Article Text
Abstract
Introduction/Background Shift in the vaginal microbiotafrom the predominant Lactobacillus spp. to the abundance of anaerobic bacteria is quite common among women of reproductive ages,approximately 40–80% of them report no complaints. However bacterial vaginosis (BV) is strongly associated with increased host susceptibility to STI (hrHPV included). Gardnerella Vaginalis (GV) might pave the way for STI causing epithelial cell (EC) damage and shedding, suppressing leukocyte recruitment, thereby leaving underlying mucosal tissue exposed to potential pathogens. Pushing regrowth of EC layers GV may make HPV-infected EC liable for persistent HPV dwelling there and than trigger viral DNA incorporation into host genome and launch neoplastic transformation. GV is a powerful biofilm-producer therefore BV often remains recalcitrant to treatment. Another input to recurrent BV can be made by host genetic variation in stress-related genes and smoking.The study examined the rate of BV among HPV-infected women with LSIL and HSIL (separately).
Methodology The study accrued 116 hrHPV-positive patients with newly recognized LSIL and HSIL who were split in two arms: LSIL (73 pts) and HSIL (43 pts). 50 HPV-negative women were taken as control group. Their vaginal swabs were assessed by Nugent score, neutrophil count, exfoliated EC/clue cell count, biofilm formation (48h-incubation).
Results It turned out that 41.9% HSIL-carriers were recognized with evident BV, 34.9% – with asymptomatic BV, whereas in among LSIL-carriers there were 24.7% and 28.8% respectively (control group: 23.1% and 30%). Furthermore HSIL vaginal swabs showed higher number of exfoliated EC (p<0.05) and GV growth (p<0.003), lower neutrophil count (p<0.001), and thicker biofilms than LSIL group.LSIL and control almost matched.
Conclusion BV, namely GV makes substantialnegative impact on female capacity to clear herself from HPV-infection raising the risk of persistent infection associated with HSIL.Therefore recognition of asymptomatic BV and its treatment is of high priority in order to prevent form HPV-related precancerous lesions.