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1.
Sciences de la santé ; 1(2): 36-37, 2015.
Article in French | AIM (Africa) | ID: biblio-1271883

ABSTRACT

Objectifs : Au cours de ces dix dernieres annees; la resistance bacterienne aux antibiotiques; particulierement par production de ?-lactamases a spectre elargi (BLSE); est devenue un probleme majeur de sante publique. L'objectif de cette etude est de determiner la prevalence des souches de Klebsiella pneumoniae BLSE au CHNU Le Dantec; Dakar; Senegal. Methodes : Il s'agit d'une etude retrospective sur une periode de 12 mois portant sur 139 souches de K. pneumoniae. La detection des BLSE a ete effectuee par la methode de diffusion par double disque. Resultats : Parmi les 139 souches de K. pneumoniae etudiees; 44 (31;7) etaient productrices de BLSE. Trente trois (75) de ces 44 souches etaient d'origine nosocomiale (p = 0;016). Ces souches etaient surtout isolees chez les patients hospitalises dans les unites de soins intensifs (USI : 45;4 ; p = 0;031) et provenaient principalement de prelevements d'urines (59) et de pus (25). Toutes les souches de K. pneumoniae etaient resistantes a l'Amoxicilline; a la Piperacilline et a la Cefalotine. La majorite des souches de K. pneumoniae BLSE avait en outre une resistance a l'association sulfamethoxazole/trimethoprime (95;2); a la Gentamicine (78;6); a la Ciprofloxacine (67;4) et a l'Amikacine (41). Par contre; elles demeurent tres sensibles a l'Imipeneme et a la Fosfomycine. Conclusion : La resistance des enterobacteries; notamment K. pneumoniae; aux fluoroquinolones par production de BLSE devient de plus en plus preoccupante. Ceci suggere une utilisation plus rationnelle des fluoroquinolones; en particulier dans les traitements de premiere intension des infections du tractus urinaire


Subject(s)
Drug Resistance, Bacterial , Enterobacteriaceae Infections , Hospitals, University , Klebsiella pneumoniae
2.
Afr J Lab Med ; 2(1): 76, 2013.
Article in English | MEDLINE | ID: mdl-29043167

ABSTRACT

BACKGROUND: Tuberculosis (TB) has been shown to accelerate the clinical course of HIV infection, but the mechanisms by which this occurs are not well understood. Regulatory T-cells (Tregs) are known to dampen hyperactivation of the immune cells, but it remains unclear whether hyperactivation of T-cells in HIV infection is associated with a decrease of Tregs and what the effect Mycobacterium tuberculosis (MTB) co-infection has on T-cell activation and Tregs. OBJECTIVES: In this study, we aim to evaluate whether active TB is associated with the increased expression of T-cell activation markers and reduced number of Treg cells in HIV-1-infected patients. METHODS: This study was conducted on 69 subjects consisting of 20 HIV-infected patients, 20 HIV and MTB co-infected patients, 19 MTB-infected patients and 10 uninfected control subjects negative for both MTB and HIV. The frequencies of T-cell activation markers (CD38 and HLA-DR) and Treg cells (CD4+CD25+CD127-) were measured by flow cytometry. RESULTS: Significantly higher expression of CD38 and HLA-DR on CD4+ and CD8+ T-cells was found in MTB and HIV co-infected patients compared with HIV-infected patients. However, no significant difference in the percentage of Treg cells was reported between HIV patients with TB and those without. The study also showed a negative correlation between regulatory T-cells frequency and CD4+ T-cell counts. CONCLUSION: These results suggest that TB enhances the expression of peripheral T-cell activation markers during HIV infection, whilst having no impact on the percentages of Treg cells.

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