Pathogenesis Of Pelvic Inflammatory Disease Research Articles

A Review of the Challenges and Complexities in the Diagnosis, Etiology, Epidemiology, and Pathogenesis of Pelvic Inflammatory Disease.

Pelvic inflammatory disease (PID) is a syndrome that causes substantial morbidity, including chronic pelvic pain, to women globally. While limited data are available from low- and middle-income countries, national databases from the United States and Europe suggest that PID incidence may be decreasing but the rate of decrease may differ by the etiologic cause. Recent studies of women with PID have reported that fewer than half of women receiving a diagnosis of PID have gonococcal or chlamydial infection, while Mycoplasma genitalium, respiratory pathogens, and the constellation of bacteria associated with bacterial vaginosis may account for a substantial fraction of PID cases. The clinical diagnosis of PID is nonspecific, creating an urgent need to develop noninvasive tests to diagnose PID. Advances in serologic testing for Chlamydia trachomatis and Neisseria gonorrhoeae could advance epidemiologic studies, while the development of vaccines against these sexually transmitted pathogens could affect incident PID and associated morbidity.

Immune Responses to Neisseria gonorrhoeae: Challenges and Opportunities With Respect to Pelvic Inflammatory Disease.

Pelvic inflammatory disease and infertility frequently develop after female genital tract infection with Neisseria gonorrhoeae, but determining their etiology from among various possibilities presents difficulties. Exploitation of serology to identify the causative agent is complicated by numerous factors, and no immunological test currently exists to determine unequivocally whether an individual currently is, or has been, infected with N. gonorrhoeae. The extensive antigenic variability of N. gonorrhoeae and its expression of antigens shared with other Neisseria species commonly carried in humans render problematic an assay that is specific for all gonococcal strains. However, novel conserved gonococcal antigens identified for potential vaccines may find additional application in diagnostic assays. N. gonorrhoeae also interferes with the adaptive immune response, and antibody responses to uncomplicated infection are usually weak. Elucidating the mechanisms whereby N. gonorrhoeae manipulates the human immune system may lead to improved understanding of the pathogenesis of pelvic inflammatory disease and infertility.

O04.6 Mycoplasma Genitalium- Is It a Pathogen in Acute Pelvic Inflammatory Disease (PID)?

BackgroundPID is a polymicrobial infectious condition of the female upper genital tract. Neisseria gonorrhoeae (GC) and Chlamydia trachomatis(CT), long considered the predominant organisms involved in the pathogenesis of PID, are...

Pelvic Inflammatory Disease

1. Maria Trent, MD, MPH* 1. *Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD. * CDC: : Centers for Disease Control and Prevention CPP: : chronic pelvic pain CT: : computed tomography IM: : intramuscular IUD: : intrauterine device IV: : intravenous KOH: : potassium hydroxide NAAT: : nucleic acid amplification testing PEACH: : Pelvic Inflammatory Evaluation and Clinical Health PID: : pelvic inflammatory disease STI: : sexually transmitted infection 1. The U. S. Centers for Disease Control and Prevention (CDC) provides evidence-based, expert-driven guidelines for effective management of pelvic inflammatory disease (PID); however, clinician adherence to the guidelines has been problematic. 2. PID practice guideline adherence is an international problem, as evidenced by a 2012 audit in the United Kingdom demonstrating that 55.5% of patients with PID did not receive care according to the British Association of Sexual Health and HIV treatment recommendations. Clinician behavior can be enhanced with the use of institutionally driven protocols, especially those that include onsite dispensing of a full course of medications. 3. Women seeking infertility services who report a history of unexplained and untreated abdominal pain are significantly more likely to have tubal infertility than women without such history; therefore caution should be used in dismissing mild symptoms (mild non-specific abdominal pain, vaginal discharge, bleeding or dyspareunia) among sexually active patients who may be at risk for PID. After completing this article, readers should be able to: 1. Describe the epidemiology and pathogenesis of pelvic inflammatory disease (PID). 2. Recognize the clinical features of PID. 3. Develop a management strategy for adolescent patients who have PID. 4. Carefully weigh the options for the disposition of patients who have PID. Justine is a 17-year-old girl who presents for evaluation of lower abdominal pain that has been increasing over the past few days. Earlier today she was eating and drinking, but has developed some nausea in the past couple of hours without vomiting. She has had soft, regular bowel movements that are free of blood and mucus. She denies dysuria, but has had some light vaginal discharge that started about 1 week ago. Justine continues to …

Does Bacterial Vaginosis Cause Pelvic Inflammatory Disease?

Pelvic inflammatory disease (PID), the infection and inflammation of the female genital tract, results in serious reproductive morbidity including infertility and ectopic pregnancy. Bacterial vaginosis (BV) is a complex alteration of the vaginal flora that has been implicated in PID. The role of BV in the etiology and pathogenesis of PID has not been studied extensively. Our objective was to extensively review data related to the relationship between BV and PID (n = 19 studies). Several studies found a link between BV and cervicitis, endometritis, and salpingitis. Furthermore, it seems that some BV-associated organisms are associated with PID, whereas others are not. However, studies demonstrating an independent association between BV-associated organisms and PID are sparse. In addition, a causal association between BV and PID has not been established. Prospective studies are needed to further delineate the role of BV in PID, with particular focus on individual BV-associated organisms.

Markedly elevated soluble E-cadherin in plasma of patient with pelvic inflammatory disease

To estimate the expression of plasma soluble E-cadherin and the gene polymorphism in patients with pelvic inflammatory disease (PID). Hospital-based case-control study. University hospital. Sixty-four women with PID. Blood specimen collection from patients before and after they received treatment. Enzyme-linked immunosorbent assay and polymerase chain reaction-restriction fragment length polymorphism were respectively used to measure the plasma soluble E-cadherin level and E-cadherin polymorphism. The level of plasma E-cadherin was significantly elevated in patients with PID as compared with that in normal controls; it decreased significantly after treatment when compared with levels noted in the same patients before they received treatment. When the cutoff level of plasma E-cadherin level was set to 20.22 ng/mL on the basis of receiver-operating characteristic curve (ROC), the sensitivity, specificity, and the area under the curve of plasma E-cadherin level for predicting PID were 0.81, 0.80, and 0.835 (95% confidence interval 0.76-0.90), respectively. The adjusted odds ratio for age, white blood cell count, and C-reactive protein levels was 19.66 (5.48-70.47). Elevated plasma soluble E-cadherin expression was involved in the pathogenesis of PID and is useful for the diagnosis of PID.

The baboon ( Papio anubis) as a novel model of Chlamydia trachomatis pelvic inflammatory disease for testing intrauterine contraception

Pelvic inflammatory disease (PID) is a major source of morbidity and infertility. The influence of intrauterine contraception (IUC) on the pathogenesis of PID is unknown. To better understand the biology of PID, and eventually study its relationship to IUC use, we sought to develop a baboon PID model.

Markedly elevated plasma myeloperoxidase protein in patients with pelvic inflammatory disease who have A allele myeloperoxidase gene polymorphism

To compared the plasma levels and the genetic polymorphism of myeloperoxidase in patients with pelvic inflammatory disease (PID) and healthy controls. A random consecutive study. University hospital. Forty-four women who were diagnosed with PID. Collected blood specimens of patients before and after they received treatment. ELISA and polymerase chain reaction-restriction fragment length polymorphism were respectively used to measure the plasma levels and genetic polymorphism of myeloperoxidase. We found the plasma level of myeloperoxidase was elevated in PID patients compared with that in normal controls and decreased significantly compared with that in the same patients after they received treatment. PID patients with myeloperoxidase G/A alleles significantly tended to have elevated plasma concentration of myeloperoxidase, whereas PID patients with G/G homozygous alleles did not. Elevated expression of myeloperoxidase may be involved in the pathogenesis of PID and could be useful for the diagnosis of PID. Furthermore, G/A alleles of myeloperoxidase may contribute to such elevation in PID patients.

Association between elevated neutrophil defensin levels and endometritis.

The role of host defenses in the pathogenesis of pelvic inflammatory disease (PID) remains largely uncharacterized. The antimicrobial peptides defensins are important components of innate host defense. To explore the relationship between neutrophil defensins and upper genital tract infection, 377 women who were at risk for PID were enrolled in a study. Women infected with Neisseria gonorrhoeae, Trichomonas vaginalis, or Chlamydia trachomatis had higher median levels of neutrophil defensins (human neutrophil peptides 1-3) in the vagina than did uninfected women. Neutrophil defensins were strongly associated with the presence of endometritis after the analysis was controlled for the presence of sexually transmitted diseases. Vaginal neutrophils were associated with endometritis only in the presence of elevated defensin levels, which highlights the importance of neutrophil activation, rather than the presence of neutrophils alone, in this inflammatory process. Neutrophil defensins appear to participate in the host defense in ascending pelvic infection and the pathogenesis of PID.

Serological investigation of Mycoplasma genitalium in infertile women.

The role of Mycoplasma genitalium in the pathogenesis of pelvic inflammatory disease has not been characterized. Sera from 308 infertile women were investigated for antibodies to M. genitalium by immunoblotting. Women with tubal factor infertility (TFI) made up 132 of the patients, 67 of the women had an infertile male partner and 109 were infertile for unknown reasons. Of the TFI patients 29 (22.0%) were seropositive to the major adhesin, MgPa, of M. genitalium versus 11 (6.3%) in the group of women with normal tubes. No cross-reactions between MgPa and P1 of the related Mycoplasma pneumoniae were found. Besides, MgPa positive sera were confirmed by immunoblotting using a cloned fragment of the C-terminal part of MgPa specific to M. genitalium. Chlamydia trachomatis is known to be able to cause infertility as a result of salpingitis. Therefore, the sera were tested against C. trachomatis using a commercial ELISA test. Seventy-five (56.8%) of the TFI patients were seropositive to C. trachomatis. Eight (27.6%) TFI patients seropositive to MgPa were negative to C. trachomatis. This study indicates that M. genitalium may be an independent risk factor in the development of an inflammatory process leading to scarring of the uterine tubes in women and thereby causing infertility.

Recovery of cytomegalovirus and herpes simplex virus from upper and lower genital tract specimens obtained from women with pelvic inflammatory disease.

Lower genital tract specimens and endometrial biopsies from 147 women with pelvic inflammatory disease (PID) and surgical specimens (fallopian tubes, ovaries, or both) from 22 women with PID and 37 women without PID were cultured for cytomegalovirus (CMV) and herpes simplex virus (HSV), as well as for organisms commonly associated with PID. CMV was isolated from 39 cervical or endometrial samples from 30 (20.4%) of 147 women with PID and from ovaries or fallopian tubes from 5 (22.7%) of 22 women with PID, but CMV was not recovered from surgical specimens obtained from 37 women undergoing surgery for tubal ligation, ectopic pregnancy, or other gynecologic conditions (P = .005). HSV was isolated from cervical samples obtained from 5 (3.4%) of 147 women with PID but not from any endometrial or surgical specimens. These data suggest that CMV, but not HSV, may contribute to the pathogenesis of PID in some patients.

Chlamydial pelvic inflammatory disease.

Pelvic inflammatory disease (PID) is the most important complication present in the female lower genital tract, causing major medical, social and economic problems. Although PID can be caused by multiple microorganisms, it results most frequently from the ascent of sexually transmitted Chlamydia.trachomatis or Neisseria gonorrhoeae infections from the cervix to the upper genital tract. The importance of cervical chlamydial infection in the pathogenesis of PID is well recognized. Recent data from many developed countries have shown a striking decrease in the incidence of gonococcal infections, while the rates of chlamydial infections remain high in most countries. Complications of PID are common and usually irreversible. Emerging evidence suggests that universal or selected screening of defined populations for cervical chlamydial infection leads to a dramatic reduction in the incidence of PID. Recent technological advances should further enhance efforts to prevent chlamydial infection and PID. Gene amplification-based diagnostic tests, screening by testing first-void urine, and single dose antimicrobial therapy greatly facilitate chlamydia control programmes. Thus, screening for chlamydia is the key approach in the secondary prevention of PID. The obvious challenge is to make screening for chlamydia the standard for health care for young, sexually active individuals. Since PID is the most important consequence of sexually transmitted bacterial infections, it is also imperative to develop better treatments to prevent the long-term sequelae of this disease. The development and implementation of new and effective intervention programmes for prevention and control of PID is one of the major challenges for the year 2000 and beyond.

Chlamydia, Gonorrhoea, and Reproductive Health

Chlamydial and gonococcal and infections are the most prevalent bacterial sexually transmitted infections. Pelvic inflammatory disease (PID) is the most important complication of chlamydial and gonococcal infections causing major medical, social, and economic problems. Worldwide, the magnitude of PID-related morbidity is enormous. Recent data from many developed countries have shown a surprisingly rapid downward trend in the incidence of gonococcal infections. This has been accompanied by a much slower downward trend in the incidence of chlamydial infections, suggesting that the epidemiologic control measures effective against gonorrhoea are generlly not effective against chlamydia. Development and implementation of safe and effective intervention programmes for the prevention and control of chlamydial infections is one of the major challenges in the 1990s. Progress in understanding the pathogenesis of PID and PID-related sequelae has come with better understanding of the immunopathogenesis of C. trachomatis infection. C. trachomatis is a strong immunogen which stimulates both humoral and cell-mediated immune responses, and can induce immune system perturbations that may assist its own survival in the infected host. Understanding the interactions of these organisms with the immune system is of paramount importance in the prevention of consequences. Gynaecologists play an important role in the primary prevention of STDs by questioning patients about high risk sexual behaviour, by encouraging screening tests for those at risk, by assuring that male sex partners are evaluated and treated, and by counselling about safer sex practices.

Pathogenesis of pelvic inflammatory disease.

Our current concept of pathogenesis of pelvic inflammatory disease (PID) is a synthesis of information from many sources. The main part is indirectly derived from epidemiological, clinical, and laboratory observations, as well as from deductions by analogy from findings in experimental systems. Documented facts are scarce, fragmentary, and in part contradictory. PID is defined as the acute clinical syndrome associated with ascending spread of microorganisms (unrelated to pregnancy or surgery) from vagina or cervix to endometrium, fallopian tubes, and/or contiguous structures.' The definition is wide and includes a multitude of inflammatory conditions of female pelvic organs. This review will focus upon infection of prognostically most important anatomical structure-the Fallopian tube; that is, on acute salpingitis.

Pathogenesis of pelvic inflammatory disease: What are the questions?

International Journal of Gynecology & ObstetricsVolume 39, Issue 1 p. 69-69 Citations from the literature infectiuos diseases Pathogenesis of pelvic inflammatory disease: What are the questions? P.A. Rice, P.A. RiceSearch for more papers by this authorJ Schachter, J SchachterSearch for more papers by this author P.A. Rice, P.A. RiceSearch for more papers by this authorJ Schachter, J SchachterSearch for more papers by this author First published: September 1992 https://doi.org/10.1016/0020-7292(92)90798-NAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume39, Issue1September 1992Pages 69-69 RelatedInformation

Pathogenesis of pelvic inflammatory disease. What are the questions?

Pathogenesis of pelvic inflammatory disease. What are the questions?

Interferon-gamma in the diagnosis and pathogenesis of pelvic inflammatory disease

International Journal of Gynecology & ObstetricsVolume 29, Issue 4 p. 386-386 Citations from the literature infectiology Interferon-gamma in the diagnosis and pathogenesis of pelvic inflammatory disease JA Grifo, JA GrifoSearch for more papers by this authorJ Jeremias, J JeremiasSearch for more papers by this authorWJ Ledger, WJ LedgerSearch for more papers by this authorSS Witkin, SS WitkinSearch for more papers by this author JA Grifo, JA GrifoSearch for more papers by this authorJ Jeremias, J JeremiasSearch for more papers by this authorWJ Ledger, WJ LedgerSearch for more papers by this authorSS Witkin, SS WitkinSearch for more papers by this author First published: August 1989 https://doi.org/10.1016/0020-7292(89)90380-9AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume29, Issue4August 1989Pages 386-386 RelatedInformation

Interferon-γ in the diagnosis and pathogenesis of pelvic inflammatory disease

Serologic markers were evaluated to determine if they could aid in the differential diagnosis of pelvic inflammatory disease in 48 consecutive women seeking evaluation for pelvic pain. On the basis of clinical and microbiologic parameters, 29 patients (60.4%) were diagnosed as having pelvic inflammatory disease. Neisseria gonorrhoeae only was isolated from the cervix of eight (27.6%) patients with pelvic inflammatory disease, five (17.2%) had only Chlamydia, and two (6.9%) had Neisseria and Chlamydia, whereas in 15 (48.3%) patients no pathogen was isolated. Interferon-gamma was present in significantly more sera (p less than 0.025) from patients with pelvic inflammatory disease (65.5%) than from women without pelvic inflammatory disease (15.8%). Sera from 10 healthy women lacked detectable interferon-gamma. In patients with only Neisseria, seven (87.5%) had circulating interferon-gamma; three (60%) of the women with only Chlamydia, one (50%) woman with Neisseria and Chlamydia, and eight (57.1%) with no identified pathogens were also positive for interferon-gamma. Sera from 11 of 28 patients with pelvic inflammatory disease (39%) but only one of 19 sera from women without pelvic inflammatory disease (5%) also inhibited the Candida-induced proliferation of control lymphocytes. This immunosuppressive activity was prevented by immunoprecipitation of interferon-gamma by anti-interferon-gamma antibody but not by treatment with anti-interferon-alpha antibody. The persistence of interferon-gamma in the sera of patients with pelvic inflammatory disease may aid in the differential diagnosis of this disease and increase our understanding of the pathogenesis of microbial-mediated tubal damage.

Mast cells in the tubal wall in women using an intrauterine contraceptive device

The number of mast cells in the tubal wall of 33 healthy nonpregnant women, 17 of whom had an intrauterine contraceptive device (IUCD), was investigated. Light microscopy showed that both the muscularis externa and the lamina propria of the tubal wall contained more mast cells in the 17 IUCD users than in the 16 non-users (control group). In both patient groups the mast cell concentration was higher in the muscularis externa than in the lamina propria. Most mast cells of the muscularis externa were more closely related to smooth muscle cells than to blood vessels. The increased number of mast cells in IUCD users may be a factor in the pathogenesis of pelvic inflammatory disease and the ectopic pregnancies that occur in IUCD users.

Mast cells in the tubal wall in women using an intrauterine contraceptive device

Summary. The number of mast cells in the tubal wall of 33 healthy non‐pregnant women, 17 of whom had an intrauterine contraceptive device (IUCD), was investigated. Light microscopy showed that both the muscularis externa and the lamina propria of the tubal wall contained more mast cells in the 17 IUCD users than in the 16 non‐users (control group). In both patient groups the mast cell concentration was higher in the muscularis externa than in the lamina propria. Most mast cells of the muscularis externa were more closely related to smooth muscle cells than to blood vessels. The increased number of mast cells in IUCD users may be a factor in the pathogenesis of pelvic inflammatory disease and the ectopic pregnancies that occur in IUCD users.