy from different endemic areas.

Animals↗
PubMed1985

Patterns of resistance of inbred mice to Trypanosoma cruzi are determined by parasite strain.

Host response and parasite behavior of three different T. cruzi strains (I-Peruvian, II-21SF, III-Colombian) were investigated by evaluating the course of infection in six inbred strains of mice (A/J, AKR, C3H/He, BALB/c, C57BL/10, DBA/1). Resistance was evaluated in terms of the harmonic mean survival time and the infection was monitored by parasitemia, histopathology and immunological parameters (immunoglobulin subclass levels and antibody titers). All six mouse strains showed high susceptibility to the Peruvian strain (Type I). However, they displayed a different spectrum of susceptibility to Types II and III. Each T. cruzi strain maintained its basic features in the different mouse strains. Despite different maximum levels, the parasitemic curves were characteristic for each type of T. cruzi strain. There was a correlation between the degree of resistance of strains DBA and B10 and their high levels of IgG2a and IgG2b, as well as the presence of the H-2d haplotype, indicating that the genetic background of the mice is also important. The inflammatory process varied with each mouse strain and was correlated with the levels of IgG2a, with resistant mice showing predominance of neutrophilic infiltration with a rise in IgG2a. The susceptible strains responded with a mild inflammatory process with predominance of mononuclear cells. These data suggest that the parasite strain is the most important factor determining the resistance of the different mouse strains to infection with T. cruzi.

Animals↗
PubMed1983

Correlation between isoenzyme patterns and biological behaviour of different strains of Trypanosoma cruzi.

Three strains of Trypanosoma cruzi, used previously as prototypes for a classification based on the host-parasite relationships, as well as several stocks isolated from different geographical areas in Brazil, were submitted to isoenzymic analysis. Their isoenzyme patterns revealed a clear correlation with the biological data. The patterns obtained with the enzymes PGM, GPI, ASAT and ALAT permitted discrimination between each of the described types. Only one type was found in each geographical area studied, indicating a possible relationship between regional patterns and clinical presentation of Chagas' disease.

Alanine Transaminase↗
PubMed1978

Histopathology of the conducting tissue of the heart in Chagas' myocarditis.

The conducting tissue of the heart was studied in 25 human cases of Chagas' myocarditis with a method which employs complete serial sections mounted on continuous transparent plastic tape. The pathological changes were correlated with electrocardiographic findings. The inflammation of the acute phase of Chagas' myocarditis, as seen in one single case, did not seem to interfere with conduction through the AV system. In chronic Chagas' myocarditis the conducting tissue showed extensive and variable changes: chronic inflammation, fibrosis, atrophy and fragmentation of specific fibers, extreme dilatation and tortuosity of veins, capillaries and lymphatics, fatty infiltration, and arterial medial and intimal fibrosis. A preferential involvement of the right bundle branch and the anterior fascicles of the left branch was observed and an excellent correlation with electrocardiographic abnormalities was found. There was also evidence presented that bundle branch block may be caused by disease proximal to the bundle branches. Complete AV block seemed to be the final result of the progressive inflammatory and degenerative changes involving the conduction system in chronic Chagas' myocarditis. Inflammation and fibrosis did also involve the sinoatrial node, Purkinje fibers, intracardiac nervous ganglia, and the contractile myocardium.

Acute Disease↗