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Pelvic inflammatory disease: Pathogenesis, microbiology,

and risk factors
Author: Jonathan Ross, MD
Section Editor: Jeanne Marrazzo, MD, MPH, FACP, FIDSA
Deputy Editor: Allyson Bloom, MD

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Jan 2020. | This topic last updated: Oct 10, 2019.

INTRODUCTION

Pelvic inflammatory disease (PID) refers to acute infection of the upper genital tract structures in
women, involving any or all of the uterus, oviducts, and ovaries; this is often accompanied by
involvement of the neighboring pelvic organs. By convention, PID is initiated by a sexually
transmitted agent, which ascends into the upper genital tract, distinguishing it from pelvic infections
caused by trans-cervical medical procedures, pregnancy, and other primary abdominal processes
that can extend to pelvic organs.

Overall, the prevalence of PID in the United States and many other resource-rich countries has
decreased in the last decade [1,2]. In the United States, PID accounts for approximately 90,000
outpatient visits and is a frequent cause for emergency department visits.

The pathogenesis and microbiology of PID as well as risk factors for PID will be reviewed here.
The clinical features, diagnosis, treatment, and sequelae of this disorder are discussed separately.
(See "Pelvic inflammatory disease: Clinical manifestations and diagnosis" and "Pelvic inflammatory
disease: Treatment in adults and adolescents".)

PATHOGENESIS
The vaginal flora of most normal, healthy women includes a variety of potentially pathogenic
bacteria [3]. Among these are species of Prevotella, Leptotrichia, Atopobium, and other anaerobes
[4]. Compared with the dominant, non-pathogenic, hydrogen peroxide-producing Lactobacillus
species, these other organisms are present in low numbers, and ebb and flow under the influence
of hormonal changes (eg, pregnancy, menstrual cycle), contraceptive method, sexual activity,
vaginal hygiene practices, and other as yet unknown forces.

The endocervical canal functions as a barrier protecting the normally sterile upper genital tract
from the organisms of the dynamic vaginal ecosystem. Endocervical infection with sexually
transmitted pathogens can disrupt this barrier. Disturbance of this barrier provides vaginal bacteria
access to the upper genital organs, infecting the endometrium, then endosalpinx, ovarian cortex,
pelvic peritoneum, and their underlying stroma. The resulting infection may be subclinical or
manifest as the clinical entity of pelvic inflammatory disease (PID). The reasons why lower genital
tract bacteria cause PID in some women but not others is not fully understood but may relate to
genetic variations in immune response, estrogen levels affecting the viscosity of cervical mucus,
and bacterial load of potential pathogens [5,6].

Patients with PID can present with clinical disease at any point along a continuum from
endometritis (with normal tubes, ovaries, and peritoneum) to salpingitis (with inflammation of the
fallopian tubes and adjacent pelvic structures). This limits the sensitivity of direct visualization of
the fallopian tubes through laparoscopy when making a diagnosis of PID because endometritis and
mild intratubal inflammation cannot be seen [7,8]. (See "Pelvic inflammatory disease: Clinical
manifestations and diagnosis".)

MICROBIOLOGY

Neisseria gonorrhoeae and Chlamydia trachomatis are commonly identified pathogens in pelvic
inflammatory disease (PID) among sexually active pre-menopausal females. Mycoplasma
genitalium is also likely to be a cause in the pre-menopausal group [9]. E. coli and colonic
anaerobes may be responsible for the rare cases of PID seen in post-menopausal women. Very
rare pathogens identified include Mycobacterium tuberculosis, Haemophilus influenzae,
Streptococcus pneumoniae, and the agents of actinomycosis. However, in most cases, the precise
microbial etiology of PID is unknown. Regardless of the initiating pathogen, PID is clinically
considered a mixed polymicrobial infection.

Neisseria gonorrhoeae — N. gonorrhoeae was the first identified cause of PID. (See
"Epidemiology and pathogenesis of Neisseria gonorrhoeae infection".)

Approximately 15 percent of women with an endocervical N. gonorrhoeae infection go on to

develop PID [10,11]. The proportion of PID caused by N. gonorrhoeae varies widely and reflects
the underlying prevalence of gonorrhea in the local population. Its importance tends to be higher in
the southeastern United States, less in the northwestern United States, and much less in western
Europe [2,12]. There has been a steady evolution of multidrug-resistant strains since the early
1980s, and treatment options are limited. (See "Treatment of uncomplicated Neisseria
gonorrhoeae infections" and "Pelvic inflammatory disease: Treatment in adults and adolescents".)

Gonococcal PID tends to be clinically more severe than chlamydia PID [13], which may lead to
earlier diagnosis and treatment. (See "Pelvic inflammatory disease: Clinical manifestations and
diagnosis".)

Chlamydia trachomatis — Genital chlamydia is the most common bacterial sexually

transmissible disease. In the United States, it is also the most common reportable infectious
disease, with over 1.5 million cases reported annually [2]. C. trachomatis accounts for about one-
third of cases of PID, with less geographic variation in the prevalence than that seen for
gonorrhea-associated PID.

As seen with genital gonococcal infections in women, about 10 to 15 percent of endocervical C.

trachomatis infections produce PID, but asymptomatic subclinical infections are also common, and
these may present years later as chronic pelvic pain or infertility. (See "Clinical manifestations and
diagnosis of Chlamydia trachomatis infections", section on 'Pelvic inflammatory disease'.)

Women aged 16 to 24 years account for most cases of chlamydia. In one report of 150,000 such
women, those at the lowest risk still had a 6 percent prevalence of genital chlamydia, which
accounted for 17 percent of infections in this sample [14]. Many, but not all studies have shown a
reduction in PID rates following the introduction of chlamydia screening in young women. As an
example, annual chlamydia screening and treatment among at-risk 18 to 34 year-old women
reduced the prevalence of PID by 56 percent (8 versus 18 per 10,000 woman-months) compared
with those managed traditionally by risk and symptomatic assessment [15]. Annual screening of
sexually active adolescent girls and young women and older women at increased risk for
chlamydia is recommended in the United States and other countries [16,17]. This is discussed in
greater detail elsewhere. (See "Screening for sexually transmitted infections", section on
'Females'.)
Mycoplasma genitalium — The role of M. genitalium in sexually transmitted infections among
women is emerging. There is growing evidence supporting an association with cervicitis and PID in
women. The proportion of PID cases that are associated with M. genitalium is uncertain; in one
study of women with mild to moderate PID in the United Kingdom, 10 percent tested positive for M.
genitalium [18-20]. (See "Mycoplasma genitalium infection in men and women", section on 'Pelvic
inflammatory disease'.)

Other initiating pathogens — Other agents that initiate PID, while almost certainly sexually
transmitted and probably infectious, remain obscure. Using molecular amplification with generic
primers, a number of novel bacteria have been identified in the fallopian tubes of women with PID,
including Atopobium, Sneathia, and Leptotrichia [21]. The role of these and other anaerobic
bacteria in the pathogenesis of PID remains to be proven, but is likely consistent with their role in
the anaerobic microbiology of bacterial vaginosis.

Mixed infection — Regardless of the initiating pathogen, the microbiology of PID, especially for
clinical purposes, should be viewed and treated as a mixed (facultative and anaerobic)
polymicrobial infection. Older studies isolated groups A and B streptococci (rarely enterococci), E.
coli, Proteus mirabilis, Haemophilus spp, Bacteroides/Prevotella spp, Peptococcus, and
Peptostreptococcus spp from women with PID [22-24]. These studies found that, among cases of
PID initiated by N. gonorrhoeae, a mixed polymicrobial infection was seen in approximately 35
percent. Another study, which employed particularly stringent microbiologic techniques, identified
other organisms in more than 50 percent of patients with gonococcal PID [25].

In a given patient with PID, different organisms can be isolated from the various levels of the
genital tract (ie, the organisms isolated from the upper genital tract may be distinct from those
isolated from the lower genital tract) [22,24-27].

RISK FACTORS

Sex is the primary risk factor for pelvic inflammatory disease (PID). Sexually abstinent women are
not at risk for PID [28], and women with longstanding monogamous relationships rarely develop
PID. On the other hand, women with multiple sexual partners are at the highest risk. Younger age,
past infection with chlamydia, a partner with a STI, and previous PID are other important risk
factors. The frequency of PID is also affected by the method of contraceptive used; barrier
contraception is protective.
African-American or Black-Caribbean ethnicity has been associated with a higher risk of STIs,
including PID, and the reasons for this are likely multifactorial [29,30]. These racial differences in
PID risk may be decreasing over time [31].

Multiple partners — The importance of multiple partners was illustrated by a study that compared
712 women hospitalized for PID with 2719 controls [32]. Having four or more sexual partners within
the prior six months increased the risk of PID 3.4 times, and having sex with a single partner six or
more times per week increased it 3.2 times. Other studies have confirmed multiple partners as a
risk factor, associated with an increased frequency of PID ranging from 3- to 20-fold [33-35]. One
report, however, did not confirm a role for coital frequency [33].

STI in the partner — Approximately a third of men with gonococcal or chlamydial urethritis are
asymptomatic. Having a symptomatic (dysuria, urethral discharge) male partner can increase a
woman's risk of PID [22].

Age — PID occurs in highest frequency among those 15 to 25 years of age [11,36]; the incidence
in women older than the age of 35 is only one-seventh that in younger women [37]. The initiating
pathogens of PID in both the United States and Europe, particularly C. trachomatis, are densely
concentrated among adolescent and young adult women, with prevalence around 3 to 5 percent
[2,38]. C. trachomatis and N. gonorrhoeae are less likely to be identified in post-menopausal
women, in whom the risk of PID is very low. In such women, it is important to consider alternate
diagnoses including ovarian cancer, fibroids, diverticulitis, and colorectal cancer [39].

Reinfection with genital C. trachomatis is also a function of age. In one series, for example, the risk
of reinfection among women whose first infection occurred at <15 years and 15 to 19 years was
eightfold (at 54 percent) and fivefold (at 30 percent) greater, respectively, compared to those
whose first infection occurred older than age 30 [40].

Previous PID — Approximately one in four women with PID will suffer recurrence [41]. In one
study, a previous episode of PID increased the risk for subsequent episodes by a factor of 2.3 [33].
However, these data must be used cautiously in practice, since PID is associated with an
increased risk of subsequent chronic pelvic pain in general, even in the absence of an identifiable
new infection.

Contraceptive method — The choice of contraceptive method does not clearly affect the risk of
pelvic infection, although consistent use of condoms offers a significant reduction of risk.
 Barrier contraception — Barrier contraception protects against PID [42]. Condoms are the
most effective form, preventing over 50 percent of endocervical gonococcal and chlamydial
infections if used correctly. One large study suggested that consistent condom use following a
diagnosis of PID can lower the rate of PID sequelae [43].

Unfortunately, most women do not consistently use condoms. According to survey data reported
by the United States Centers for Disease Control and Prevention from 2002 to 2007, consistent
condom use was reported in only 31 percent of never-married women aged 20 to 24 years [44].

Oral contraceptives — Oral contraceptives (OCs) have a complex interaction with PID.
Several studies have shown that OC use nearly doubles the prevalence of both chlamydia and
gonococcal infection of the cervix [45]. However, OC use has traditionally been associated with a
50 percent reduction in PID risk [46].

Among OC users with cervical infection, asymptomatic endometritis is fourfold more common than
among their counterparts not using OCs [47], although gross salpingitis is reduced fivefold [48].
Thus, women using OCs appear to develop PID about as frequently as other women, but the
severity of the infection is substantially diminished.

Intrauterine device and tubal ligation — Modern intrauterine devices cause little, if any,
increased risk for PID [49-51]. The risk of PID is primarily limited to the first three weeks after IUD
insertion and is uncommon thereafter [50]. One methodologically limited trial suggested that IUD
removal in the setting of PID results in better clinical outcomes [52], but most guidelines note that
leaving the IUD in place while treating acute PID with antibiotics is acceptable with close follow-up
[51]. The IUD should be removed if clinical improvement is delayed beyond a few days.

Long-term indwelling IUDs have been associated with pelvic actinomycosis, a rare disease that
can present as a pelvic mass with weight loss and constitutional symptoms [53]. In a study of 475
isolates of actinomyces species, 30 percent of the clinical specimens originated in association with
IUDs [54]. The decision to treat a patient for possible pelvic actinomycosis is influenced by the
presence or absence of clinical symptoms, since actinomyces are part of normal vaginal flora. This
is discussed elsewhere. (See "Intrauterine contraception: Management of side effects and
complications", section on 'Actinomyces and related organisms'.)

Tubal ligation may protect the distal oviducts from involvement, but the clinical syndrome of PID is
otherwise unaffected.
Other conditions — Complete disruption of the vaginal ecosystem can occur, in which anaerobic
bacteria assume predominance over the desirable strains of lactobacilli. This condition is known as
bacterial vaginosis and affects 15 to 30 percent of American women, one-half of whom are
asymptomatic [55]. Overall, bacterial vaginosis does not increase the risk of developing PID, but
the risk is higher with certain subtypes of bacterial vaginosis (based on the specific pattern of
bacteria present) [56]. Cultivation-independent methods of characterizing vaginal bacteria may
clarify this relationship in the future.

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics."
The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading
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These articles are best for patients who want a general overview and who prefer short, easy-to-
read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and
more detailed. These articles are written at the 10th to 12th grade reading level and are best for
patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or
e-mail these topics to your patients. (You can also locate patient education articles on a variety of
subjects by searching on "patient info" and the keyword(s) of interest.)

● Basics topic (see "Patient education: Pelvic inflammatory disease (The Basics)")

SUMMARY AND RECOMMENDATIONS

● Pelvic inflammatory disease (PID) is initiated by a sexually transmitted agent, distinguishing it

from pelvic infections caused by medical procedures, pregnancy, and primary abdominal
processes. (See 'Introduction' above and 'Pathogenesis' above.)

● Anatomically, PID refers to acute infection of the upper genital tract structures in women,
involving any or all of the uterus, oviducts, and ovaries and sometimes other surrounding
pelvic organs. (See 'Introduction' above.)

● Initiating pathogens in PID include Neisseria gonorrhoeae, Chlamydia trachomatis, and likely
Mycoplasma genitalium, which account for an estimated 30 to 40 percent of all cases,
 although in the majority of cases the specific microbial etiology of PID is unknown. Regardless
of the initiating event, the microbiology of PID should be viewed and treated as a mixed
(facultative and anaerobic) polymicrobial infection. (See 'Microbiology' above.)

● The main risk factor for pelvic inflammatory disease is having unprotected intercourse with
multiple sex partners. The choice of contraceptive method does not clearly affect the risk of
pelvic infection, though consistent use of condoms offers a significant reduction of risk. (See
'Risk factors' above.)

ACKNOWLEDGMENT — The editorial staff at UpToDate would like to acknowledge Charles

Livengood, MD, who contributed to an earlier version of this topic review.

Use of UpToDate is subject to the Subscription and License Agreement.

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Topic 7580 Version 23.0

Contributor Disclosures
Jonathan Ross, MD Grant/Research/Clinical Trial Support: Janssen [HIV (educational support)].
Consultant/Advisory Boards: GlaxoSmithKlein [Gonorrhea, Mycoplasma genitalium [Development of new
antimicrobials)]; Hologic [Mycoplasma genitalium (diagnostics)]. Equity Ownership/Stock Options:
GlaxoSmithKlein; AstraZeneca. Jeanne Marrazzo, MD, MPH, FACP, FIDSA Grant/Research/Clinical Trial
Support: BD Diagnostics [Vaginal infections, STI (diagnostic tests)]. Consultant/Advisory Boards: BD
Diagnostics [Vaginitis (diagnostic testing strategies)]; Gilead [HIV (pre-exposure prophylaxis)]. Other Financial
Interest: Gilead [HIV (Data and Safety Monitoring Board member)]. Allyson Bloom, MD Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
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