Nasreen Kirmani ( PMRC Research Centre, Jinnah Postgraduate Medical Centre, Karachi. )
Pelvic inflammatory disease (PD) is a general term which refers to an inflammatory con-dillon of the female upper genital tract. Clinically the term ND is most often used to denote acute or chronic infectious condition of the fallopian tubes and the sequelae of such infection such as tuboovarian adhesions, hypersalpinx or tuboovarian abscesses1. Acute PID usually results from salpingitis, which is the most common and serious genital infection. Occurring in an estimated 500,000 Americans2, the infection causes serious morbidity, stcrility3, chronic pelvic pain4 and is associated with subsequent episodes of PID. Salpingitis may follow intrauterine procedures such as curettage or the insertion of a contraceptive device. The disease is usually due to an ascending infection which is often sexually transmitted. A variety of organisms cause pelvic sepsis with superadded secondary infection and that is why the primary pathogen remains unidentified. Gonococci, coliforms, anaerobes (principally bacteroides, Gram’s positive pyogenes, gas forming organisms or mycoplasma), and enterobacter may be responsible and recently chlamydia have also been found to produce a significant proportion of PID and infection of lower genital urinary tract. A recent study by Wasserheit in 22 women with proven salpingitis found c. trachornatis infection more prevalent than N. gonorrhoeae5. Chlamydial antigen was studied in 221 women in Karachi by ELISA method and 14 (63%) cases were found to be positive for the antigen. The frequency of a chlamydial antigen positivity varied in various groups, being maximally positive in infertile group (9.4%), followed by JUD users (7.7%) and PJD patients (25%). None of the pregnant females were positive for the antigen6. Occasionally ascending pelvic infection is tuberculous or actinomycotic in origin. The role of mycoplasma or of other bacteria in PID is less certain. M. hominis and plasma, urealyticum are common components of the normal vaginal flora, together with other aerobic and anaerobicbacteria, but theymaycause opportunistic infection following alterations in lower genital tract ecology7,8 as a result of infection with a primary pathogen (chlamydia or gonococci), presence of intra uterine contraceptive devices, surgical intervention and manipulation or trauma to genital tract during delivery or abortion. The route ofinfectioñformycoplasma salpingitis differs from gonococcal or Chlamydial infection. Mycoplasma spreads from the cervix to uterus via blood vessels orlymphatics tocause parametritis and exosalpingills whereas Chlamydiac and gono-cocci ascend canalicularly via the uterus to cause upper genital tract infection. Acute pelvic inflaniniatory disease can be divided, on the basis of microbial etiology, into those casçs caused by N. gonorrhoeae alone, those caused by N. gonorrhoeae alongwith other bacteria and those caused by other bacteria9. In Seattle, approximately one half of all women with PH) have evidence of endocervical gonococcal infection. Peritoneal exudates from these cases usually reveal N. gonorrhoeae alone, but occasionally they appear alongwith other cervico-vaginal bacteria or only other bacteria are recovered. Among patients without endocervical gonococcal infection pentoneal cultures and gram stain show bacteria other than N. gonorrboeae, most commonlybacteroides, fragitis and anaerobic gram’s positive cocci9. Although gonorrhoeae has long been considered the major cause of PID, but recent studies have found a rising proportion of non- gonococcal PID; by improved culture technique, workers have isolated chlamydia trachomatis, anaerobic bacteria, enterobacteria and mycoplasma hominis as bacterial pathogenesis of acute salpingitis7, but the relative importance of these as primary or secoñdary pathogens is not dear: Anaerobic organisms are important as secondaryinvaders than as a primary cause f PH), but the possibility that they may initiate infection is not excluded. Anaerobic bacteria are often recovered from pelvic abscesse% post partum endometnitis and septic abortions10, but Westron and Mardh were unable to isolate anaerobes from any tubal specimen from twenty women with acute salpingills11. The best explanation of these conflicting data seems to be that patients, who have PH) without any previous intrauterine procedure, first develop infection of the lower genital tract by sexually transmitted organisms, of which N. gonorrhoeae and chiamydia trachomatis are the most important. These organisms ascend in the epithelium, subepitheliuni, connective tissues or lymphatics and initiate salpingitis; they also cause secondary invasion by the normal vaginal flora, including aerobic andanaerobic bacteria. This implies that correlation between tubal cervical cultures can onlybe expected earlybefore super infection has occurredbecause later mixed infection are more likely to occur. After abortion, especially in second trimester infection is likely to occur and may spread rapidly to the adnexae. In these circumstances the most common infecting organisms are E. coil; others indude, gram negative bacilli including bacteroides fragilis, the clostridil, streptococci and staphylococci. Bacteremia and toxemia occur re-suiting in septic shock, and even death if the treatment is not prompt and effective. Pelvic infection associated with intrauterine contraceptive device (IUCD), is an ascending infectioñ. The thread tail of the device probably act as a ‘wick’. In vitro tests have isolated pathogens like beta haemolytic streptococci and bacteroides fragitis in such cases. A three to four fold increase in PID is encountered in IUCD users7. Recently, association between an acute and potentially lethal shock syndrome caused by staphylococcal exotoxin and the use of vaginal tampons during menstruation12 has been observed. Staph. aureus is the causative agent which multiplies inthe retained menstrual blood producing exotoxin which is absorbed through the vaginal epithellum into the circulation and may also ascend into the uterus to be carried by retrograde menstrual flow into the peritoneal cavity. Infection of the female genital tract by the grain’s positive (nonacid fast) mycelium bearing anaerobic fungus actinomyces Israelii was considered rare until recently. This organism is a normal commensal of the mouth and gut, but now it is more often associated with presence of an IUCD. In these cases the route of infection is from the anus across the perineum and upward through the vagina and cervix and there is often coexistent infection by other anaerobes, the combination of a foreign body causing chronic trauma and the adjacent heavy anaerobic flora of vagina provides ideal conditions for opportunistic colonization and occasionally frank infection by actinomyces13. Actinomyces may be difficult to culture but microscopic tissue diagnosis canbe made by recognizing typical sulphur body colonies surrounded by pus containing lipid histiocytes and by special staining7. The control and prevention of PID andits sequelae are through the control of sexually transmitted diseases (5Th), for which three main elements, namely, (1) education of the public in kehavioural and physical method of reducing the transmission of STD, (2) improved laboratory and clinical methods for the diagnosis of P11) and (3) development of new vaccines against gonococcal and chlamydial infections need to be stressed.
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2. Eschenbach, D.A., Harnisch, J.P. and Holmes, KK. Pathogenesis of pelvic inflammatory disease; role of contraception and other risk factors. Am. 3. Obstet. Gynecol., 1977; 128 : 838.
3. Westron, L Effect of acute pelvic inflammatory disease on fertility. Am. J. Obstet. Gynecol., 1975; 121 : 707.
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5. Wasserheit, J.N., Bell, T.A., Kiviate, N.B., et al. Microbial causes of proven pelvic inflammatory disease and efficacyof clindemycin and tobramycin. Ann. Intern. Med., 1986; 104:187.
6. Suleman, N. Surveillance of chlamydial infections in different groups of women. Karachi, Karachi University, 1988, p. 34. Karachi.
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11. Westron, L and Mardh, P.A. In genital infection and their complication. Edited by D. Danietsson, L Juhlin, and Mardh, P.A. Stockholm, Almqvist and Wiksell, 1975, p. 157.
12. Schrock, CO. Disease alert. JAMA., 1980; 243:1231.
13. Lomax, C.W., Harbert, G.M. Jr. and Thornton, W.N.Jr. Actinomycosis of the female genital tract. Obstet. Gynecol., 1976; 48:341.