Pathophysiology of Pelvic Inflammatory Disease
Primary Mechanism of Infection
PID results from direct canalicular (ascending) spread of organisms from the endocervix to the endometrium and fallopian tube mucosa 1
Noncanalicular spread via parametrial lymphatics has also been observed, though less commonly 1
Initial Infection Site
Both N. gonorrhoeae and C. trachomatis commonly cause endocervicitis as the initial infection 1
10-40% of women with untreated gonococcal or chlamydial cervicitis develop clinical symptoms of acute PID 1, 2
Even higher percentages of ascending infection are detected when endometrial biopsies are used to diagnose subclinical endometritis 1
Microbial Etiology
Most cases of PID are polymicrobial, involving multiple organisms simultaneously 1, 3, 2
C. trachomatis recovered from cervix in 5-39% of women with PID 1, 3, 2
N. gonorrhoeae isolated from cervix in 27-80% of women with PID 1, 3, 2
Anaerobic bacteria (Bacteroides, Peptostreptococcus, Peptococcus species) isolated from upper genital tract in 25-50% of acute PID cases 1
Aerobic/facultative bacteria (Gardnerella vaginalis, Streptococcus species, E. coli, H. influenzae) also commonly involved 1
Bacterial vaginosis serves as an antecedent to lower genital tract infection leading to polymicrobial acute PID 1, 2
Contributing Factors to Bacterial Ascent
Uterine instrumentation (e.g., IUD insertion) facilitates upward spread of vaginal and cervical bacteria 1, 2
Hormonal changes during menses and menstruation itself cause cervical alterations resulting in loss of mechanical barrier preventing ascent 1, 2
Bacteriostatic effect of cervical mucus is lowest at onset of menses 1
Retrograde menstruation may favor ascent to tubes and peritoneum 1, 2
Individual organisms possess virulence factors associated with pathogenesis of acute chlamydial and gonococcal PID 1, 2
Immune Evasion and Inflammatory Response
Both N. gonorrhoeae and C. trachomatis survive within host epithelial cells and neutrophils, requiring T-cell-mediated interferon-γ production for protection 4
Activation of myeloid cell, cell death, and innate inflammatory pathways occurs in conjunction with dampening of T-cell activation pathways in women with histologic endometritis 4
Both pathogens exert multiple immune evasion mechanisms that benefit themselves and each other at the host's expense 4