26/2/2018 Enfermedad pélvica inflamatoria: patogénesis, microbiología y factores de riesgo - UpToDate

Autor: Jonathan Ross, MD

Editor de sección: Noreen A Hynes, MD, MPH, DTM y H
Editor Adjunto: Allyson Bloom, MD

Divulgaciones del colaborador

Todos los temas se actualizan a medida que hay nuevas pruebas disponibles y nuestro proceso de revisión
por pares está completo.
Revisión de literatura actual hasta: enero 2018. | Este tema se actualizó por última vez el 13 de
febrero de 2018.

INTRODUCCIÓN - La enfermedad inflamatoria pélvica (EPI) se refiere a la infección aguda de las

estructuras del tracto genital superior en mujeres, que afecta a algunos o todos los úteros, oviductos y
ovarios; esto a menudo va acompañado de la participación de los órganos pélvicos vecinos. Por
convención, el PID es iniciado por un agente de transmisión sexual, que asciende al tracto genital superior,
distinguiéndolo de las infecciones pélvicas causadas por procedimientos médicos transcervicales, el
embarazo y otros procesos abdominales primarios que pueden extenderse a los órganos pélvicos.

En general, la prevalencia de EIP en los Estados Unidos y muchos otros países ricos en recursos ha
disminuido en la última década [ 1,2 ]. En los Estados Unidos, el PID representa aproximadamente 106,000
consultas ambulatorias y 60,000 hospitalizaciones cada año, y es una causa frecuente de visitas al
departamento de emergencias [ 1 ]. Cada mujer con PID cuesta alrededor de $ 2000 USD para tratar,
llegando a $ 6000 si desarrolla dolor pélvico crónico [ 3 ].

La patogénesis y la microbiología de la EPI, así como los factores de riesgo para la EIP serán revisados
aquí. Las características clínicas, el diagnóstico, el tratamiento y las secuelas de este trastorno se tratan
por separado. (Consulte "Enfermedad inflamatoria pélvica: manifestaciones clínicas y diagnóstico" y
"Enfermedad inflamatoria pélvica: tratamiento" ).

PATOGENIA : la flora vaginal de la mayoría de las mujeres sanas y normales incluye una variedad de
bacterias potencialmente patógenas [ 4 ]. Entre ellos se encuentran especies de estreptococos,
estafilococos, Enterobacteriaceae (más comúnmente Klebsiella spp, Escherichia coli y Proteus spp) y una
variedad de anaerobios. En comparación con las especies de Lactobacillus dominantes, no patógenas
productoras de peróxido de hidrógeno , estos otros organismos están presentes en cantidades bajas, y el
flujo y reflujo bajo la influencia de cambios hormonales (por ejemplo, embarazo, ciclo menstrual), método
anticonceptivo, actividad sexual, y otras fuerzas aún desconocidas.

El canal endocervical funciona como una barrera que protege el tracto genital superior normalmente estéril
de los organismos del ecosistema vaginal dinámico. La infección endocervical con patógenos de
transmisión sexual puede alterar esta barrera. La alteración de esta barrera proporciona acceso a las
bacterias vaginales a los órganos genitales superiores, infectando el endometrio, luego endosalpinx,
corteza ovárica, peritoneo pélvico y su estroma subyacente. La infección resultante puede ser subclínica o
manifestarse como la entidad clínica de la enfermedad inflamatoria pélvica (EIP). Las razones por las que
las bacterias del tracto genital inferior causan PID en algunas mujeres pero no en otras no se conocen
completamente, pero pueden relacionarse con variaciones genéticas en la respuesta inmune, niveles de
estrógenos que afectan la viscosidad del moco cervical y la carga bacteriana [ 5,6 ].

Los pacientes con EPI pueden presentar una enfermedad clínica en cualquier punto a lo largo de un
continuo de endometritis (con tubos normales, ovarios y peritoneo) a salpingitis (con inflamación de las
trompas de Falopio y las estructuras pélvicas adyacentes). Esto limita la sensibilidad de la visualización
directa de las trompas de Falopio a través de la laparoscopia cuando se hace un diagnóstico de EPI debido
a que no se puede ver la endometritis y la inflamación intratubular leve [ 7,8 ]. (Consulte "Enfermedad
inflamatoria pélvica: manifestaciones clínicas y diagnóstico" ).
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MICROBIOLOGÍA - Neisseria gonorrhoeae y Chlamydia trachomatis son los patógenos identificados con
mayor frecuencia en la enfermedad pélvica inflamatoria (EIP) entre las mujeres premenopáusicas
sexualmente activas. Mycoplasma genitalium también es probable que sea una causa en el grupo
premenopáusico. E. coli y anaerobios colónicos pueden ser responsables de los raros casos de PID
observados en mujeres posmenopáusicas. Los patógenos muy raros identificados incluyen Mycobacterium
tuberculosis y los agentes de la actinomicosis. Sin embargo, en la mayoría de los casos, se desconoce la
etiología microbiana precisa de la EPI. Independientemente del patógeno iniciador, la PID se considera
clínicamente una infección mixta.

Neisseria gonorrhoeae - N. gonorrhoeae fue la primera causa identificada de PID. (Ver "Epidemiología y
patogénesis de la infección por Neisseria gonorrhoeae" ).

Aproximadamente el 15 por ciento de las mujeres con una infección endocervical de N. gonorrhoeae
continúan desarrollando EPI [ 9,10 ]. La proporción de PID causada por N. gonorrhoeae varía ampliamente
y refleja la prevalencia subyacente de gonorrea en la población local. Su importancia tiende a ser mayor en
el sudeste de los Estados Unidos, menos en el noroeste de los Estados Unidos y mucho menos en Europa
occidental [ 11,12 ]. Ha habido una evolución constante de las cepas resistentes a múltiples fármacos
desde principios de los años ochenta, y un tercio de los aislamientos de los Estados Unidos actualmente
tienen algún tipo de resistencia a los medicamentos. (Ver "Tratamiento de infecciones no complicadas por
Neisseria gonorrhoeae" .)

La PID gonocócica tiende a ser clínicamente más severa que la EPI por clamidia [ 13 ], lo que puede
conducir a un diagnóstico y tratamiento más precoz. (Consulte "Enfermedad inflamatoria pélvica:
manifestaciones clínicas y diagnóstico" ).

Chlamydia trachomatis : la clamidia genital es la enfermedad bacteriana sexualmente transmisible más

común. En los Estados Unidos, también es la enfermedad infecciosa reportable más común, con
aproximadamente 1,5 millones de casos informados anualmente [ 11 ]. C. trachomatis representa
aproximadamente un tercio de los casos de EIP, con una variación geográfica menor en la prevalencia que
la observada para la EIP asociada a la gonorrea.

Como se observó con las infecciones gonocócicas genitales en mujeres, aproximadamente del 10 al 15 por
ciento de las infecciones por C. trachomatis endocervicales producen PID, pero las infecciones subclínicas
asintomáticas también son comunes, y pueden presentarse años más tarde como dolor pélvico crónico o
infertilidad. (Consulte "Manifestaciones clínicas y diagnóstico de infecciones por Chlamydia trachomatis",
sección sobre "Enfermedad inflamatoria pélvica" ).

Las mujeres de 16 a 24 años representan la mayoría de los casos de clamidia. En un informe de 150,000
de esas mujeres, aquellas con el riesgo más bajo aún tenían una prevalencia del 6 por ciento de clamidia
genital, que representaba el 17 por ciento de las infecciones en esta muestra [ 14 ]. Muchos, pero no todos,
los estudios han mostrado una reducción en las tasas de PID después de la introducción del cribado de
clamidia en mujeres jóvenes. Como ejemplo, el cribaje y el tratamiento anual de clamidia entre mujeres de
18 a 34 años con riesgo redujo la prevalencia de PID en un 56 por ciento (8 versus 18 por 10.000 meses)
en comparación con los administrados tradicionalmente por riesgo y evaluación sintomática [ 15].] Se
recomienda el cribado anual de adolescentes y mujeres jóvenes sexualmente activas y mujeres mayores
con mayor riesgo de clamidia en los Estados Unidos y en otros países [ 16,17 ]. Esto se discute con mayor
detalle en otro lugar. (Consulte "Detección de infecciones de transmisión sexual", sección sobre "Mujeres"
).

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]. (See
"Mycoplasma genitalium infection in men and women", section on 'Pelvic inflammatory disease'.)

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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 [19]. The role of these and other anaerobic bacteria in the pathogenesis of PID
remains to be proven.

Investigations of various other mycoplasma species, such as Mycoplasma hominis, have been fueled by the
ability of these organisms to cause urethritis in the male, but their relevance to PID is not yet clear. (See
"Mycoplasma hominis and Ureaplasma urealyticum infections".)

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, Klebsiella spp, Proteus
mirabilis, Haemophilus spp, Bacteroides/Prevotella spp, Peptococcus, and Peptostreptococcus spp from
women with PID [20-22]. 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 [23].

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) [20,22-25].

RISK FACTORS — Sex is the primary risk factor for pelvic inflammatory disease (PID). Celibate women are
not at risk for PID [26], 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.

In the United States, African-American or Black-Caribbean ethnicity has been associated with a higher risk
of PID. The reasons for this are likely multifactorial, possibly related to access to care or behavioral
differences. These racial differences in PID risk may be decreasing over time [27].

Multiple partners — The importance of multiple partners was illustrated by a study that compared 712
women hospitalized for PID with 2719 controls [28]. 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 [29-31]. One report, however, did not confirm a role
for coital frequency [29].

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 [20].

Age — PID occurs in highest frequency among those 15 to 25 years of age [10,32]; the incidence in women
older than the age of 35 is only one-seventh that in younger women [33]. 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 [11,34]. 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 [35].

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

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54 percent) and fivefold (at 30 percent) greater, respectively, compared to those whose first infection
occurred older than age 30 [36].

Previous PID — Approximately one in four women with PID will suffer recurrence [37]. In one study, a
previous episode of PID increased the risk for subsequent episodes by a factor of 2.3 [29]. 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 [38]. 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 [39].

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 [40].

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 [41]. However, OC use has traditionally been associated with a 50 percent reduction in PID risk [42].

Among OC users with cervical infection, asymptomatic endometritis is fourfold more common than among
their counterparts not using OCs [43], although gross salpingitis is reduced fivefold [44]. 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 [45-47]. The risk of PID is primarily limited to the first three weeks after IUD insertion and is
uncommon thereafter [46]. One low quality trial suggested that IUD removal in the setting of PID results in
better clinical outcomes [48], but most guidelines note that leaving the IUD in place while treating acute PID
with antibiotics is acceptable with close follow-up [47]. 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 [49]. In a study of 475 isolates of
actinomyces species, 30 percent of the clinical specimens originated in association with IUDs [50]. 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 [51].
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) [52].

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 level, and they answer the four or five key questions a patient might have about a given
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condition. 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 and Chlamydia trachomatis, which account
for an estimated one-third 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.

REFERENCES

1. Centers for Disease Control and Prevention (CDC). Pelvic Inflammatory Disease (PID). http://www.cd
c.gov/std/pid/stats.htm (Accessed on January 05, 2015).
2. French CE, Hughes G, Nicholson A, et al. Estimation of the rate of pelvic inflammatory disease
diagnoses: trends in England, 2000-2008. Sex Transm Dis 2011; 38:158.
3. Yeh JM, Hook EW 3rd, Goldie SJ. A refined estimate of the average lifetime cost of pelvic
inflammatory disease. Sex Transm Dis 2003; 30:369.
4. Galask RP, Larsen B, Ohm MJ. Vaginal flora and its role in disease entities. Clin Obstet Gynecol 1976;
19:61.
5. Morré SA, Karimi O, Ouburg S. Chlamydia trachomatis: identification of susceptibility markers for
ocular and sexually transmitted infection by immunogenetics. FEMS Immunol Med Microbiol 2009;
55:140.
6. Ness RB, Kip KE, Hillier SL, et al. A cluster analysis of bacterial vaginosis-associated microflora and
pelvic inflammatory disease. Am J Epidemiol 2005; 162:585.
7. Molander P, Finne P, Sjöberg J, et al. Observer agreement with laparoscopic diagnosis of pelvic
inflammatory disease using photographs. Obstet Gynecol 2003; 101:875.

https://www.uptodate.com/contents/pelvic-inflammatory-disease-pathogenesis-microbiology-and-risk-factors?search=ENFERMEDAD%20PELVIC… 5/8
26/2/2018 Enfermedad pélvica inflamatoria: patogénesis, microbiología y factores de riesgo - UpToDate

8. Gaitán H, Angel E, Diaz R, et al. Accuracy of five different diagnostic techniques in mild-to-moderate
pelvic inflammatory disease. Infect Dis Obstet Gynecol 2002; 10:171.
9. Rendtroff RC, Curran JW, Chandler RW, et al. Economic consequences of gonorrhea in women:
experience from an Urban hospital. J Am Vener Dis Assoc 1974; 1:40.
10. Forslin L, Falk V, Danielsson D. Changes in the incidence of acute gonococcal and nongonococcal
salpingitis. A five-year study from an urban area of central Sweden. Br J Vener Dis 1978; 54:247.
11. Centers for Disease Control and Prevention. Sexually Transmitted Disease Surveillance, 2015. Atlant
a, GA: US Department of Health and Human Services; October 2016.
12. HIV and Sexually Transmitted Infections Department. STI diagnoses and rates in England by gender,
2004-2013. Public Health England, 2014. https://www.gov.uk/government/uploads/system/uploads/atta
chment_data/file/340430/Table_1_STI_diagnoses_and_rates_in_England_by_gender.pdf (Accessed o
n January 21, 2015).
13. Reekie J, Donovan B, Guy R, et al. Risk of Pelvic Inflammatory Disease in Relation to Chlamydia and
Gonorrhea Testing, Repeat Testing, and Positivity: A Population-Based Cohort Study. Clin Infect Dis
2018; 66:437.
14. Mosure DJ, Berman S, Fine D, et al. Genital Chlamydia infections in sexually active female
adolescents: do we really need to screen everyone? J Adolesc Health 1997; 20:6.
15. Scholes D, Stergachis A, Heidrich FE, et al. Prevention of pelvic inflammatory disease by screening
for cervical chlamydial infection. N Engl J Med 1996; 334:1362.
16. National Chlamydia Screening Programme. http://www.chlamydiascreening.nhs.uk/ (Accessed on Jan
uary 05, 2015).
17. U.S. Preventive Services Task Force (USPSTF). http://www.uspreventiveservicestaskforce.org/Page/N
ame/tools-and-resources-for-better-preventive-care (Accessed on January 05, 2015).
18. Dean G, Whetham J, Soni S, et al. Mycoplasma genitalium and macrolide resistance in pelvic inflamm
atory disease (PID) presented at the Annual Conference for the British Association for Sexual Health a
nd HIV, Oxford, England, July 10-12, 2016.
19. Hebb JK, Cohen CR, Astete SG, et al. Detection of novel organisms associated with salpingitis, by use
of 16S rDNA polymerase chain reaction. J Infect Dis 2004; 190:2109.
20. Eschenbach DA, Buchanan TM, Pollock HM, et al. Polymicrobial etiology of acute pelvic inflammatory
disease. N Engl J Med 1975; 293:166.
21. Thompson SE 3rd, Hager WD, Wong KH, et al. The microbiology and therapy of acute pelvic
inflammatory disease in hospitalized patients. Am J Obstet Gynecol 1980; 136:179.
22. Chow AW, Malkasian KL, Marshall JR, Guze LB. The bacteriology of acute pelvic inflammatory
disease. Am J Obstet Gynecol 1975; 122:876.
23. Sweet RL, Draper DL, Hadley WK. Etiology of acute salpingitis: influence of episode number and
duration of symptoms. Obstet Gynecol 1981; 58:62.
24. Soper DE, Brockwell NJ, Dalton HP, Johnson D. Observations concerning the microbial etiology of
acute salpingitis. Am J Obstet Gynecol 1994; 170:1008.
25. Sweet RL, Mills J, Hadley KW, et al. Use of laparoscopy to determine the microbiologic etiology of
acute salpingitis. Am J Obstet Gynecol 1979; 134:68.
26. Stemmer W. Uber die ursachen von eileiterentzundungen. Gentral fur Gynnak 1941; 65:1062.
27. Leichliter JS, Chandra A, Aral SO. Correlates of self-reported pelvic inflammatory disease treatment in
sexually experienced reproductive-aged women in the United States, 1995 and 2006-2010. Sex
Transm Dis 2013; 40:413.
28. Lee NC, Rubin GL, Grimes DA. Measures of sexual behavior and the risk of pelvic inflammatory
disease. Obstet Gynecol 1991; 77:425.
https://www.uptodate.com/contents/pelvic-inflammatory-disease-pathogenesis-microbiology-and-risk-factors?search=ENFERMEDAD%20PELVIC… 6/8
26/2/2018 Enfermedad pélvica inflamatoria: patogénesis, microbiología y factores de riesgo - UpToDate

29. Flesh G, Weiner JM, Corlett RC Jr, et al. The intrauterine contraceptive device and acute salpingitis: a
multifactor analysis. Am J Obstet Gynecol 1979; 135:402.
30. Rein MF. Epidemiology of gonococcal infection. In: The Gonococcus, Roberts RB (Ed), Wiley and Son
s, New York 1977. p.1.
31. Kreisel K, Torrone E, Bernstein K, et al. Prevalence of Pelvic Inflammatory Disease in Sexually
Experienced Women of Reproductive Age - United States, 2013-2014. MMWR Morb Mortal Wkly Rep
2017; 66:80.
32. Westrom, L, Mardh PA. Epidemiology, etiology, and prognosis of acute salpingitis: A study of 1,457 lap
aroscopically verified cases. In: Nongonococcal Urethritis and Related Diseases, Hobson D, Holmes K
K (Eds), Am Soc Microbiol, Washington DC 1977. p.84.
33. Weström L. Incidence, prevalence, and trends of acute pelvic inflammatory disease and its
consequences in industrialized countries. Am J Obstet Gynecol 1980; 138:880.
34. Sonnenberg P, Clifton S, Beddows S, et al. Prevalence, risk factors, and uptake of interventions for
sexually transmitted infections in Britain: findings from the National Surveys of Sexual Attitudes and
Lifestyles (Natsal). Lancet 2013; 382:1795.
35. Jackson SL, Soper DE. Pelvic inflammatory disease in the postmenopausal woman. Infect Dis Obstet
Gynecol 1999; 7:248.
36. Hillis SD, Nakashima A, Marchbanks PA, et al. Risk factors for recurrent Chlamydia trachomatis
infections in women. Am J Obstet Gynecol 1994; 170:801.
37. Weström L. Effect of acute pelvic inflammatory disease on fertility. Am J Obstet Gynecol 1975;
121:707.
38. Eschenbach DA, Harnisch JP, Holmes KK. Pathogenesis of acute pelvic inflammatory disease: role of
contraception and other risk factors. Am J Obstet Gynecol 1977; 128:838.
39. Ness RB, Randall H, Richter HE, et al. Condom use and the risk of recurrent pelvic inflammatory
disease, chronic pelvic pain, or infertility following an episode of pelvic inflammatory disease. Am J
Public Health 2004; 94:1327.
40. Gavin L, MacKay AP, Brown K, et al. Sexual and reproductive health of persons aged 10-24 years -
United States, 2002-2007. MMWR Surveill Summ 2009; 58:1.
41. Louv WC, Austin H, Perlman J, Alexander WJ. Oral contraceptive use and the risk of chlamydial and
gonococcal infections. Am J Obstet Gynecol 1989; 160:396.
42. Rubin GL, Ory HW, Layde PM. Oral contraceptives and pelvic inflammatory disease. Am J Obstet
Gynecol 1982; 144:630.
43. Ness RB, Keder LM, Soper DE, et al. Oral contraception and the recognition of endometritis. Am J
Obstet Gynecol 1997; 176:580.
44. Wølner-Hanssen P, Svensson L, Mårdh PA, Weström L. Laparoscopic findings and contraceptive use
in women with signs and symptoms suggestive of acute salpingitis. Obstet Gynecol 1985; 66:233.
45. Lee NC, Rubin GL, Borucki R. The intrauterine device and pelvic inflammatory disease revisited: new
results from the Women's Health Study. Obstet Gynecol 1988; 72:1.
46. Grimes DA. Intrauterine device and upper-genital-tract infection. Lancet 2000; 356:1013.
47. Workowski KA, Bolan GA, Centers for Disease Control and Prevention. Sexually transmitted diseases
treatment guidelines, 2015. MMWR Recomm Rep 2015; 64:1.
48. Altunyurt S, Demir N, Posaci C. A randomized controlled trial of coil removal prior to treatment of
pelvic inflammatory disease. Eur J Obstet Gynecol Reprod Biol 2003; 107:81.
49. Lee YC, Min D, Holcomb K, et al. Computed tomography guided core needle biopsy diagnosis of
pelvic actinomycosis. Gynecol Oncol 2000; 79:318.

https://www.uptodate.com/contents/pelvic-inflammatory-disease-pathogenesis-microbiology-and-risk-factors?search=ENFERMEDAD%20PELVIC… 7/8
26/2/2018 Enfermedad pélvica inflamatoria: patogénesis, microbiología y factores de riesgo - UpToDate

50. Hall V, Talbot PR, Stubbs SL, Duerden BI. Identification of clinical isolates of actinomyces species by
amplified 16S ribosomal DNA restriction analysis. J Clin Microbiol 2001; 39:3555.
51. Fleury FJ. Adult vaginitis. Clin Obstet Gynecol 1981; 24:407.
52. Ness RB, Hillier SL, Kip KE, et al. Bacterial vaginosis and risk of pelvic inflammatory disease. Obstet
Gynecol 2004; 104:761.

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