Pathophysiology

Infection begins in the cervix and, if untreated, may ascend to the upper genital tract. Epithelial damage,
usually caused by N gonorrhoea and C trachomatis may allow opportunistic entry of other micro-
organisms. [5] Spread to the upper genital tract can also be caused by instrumentation of the cervix such as
D&C, termination of pregnancy or insertion of an IUD. [5]Infection is thought to be caused by disruption of
the protective cervical barrier and direct introduction of bacteria into the endometrial cavity from the vagina
or cervix. [6]

Abstract
The pathophysiology of pelvic inflammatory disease (PID) involves an ascending infection of cervicovaginal
microorganisms, of which the most important pathogens are Neisseria gonorrhoeae and Chlamydia
trachomatis. The clinician should recognize that not all women with PID will present with abdominal pain and
that associated atypical symptoms such as meteorrhagia and dyspareunia should suggest diagnosis. The
documentation of lower genital tract inflammation is helpful in making the diagnosis of PID. Treatment with
broad spectrum antibiotic regimens is currently recommended. Prevention of sexually transmitted diseases
and ascending infection remains of utmost importance to decrease the sequelae, such as tubal factor
infertility and ectopic pregnancy associated with PID.

Pathophysiology
Pelvic inflammatory disease (PID) most commonly occurs as a result of Chlamydia
trachomatis or Neisseria gonorrhoeae infection of the cervix or vagina that then spreads into the
endometrium, fallopian tubes, ovaries, and adjacent structures. Less commonly, direct spread
from a nearby infection such as appendicitis or diverticulitismay occur. Hematogenous infection is
a rare cause of PID except in cases of tuberculous PID.10

Definition
Pelvic inflammatory disease is a general term for infection of the uterus lining, fallopian tubes,
or ovaries.
See also: Endometritis
Alternative Names
PID; Oophoritis; Salpingitis; Salpingo-oophoritis; Salpingo-peritonitis
Causes, Incidence, And Risk Factors
Most cases of pelvic inflammatory disease are caused by bacteria that move from the vagina
or cervix into the uterus, fallopian tubes, ovaries, or pelvis.
The most common cause of PID is sexual contact without using a condom or other protection.
This is called a sexually transmitted disease (STD). Chlamydia and gonorrhea are the two
bacteria that cause most cases of PID.
However, bacteria may also enter the body during some surgical or office procedures, such as:
• Childbirth
• Endometrial biopsy
• Insertion of an intrauterine device (IUD)
• Miscarriage
• Therapeutic or elective abortion
In the United States, nearly 1 million women develop PID each year. About 1 in 8 sexually active
adolescent girls will develop PID before age 20.
Risk factors include:
• Male sexual partner with gonorrhea or chlamydia
 • Multiple sexual partners
• Past history of any sexually transmitted disease
• Past history of PID
• Recent insertion of an IUD
• Sexual activity during adolescence
Symptoms
The most common symptoms of PID include:
• Fever (not always present; may come and go)
• Pain or tenderness in the pelvis, lower abdomen, or sometimes the lower back
• Vaginal discharge with abnormal color, texture, or smell
Other symptoms that may occur with PID:
• Bleeding after intercourse
• Chills
• Fatigue
• Frequent or painful urination
• Increased menstrual cramping
• Irregular menstrual bleeding or spotting
• Lack of appetite
• Nausea, with or without vomiting
• No menstruation
• Painful sexual intercourse
Note: There may be no symptoms. People who experience an ectopic
pregnancy or infertility often have had silent PID, which is usually caused
by chlamydia infection.
Signs And Tests
You may have a fever and abdominal tenderness. A pelvic examination may show:
• A cervix that bleeds easily
• Cervical discharge
• Pain with movement of the cervix
• Tenderness in the uterus or ovaries
Lab tests that look for signs of infection are:
• C-reactive protein (CRP)
• Erythrocyte sedimentation rate (ESR)
• WBC count
Other tests include:
• Culture of your vagina or cervix to look for gonorrhea, chlamydia, or other causes of PID
• Pelvic ultrasound or CT scan to look for other causes of your symptoms, such
as appendicitis or pregnancy, and to look for abscesses or pockets of infection around
the tubes and ovaries
• Serum HCG (pregnancy test)

Read more: http://www.righthealth.com/topic/Pelvic_Inflammatory_Diseases/overview/adam20?

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Pathophysiology
Most cases of PID occur in 2 stages. The first stage involves acquisition of a vaginal or cervical
infection. The original sexually transmitted infection (STI) may be asymptomatic. An estimated
10-20% of untreated chlamydial or gonorrheal infections progress to PID.

In PID, the second stage of upper female genital tract infection occurs by direct ascent of micro-
organisms from the vagina and cervix. Although the exact mechanism of ascent is unknown,
studies have suggested that a number of factors may be involved. Cervical mucus provides a
functional barrier against upward spread; however, the efficacy of this mechanism may be
decreased by hormonal changes that occur during ovulation and menstruation. Alterations in the
cervicovaginal microenvironment may result from antibiotic treatment and STIs that can disrupt
the balance of endogenous flora, causing normally nonpathogenic organisms to overgrow and
ascend. Opening of the cervix during menstruation with retrograde menstrual flow may facilitate
ascent of micro-organisms. Intercourse may contribute to the ascent of infection due to rhythmic
mechanical uterine contractions. Bacteria may be carried along with sperm into the uterus and
tubes.

Risk factors for PID include multiple sexual partners, a history of prior STIs, and a history of
sexual abuse.3Frequent vaginal douching has also been implicated.4,5 Younger age has been
found to be associated with increased risk, suggested to be due to some combination of
increased cervical mucosal permeability, a larger zone of cervical ectopy, a lower prevalence of
protective chlamydial antibodies, and increased risk-taking behaviors. Surgical procedures, such
as endometrial biopsy, curettage, and hysteroscopies break the cervical barrier, predisposing
women to ascending infections.

The organisms most commonly isolated in many, if not most, cases of acute PID are Neisseria
gonorrhoeae andChlamydia trachomatis. As such, therapy has been directed primarily against
these organisms. However, unlike infections in other areas of the body, newer studies obtaining
more sensitive and specific laparoscopic cultures have found acute PID to be polymicrobial in up
to 30-40% of cases. Organisms involved include Gardnerella vaginalis, Mycoplasma hominis,
Ureaplasma urealyticum, herpes simplex virus-2 (HSV-2), Trichomonas
vaginalis,cytomegalovirus, Haemophilus influenzae, Streptococcus agalactiae, enteric gram-
negative rods, and anaerobes.N gonorrhoeae and C trachomatis may be instrumental in the initial
infection of the upper tract, with anaerobes, facultative anaerobes, and other bacteria increasingly
isolated as inflammation increases and abscesses form.

The microbiology of PID has also been found to reflect both the predominant STIs prevalent
within a specific population and also less common organisms seen in specific populations.
Bacterial vaginosis (BV) is suggested to play a role in the initiation of ascending infection in a
subset of women with heavy growth of BV-associated organisms, such as G vaginalis, more than
2 recent sexual partners, and especially after recent abortion or gynecologic surgery.6,7

A 2006 cross-sectional study examined the role of HSV-2 and T vaginalis in PID. In this study of
736 women, those with T vaginalis demonstrated a 4-fold increase in the histologic evidence of
acute endometritis. Co-infection of HSV-2 with N gonorrhoeae, C trachomatis, and BV was also
associated with histologic evidence of acute endometritis. HSV-2 was demonstrated to be
associated with fallopian tube inflammation and lower tract ulcerations that may contribute to
disruption of the endocervical canal mucus barrier.8

HIV infection has been found to be associated with an increased incidence of C

trachomatis infection, Candida, and human papillomavirus. Those with HIV infection also have an
increased risk of progression to PID and tubo-ovarian abscess.9

Actinomycete species have been identified almost exclusively in those patients with IUDs.2
PID may result from Mycobacterium tuberculosis in endemic areas.10

Different forms of contraception may affect PID incidence and severity. Appropriately used barrier
contraception has clearly been shown to decrease the acquisition of most STIs. The CDC
recommends that spermicides and condoms containing nonoxynol-9 should be avoided, as a
number of African studies have demonstrated that nonoxynol-9 can cause vaginal lesions and
may increase the risk of HIV transmission. While the level of nonoxynol-9 in condoms is lower
than the level associated with vaginal lesions, these are also not recommended because they are
more expensive, have a shorter shelf life, and have been associated with urinary tract infections.

Oral contraceptive pills (OCPs) have been found to have differing effects on PID risks. Oral
contraceptives are thought to increase the risk of endocervical infection, probably by increasing
the zone of cervical ectopy. OCPs have been found to decrease the risk of symptomatic PID,
possibly by increasing cervical mucous viscosity, decreasing menstrual anterograde and
retrograde flow, and modifying local immune responses. More recent data suggest that OCPs
may not have any effect on PID incidence.4

Bilateral tubal ligation (BTL) has not been found to provide protection against PID; however,
patients with BTL may have delayed or milder forms of PID.11

Intrauterine device (IUD) use has been associated with a 2- to 9-fold increased risk for PID, but
recent data suggest that the risk with current IUDs may be significantly less.12 Kelly et al found a
rate of 9.6 cases of PID per 1000 IUD insertions, with the most significant risk in the first 20
days.13 Meirik et al validated early risk of PID within the first month after insertion and also found
that the risk appears to be modified by the number of patient sexual partners, the age of the user,
and the community prevalence of STIs.14

Pregnancy decreases the risk of PID once the cervical os is protected by the mucous plug.
However, PID can occur during the early first trimester until the mucous plug is solidified, and it
may produce fetal loss.

In the upper tract, a number of microbial and host factors appear to play a role in the degree of
host inflammation and resultant scarring. Uterine infection is usually limited to the endometrium,
but may be more invasive in a gravid or postpartum uterus. Tubal infection initially affects the
mucosa, but acute, complement-mediated transmural inflammation may develop rapidly and
increase in intensity with subsequent infections. Inflammation may extend to uninfected
parametrial structures, including the bowel. Infection may extend by spillage of purulent materials
from the fallopian tubes or via lymphatic spread beyond the pelvis to produce acute peritonitis
and acute perihepatitis (Fitz-Hugh-Curtis syndrome).

Bjartling et al have found less symptomatic urethral infection and decreased lower abdominal
findings produced by a less virulent variant strain of Chlamydia trachomatis.15 Den Hartog
examined the role of 5 single nucleoside polymorphisms (SNPs) in 4 genes encoding pattern
recognition receptors in local tubal cells and circulating immune cells (eg, macrophages). The
presence of 2 or more SNPs in patients appeared to correlate with increased laparoscopically
identifiable tubal pathology.16 Genetic polymorphisms of PID pathogens has been suggested to
affect the likelihood that a lower tract infection will progress to frank PID. CHSP60 antigen
expression in C trachomatis17 and P9Opa(b) protein expression in N gonorrhoeae18 are examples
of specific bacterial genes implicated in the pathology of PID.