First detection of mutated ERG11 gene in vulvovaginal Candida albicans isolates at Ouagadougou/Burkina Faso.

BACKGROUND: Vulvovaginal candidiasis is an important cause of morbidity among women due to Candida species. In the last decades, resistance to azoles, first-line antifungals has increased. One molecular mechanism of azole resistance by Candida involves mutations in the ERG11 gene encoding lanosterol 14-α-demethylase, the target enzyme. This study was conducted to identify the clinical Candida species associated in vulvovaginal candidiasis; to determine the rate of antifungal resistance among Candida albicans isolates and to determine mutated ERG11 gene at Saint Camille Hospital in Ouagadougou, Burkina Faso. METHODS: Antifungals susceptibility were performed using Kirby-Bauer disk diffusion method. ERG11 gene was detected using conventional PCR in C. albicans isolates resistant to at least one azole. RESULTS: Out of 262 clinical strains isolated, C. albicans accounted for 59.90%, followed by Candida glabrata 27.86%, Candida famata 7.25%, Candida tropicalis 3.05% and Saccharomyces cerevisiae 1.91%. Resistance rate of fluconazole to C. albicans was 59.54%. ERG11 gene was found in 9.79% of 92 C. albicans strains resistant to azoles. CONCLUSIONS: This detection of mutated ERG11 gene in C. albicans is the first in Burkina Faso and may be a cause of azole resistance in recurrent Candida vulvovaginitis.

Carriage of mutations R462Q (rs 486907) and D541E (rs 627928) of the RNASEL gene and risk factors in patients with prostate cancer in Burkina Faso.

BACKGROUND: Prostate cancer (Pca) is a public health problem that affects men, usually of middle age or older. It is the second most common cancer diagnosed in men and the fifth leading cause of death. The RNASEL gene located in 1q25 and identified as a susceptibility gene to hereditary prostate cancer, has never been studied in relation to prostate cancer in Burkina Faso. The aim of this study was to analyze the carriage of RNASEL R462Q and D541E mutations and risks factors in patients with prostate cancer in the Burkina Faso. METHODS: This case-control study included of 38 histologically diagnosed prostate cancer cases and 53 controls (cases without prostate abnormalities). Real-time PCR genotyping of R462Q and D541E variants using the TaqMan® allelic discrimination technique was used. Correlations between different genotypes and combined genotypes were investigated. RESULTS: The R462Q variant was present in 5.3% of cases and 7.5% of controls. The D541E variant was present in 50.0% of cases and 35% of controls. There is no association between R462Q variants (OR = 0.60; 95%IC, 0.10-3.51; p = 0.686) and D541E variants (OR = 2.46; 95%IC, 0.78-7.80; p = 0.121) and genotypes combined with prostate cancer. However, there is a statistically significant difference in the distribution of cases according to the PSA rate at diagnosis (p ˂ 0.001). For the Gleason score distribution, only 13.2% of cases have a Gleason score greater than 7. There is a statistically significant difference in the Gleason score distribution of cases (p ˂ 0.001). CONCLUSIONS: These variants, considered in isolation or in combination, are not associated with the risk of prostate cancer.

Carriage of Ser217Leu and Ala541Thr Variants of ELAC2 Gene and Risk Factors in Patients with Prostate Cancer in Burkina Faso.

Background: Genetic factors are one of the significant contributors to prostate cancer (PCa) development, and hereditary prostate cancer 2 (HPC2) locus gene ELAC2 is considered a PCa susceptibility region. The HPC2/ELAC2 gene has been identified by linkage analysis in familial prostate cancer patients in the United States but has never been studied in Burkina Faso. The objective of the present study was to analyze the carriage of the C650T (Ser217Leu) and G1621A (Ala541Thr) mutations of the ELAC2 gene and the risk factors in prostate cancer patients in Burkina Faso. Methods: This case-control study included 76 participants, including 38 histologically confirmed prostate cancer cases and 38 healthy controls without prostate abnormalities. PCR combined with restriction fragment length polymorphism (RFLP) was used to characterize the genotypes of the Ser217Leu and Ala541Thr polymorphisms of the ELAC2 gene. The correlations between the different genotypes and risk factors for prostate cancer were investigated. Results: The C650T mutation was present in 44.73% of prostate cancer cases and 47.37% of controls. The G1621A mutation was present in 26.32% of prostate cancer cases and 15.79% of controls. We did not detect an association between prostate cancer risk and the Ser217Leu (p=0.972) and Ala541Thr (p=0.267) variants of the ELAC2 gene. Also, the two ELAC2 SNPs did not correlate with clinical stage, prostate-specific antigen (PSA) level at diagnosis, or the Gleason score on biopsies. However, we found that 100% of homozygous carriers of the T650 mutation have an A1621 mutation (p ≤ 0.001). Conclusion: Ser217Leu and Ala541Thr polymorphisms of ELAC2, considered alone or in combination, are not associated with prostate cancer risk.

Molecular Epidemiology of Human Papillomaviruses, Neisseria gonorrhoeae, Chlamydia trachomatis and Mycoplasma genitalium among Female Sex Workers in Burkina Faso: Prevalence, Coinfections and Drug Resistance Genes.

Viral and bacterial infections represent an occupational risk for female sex workers. This study aimed at determining HPV coinfection with genital pathogens among female sex workers in West and Central Africa and identifying antibiotic resistance genes. A total of 182 samples from female sex workers were analyzed by real-time PCR and classic PCR. For the molecular diagnosis of HPV, the real-time multiplex amplification kit "HPV Genotypes 14 Real-TM Quant" from SACACE Biotechnologies®, detecting 14 high-risk HPV genotypes, was used, while for other pathogens, the real-time multiplex amplification kit N. gonorrhoeae/C. trachomatis/M. genitalium/T. vaginalis Real-TM, allowing their simultaneous detection, was used. The women were aged 17-50 years with an average age of 27.12 ± 6.09 years. The pathogens identified were HPV 54.94% (100/120), Neisseria gonorrhoeae (13.74%), Chlamydia trachomatis (11.54%) and Mycoplasma genitalium (11.54%). The most common HPV genotypes were HPV68, HPV38 and HPV52. The antibiotic resistance genes identified were bla QNR B 24.00%, bla GES 22.00%, bla SHV 17.00%, blaCTX-M 13.00% and bla QNR S 1.00%. This study revealed the presence of various HPV genotypes associated with other pathogens with problems of antibiotic resistance among sex workers of West and Central African origin working in Ouagadougou.

Glutathione S-transferase M1 (GSTM1) and T1 (GSTT1) variants and breast cancer risk in Burkina Faso.

Background and objective Breast cancer remains the most common cause of cancer mortality in women. The aim of this study was to investigate associations between genetic variability in GSTM1 and GSTT1 and susceptibility to breast cancer. Methods Genomic DNA was extracted from blood samples for 80 cases of histologically diagnosed breast cancer and 100 control subjects. Genotyping analyses were performed by PCR-based methods. Associations between specific genotypes and the development of breast cancer were examined using logistic regression to calculate odds ratios [1] and 95% confidence intervals (95%CI). Results No correlation was found between GSTM1-null and breast cancer (OR = 1.83; 95%CI 0.90-3.71; p = 0.10), while GSTT1-null (OR = 2.42; 95%CI 1.17-5.02; p= 0.01) was associated with increased breast cancer risk. The GSTM1/GSTT1 double null was not associated with an increased risk of developing breast cancer (OR = 2.52; 95%CI 0.75-8.45; p = 0.20). Furthermore, analysis found no association between GSTM1-null (OR =1.12; 95%CI 0.08-15.50; p = 1.00) or GSTT1-null (OR = 1.71; 95%CI 0.13-22.51; p = 1.00) and the disease stage of familial breast cancer patients or sporadic breast cancer patients (GSTM1 (OR = 0.40; 95%CI 0.12-1.32; p = 0.20) and GSTT1 (OR = 1.41; 95%CI 0.39-5.12; p = 0.75)). Also, body mass index (BMI) was not associated with increased or decreased breast cancer risk in either GSTM1-null (OR = 0.60; 95%CI 0.21-1.68; p = 0.44) or GSTT1-null (OR = 0.60; 95%CI 0.21-1.68; p =0.45). Conclusion Our results suggest that only GSTT1-null is associated with increased susceptibility to breast cancer development.