Shigellosis in Ethiopia: Review of studies conducted since 1974

No Abstract. Keywords: Antibiotic resistance; Ethiopia; Prevalence; Shingella Ethiop. J. Bio. Sci. Vol. 3 (2) 2004: pp. 191-23

Antimicrobial responses of Yersinia enterocolitica isolates in comparison to other commonly encountered bacteria that causes diarrhoea

Objective: To determine antimicrobial susceptibility and resistance of Yersinia enterocolitica, Shigella, E.coli and Salmonella isolated strains from diarrhoeal out-patients. Design: A cross-sectional study.Setting: Ethiopian Health and Nutrition Research Institute (EHNRI) in Addis Ababa Ethiopia. Subjects: Fifty one strains of enteric pathogenic bacterial isolates from 205 diarrhoeal out-patient cases. Results: All fifty one strains of enteric pathogenic bacterial isolates were sensitive to nalidixic acid, norfloxacin, and polymyxin B and 46 strains were resistant to cephalothin. Sensitivity to gentamycin, nalidixic acid, norfloxacin and polymyxin B is greater than 90% for the tested strains, while resistance to cephalothin, ampicillin and tetracycline was greater than 50%. All strains of Yersinia enterocolitica were sensitive to carbenicillin, chloramphenicol, gentamycin, kanamycin, nalidixic acid, norfloxacin, polymyxin B, streptomycin, sulphadiazene and trimethoprim-sulphamethoxazole. All strains of Yersinia enterocolitica were resistant to ampicillin. All of the 12 strains of Shigella were sensitive to nalidixic acid, norfloxacin, polymyxin B, gentamycin and kanamycin. Ampicillin, carbenicillin, cephalothin, streptomycin sulphadiazene, tetracycline and trimethoprimsulphamethoxazole were sensitive agains

Development of research capability in Ethiopia: the Ethio-Netherlands AIDS research project (ENARP): 1994-2002, achievements, scientific findings and project goals.

In 1992, HIV/AIDS researchers in Amsterdam, the Netherlands, were invited to work in partnership with researchers in Ethiopia to build an HIV/AIDS research infrastructure in Addis Ababa. This project, which began in 1994, was envisioned to contribute meaningfully to fighting the HIV pandemic in the decades to come. Its immediate objective was to establish an HIV research laboratory to serve international partnerships pursuing HIV vaccine research in Ethiopia and to support national health authorities fighting the HIV epidemic in Ethiopia. The overall goal was to develop research capacity at the Ethiopian Health and Nutrition Research Institute (EHNRI) by improving facilities, training technical and academic personnel (at PhD, MSc, and MPH level), establishing cohort studies to study HIV infection progression, and helping the government to implement a national HIV surveillance program. In the period 1994-2002, the projected HIV/AIDS research laboratory was built and several existing sections of EHNRI were renovated and upgraded. An active HIV-research program was established. Staff grew to more than 60, including three Ethiopian and three expatriate research/managers. Two PhD. students have graduated in immunology and virology (University of Amsterdam, 2000), and five are currently in training. Several technical persons were trained and over 19 MSc/MPH-programs were supported at Addis Ababa University (AAU). The first Ethiopian PhD graduate became the national program manager for ENARP. Two ENARP cohort studies and several HIV-prevalence studies have helped to document the severity of the HIV epidemic in Ethiopia, assisting national authorities in formulation of national and regional policies to prevent HIV transmission. Initial funding for ENARP from the Netherlands government was projected for eight years, to end by 2003. It was expected that management responsibilities would then be transferred from expatriate to Ethiopian staff and all ENARP activities integrated into EHNRI

Risk factors associated with failure of syndromic treatment of sexually transmitted diseases among women seeking primary care in Addis Ababa

Methods: Women with symptomatic STDs seeking care in a health centre were prospectively enrolled. A total of 259 women were interviewed and underwent clinical examination; 106 were enrolled and received syndromic STD treatment and 91% returned for follow up. Logistic regression analysis was used to identify risk factors associated with treatment failure. Results: Of the 106 women enrolled and presenting with symptomatic STDs 67% were HIV seropositive. Syndromic STD treatment did not result in clinical improvement in 30% of the women. Having genital ulcer disease, genital ulcer disease with genital discharge, genital warts, bacterial vaginosis and plasma HIV-1 load >10 000 copies RNA/ml or being HIV seropositive were all significantly associated with treatment failure. In multivariate analysis, however, only genital ulcer disease was significantly associated with treatment failure. Conclusion: In our setting, the association between HIV and genital ulcer disease caused by herpes may, therefore, be the reason for the failure of treatment

The impact of syndromic treatment of sexually transmitted diseases on genital shedding of HIV-1.

OBJECTIVES: To examine the impact of sexually transmitted diseases (STD) syndromic treatment on genital shedding of HIV and the impact among women in whom STD treatment was not successful. DESIGN: Seventy-one HIV-infected women were included; 60 had symptomatic STD [72% with genital discharge syndrome (GDS) and 28% with genital ulcer syndrome (GUS)] and 11 controls did not have symptomatic STD. Cervical HIV load in 94% women was measured at baseline and after STD treatment. RESULTS: Cervical HIV load at entry was significantly higher in women with symptomatic STD than in controls [median, 3.15; interquartile range (IQR), 1.90-3.34 versus median, 1.90; IQR, 1.90-2.19 log10 RNA copies/swab, respectively; P = 0.024]. Women with STD were also more likely to have detectable cervical HIV RNA (68% versus 27%; P = 0.016). Cervical HIV load was significantly higher in women with GUS than in those with GDS (median 3.46; IQR, 2.84-4.18 versus median, 2.83; IQR, 1.90-3.31 log10 copies/swab; P = 0.019). There was no significant reduction in genital HIV shedding after syndromic treatment of GDS or GUS. However, significant decreases were limited to only those with clinical improvement (median, 2.91; IQR, 1.90-3.45 versus median, 2.25; IQR, 1.90-3.08 log10 RNA copies/swab, respectively; P = 0.006). GUS was significantly associated with treatment failure, independent of plasma HIV RNA load and CD4 T-cell count (odds ratio, 4.79; 95% confidence interval, 1.32-17.46). CONCLUSIONS: The fact that STD syndromic treatment impacts very little in reducing genital HIV shedding underscores the need for appropriate validation of STD syndromic diagnosis and management to control heterosexual transmission of HIV