Most cases of PID are presumed to originate with sexually transmitted disease (STD) of the lower genital tract followed by ascending infection of the upper tract. The original STD may not be symptomatic. It is estimated that 10 to 20 percent of untreated gonococcal or chlamydial cervicitis may progress to PID. The precise mechanisms by which infection in the upper genital tract is initiated and propagated remain unclear. The female genital tract is an open system; therefore a vehicle to transport potential pathogens is unnecessary. Although the cervical mucus serves as a functional barrier to ascending infection much of the time, its efficacy may be decreased by hormonal changes during ovulation and by retrograde menstruation. Bacteria may also be carried by or along with sperm into the uterus and tubes. Uterine infection is usually limited to the endometrium but may be more invasive in a gravid or post-partum uterus. Initial gonorrheal adherence is to non-ciliated cells, but it is felt that surface components of the organism affect neighboring ciliated cells. Tubal infection initially affects only the mucosa, but acute, complement-mediated transmural inflammation may develop rapidly. Inflammation may extend to uninfected parametrial structures including the bowel. If purulent material from the tubes spills into the abdomen, frank pelvic peritonitis may result. Infection may extend via direct or lymphatic spread beyond the pelvis to involve the hepatic capsule with acute perihepatitis and focal peritonitis (Fitzhugh-Curtis syndrome).
Risk factors for PID within a sexually active population include multiple sexual partners, history of other STDs, substance abuse, and frequent vaginal douching. Younger age is associated with increased risk, possibly because of a larger zone of cervical ectopy in young women, increased cervical mucosal permeability, lower prevalence of protective chlamydial antibodies, risk-taking behavior, or a combination of these factors. 4 Barrier contraception is associated with lower risk of PID. IUD use is associated with a 2 to 9 fold increased risk for PID, with the highest risk in the first four months after insertion. 56 Oral contraceptive pills (OCPs) increase the risk of endocervical infection, probably by increasing the zone of cervical ectopy. However, OCPs decrease the risk of symptomatic PID, possibly by increasing the viscosity of cervical mucus, decreasing menstrual blood flow (and hence decreasing retrograde menstruation), or modifying local immune responses. 7 Bilateral tubal ligation (BTL) does not provide protection from PID, but patients with BTL may have a clinically milder form of the disease. 8 Bacterial vaginosis (BV) is associated with an increased risk of PID, and BV organisms are frequently cultured from upper genital tract specimens in PID. Pregnancy decreases the risk of PID as the cervical os is protected by a mucous "plug." However, PID can occur during the first trimester and may cause fetal loss.
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