eMedicine Specialties > Obstetrics and Gynecology > Infections

Salpingitis

Author: Suzanne Moore Shepherd, MD, MS, DTM&H, FACEP, FAAEM, Associate Professor, Department of Emergency Medicine, Hospital of the University of Pennsylvania; Director of Education and Research, PENN Travel Medicine
Coauthor(s): Clarisa R Gracia, MD, Staff Physician, Department of Obstetrics and Gynecology, University of Pennsylvania; Evan M Meiner, MD, Director of Emergency Medicine Trauma Care, Department of Emergency Medicine, North Shore University Hospital; William H Shoff, MD, DTM&H, Director, PENN Travel Medicine, Associate Professor, Department of Emergency Medicine, Hospital of the University of Pennsylvania
Contributor Information and Disclosures

Updated: Aug 16, 2007

Introduction

Background

Acute salpingitis is a gynecologic condition consisting of infection and inflammation of the oviducts. In most clinical situations, the terms acute salpingitis and pelvic inflammatory disease (PID) are used synonymously to describe acute infection of the female upper genital tract. PID is a condition that lacks a precise definition and may include infection of any or all of the following anatomic locations: the endometrium (endometritis), the oviducts (salpingitis), the ovaries (oophoritis), the uterine wall (myometritis), the uterine serosa and broad ligaments (parametritis), and the pelvic peritoneum. In addition, a tuboovarian abscess (TOA) may form. Many authors prefer the term salpingitis because, at a minimum, the oviduct (fallopian tube) is involved, and most of the long-term sequelae of PID result from destruction of the tubal architecture.

Pathophysiology

Most cases of acute salpingitis occur in 2 stages. The first involves acquisition of a vaginal or cervical infection. The second involves ascent of the infection to the upper genital tract. Although the exact mechanism of ascent is unknown, retrograde menstrual flow and opening of the cervix during menstruation has been theorized to facilitate ascent of infection. Surgical procedures, such as endometrial biopsy, curettage, and hysteroscopies, break the cervical barrier, predisposing women to these infections. Also, alterations in the cervicovaginal microenvironment resulting from antibiotic treatment, ovulation, menstruation, or sexually transmitted disease (STD) can disrupt the balance of endogenous flora, causing normally nonpathogenic organisms to overgrow and ascend to the upper genital tract.

These factors also may facilitate the ascent of pathogens, such as Neisseria gonorrhoeae or Chlamydia trachomatis. Intercourse also may contribute to ascent of infection, with uterine coital contractions mechanically inducing organisms to ascend. In addition, sperm can carry organisms into the upper genital tract following intercourse.

Once ascended, both microbial and host factors appear to play a role in the degree of host inflammation and scarring produced. These processes remain poorly understood. One area of research that has provided some insight is the interaction of chlamydia with host cells. Both clinical and histologic studies have shown significant host variability in response to chlamydial infection. 

An intriguing preliminary study by den Hartog et al, examined 5 single nucleoside polymorphisms (SNPs) in 4 genes that encode for pattern recognition receptors (PRRs) on circulating immune cells (such as macrophages) and local tubal cells.1  These PRRs recognize specific chlamydial pathogen-associated molecular patterns (PAMPs), facilitating the ability of the host cell to recognize the presence of a pathogen. PAMPs are unique microorganism cell wall components or intracellular components. The authors found that the presence of 2 or more SNPs in a patient appeared to correlate with an increase in laparoscopically identified tubal pathology. The authors suggested several possible mechanisms for this effect, including synthesis of aberrant PRRs or change in regulation of these PRRs.   

The organisms most commonly associated with acute salpingitis are N gonorrhoeae and C trachomatis (15-75%). Unlike infection in many other areas of the body, acute salpingitis is usually polymicrobial in nature. Other associated organisms include Ureaplasma urealyticum, Mycoplasma genitalium, Trichomonas vaginalis, Gardnerella vaginalis, and mixed anaerobic and aerobic bacteria; however, the exact roles of these organisms remain poorly understood.

The contribution of non-STD acute salpingitis is unknown but may be as high as 20%. Controversy surrounds the role of bacterial vaginosis (BV) and salpingitis. Multiple studies, including a large (N = 1179) multicenter US study2 , have not supported an association between baseline G vaginalis and BV and the development of PID except in a subgroup of women with heavy growth of BV-associated microorganisms, especially if they had more than 2 recent sexual partners. 

A cross-sectional study from the University of Pittsburgh3 looked at the roles of T vaginalis and herpes simplex virus 2 (HSV-2) in PID. Both had previously been shown to be associated with PID or tubal scarring and ectopic pregnancy. In this study, involving 736 women, those with T vaginalis were found to have increased histologic evidence of acute endometritis. Co-infection of HSV-2 with C trachomatis, N gonorrhoeae, T vaginalis, or BV was also associated with acute endometritis. HSV-2 was also the only microorganism directly associated with fallopian tube obstruction.

The authors proposed several hypotheses for the role of HSV-2 in infection and inflammation, including (1) lower tract ulcerations produced by HSV-2 might disrupt the endocervical canal barrier, facilitating the spread of lower tract organisms to the upper tract, (2) presence of inflammatory cells in the upper tract in response to HSV-2 might increase the likelihood of fallopian tube damage, or (3) presence of these organisms might be a marker for sexual activity and the coacquisition of a PID-associated STD.

Frequency

United States

PID is the most common gynecologic reason for emergency medicine visits in the United States. From 1995-2001, approximately 769,859 cases of acute salpingitis were reported annually in the United States. Of these, 91% were diagnosed in the ambulatory setting, with an average of 25,235 (4 of 1000 women aged 15-44 y) seen in emergency departments.4  However, the true incidence is probably much higher because of incomplete and untimely conventional nonelectronic reporting methods and because many cases of silent or smoldering salpingitis occur and are discovered only when patient develops late chronic complications of the disease. The annual direct cost of care for PID and its sequelae has been estimated at $2 billion, with an estimate of $10 billion annually when indirect costs are considered.5

The 2002 CDC revised diagnostic and treatment guidelines for PID, requiring only adnexal, cervical motion, or uterine tenderness rather than both adnexal and cervical motion tenderness, have made a clinically significant increase in the reported prevalence and incidence of PID. The actual incidence, based on National Center for Health Statistics Data sets, has declined from 1985-2001. Hospitalization for PID has declined approximately 68% (from 4.4 to 1.4 per 1000 women aged 15-44 y, P =.0001), with the rate of hospitalization highest for women aged 20-24. This decline correlates with national declines in reported chlamydial and gonorrheal infections in areas with long-term programs for screening and treatment.

Salpingitis is the most common serious infection of women aged 16-25 years. The estimated annual incidence is approximately 1% for women aged 15-34 years, and the risk that a sexually active adolescent will develop the disease is 1 in 8. Ultimately, salpingitis affects approximately 11% of reproductive-aged women. A midwestern study reported PID in 1% of women in the post-partum year, with young age and positive gonorrhea screening independent predictors of disease.6  TOA occurs in 4-15% of women hospitalized with salpingitis.

International

Worldwide frequency of salpingitis is difficult to estimate. Access to health care, diagnostic and lab techniques, medical data collection methods, and other factors vary in different regions of the world, making accurate estimates difficult and leading to underestimates of disease. Although no good data exist on salpingitis, the World Health Organization has published data on the number of new cases of gonorrhea and chlamydia worldwide as of 1995. In that year, approximately 31 million cases of Gonorrhea infection and 22.5 million cases of Chlamydia infection, the major causative organisms of salpingitis, occurred in women worldwide. Geographically, the vast majority of these cases were in the developing world. The highest prevalences were in sub-Saharan Africa and Southeast Asia, with the lowest in East Asia and the Pacific. In addition, complications of STDs, including salpingitis, are more common in countries with poorer resources.

Mortality/Morbidity

The mortality rate directly related to salpingitis and/or PID has been estimated at 0.29 patients per 100,000 cases for patients aged 15-44 years. Most deaths result from rupture of a TOA, with the mortality rate of rupture being 5-10% despite modern medical treatment. Most importantly, salpingitis results in long-term sequelae in 25% of patients. The most common and serious among these sequelae are tubal factor infertility and ectopic pregnancy. Other sequelae include chronic pelvic pain, dyspareunia, menstrual disturbances, and pelvic adhesions. Chronic pelvic pain has been associated with reduced mental and physical health. Early diagnosis and treatment effectively reduces the incidence of complications.

Salpingitis causes approximately 75,000-225,000 cases of infertility annually in the United States. Infertility is thought to be the result of inflammatory damage to the oviduct. Oviduct damage is estimated to occur in 8-17% of all women with 1 episode of disease, and the percentage increases dramatically with repeat episodes of salpingitis. Infertility rates approach 40-60% in women with 3 episodes of disease. The percentage also increases with the severity of scarring.

The other major sequela of salpingitis is ectopic pregnancy. Histologic studies estimate that approximately 50% of ectopic pregnancies occur in tubes damaged by salpingitis. One episode of salpingitis increases the risk of ectopic pregnancy by 7- to 10-fold. The number of reported ectopic pregnancies has increased 3-5 times over the past 20 years, and the rate of increase has been attributed to an increase in reported STDs and acute salpingitis. However, this may be misleading because physician awareness of ectopic pregnancy and its potential for mortality has increased, which may have contributed to an increase in diagnosis. Of interest, from 1985-2001 the number of hospitalizations for ectopic pregnancy has decreased, with more outpatient management. This may be a reflection of earlier PID management.

Race

Salpingitis is more common among blacks and members of lower socioeconomic classes. Black women are diagnosed with PID 2.3 times the rate of diagnosis in white women. However, no data indicate that race or socioeconomic class is an independent risk factor for salpingitis. Instead, individuals in these groups have been found to have an increased number of other risk factors, including early coitarche, single marital status, delayed medical care seeking, and multiple sexual partners.

Due to the subjective method by which PID is diagnosed, racial and socioeconomic biases may influence the diagnosis at a number of levels and selection bias is likely in studies determining such data. These groups have decreased access to health care and are more likely to seek care in STD clinics and emergency departments, where such data are collected. Other groups may seek treatment in private physician's offices, and the true incidence of salpingitis is likely to be underreported in these groups.

Sex

Acute salpingitis, by definition, occurs in female patients.

Age

The rate of acute salpingitis is highest in sexually active women aged 15-24 years. Studies indicate that people in this age group often exhibit high-risk behaviors, including multiple sexual partners, less consistent condom use, less barrier contraceptive use, coincident use of alcohol and drugs, and delay in access to medical care, and they are also less aware of their symptoms.

Physiologic factors in young women that increase the risk of PID include lower levels of protective antibodies and cervical ectopy. The disease is extremely rare in women without menstrual periods, such as pregnant, premenarchal, or postmenarchal women, but it can, and does, occur. If disease occurs during pregnancy, it usually is early in pregnancy, prior to changes in the cervical mucous barrier that prevent ascent of infection. Similarly, hormonal contraceptives, which some studies attribute to the progesterone component, have been shown to reduce the risk of salpingitis by causing a thickening in cervical mucus and shortening the duration of menstrual flow. The risk of PID doubles in young women with coitarche before 16 years of age. 

Clinical

History

A constellation of signs and symptoms define acute salpingitis, and establishing its diagnosis may be difficult. Great variation may be observed in clinical presentation, ranging from relatively asymptomatic women to those with diffuse peritonitis and life-threatening illness.

  • Pain in the lower abdomen and pelvis by far is the most common symptom of acute salpingitis. More than 90% of patients with the disease present with diffuse bilateral lower abdominal pain. The pain often is described as constant and dull but may be described as cramping. Pain may be accentuated by motion or sexual activity. Generally, the pain is of less than 7 days in duration at presentation.
  • Approximately 75% of patients will have a coexisting purulent vaginal discharge.
  • Abnormal vaginal bleeding, especially spotting or menorrhagia, is noted in more than one third of patients.
  • Nausea and vomiting are relatively late findings in the course of the disease.
  • Patients may complain of fever.
  • As many as 5-10% of patients may develop symptoms of perihepatic inflammation (the Fitz-Hugh-Curtis syndrome), including right upper quadrant or pleuritic pain.
  • Symptoms occur more frequently toward the end of menses or early in the menstrual cycle. The temporal clustering of symptoms soon after menses may be due to low progesterone levels influencing the cervical mucus barrier, making the barrier less thick and, therefore, less effective after menstruation.

Physical

  • The diagnosis of acute salpingitis usually is based on clinical findings. Clinical diagnosis is imprecise, and, in all settings, no single historical, physical, or lab finding is both sensitive and specific for disease. Most women with acute salpingitis have tenderness to direct palpation in the lower abdomen and sometimes may have rebound tenderness. On pelvic examination, tenderness of the adnexa, which usually is bilateral, is noted. Tenderness is noted on movement of the cervix or uterus. Patients most often have mucopurulent endocervical discharge. Patients with Fitz-Hugh-Curtis syndrome may have tenderness to palpation in the right upper quadrant. Physical examination also may reveal adnexal fullness or mass, which may represent a TOA, although TOA may be present without obvious localizing findings. Patients may exhibit signs of peritonitis on examination.
  • In the last 15 years, awareness of a sizable proportion of patients with salpingitis who may have an atypical presentation and may express few or no symptoms has increased. Studies of women with tubal infertility have demonstrated that many women who were never diagnosed with salpingitis have had chlamydial infection of the upper genital tract. More than one fourth of patients presenting with atypical presentations have objective criteria for upper tract disease when examined by laparoscope. A study from the University of Lund, Sweden found 3 variables to be significant predictors for the diagnosis of salpingitis: erythrocyte sedimentation rate (ESR) (P <.0001), fever (P <.0001), and adnexal tenderness (P <.0001). In this study, these variables correctly classified 65% of patients with laparoscopically proven PID (95% CI, 61-99%).
  • Because of the poor sensitivity and specificity of history and physical examination in diagnosing salpingitis and due to the potentially large number of patients with mild or atypical symptoms, the Centers for Disease Control and Prevention (CDC) has established minimal criteria for the diagnosis of acute salpingitis. These criteria were developed in an attempt to prevent many of the complications that are caused by this disease. According to the CDC 1998 Guidelines for Treatment of Sexually Transmitted Diseases, initiate empiric antibiotic coverage in sexually active young women and others at risk for STDs if all of the following minimum criteria are present and no other causes for the illness can be identified:
    • Lower abdominal tenderness
    • Adnexal tenderness
    • Cervical motion tenderness
  • Additional criteria specified by the CDC recommendations that may be used to enhance the specificity of the minimum criteria to support the diagnosis include the following:
    • Oral temperature greater than 38.3°C or 101°F
    • Abnormal cervical or vaginal discharge
    • Elevated erythrocyte sedimentation rate (ESR)
    • Elevated C-reactive protein
    • Laboratory documentation of cervical infection with N gonorrhoeae or C trachomatis

Causes

Acute salpingitis has been thought to occur as a result of infection with N gonorrhoeae, C trachomatis, or both. C trachomatis is recovered from the upper genital tract of 15-40% of patients with disease. However, utilizing laparoscopic specimens, recent studies demonstrate that as many as 30-50% of patients may not be infected with either organism.

Unlike many other infections in the body, salpingitis is most often polymicrobial in nature. Anaerobic organisms tend to predominate, the most common of which are Bacteroides species, Peptostreptococcus species, and Peptococcus species, which are organisms that are part of the normal flora of the vagina and perineum. Many other organisms have been recovered and include G vaginalis, facultative streptococci, alpha-hemolytic streptococci, Escherichia coli, U urealyticum, HSV-2, Mycoplasma genitalium, and Mycoplasma hominis. Less common infectious etiologies include Haemophilus influenzae and other respiratory pathogens.

Until 2002, CDC guidelines recommended that HIV-positive women with PID be admitted for treatment. A large US study found no difference in outcome between inpatient and outpatient management in these patients. Worldwide, greater than 90% of HIV-positive patients are treated as outpatients. A recent study in HIV co-infected women in Nairobi, with study investigators blinded to HIV status, found that severe PID was more common in the HIV-positive group, irrespective of CD4 count. This group with severe PID tended to take longer to meet criteria for clinical improvement. No change in antibiotic management was found necessary in the HIV-positive patients. 

Outside of the United States, Mycobacterium tuberculosis may be a cause of chronic salpingitis. Actinomycetes species also have been found, but this species is identified almost exclusively in patients with an intrauterine device (IUD) in place. These patients are at increased risk for salpingitis within the first 4 months after the device is inserted. A recent study by Viberga et al, found that IUD users with PID had increased Fusobacteria and Peptostreptococcus species compared with non-IUD users with PID, and that IUD use increased the risk of complicated PID irrespective of duration of use.7  Other gynecologic procedures that breach the cervicovaginal barrier increase the risk of ascending infection as well. Vaginal douching also has been associated with an increased risk of upper genital tract infection.

More on Salpingitis

Overview: Salpingitis
Differential Diagnoses & Workup: Salpingitis
Treatment & Medication: Salpingitis
Follow-up: Salpingitis
References
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Further Reading

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Keywords

salpingitis, pelvic inflammatory disease, PID, pelvic inflammation, oviduct inflammation, oviduct infection, gynecologic infection, fallopian tube inflammation, fallopian tube infection, tuboovarian abscess, TOA, tubo-ovarian abscess, infertility, Neisseria gonorrhoeae, N gonorrhoeae, C trachomatis, Chlamydia trachomatis, Bacteroides, Peptostreptococcus, Peptococcus, gonorrhea, chlamydia, sexually transmitted disease, STD complication, STD

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Contributor Information and Disclosures

Author

Suzanne Moore Shepherd, MD, MS, DTM&H, FACEP, FAAEM, Associate Professor, Department of Emergency Medicine, Hospital of the University of Pennsylvania; Director of Education and Research, PENN Travel 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, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Coauthor(s)

Clarisa R Gracia, MD, Staff Physician, Department of Obstetrics and Gynecology, University of Pennsylvania
Clarisa R Gracia, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Obstetricians and Gynecologists, and American Society for Reproductive Medicine
Disclosure: Nothing to disclose.

Evan M Meiner, MD, Director of Emergency Medicine Trauma Care, Department of Emergency Medicine, North Shore University Hospital
Evan M Meiner, MD is a member of the following medical societies: Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

William H Shoff, MD, DTM&H, Director, PENN Travel Medicine, Associate Professor, Department of Emergency Medicine, Hospital of the University of Pennsylvania
William H Shoff, MD, DTM&H is a member of the following medical societies: American College of Physicians, American Society of Tropical Medicine and Hygiene, International Society of Travel Medicine, Society for Academic Emergency Medicine, and Wilderness Medical Society
Disclosure: Glaxo Smith Kline Consulting fee Consulting; Glaxo Smith Kline Honoraria Speaking and teaching

Medical Editor

Bruce A Meyer, MD, MBA, Vice President for Medical Affairs, Associate Dean for Health System Affairs and Director of the Faculty Practice Plan, Professor, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical School
Bruce A Meyer, MD, MBA is a member of the following medical societies: American College of Obstetricians and Gynecologists, American College of Physician Executives, American Institute of Ultrasound in Medicine, Association of Professors of Gynecology and Obstetrics, Massachusetts Medical Society, Medical Group Management Association, and Society for Maternal-Fetal Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Gail F Whitman-Elia, MD, Professor, Department of Obstetrics and Gynecology, University of South Carolina School of Medicine
Gail F Whitman-Elia, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Clinical Endocrinologists, American College of Obstetricians and Gynecologists, American Institute of Ultrasound in Medicine, American Medical Association, American Medical Women's Association, American Public Health Association, American Society for Reproductive Medicine, Endocrine Society, and South Carolina Medical Association
Disclosure: Nothing to disclose.

CME Editor

Frederick B Gaupp, MD, Consulting Staff, Department of Family Practice, Hancock Medical Center
Frederick B Gaupp, MD is a member of the following medical societies: American Academy of Family Physicians
Disclosure: Nothing to disclose.

Chief Editor

Michel E Rivlin, MD, Professor, Coordinator of Quality Assurance/Quality Improvement, 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, and Royal College of Surgeons of Edinburgh
Disclosure: Nothing to disclose.

 
 
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