Pathophysiology 1g6i71

Pathophysiology Infection begins in the cervix and, if untreated, may ascend to the upper genital tract. Epithelial damage, usually caused by N gonorrhoea and C trachomatis may allow opportunistic entry of other microorganisms. [5] Spread to the upper genital tract can also be caused by instrumentation of the cervix such as D&C, termination of pregnancy or insertion of an IUD. [5]Infection is thought to be caused by disruption of the protective cervical barrier and direct introduction of bacteria into the endometrial cavity from the vagina or cervix. [6] Abstract The pathophysiology of pelvic inflammatory disease (PID) involves an ascending infection of cervicovaginal microorganisms, of which the most important pathogens are Neisseria gonorrhoeae and Chlamydia trachomatis. The clinician should recognize that not all women with PID will present with abdominal pain and that associated atypical symptoms such as meteorrhagia and dyspareunia should suggest diagnosis. The documentation of lower genital tract inflammation is helpful in making the diagnosis of PID. Treatment with broad spectrum antibiotic regimens is currently recommended. Prevention of sexually transmitted diseases and ascending infection remains of utmost importance to decrease the sequelae, such as tubal factor infertility and ectopic pregnancy associated with PID.

Pathophysiology Pelvic inflammatory disease (PID) most commonly occurs as a result of Chlamydia trachomatis or Neisseria gonorrhoeae infection of the cervix or vagina that then spreads into the endometrium, fallopian tubes, ovaries, and adjacent structures. Less commonly, direct spread from a nearby infection such as appendicitis or diverticulitismay occur. Hematogenous infection is a rare cause of PID except in cases of tuberculous PID.10

Definition Pelvic inflammatory disease is a general term for infection of the uterus lining, fallopian tubes, or ovaries. See also: Endometritis Alternative Names PID; Oophoritis; Salpingitis; Salpingo-oophoritis; Salpingo-peritonitis Causes, Incidence, And Risk Factors Most cases of pelvic inflammatory disease are caused by bacteria that move from the vagina or cervix into the uterus, fallopian tubes, ovaries, or pelvis. The most common cause of PID is sexual without using a condom or other protection. This is called a sexually transmitted disease (STD). Chlamydia and gonorrhea are the two bacteria that cause most cases of PID. However, bacteria may also enter the body during some surgical or office procedures, such as: • Childbirth • Endometrial biopsy • Insertion of an intrauterine device (IUD) • Miscarriage • Therapeutic or elective abortion In the United States, nearly 1 million women develop PID each year. About 1 in 8 sexually active adolescent girls will develop PID before age 20. Risk factors include: • Male sexual partner with gonorrhea or chlamydia

• Multiple sexual partners • Past history of any sexually transmitted disease • Past history of PID • Recent insertion of an IUD • Sexual activity during adolescence Symptoms The most common symptoms of PID include: • Fever (not always present; may come and go) • Pain or tenderness in the pelvis, lower abdomen, or sometimes the lower back • Vaginal discharge with abnormal color, texture, or smell Other symptoms that may occur with PID: • Bleeding after intercourse • Chills • Fatigue • Frequent or painful urination • Increased menstrual cramping • Irregular menstrual bleeding or spotting • Lack of appetite • Nausea, with or without vomiting • No menstruation • Painful sexual intercourse Note: There may be no symptoms. People who experience an ectopic pregnancy or infertility often have had silent PID, which is usually caused by chlamydia infection. Signs And Tests You may have a fever and abdominal tenderness. A pelvic examination may show: • A cervix that bleeds easily • Cervical discharge • Pain with movement of the cervix • Tenderness in the uterus or ovaries Lab tests that look for signs of infection are: • C-reactive protein (CRP) • Erythrocyte sedimentation rate (ESR) • WBC count Other tests include: • Culture of your vagina or cervix to look for gonorrhea, chlamydia, or other causes of PID • Pelvic ultrasound or CT scan to look for other causes of your symptoms, such as appendicitis or pregnancy, and to look for abscesses or pockets of infection around the tubes and ovaries • Serum HCG (pregnancy test) Read more: http://www.righthealth.com/topic/Pelvic_Inflammatory_Diseases/overview/adam20? fdid=Adamv2_000888#ixzz0wHlzUsUv

Pathophysiology Most cases of PID occur in 2 stages. The first stage involves acquisition of a vaginal or cervical infection. The original sexually transmitted infection (STI) may be asymptomatic. An estimated 10-20% of untreated chlamydial or gonorrheal infections progress to PID. In PID, the second stage of upper female genital tract infection occurs by direct ascent of micro-

organisms from the vagina and cervix. Although the exact mechanism of ascent is unknown, studies have suggested that a number of factors may be involved. Cervical mucus provides a functional barrier against upward spread; however, the efficacy of this mechanism may be decreased by hormonal changes that occur during ovulation and menstruation. Alterations in the cervicovaginal microenvironment may result from antibiotic treatment and STIs that can disrupt the balance of endogenous flora, causing normally nonpathogenic organisms to overgrow and ascend. Opening of the cervix during menstruation with retrograde menstrual flow may facilitate ascent of micro-organisms. Intercourse may contribute to the ascent of infection due to rhythmic mechanical uterine contractions. Bacteria may be carried along with sperm into the uterus and tubes. Risk factors for PID include multiple sexual partners, a history of prior STIs, and a history of sexual abuse.3Frequent vaginal douching has also been implicated.4,5 Younger age has been found to be associated with increased risk, suggested to be due to some combination of increased cervical mucosal permeability, a larger zone of cervical ectopy, a lower prevalence of protective chlamydial antibodies, and increased risk-taking behaviors. Surgical procedures, such as endometrial biopsy, curettage, and hysteroscopies break the cervical barrier, predisposing women to ascending infections. The organisms most commonly isolated in many, if not most, cases of acute PID are Neisseria gonorrhoeae andChlamydia trachomatis. As such, therapy has been directed primarily against these organisms. However, unlike infections in other areas of the body, newer studies obtaining more sensitive and specific laparoscopic cultures have found acute PID to be polymicrobial in up to 30-40% of cases. Organisms involved include Gardnerella vaginalis, Mycoplasma hominis, Ureaplasma urealyticum, herpes simplex virus-2 (HSV-2), Trichomonas vaginalis,cytomegalovirus, Haemophilus influenzae, Streptococcus agalactiae, enteric gramnegative rods, and anaerobes.N gonorrhoeae and C trachomatis may be instrumental in the initial infection of the upper tract, with anaerobes, facultative anaerobes, and other bacteria increasingly isolated as inflammation increases and abscesses form. The microbiology of PID has also been found to reflect both the predominant STIs prevalent within a specific population and also less common organisms seen in specific populations. Bacterial vaginosis (BV) is suggested to play a role in the initiation of ascending infection in a subset of women with heavy growth of BV-associated organisms, such as G vaginalis, more than 2 recent sexual partners, and especially after recent abortion or gynecologic surgery.6,7 A 2006 cross-sectional study examined the role of HSV-2 and T vaginalis in PID. In this study of 736 women, those with T vaginalis demonstrated a 4-fold increase in the histologic evidence of acute endometritis. Co-infection of HSV-2 with N gonorrhoeae, C trachomatis, and BV was also associated with histologic evidence of acute endometritis. HSV-2 was demonstrated to be associated with fallopian tube inflammation and lower tract ulcerations that may contribute to disruption of the endocervical canal mucus barrier.8 HIV infection has been found to be associated with an increased incidence of C trachomatis infection, Candida, and human papillomavirus. Those with HIV infection also have an increased risk of progression to PID and tubo-ovarian abscess.9 Actinomycete species have been identified almost exclusively in those patients with IUDs.2

PID may result from Mycobacterium tuberculosis in endemic areas.10 Different forms of contraception may affect PID incidence and severity. Appropriately used barrier contraception has clearly been shown to decrease the acquisition of most STIs. The CDC recommends that spermicides and condoms containing nonoxynol-9 should be avoided, as a number of African studies have demonstrated that nonoxynol-9 can cause vaginal lesions and may increase the risk of HIV transmission. While the level of nonoxynol-9 in condoms is lower than the level associated with vaginal lesions, these are also not recommended because they are more expensive, have a shorter shelf life, and have been associated with urinary tract infections. Oral contraceptive pills (Os) have been found to have differing effects on PID risks. Oral contraceptives are thought to increase the risk of endocervical infection, probably by increasing the zone of cervical ectopy. Os have been found to decrease the risk of symptomatic PID, possibly by increasing cervical mucous viscosity, decreasing menstrual anterograde and retrograde flow, and modifying local immune responses. More recent data suggest that Os may not have any effect on PID incidence.4 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.11 Intrauterine device (IUD) use has been associated with a 2- to 9-fold increased risk for PID, but recent data suggest that the risk with current IUDs may be significantly less.12 Kelly et al found a rate of 9.6 cases of PID per 1000 IUD insertions, with the most significant risk in the first 20 days.13 Meirik et al validated early risk of PID within the first month after insertion and also found that the risk appears to be modified by the number of patient sexual partners, the age of the , and the community prevalence of STIs.14 Pregnancy decreases the risk of PID once the cervical os is protected by the mucous plug. However, PID can occur during the early first trimester until the mucous plug is solidified, and it may produce fetal loss. In the upper tract, a number of microbial and host factors appear to play a role in the degree of host inflammation and resultant scarring. Uterine infection is usually limited to the endometrium, but may be more invasive in a gravid or postpartum uterus. Tubal infection initially affects the mucosa, but acute, complement-mediated transmural inflammation may develop rapidly and increase in intensity with subsequent infections. Inflammation may extend to uninfected parametrial structures, including the bowel. Infection may extend by spillage of purulent materials from the fallopian tubes or via lymphatic spread beyond the pelvis to produce acute peritonitis and acute perihepatitis (Fitz-Hugh-Curtis syndrome). Bjartling et al have found less symptomatic urethral infection and decreased lower abdominal findings produced by a less virulent variant strain of Chlamydia trachomatis.15 Den Hartog examined the 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 in patients appeared to correlate with increased laparoscopically identifiable tubal pathology.16 Genetic polymorphisms of PID pathogens has been suggested to affect the likelihood that a lower tract infection will progress to frank PID. CHSP60 antigen

expression in C trachomatis17 and P9Opa(b) protein expression in N gonorrhoeae18 are examples of specific bacterial genes implicated in the pathology of PID.