Several studies on vulvovaginal candidiasis have shown that C. albicans is the commonest species isolated. In our study, out of 262 Candida clinical isolates, C. albicans remains to be the most common species at 59.90% followed by Candida glabrata 27.86%. This results are similited to Zida et al. study who obtained a prevalence of 59.36% of C. albicans  and also Kouadio-Yapo et al., a high prevalence of 64.8% in Ivory Coast .
In our study, younger women, between 11 and 24 years had a lower prevalence 35.1% of vulvovaginal candidiasis, while the prevalence was 47.8% in the 25–35 age group. In every age group, C. albicans has the highest prevalence: 57.29% in 11–24 years; 62.0 in 25–35 years and 60.01% in over 35 years which are statistically signifiant. It is similar to Chuku et al study with a prevalence rates of 52.03% recorded among women who were within the age group of 21–30 years . It is in concordance with the findings of Nadembega et al. who reported a prevalence rates of 59% of C. albicans in a study of vaginal infections in women aged 15–24 in Ouagadougou . This may be due to many risks factors such as hormonal influences, predominant nutritional types or sexual activities. The high prevalence of C. albicans isolates may be due to its ability of adaptation to the human being which constitutes its main reservoir and its virulence factors such as colonization of human tissues, biofilm formation, hyphae formation as reported by Gonçalves et al. .
Sangaré et al., in their study on Candida species isolated from pregnant women in Burkina Faso, a prevalence rate of 40.39% for C. albicans and a rate of 59.61% for NCA with C. glabrata (32.69%) followed by Candida tropicalis (C. tropicalis) (15.38%) and Candida krusei (C. krusei) (11.54%) . We did not isolate C. krusei in our study. In China, a study conducted by Xiang et al. showed that C. albicans isolates were 50% followed by 18% C. glabrata, 17% C. parapsilosis, 11% C. tropicalis and 2% C. krusei . Similar studies have shown that the prevalence rates of other species are variable from one study population to another, from one region to another but C. glabrata is the most isolated on the non-C. albicans species [18,19,20,21]. This may be attributed to the ability of C. glabrata to adapt and survive in macrophages as an immune evasion strategy. The incidence of non-C. albicans species such as C. glabrata, C. tropicalis, C. parapsilosis… has increased probably due to the use of narrow-spectrum antifungals only act on C. albicans [19, 22].
We isolated S. cerevisiae at 1.91%. This is extremely rare. In South America, Papaemmanouil et al. study obtained a rate prevalence of 2.17% on recurrent vaginal candidiasis in sexually active adult women ; in Asia, Guo et al. obtained similar prevalence rate of 2.3% in their study on Candida involved in vaginitis and their susceptibility tests to antifungals . This could also be one of the causal agents of recurrent CVV.
In our study, results of the antifongigram are similarly to those of Zida et al., in 2017 where Fluconazole was resistant at 66.5% and Nystatin very active on C. albicans at 94.7% (p < 0.05). Kouadio-Yapo et al. in 2017, obtained resistance rate of 39.7% for Itraconazole and a rate of 26.3% for Fluconazole (p < 0.05) at Pasteur Institute of Ivory Coast. This difference can be explained by the fact that Fluconazole is the widely used molecule among azoles. In recent years, many studies have shown resistance of C. albicans and NCA to azoles specifically to Fluconazole . In the United States, a study on the resistance of Candida to azoles in vaginal infections have shown 11% in C. glabrata (p < 0.05) . In our study, we obtained co-resistance in C. albicans isolates, a prevalence rate of 25% of co-resistance to Clotrimazole–Miconazole and 19.56% of co-resistance to Clotrimazole–Fluconazole–Miconazole. Our results differ from those of Das et al. and Farhan et al., who obtained respectively co-resistance for Fluconazole–Ketoconazole and for Clotrimazole–Ketoconazole [27, 28]. In our study, 25.5% of strains of C. albicans were resistant to Ketoconazole. All this testify the global distribution of resistance to azoles and the very great variability of their prevalence according to country, biological samples and species; and therefore, a global public health problem.
In our study, the ERG11 gene was detected in C. albicans isolates resistant to azoles. In Nigeria, similar studies were carried out showing the presence of the ERG11 gene at 11.18% in strains of Candida resistant to Fluconazole isolated from vulvovaginitis (p > 0.05) and 88.89% in C. albicans strains all resistant to the azoles Fluconazole and Voriconazole isolated only in pregnant women . In China, studies on ERG11 gene mutations in C. albicans isolated in vulvovaginitis (p < 0.05) showed a prevalence of the detected gene of 8.4%  and 12.2% ; which is similar to ours. In United States, White et al. obtained a prevalence of 10.52% of the ERG11 gene by sequencing in their study on the molecular mechanisms of resistance of C. albicans to azoles . Our results can be explained by the fact that there are other mechanisms of azoles resistance which are not yet explore in our country.
Because of the toxicity of others antifungal drugs and the multiples Candida Drugs Resistant, there is a need for new antifungal agents for the efficient management of C. albicans infections . Natural drugs, microbial natural products from plants have shown their efficiency on Candida strains. Their antifungal mechanisms are: interaction with ergosterol, inhibition of the synthesis of cell wall components, inhibition of sphingolipid synthesis and inhibition of protein synthesis. Natural products from plants mostly exert their antifungal effects by membrane-active mechanism .
Our study was limited to find relationship between Candida burden with/without ERG11 mutation and comorbidities/factors because of the lack of patients informations. Due to the non-availability of sequencing in our environment, the specify mutations in ERG11 gene were not determine (Additional file 1).