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EP338 Cervical cancer and vaginal flora changes
  1. S Kovachev
  1. Gynecology, Military Institute of Medicine, Sofia, Bulgaria

Abstract

Introduction/Background Microbial changes in vaginal ecosystem may accelerate the process of cervical carcinogenesis. The developed cervical cancer can lead to changes in the vaginal flora. The aim of our study is to determine the vaginal flora changes at women with cervical cancer.

Methodology We conducted an open, single-site survey in the Department of gynecology of the Military Medical Academy in Sofia, Bulgaria, from 2013 to 2018 year. The study included a total of 32 women aged 38–55 years with clinical and pathology established cervical cancer (FIGO I stage). The underlying clinical and microbiological studies indicated presence or absence of bacterial vaginosis, other vaginal infections or normal vaginal flora.

Results Of 32 (100%) women enrolled in our study, 19 (59.4%) was with FIGO IA stage cervical cancer and 13 (40.6%) with IB stage. Disturbances of vaginal flora in we found at 23 (71.9%) of women with cancer cancer included in our study. At the rest of 9 (28.1%) women we found out normal vaginal flora. Bacterial vaginosis was determined clinically and microbiologically in 15 (46.9%) women enrolled in the study. Aerobic vaginitis caused by Group B Streptococcus we establish at 4 (12.5%) of women: (Enterococcus faecalis -3/9.4%; Escherichia coli - 1/3.1%). Trichomonas vaginalis infection have 1 (3.1%) women and Candida Albicans the last one 1 (3.1%) from this group with disturbed vaginal microbial balance.

Conclusion Bacterial dysbiosis, characterized by a predominance of Gardnerella vaginalis alone or in complex with other anaerobic bacteria, aerobic vaginitis and other sexually transmitted vaginal pathogens from one side and a concomitant paucity of vaginal Lactobacillus species may be an HPV-dependent cofactor for cervical neoplasia development. Only with this single observation it is difficult to confirm that microbiota dysbiosis contributes to HPV infection and carcinogenesis.

Disclosure Authors declare no conflict of interest. This is an author’s own work.

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