The changes of antifungal susceptibilities caused by the phenotypic switching of Candida species in 229 patients with vulvovaginal candidiasis.

OBJECTIVE: This study was to investigate the changes of antifungal susceptibilities caused by the phenotypic switching in patients with vulvovaginal candidiasis (VVC). METHODS: 229 women were enrolled in this study. The vaginal smears of these patients were collected and gram stained for fungal microscopic observation. The vaginal discharge of them in cotton swabs was cultured in sabouraud's agar with chloramphenicol medium. After fungal culture, fungal identification was analyzed using CHROM agar Candida chromogenic and identification medium. Then, the in vitro antifungal susceptibility testing was carried out using the standardized CLSI M27-A2 broth microdilution method. RESULTS: 64.63% of Candia species in patients with VVC were Candida albicans and the remainders were non-albicans Candida species. The phenotypic switching was observed in 91.22% of C. albicans infection. In antifungal susceptibility testing, the susceptible rates of C. albicans to voriconazole, fluconazole and itraconazole were significantly higher than that of non-albicans Candida species (P = 0.00, 0.00, 0.00). No matters in patients infected with C. albicans or with non-albicans Candida species, the susceptible rate to fluconazole of the clinical isolates with phenotypic switching was significantly higher than that without phenotypic switching (P = 0.01, 0.01). CONCLUSIONS: In the study, C. albicans was the commonest pathogenic species in patients with VVC, in which the phenotypic switching was easy to occur. The susceptible rates of C. albicans to all antifungal drugs were higher than that of non-albicans Candida species. The susceptible rate to fluconazole was all influenced by the phenotypic switching in C. albicans and non-albicans Candida species.

[Influence of chronic lead exposure in rats during the developmental stage on expression of leptin in plasma, cerebrospinal fluid, and hippocampus].

OBJECTIVE: To investigate the influence of lead exposure in rats during the developmental stage on the expression of leptin in plasma, cerebrospinal fluid, and hippocampus, as well as investigating whether leptin is associated with the mechanism of cognitive impairment induced by lead exposure. METHODS: The rat model of cognitive impairment after chronic lead exposure was established by adding lead acetate into drinking water. According to the concentration of lead acetate in drinking water, the rats were divided into control (0 ppm), low-lead (50 ppm), medium-lead (200 ppm), and high-lead groups (1 000 ppm), with 16 rats in each group. Atomic absorption spectrometry was used to measure the content of lead in the plasma, cerebrospinal fluid and hippocampus. ELISA was used to measure the level of leptin in the plasma and cerebrospinal fluid. Immunohistochemistry was used to observe the distribution of leptin protein in the hippocampus. Western blot was used for relative quantification of leptin proteins in the hippocampus. RESULTS: Compared with the control group, the lead exposure groups showed significant increases in the content of lead in blood, cerebrospinal fluid, and hippocampus (P<0.01), as well as significant reductions in the levels of leptin in plasma and cerebrospinal fluid (P<0.05). The results of immunohistochemical staining showed that leptin was mainly distributed in the cytoplasm of pyramidal neurons in the hippocampal CA region. The results of Western blot showed that compared with the control group, the three lead exposure groups showed a slight increase in the protein expression of leptin in the hippocampus (P>0.05). CONCLUSIONS: Lead exposure can reduce the levels of leptin in plasma and cerebrospinal fluid in rats, which may be associated with the mechanism of cognitive impairment induced by lead exposure.