PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Trypanosomiasis, African”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1992

Study of evoked potentials in human African trypanosomiasis.

Human African trypanosomiasis or sleeping sickness has a stage of neurological involvement characterized by the onset of diffuse meningoencephalitis with sleep disturbances and decreased wakefulness. The pathogenesis of this disease is not well understood. We studied auditory, visual, sensory, and motor evoked potentials in 16 patients with trypanosomiasis in the early stage of meningoencephalitis. In all patients, the brain-stem auditory evoked response (BAER) and the pattern-reversal visual evoked response (PVER) were normal. On the other hand, abnormalities of the somatosensory evoked response (SSER) or the motor evoked response (MER) were found in only five cases; however, their relationship to the illness could not be definitely confirmed. The study results indicate that the evaluated pathways were essentially intact, in particular at the level of the brain-stem in the early stage of the disease. Sleep disturbances and decreased wakefulness noted at this stage were thus linked more closely to functional involvement at the level of the sleep centres than to any detectable specific anatomic lesion.

Adolescent↗
PubMed1977

An improved parasitological technique for the diagnosis of African trypanosomiasis.

Light microscopic examination of the buffy coat zone of a microhaematocrit capillary tube expressed on to a slide was found to be consistently more reliable than other standard techniques in detecting trypanosomes in the circulation of cattle. This method alaos allowed identification of different trypanosome species. Optimal results were obtained using darkground illumination.

Animals↗
PubMed1979

The complement fixation test and African trypanosomiasis: I. Experimental infection and re-infection in cattle before and after treatment.

The complement fixation test was applied to assess antibody responses in cattle infected with T. brucei, T. congolense, and T. vivax which had been treated and re-infected. After the first infection, the specificity of the results was low in T. congolense, fair in T. brucei, and high in T. vivax infected animals. After re-infection with the same trypanosoma species as used for previous infections, the specificity of CF results was high in all cases. After a foregoing T. vivax infection, specific titres of T. congolense and to a lesser degree of T. brucei infections were frequently masked by residual T. vivax titres. After treatment of trypanosoma-infected cattle the fasted drop of CF antibody titres occurred in T. congolense cases, followed by T. brucei infections. T. vivax titres persisted over prolonged periods.

Animals↗
PubMed1977

Free fatty acids, complement activation, and polyclonal B-cell stimulation as factors in the immunopathogenesis of African trypanosomiasis.

Human and animal forms of African trypanosomiasis are characterised by sustained hypocomplementaemia, gross hypergammaglobulinaemia M, and profound immunosuppression. It is suggested that this hypocomplementaemia is probably due to the action of a trypanosome-derived complement-activating factor and that the elevated IgM levels may be the combined result of this decomplementation, together with a subsequent failure of the normal IgM-to-IgG antibody switch mechanism and polyclonal B-lymphocyte activation by a trypanosome-generated mitogen. The immunosuppression in this disease may be a result of the collective immunosuppressive effects of trypanosome-derived immune-modulating free fatty acids, polyclonally stimulating B-cell mitogen, and complement-activating factors.

Animals↗
PubMed1992

Subcurative chemotherapy and fatal post-treatment reactive encephalopathies in African trypanosomiasis.

The treatment of late-stage African sleeping sickness in man is often complicated by a post-treatment reactive encephalopathy. The bases of this pathological reaction was investigated in a mouse model of African trypanosomiasis. Subcurative treatment with diminazene aceturate, which did not clear parasites from the central nervous system, resulted in a post-treatment meningoencephalitis similar to that seen in man. By contrast, a curative regimen of melaminylthioarsenite and 5-nitroimidazole, which cleared parasites from the central nervous system, did not cause any pathological reaction in the mice. This result indicates that subcurative treatment leads to the development of the post-treatment encephalopathy. Evidence that this may also be the case in man was provided by the detection of trypanosome DNA with the polymerase chain reaction in the brains of 9 patients who had died as the result of a post-treatment reaction. Our findings suggest that more aggressive treatment regimens, which ensure the elimination of trypanosomes from the central nervous system, may prevent post-treatment reactions in patients.

Adolescent↗
PubMed1977

Pathological aspects of human African trypanosomiasis (HAT) in Uganda. A post-mortem survey of fourteen cases.

The pathological features of 14 cases of human African trypanosomiasis (HAT) occurring in Uganda over an 8 year period are described. Three cases were clinically proven and in all 14 cases a chronic meningoencephalitis was found. In 2 cases there was histological evidence of ganglion radiculitis and in one of these chronic choroiditis and peripheral neuritis associated with chronic myositis were present. The cardiac lesions consisted of a chronic pancarditis of varying degree in 8 cases and in 3 a generalized valvulitis was observed. In 2 cases, specially investigated, generalized lesions of the conducting system were noticed. Previous histopathological descriptions of HAT are briefly reviewed. The present findings are compared with some of those recorded in human american trypanosomiasis and experimental African trypanosomiasis.

Adolescent↗
PubMed1978

The role of the host immune response in the development of tissue lesions associated with African trypanosomiasis in mice.

A variety of tissue lesions occurs in African trypanosomiasis, in the pathogenesis of which direct toxic effects of the parasite as well as immunological mechanisms may be involved. The purpose of the present study was to evaluate the role of the host immune response in inducing tissue damage in this disease and particularly in the production of lesions in striated muscle. The development of muscle lesions in T. brucei infection was studied in several groups of mice with different forms of immunodeficiency, as well as in normal mice. In the normal mice, foci of intense inflammation and necrosis were found in the cardiac and skeletal muscles 2 weeks or more after infection. In these lesions, there was a heavy deposition of IgG and IgM, and of trypanosomal antigens. In irradiated, newborn mice, and athymic nude mice infected with T. brucei, these inflammatory lesions were not found, although large numbers of trypanosomes were present between the muscle fibres. The characteristic lesions could be induced in athymic nude mice by transfer of normal spleen cells or of normal T lymphocytes 1 week after the onset of infection. The lesions were also partly induced by transfer of antibody to T. brucei. No antibodies to tissue components, particularly to cardiac myofibrils, were found in any of the infected mice. The results of this study show that immunodeficiency suppresses the development of the characteristic muscle lesions of African trypanosomiasis. The relative importance of humoral and cellular immune mechanisms in the pathogenesis of these lesions is not year clear.

Animals↗
PubMed1978

Growth of infective forms of Trypanosoma rhodesiense in vitro, the causative agent of African trypanosomiasis.

A new approach to the culture of African trypanosomes led to the growth of the infective forms of the causative agent of human African trypanosomiasis. Infective cultures of Trypanosoma rhodesiense were initiated and maintained in vitro on Chinese hamster lung cells. By changing daily one-third of the Hepes-buffered RPMI 1640 medium containing 20 percent fetal bovine serum, the trypanosome numbers increased to 3 X 10(6) to 5 X 10(6) cells per milliliter. After 80 days in vitro at 37 degrees C, the cultured trypomastigotes are infective for mice and rats and morphologically similar to bloodstream trypomastigotes in having a subterminal kinetoplast and a surface coat. In addition, they possess L-alpha-glycerophosphate oxidase, the predominant steady-state terminal oxidase of bloodstream trypomastigotes.

Animals↗
PubMed1992

Human African trypanosomiasis: presence of antibodies to galactocerebrosides.

Improvements were made in the immunodetection of anti-galactocerebroside (anti-GalC) antibody in sera of patients with human African trypanosomiasis by thin-layer chromatography, enzyme-linked immunosorbent assay, and immunoadsorption. Rabbit anti-GalC antibodies were used to standardize these techniques and demonstrate their specificity. Anti-GalC antibodies were found in the sera of 42.8% of 63 patients with human African trypanosomiasis. Thirty-four control subjects living in the same endemic area were also tested. Anti-GalC levels were higher in human African trypanosomiasis patients with neurologic disturbances compared with patients without such disturbances. These antibodies were distributed mainly between the IgG and IgM classes, but 28% of the patients with human African trypanosomiasis had increased IgA levels without anti-GalC antibody activity.

Agglutination Tests↗
PubMed1976

Pancarditis affecting the conducting system and all valves in human African trypanosomiasis.

This paper describes the pathological features of 10 cases of human African trypanosomiasis occurring in Uganda over an 8-year period. Three cases were clinically proved, and in all 10 cases chronic meningoencephalitis and myocarditis were present. There was chronic pancarditis in 6 cases, and in 3 of these there was a generalized focal valvulitis and in 2 lesions of the conducting system. Previous descriptions of carditis in human African trypanosomiasis are briefly reviewed, and the present findings are compared with some cardiomyopathies as well as American human and experimental trypanosomiasis.

Adolescent↗
PubMed1977

Application of the enzyme-linked immunosorbent assay (ELISA) for the serodiagnosis of human African trypanosomiasis (sleeping sickness).

An enzyme-linked immunosorbent assay (ELISA) for the serodiagnosis of human African trypanosomiasis (sleeping sickness) is described. A crude extract of a Trypanosoma brucei suspension which was purified from all blood components was used as antigen. In rabbits experimentally infected with T. brucei or T. rhodesiense both homologous (anti-T. brucei) and heterologous (anti-T. rhodesiense) Trypanosoma antibodies could be detected with ELISA using T. brucei as antigen. The sensitivity of ELISA was comparable with that of the immunofluorescence (IF) technique. Sera of patients with sleeping sickness were examined with ELISA and IF. It proved possible to discriminate between groups of individuals with and without trypanosomiasis. Cross reactions were only observed with serum from a patient in which antibodies to Leishmania were detected. No cross reactions were observed in sera from patients with malaria, toxoplasmosis, schistosomiasis, or echinococcosis. ELISA represents a good alternative to IF in the serology of African trypanosomiasis, and may be particularly suitable for mass screening purposes.

Animals↗
PubMedDate not supplied

[An ELISA technic for the diagnosis of human African trypanosomiasis].

The authors studied several factor influencing the serodiagnosis of human african trypanosomiasis using the microplate enzyme immunoassay ("micro E.L.I.S.A."). They used an antigenic extract obtained by sonic disruption of purified suspensions of trypanosomes of a Trypanosoma brucei brucei strain. the conjugate was a peroxidase-conjugate anti-human immunoglobulin and the chromogen was orthodianisidine. Spectrophotometric reading was used. Although this method may have some advantaged, its specificity needs further study because of few false positive and negative reactions. Moreover its reproducibility as quantitative reaction has proved to be delicate.

Antibody Specificity↗