Pelvic Inflammatory Disease: Background, Pathophysiology, Etiology

12/11/15, 12:32 AM

Pelvic Inflammatory Disease

Author: Suzanne Moore Shepherd, MD, MS, DTM&H, FACEP, FAAEM; Chief Editor: Michel E Rivlin, MD
more...
Updated: Sep 28, 2015

Background
Pelvic inflammatory disease (PID) is an infectious and inflammatory disorder of the upper female genital tract,
including the uterus, fallopian tubes, and adjacent pelvic structures. Infection and inflammation may spread to the
abdomen, including perihepatic structures (Fitz-HughCurtis syndrome). The classic high-risk patient is a
menstruating woman younger than 25 years who has multiple sex partners, does not use contraception, and lives
in an area with a high prevalence of sexually transmitted disease (STD).
PID is initiated by infection that ascends from the vagina and cervix into the upper genital tract. Chlamydia
trachomatis is the predominant sexually transmitted organism associated with PID. Other organisms implicated in
the pathogenesis of PID include Neisseria gonorrhoeae, Gardnerella vaginalis, Haemophilus influenzae, and
anaerobes such as Peptococcus and Bacteroides species. Laparoscopic studies have shown that in 30-40% of
cases, PID is polymicrobial. (See Etiology.)
The diagnosis of acute PID is primarily based on historical and clinical findings. Clinical manifestations of PID vary
widely, however: Many patients exhibit few or no symptoms, whereas others have acute, serious illness. The most
common presenting complaint is lower abdominal pain. Many women report an abnormal vaginal discharge. (See
Presentation.)
The differential diagnosis includes appendicitis, cervicitis, urinary tract infection, endometriosis, and adnexal
tumors. Ectopic pregnancy can be mistaken for PID; indeed, PID is the most common incorrect diagnosis in cases
of ectopic pregnancy. Consequently, a pregnancy test is mandatory in the workup of women of childbearing age
who have lower abdominal pain. (See DDx.)
PID may produce tubo-ovarian abscess (TOA) and may progress to peritonitis and Fitz-HughCurtis syndrome
(perihepatitis; see the image below).[1] Note that a rare but life-threatening complication of acute rupture of a TOA
may result in diffuse peritonitis and necessitate urgent abdominal surgery.[2, 3, 4, 5] See Imaging in Pelvic
Inflammatory Disease and Tubo-Ovarian Abscess for more information.

"Violin-string" adhesions of chronic Fitz-Hugh-Curtis syndrome.

Laparoscopy is the current criterion standard for the diagnosis of PID. No single laboratory test is highly specific or
sensitive for the disease, but studies that can be used to support the diagnosis include the erythrocyte
sedimentation rate (ESR), the C-reactive protein (CRP) level, and chlamydial and gonococcal DNA probes and
cultures. Imaging studies (eg, ultrasonography, computed tomography [CT], and magnetic resonance imaging
[MRI]) may be helpful in unclear cases. (See Workup.)
Most patients with PID are treated in an outpatient setting. In selected cases, however, physicians should consider
hospitalization. (See Treatment.)
Empirical antibiotic treatment is recommended for patients with otherwise unexplained uterine or adnexal
tenderness and cervical motion tenderness, according to guidelines from the Centers for Disease Control and
Prevention (CDC).[6] Antibiotic regimens for PID must be effective against C trachomatis and N gonorrhoeae, as
well as against gram-negative facultative organisms, anaerobes, and streptococci. (See Treatment and
Medication.)

Pathophysiology
Most cases of PID are presumed to occur in 2 stages. The first stage is acquisition of a vaginal or cervical
infection. This infection is often sexually transmitted and may be asymptomatic. The second stage is direct ascent
of microorganisms from the vagina or cervix to the upper genital tract, with infection and inflammation of these
structures.

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The mechanism (or mechanisms) by which microorganisms ascend from the lower genital tract is unclear. Studies
suggest that multiple factors may be involved. Although cervical mucus provides a functional barrier against
upward spread, the efficacy of this barrier may be decreased by vaginal inflammation and by hormonal changes
that occur during ovulation and menstruation.
In addition, antibiotic treatment of sexually transmitted infections can disrupt the balance of endogenous flora in
the lower genital tract, causing normally nonpathogenic organisms to overgrow and ascend. Opening of the cervix
during menstruation, along with retrograde menstrual flow, may also facilitate ascent of microorganisms.
Intercourse may contribute to the ascent of infection through rhythmic uterine contractions occurring during
orgasm. Bacteria may also be carried along with sperm into the uterus and fallopian tubes.[7]
In the upper tract, a number of microbial and host factors appear to influence the degree of inflammation that
occurs and, thus, the amount of subsequent scarring that develops. Infection of the fallopian tubes initially affects
the mucosa, but inflammation may rapidly become transmural. This inflammation, which appears to be mediated
by complement, may increase in intensity with subsequent infections.
Inflammation may extend to uninfected parametrial structures, including the bowel. Infection may extend via
spillage of purulent materials from the fallopian tubes or via lymphatic spread beyond the pelvis to produce acute
peritonitis and acute perihepatitis (Fitz-HughCurtis syndrome).

Pregnancy-related factors
PID rarely occurs in pregnancy; however, chorioamnionitis can occur in the first 12 weeks of gestation, before the
mucous plug solidifies and seals off the uterus from ascending bacteria. Fetal loss may result. Concurrent
pregnancy influences the choice of antibiotic therapy for PID and demands that an alternative diagnosis of ectopic
pregnancy be excluded. Uterine infection is usually limited to the endometrium but may be more invasive in a
gravid or postpartum uterus.

Genetic factors
Genetically mediated variation in immune response plays an important role in susceptibility to PID.[8] Variants in
the genes that regulate toll-like receptors (TLRs), an important component in the innate immune system, have
been associated with an increased progression of C trachomatis infection to PID.[9]
Den Hartog et al found a possible contributing 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 appeared to correlate with increased laparoscopically identifiable tubal pathology.[10]

Etiology
The organisms most commonly isolated in cases of acute PID are N gonorrhoeae and C trachomatis.[11] C
trachomatis is an intracellular bacterial pathogen and the predominant sexually transmitted organism that causes
PID.
In the United States, N gonorrhoeae is no longer the primary organism associated with PID, but gonorrhea
remains the second most frequently reported sexually transmitted disease, after chlamydial infection. Clinically,
gonorrheal infection may be asymptomatic or may manifest similarly to chlamydial infection; however, it more often
produces more acute symptomatic disease. An estimated 10-20% of untreated chlamydial or gonorrheal infections
progress to PID.[12, 13, 14]
Cultures of specimens collected during laparoscopy have demonstrated that PID is a polymicrobial infection in as
many as 30-40% of cases. Polymicrobial PID may begin as an isolated infection with N gonorrhoeae or C
trachomatis, which causes inflammation of the upper genital tract that facilitates the involvement of other
pathogens (anaerobes, facultative anaerobes, and other bacteria). These other organisms are increasingly
isolated as inflammation increases and abscesses form.
In addition to N gonorrhoeae and C trachomatis,[15] organisms involved in PID include the following:
Gardnerella vaginalis
Mycoplasma hominis
Mycoplasma genitalium [16, 17]
Ureaplasma urealyticum
Herpes simplex virus 2 (HSV-2)
Trichomonas vaginalis
Cytomegalovirus (CMV)
Haemophilus influenzae
Streptococcus agalactiae
Enteric gram-negative rods (eg, Escherichia coli)
Enterococcus, described in 2 individuals post IUD insertion [18]
Peptococcus species
Anaerobes
The microbiology of PID reflects the predominant sexually transmitted pathogens within a specific population, as
well as some organisms less commonly seen in that population. Bacterial vaginosis (BV) may lead to vaginal
inflammation, which could facilitate ascending infection with BV-associated organisms (eg, G vaginalis). In some
regions, PID may be from a granulomatous salpingitis caused by Mycobacterium tuberculosis or Schistosoma
species.[19]
In a cross-sectional study of 736 women with PID, patients with Trichomonas infections demonstrated a 4-fold
increase in the histologic evidence of acute endometritis. Coinfection with HSV-2, N gonorrhoeae, C trachomatis,
and BV were associated with histologic evidence of acute endometritis. HSV-2 was associated with fallopian tube
inflammation and lower tract ulcerations that may contribute to disruption of the endocervical canal mucous barrier.
[20]

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HIV infection is associated with an increased incidence of infection with C trachomatis, Candida, and human
papillomavirus (HPV). N gonorrhoeae can facilitate HIV transmission via modulation of HIV-specific immune
responses.[21] Women with HIV infection also have an increased risk of progression to PID and TOA.[22]
Microbial virulence appears to play a significant role in PID. Bjartling et al studied different chlamydial strains
recovered from patients with PID and found less symptomatic disease in infection produced by a less virulent
variant strain.[23] Features that may increase the likelihood that a lower tract infection will progress to frank PID
include expression of chlamydial heat shock protein 60 (CHSP60) in C trachomatis[24] and expression of P9Opa(b)
protein in N gonorrhoeae.[25]

Risk factors
Risk factors for PID include multiple sexual partners, a history of prior STIs, and a history of sexual abuse.[26]
Frequent vaginal douching has been considered a risk factor for PID,[27] but studies reveal no clear association.[28]
Gynecologic surgical procedures such as endometrial biopsy, curettage, and hysteroscopy break the cervical
barrier, predisposing women to ascending infections.[29, 30]
Younger age has been found to be associated with an increased risk of PID. Likely reasons include increased
cervical mucosal permeability, a larger zone of cervical ectopy, a lower prevalence of protective antichlamydial
antibodies, and increased risk-taking behaviors.

Contraception
Different forms of contraception may affect the incidence and severity of PID. Appropriately used barrier
contraception has clearly been shown to decrease the acquisition of most STIs.[31]
Studies of oral contraceptive pills (OCPs) have found differing effects on PID risks. On one hand, some authors
suggest that OCPs increase the risk of endocervical infection, probably by increasing the zone of cervical ectopy.
On the other hand, some evidence indicates that OCPs can decrease the risk of symptomatic PID, possibly by
increasing cervical mucus viscosity, decreasing menstrual anterograde and retrograde flow, and modifying local
immune responses. Still other studies have suggested that OCPs may not have any effect on PID incidence.[31]
Use of an intrauterine device (IUD) has been linked to a 2- to 9-fold increased risk of PID, but current IUDs may
pose a substantially lower risk.[32] In a large retrospective cohort study from 2012, the overall risk of PID in women
receiving IUDs was 0.54%.[33]
Kelly et al reported 9.6 cases of PID per 1,000 IUD insertions, with the most significant risk in the first 20 days.[34]
Meirik et al validated the risk of PID within the first month after insertion and also found that the risk appears to be
modified by the patients number of sexual partners and age and by the community prevalence of STIs.[35] The
CDC notes that the risk of PID is greatly reduced by testing forand, if necessary, treatingSTD before IUD
insertion.[36, 37] }
PID may have a different microbial profile in IUD users. Viberga et al found that in women with PID, Fusobacterium
and Peptostreptococcus species were significantly more common in IUD users than in non-IUD users.
Actinomyces species were found almost exclusively in patients with IUDs.[38]
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.[39]

Epidemiology
United States statistics
From 1995 to 2001, 769,859 cases of PID were reported in the United States annually.[40] The true incidence was
probably much higher; cases likely went unreported as a consequence of incomplete and untimely conventional
nonelectronic reporting methods and because many cases of silent and smoldering PID occur and are discovered
only when chronic complications develop.
The CDC has estimated that more than 1 million women experience an episode of PID every year. The disease
leads to approximately 2.5 million office visits and 125,000-150,000 hospitalizations yearly.[41, 42]

International statistics
No specific international data are available for PID incidence worldwide. In 2005, however, the World Health
Organization (WHO) estimated that approximately 448 million new cases of curable STIs occur annually in
individuals aged 15-49 years.[43] Factors contributing to the difficulty of determining the actual worldwide incidence
and prevalence of PID include the following[44] :
Nonrecognition of disease on the part of patients
Difficulties in obtaining access to care
The often subjective method of disease diagnosis
The lack of diagnostics and laboratory facilities in many developing countries
Underfunded and overstretched public health systems
Worldwide, WHO has determined that STIs rank in the top 5 disease categories for which adults seek care.
Women in resource-poor countries, especially those in sub-Saharan Africa and Southeast Asia, experience an
increased rate of complications and sequelae.
The annual rate of PID in high-income countries has been reported to be as high as 10-20 per 1000 women of
reproductive age. Public health efforts implemented in Scandinavia to decrease the prevalence of STIs have been
quite effective in reducing the incidence of PID.[45, 46]

Prognosis
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PID has 3 principal complications, as follows:

Chronic pelvic pain
Infertility
Ectopic pregnancy
Chronic pelvic pain occurs in approximately 25% of patients with a history of PID. This pain is thought to be related
to cyclic menstrual changes, but it also may be the result of adhesions or hydrosalpinx.
Impaired fertility is a major concern in women with a history of PID. Infection and inflammation can lead to scarring
and adhesions within tubal lumens. Of women with tubal factor infertility, 50% have no history of PID but have
scarring of the fallopian tubes and exhibit antibodies to C trachomatis. The rate of infertility increases with the
number of episodes of infection.
The risk of ectopic pregnancy is increased 15-50% in women with a history of PID. Ectopic pregnancy is a direct
result of damage to the fallopian tube.
PID may produce TOA and extend to produce pelvic peritonitis and Fitz-HughCurtis syndrome (perihepatitis).[47,
48]
TOA is reported in as many as one third of women hospitalized for PID. Acute rupture of a TOA with resultant
diffuse peritonitis is a rare but life-threatening event that calls for urgent abdominal surgery.[2, 3, 4, 5]
Approximately 125,000-150,000 hospitalizations occur yearly in the United States because of PID.[41] Women in
resource-poor countries, especially those in sub-Saharan Africa and Southeast Asia, experience an increased rate
of complications and sequelae; reasons for these higher rates include lack of access to care and inability to afford
optimal care.
Studies of Taiwanese databases that included more than 60,000 women diagnosed with PID found that PID was
an independent risk factor for myocardial infarction in patients older than 55 years[49] and that risk of stroke was
increased in the 3 years following PID.[50] Another large-scale study from Taiwan found that the risk of ovarian
cancer is also increased, particularly in women who have had at least 5 episodes of PID.[51]

Patient Education
Patient education should focus on methods of preventing PID and STIs, including reducing the number of sexual
partners, avoiding unsafe sexual practices, and routinely using appropriate barrier protection. Adolescents are at
increased risk for PID and should therefore be advised to delay the onset of sexual activity until age 16 years or
older.[52]
After treatment, women should be counseled to abstain from sexual activity or educated to use barrier protection
strictly and appropriately until their symptoms have fully abated and they have completed their antibiotic regimen.
The womans sexual partner should also be treated for STI if necessary.
For patient education information, see the Pelvic Inflammatory Disease (PID) Directory, Womens Health Center,
Sexual Health Center, and Pregnancy Center, as well as Pelvic Inflammatory Disease, Ectopic Pregnancy, Birth
Control Overview, Birth Control Methods, and Female Sexual Problems.
Clinical Presentation

Contributor Information and Disclosures

Author
Suzanne Moore Shepherd, MD, MS, DTM&H, FACEP, FAAEM Professor of Emergency Medicine, Education
Officer, Department of Emergency Medicine, Hospital of the University of Pennsylvania; Director of Education
and Research, PENN Travel Medicine; Medical Director, Fast Track, Department of Emergency Medicine
Suzanne Moore Shepherd, MD, MS, DTM&H, FACEP, FAAEM is a member of the following medical societies:
Alpha Omega Alpha, American Academy of Emergency Medicine, American Society of Tropical Medicine and
Hygiene, International Society of Travel Medicine, Society for Academic Emergency Medicine, Wilderness
Medical Society
Disclosure: Nothing to disclose.
Specialty Editor Board
Nicole W Karjane, MD Associate Professor, Department of Obstetrics and Gynecology, Virginia
Commonwealth University Medical Center
Nicole W Karjane, MD is a member of the following medical societies: American College of Obstetricians and
Gynecologists, Association of Professors of Gynecology and Obstetrics, North American Society for Pediatric
and Adolescent Gynecology
Disclosure: Received honoraria from Merck for speaking and teaching.
Chief Editor
Michel E Rivlin, MD Former Professor, Department of Obstetrics and Gynecology, University of Mississippi
School of Medicine
Michel E Rivlin, MD is a member of the following medical societies: American College of Obstetricians and
Gynecologists, American Medical Association, Mississippi State Medical Association, Royal College of
Surgeons of Edinburgh, Royal College of Obstetricians and Gynaecologists
Disclosure: Nothing to disclose.
Acknowledgements
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center
College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
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References
1. Wiesenfeld HC, Hillier SL, Meyn LA, Amortegui AJ, Sweet RL. Subclinical pelvic inflammatory disease
and infertility. Obstet Gynecol. 2012 Jul. 120(1):37-43. [Medline].
2. Rivlin ME, Hunt JA. Ruptured tuboovarian abscess. Is hysterectomy necessary?. Obstet Gynecol. 1977
Nov. 50 (5):518-22. [Medline].
3. Laohaburanakit P, Treevijitsilp P, Tantawichian T, Bunyavejchevin S. Ruptured tuboovarian abscess in late
pregnancy. A case report. J Reprod Med. 1999 Jun. 44 (6):551-5. [Medline].
4. De Temmerman G, Villeirs GM, Verstraete KL. Ruptured tuboovarian abscess causing peritonitis in a
postmenopausal woman. A difficult diagnosis on imaging. JBR-BTR. 2003 Mar-Apr. 86 (2):72-3. [Medline].
5. Powers K, Lazarou G, Greston WM, Mikhail M. Rupture of a tuboovarian abscess into the anterior
abdominal wall: a case report. J Reprod Med. 2007 Mar. 52 (3):235-7. [Medline].
6. Workowski KA, Berman S. Sexually transmitted diseases treatment guidelines, 2010. MMWR Recomm
Rep. 2010 Dec 17. 59:1-110. [Medline]. [Full Text].
7. Patton DL, Wolner-Hanssen P, Zeng W, Lampe M, Wong K, Stamm WE, et al. The role of spermatozoa in
the pathogenesis of Chlamydia trachomatis salpingitis in a primate model. Sex Transm Dis. 1993 Jul-Aug.
20(4):214-9. [Medline].
8. Paavonen J. Chlamydia trachomatis infections of the female genital tract: state of the art. Ann Med. 2012
Feb. 44(1):18-28. [Medline].
9. Taylor BD, Darville T, Ferrell RE, Kammerer CM, Ness RB, Haggerty CL. Variants in toll-like receptor 1
and 4 genes are associated with Chlamydia trachomatis among women with pelvic inflammatory disease.
J Infect Dis. 2012 Feb 15. 205(4):603-9. [Medline]. [Full Text].
10. den Hartog JE, Ouburg S, Land JA, et al. Do host genetic traits in the bacterial sensing system play a role
in the development of Chlamydia trachomatis-associated tubal pathology in subfertile women?. BMC
Infect Dis. Jul 21 2006. 6:122.
11. [Guideline] Royal College of Obstetricians and Gynaecologists (RCOG). Management of acute pelvic
inflammatory disease. London (UK): Royal College of Obstetricians and Gynaecologists (RCOG).; 2008
Nov. [Full Text].
12. Herzog SA, Althaus CL, Heijne JC, Oakeshott P, Kerry S, Hay P, et al. Timing of progression from
Chlamydia trachomatis infection to pelvic inflammatory disease: a mathematical modelling study. BMC
Infect Dis. 2012 Aug 11. 12:187. [Medline]. [Full Text].
13. Hillis SD, Wasserheit JN. Screening for chlamydia--a key to the prevention of pelvic inflammatory disease.
N Engl J Med. 1996 May 23. 334(21):1399-401. [Medline].
14. Hook EW, Handsfield HH. Gonococcal infections in the adult. Holmes KK, Sparling PF, Stamm WE, et al.
eds. Sexually Transmitted Diseases. 4th edition. New York: McGraw Hill, Inc; 2008. 627-645.
15. Mylonas I. Female genital Chlamydia trachomatis infection: where are we heading?. Arch Gynecol Obstet.
2012 May. 285(5):1271-85. [Medline].
16. Ross JD. Is Mycoplasma genitalium a cause of pelvic inflammatory disease?. Infect Dis Clin North Am.
2005 Jun. 19(2):407-13. [Medline].
17. Bjartling C, Osser S, Persson K. Mycoplasma genitalium in cervicitis and pelvic inflammatory disease
among women at a gynecologic outpatient service. Am J Obstet Gynecol. 2012 Jun. 206(6):476.e1-8.
[Medline].
18. Bravender T, Matson SC. Adolescents, IUDs, PID, and Enterococcus: a report of two cases. J Pediatr
Adolesc Gynecol. 2012 Jun. 25(3):e73-4. [Medline].
19. Avan BI, Fatmi Z, Rashid S. Comparison of clinical and laparascopic features of infertile women suffering
from genital tuberculosis (TB) or pelvic inflammatory disease (PID) or endometriosis. J Pak Med Assoc.
2001 Nov. 51(11):393-9. [Medline].
20. Cherpes TL, Wiesenfeld HC, Melan MA, Kent JA, et al. The associations between pelvic inflammatory
disease, Trichomonas vaginalis infection, and positive herpes simplex virus type 2 serology. Sex Transm
Dis. 2006. 33:747-52.
21. Jarvis GA, Chang TL. Modulation of HIV transmission by Neisseria gonorrhoeae: molecular and
immunological aspects. Curr HIV Res. 2012 Apr. 10(3):211-7. [Medline].
22. Brunham RC, Kimani J, Bwayo J, Maitha G, Maclean I, Yang C, et al. The epidemiology of Chlamydia
trachomatis within a sexually transmitted diseases core group. J Infect Dis. 1996 Apr. 173(4):950-6.
[Medline].
23. Bjartling C, Osser S, Johnsson A, Persson K. Clinical manifestations and epidemiology of the new genetic
variant of Chlamydia trachomatis. Sex Transm Dis. 2009 Sep. 36(9):529-35. [Medline].
24. Kinnunen A, Molander P, Morrison R, Lehtinen M, Karttunen R, Tiitinen A, et al. Chlamydial heat shock
protein 60--specific T cells in inflamed salpingeal tissue. Fertil Steril. 2002 Jan. 77(1):162-6. [Medline].
25. Makepeace BL, Watt PJ, Heckels JE, Christodoulides M. Interactions of Neisseria gonorrhoeae with
mature human macrophage opacity proteins influence production of proinflammatory cytokines. Infect
Immun. 2001 Mar. 69(3):1909-13. [Medline]. [Full Text].
26. Champion JD, Piper J, Shain RN, Perdue ST, Newton ER. Minority women with sexually transmitted

http://emedicine.medscape.com/article/256448-overview#showall

Page 5 of 8

Pelvic Inflammatory Disease: Background, Pathophysiology, Etiology

12/11/15, 12:32 AM

diseases: sexual abuse and risk for pelvic inflammatory disease. Res Nurs Health. 2001 Feb. 24(1):38-43.
[Medline].
27. Ness RB, Soper DE, Holley RL, Peipert J, Randall H, Sweet RL, et al. Douching and endometritis: results
from the PID evaluation and clinical health (PEACH) study. Sex Transm Dis. 2001 Apr. 28(4):240-5.
[Medline].
28. Ness RB, Hillier SL, Kip KE, Richter HE, Soper DE, Stamm CA, et al. Douching, pelvic inflammatory
disease, and incident gonococcal and chlamydial genital infection in a cohort of high-risk women. Am J
Epidemiol. 2005 Jan 15. 161(2):186-95. [Medline].
29. Koumans EH, Kendrick JS. Preventing adverse sequelae of bacterial vaginosis: a public health program
and research agenda. Sex Transm Dis. 2001 May. 28(5):292-7. [Medline].
30. Ness RB, Hillier SL, Kip KE, Soper DE, Stamm CA, McGregor JA, et al. Bacterial vaginosis and risk of
pelvic inflammatory disease. Obstet Gynecol. 2004 Oct. 104(4):761-9. [Medline].
31. Ness RB, Soper DE, Holley RL, Peipert J, Randall H, Sweet RL, et al. Hormonal and barrier contraception
and risk of upper genital tract disease in the PID Evaluation and Clinical Health (PEACH) study. Am J
Obstet Gynecol. 2001 Jul. 185(1):121-7. [Medline].
32. Shelton JD. Risk of clinical pelvic inflammatory disease attributable to an intrauterine device. Lancet. 2001
Feb 10. 357(9254):443. [Medline].
33. [Guideline] CDC, Workowski KA, Berman SM. Sexually transmitted diseases treatment guidelines, 2006.
MMWR Recomm Rep. Aug 4 2006. 55(RR-11):1-94.
34. Kelly EK, Rudinsky SW. Intrauterine contraception: current evidence-based recommendations. J
Midwifery Womens Health. 2007 Sep-Oct. 52(5):505-7. [Medline].
35. Meirik O. Intrauterine devices - upper and lower genital tract infections. Contraception. 2007. 06;75(6
Suppl/):S41-7.
36. Centers for Disease Control and Prevention. Pelvic Inflammatory Disease PID. CDC Fact Sheet.
Available at http://www.cdc.gov/std/pid/stdfact-pid.htm. Accessed: December 9, 2012.
37. Sufrin CB, Postlethwaite D, Armstrong MA, Merchant M, Wendt JM, Steinauer JE. Neisseria gonorrhea
and Chlamydia trachomatis screening at intrauterine device insertion and pelvic inflammatory disease.
Obstet Gynecol. 2012 Dec. 120(6):1314-21. [Medline].
38. Viberga I, Odlind V, Lazdane G, Kroica J, Berglund L, Olofsson S. Microbiology profile in women with
pelvic inflammatory disease in relation to IUD use. Infect Dis Obstet Gynecol. 2005 Dec. 13(4):183-90.
[Medline]. [Full Text].
39. Levgur M, Duvivier R. Pelvic inflammatory disease after tubal sterilization: a review. Obstet Gynecol Surv.
2000 Jan. 55(1):41-50. [Medline].
40. Sutton MY, Sternberg M, Zaidi A, St Louis ME, Markowitz LE. Trends in pelvic inflammatory disease
hospital discharges and ambulatory visits, United States, 1985-2001. Sex Transm Dis. 2005 Dec.
32(12):778-84. [Medline].
41. Ness RB, Smith KJ, Chang CC, Schisterman EF, Bass DC. Prediction of pelvic inflammatory disease
among young, single, sexually active women. Sex Transm Dis. 2006 Mar. 33(3):137-42. [Medline].
42. Sorbye IK, Jerve F, Staff AC. Reduction in hospitalized women with pelvic inflammatory disease in Oslo
over the past decade. Acta Obstet Gynecol Scand. 2005 Mar. 84(3):290-6. [Medline].
43. World Health Organization. Sexually transmitted infections. Available at
http://www.who.int/mediacentre/factsheets/fs110/en/. Accessed: February 2, 2010.
44. Low N, Broutet N, Adu-Sarkodie Y, Barton P, Hossain M, Hawkes S. Global control of sexually transmitted
infections. Lancet. 2006 Dec 2. 368(9551):2001-16. [Medline].
45. Kamwendo F, Forslin L, Bodin L, Danielsson D. Programmes to reduce pelvic inflammatory disease--the
Swedish experience. Lancet. 1998. 351 Suppl 3:25-8. [Medline].
46. Kamwendo F, Forslin L, Bodin L, Danielsson D. Decreasing incidences of gonorrhea- and chlamydiaassociated acute pelvic inflammatory disease. A 25-year study from an urban area of central Sweden. Sex
Transm Dis. 1996 Sep-Oct. 23(5):384-91. [Medline].
47. Banikarim C, Chacko MR. Pelvic inflammatory disease in adolescents. Adolesc Med Clin. 2004 Jun. 15
(2):273-85, viii. [Medline].
48. Zeger W, Holt K. Gynecologic infections. Emerg Med Clin North Am. 2003 Aug. 21 (3):631-48. [Medline].
49. Liou TH, Wu CW, Hao WR, Hsu MI, Liu JC, Lin HW. Risk of myocardial infarction in women with pelvic
inflammatory disease. Int J Cardiol. 2012 Jan 20. [Medline].
50. Chen PC, Tseng TC, Hsieh JY, Lin HW. Association between stroke and patients with pelvic inflammatory
disease: a nationwide population-based study in Taiwan. Stroke. 2011 Jul. 42(7):2074-6. [Medline].
51. Lin HW, Tu YY, Lin SY, Su WJ, Lin WL, Lin WZ, et al. Risk of ovarian cancer in women with pelvic
inflammatory disease: a population-based study. Lancet Oncol. 2011 Sep. 12(9):900-4. [Medline].
52. Simms I, Stephenson JM, Mallinson H, Peeling RW, Thomas K, Gokhale R, et al. Risk factors associated
with pelvic inflammatory disease. Sex Transm Infect. 2006 Dec. 82(6):452-7. [Medline]. [Full Text].
53. Toth M, Patton DL, Esquenazi B, Shevchuk M, Thaler H, Divon M. Association between Chlamydia
trachomatis and abnormal uterine bleeding. Am J Reprod Immunol. 2007 May. 57(5):361-6. [Medline].
54. Peipert JF, Ness RB, Blume J, Soper DE, Holley R, Randall H, et al. Clinical predictors of endometritis in
http://emedicine.medscape.com/article/256448-overview#showall

Page 6 of 8

Pelvic Inflammatory Disease: Background, Pathophysiology, Etiology

12/11/15, 12:32 AM

women with symptoms and signs of pelvic inflammatory disease. Am J Obstet Gynecol. 2001 Apr.
184(5):856-63; discussion 863-4. [Medline].
55. Molander P, Finne P, Sjoberg J, Sellors J, Paavonen J. Observer agreement with laparoscopic diagnosis
of pelvic inflammatory disease using photographs. Obstet Gynecol. 2003 May. 101(5 Pt 1):875-80.
[Medline].
56. Risser WL, Risser JM, Benjamins LJ, Feldmann JM. Incidence of Fitz-Hugh-Curtis syndrome in
adolescents who have pelvic inflammatory disease. J Pediatr Adolesc Gynecol. 2007 Jun. 20(3):179-80.
[Medline].
57. Sanfilippo JS. The silent epidemic of Chlamydia: what are we missing here?. J Pediatr Adolesc Gynecol.
2008 Oct. 21(5):231-2. [Medline].
58. Haggerty CL, Ness RB. Newest approaches to treatment of pelvic inflammatory disease: a review of
recent randomized clinical trials. Clin Infect Dis. 2007 Apr 1. 44(7):953-60. [Medline].
59. Tukeva TA, Aronen HJ, Karjalainen PT, Molander P, Paavonen T, Paavonen J. MR imaging in pelvic
inflammatory disease: comparison with laparoscopy and US. Radiology. 1999 Jan. 210(1):209-16.
[Medline].
60. Burnett AM, Anderson CP, Zwank MD. Laboratory-confirmed gonorrhea and/or chlamydia rates in
clinically diagnosed pelvic inflammatory disease and cervicitis. Am J Emerg Med. 2012 Sep. 30(7):1114-7.
[Medline].
61. Schoeman SA, Stewart CM, Booth RA, Smith SD, Wilcox MH, Wilson JD. Assessment of best single
sample for finding chlamydia in women with and without symptoms: a diagnostic test study. BMJ. 2012
Dec 12. 345:e8013. [Medline]. [Full Text].
62. Taylor-Robinson D, Stacey CM, Jensen JS, Thomas BJ, Munday PE. Further observations, mainly
serological, on a cohort of women with or without pelvic inflammatory disease. Int J STD AIDS. 2009 Oct.
20(10):712-8. [Medline].
63. Thomassin-Naggara I, Darai E, Bazot M. Gynecological pelvic infection: what is the role of imaging?.
Diagn Interv Imaging. 2012 Jun. 93(6):491-9. [Medline].
64. Horrow MM. Ultrasound of pelvic inflammatory disease. Ultrasound Q. 2004 Dec. 20(4):171-9. [Medline].
65. Goharkhay N, Verma U, Maggiorotto F. Comparison of CT- or ultrasound-guided drainage with
concomitant intravenous antibiotics vs. intravenous antibiotics alone in the management of tubo-ovarian
abscesses. Ultrasound Obstet Gynecol. 2007 Jan. 29(1):65-9. [Medline].
66. Del Frate C, Girometti R, Pittino M, et al. Deep retroperitoneal pelvic endometriosis: MR imaging
appearance with laparoscopic correlation. Radiographics. 2006. 26(6):1705-18.
67. Romero R, Espinoza J, Mazor M. Can endometrial infection/inflammation explain implantation failure,
spontaneous abortion, and preterm birth after in vitro fertilization?. Fertil Steril. 2004 Oct. 82(4):799-804.
[Medline].
68. Liu B, Donovan B, Hocking JS, Knox J, Silver B, Guy R. Improving adherence to guidelines for the
diagnosis and management of pelvic inflammatory disease: a systematic review. Infect Dis Obstet
Gynecol. 2012. 2012:325108. [Medline]. [Full Text].
69. Simms I, Vickers MR, Stephenson J, Rogers PA, Nicoll A. National assessment of PID diagnosis,
treatment and management in general practice: England and Wales. Int J STD AIDS. 2000 Jul. 11(7):4404. [Medline].
70. Shih TY, Gaydos CA, Rothman RE, Hsieh YH. Poor provider adherence to the Centers for Disease
Control and Prevention treatment guidelines in US emergency department visits with a diagnosis of pelvic
inflammatory disease. Sex Transm Dis. 2011 Apr. 38(4):299-305. [Medline].
71. Scholes D, Stergachis A, Heidrich FE, Andrilla H, Holmes KK, Stamm WE. Prevention of pelvic
inflammatory disease by screening for cervical chlamydial infection. N Engl J Med. 1996 May 23.
334(21):1362-6. [Medline].
72. Trent M, Haggerty CL, Jennings JM, Lee S, Bass DC, Ness R. Adverse adolescent reproductive health
outcomes after pelvic inflammatory disease. Arch Pediatr Adolesc Med. 2011 Jan. 165(1):49-54.
[Medline].
73. Anschuetz GL, Asbel L, Spain CV, et al. Association between enhanced screening for Chlamydia
trachomatis and Neisseria gonorrhoeae and reductions in sequelae among women. J Adolesc Health.
2012 Jul. 51(1):80-5. [Medline].
74. US Preventive Services Task Force. Available at . Screening for Chlamydial Infection. Available at
http://www.ahrq.gov/clinic/uspstf/uspschlm.htm. Accessed: March 26, 2010.
75. Gift TL, Gaydos CA, Kent CK, Marrazzo JM, Rietmeijer CA, Schillinger JA, et al. The program cost and
cost-effectiveness of screening men for Chlamydia to prevent pelvic inflammatory disease in women. Sex
Transm Dis. 2008 Nov. 35(11 Suppl):S66-75. [Medline].
76. Irwin KL, Moorman AC, O'Sullivan MJ, Sperling R, Koestler ME, Soto I, et al. Influence of human
immunodeficiency virus infection on pelvic inflammatory disease. Obstet Gynecol. 2000 Apr. 95(4):525-34.
[Medline].
77. Mugo NR, Kiehlbauch JA, Nguti R, Meier A, Gichuhi JW, Stamm WE, et al. Effect of human
immunodeficiency virus-1 infection on treatment outcome of acute salpingitis. Obstet Gynecol. 2006 Apr.
107(4):807-12. [Medline].
78. Trent M, Ellen JM, Walker A. Pelvic inflammatory disease in adolescents: care delivery in pediatric
ambulatory settings. Pediatr Emerg Care. 2005 Jul. 21(7):431-6. [Medline].

http://emedicine.medscape.com/article/256448-overview#showall

Page 7 of 8

Pelvic Inflammatory Disease: Background, Pathophysiology, Etiology

12/11/15, 12:32 AM

79. Ness RB, Soper DE, Holley RL, et al. for the Pelvic Inflammatory Disease Evaluation and Clinical Health
(PEACH) Study Investigators. Effectiveness of inpatient and outpatient treatment strategies for women
with pelvic inflammatory disease: Results from the pelvic inflammatory disease evaluation and clinical
health (PEACH) randomized trial. Am J Obstet Gynecol. 2001. 186:929-37.
80. Savaris RF, Teixeira LM, Torres TG, Edelweiss MI, Moncada J, Schachter J. Comparing ceftriaxone plus
azithromycin or doxycycline for pelvic inflammatory disease: a randomized controlled trial. Obstet
Gynecol. 2007 Jul. 110(1):53-60. [Medline].
81. Bevan CD, Ridgway GL, Rothermel CD. Efficacy and safety of azithromycin as monotherapy or combined
with metronidazole compared with two standard multidrug regimens for the treatment of acute pelvic
inflammatory disease. J Int Med Res. 2003 Jan-Feb. 31(1):45-54. [Medline].
82. Bradshaw CS, Chen MY, Fairley CK. Persistence of Mycoplasma genitalium following azithromycin
therapy. PLoS One. 2008. 3(11):e3618. [Medline]. [Full Text].
83. [Guideline] CDC. Update to CDC's sexually transmitted diseases treatment guidelines, 2006.
fluoroquinolones no longer recommended for treatment of gonococcal infections. MMWR Morb Mortal
Wkly Rep. Apr 13 2007. 56(14):332-6.
84. [Guideline] Centers for Disease Control and Prevention (CDC). Update to CDCs Sexually transmitted
diseases treatment guidelines, 2010: oral cephalosporins no longer a recommended treatment for
gonococcal infections. MMWR Morb Mortal Wkly Rep. 2012 Aug 10;61(31):. 590-4. [Medline]. [Full Text].
85. Bakken IJ, Ghaderi S. Incidence of pelvic inflammatory disease in a large cohort of women tested for
Chlamydia trachomatis: a historical follow-up study. BMC Infect Dis. Aug 14 2009. 9(1):130.
Medscape Reference 2011 WebMD, LLC

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