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 ecology^7,8 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.

1. Edelmen, D.A., Berger, G.S., and Keith, LG. In­trauterine devices and their complications. Boston, Hall, 1979, p.93.
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.
4. Falk, V. Treatment of acute nontuberculous salpingitis with antibiotics alone and in combinationwithgtucocor­ticoids. A prospective double blind controlled study of the clinical course and prognosis. Acta Obstet. GynecoL Scand., 1965; 44 (Suppl. 6): 3.
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.
7. Mardh, PA. An overview of infectious agents of salpin­gitis, their biology, and recent advances in methods of detection. Am. 3. Obstet. Gynecol., 1980 138:933.
8. Wasserheit, J.N. Pelvic inflammatory disease and fer­tility. Md. Med. J., 1987; 36:58.
9. Eschenbach, D.A., Buchanan, TM., Pollock, H.M., For­syth, P.S., Alexander, E.R., Lin,J.,Wang,S.,Wentworth, B.B., Mc Cormack, W.M. and Holmes, K.K. Poly­microbial etiology of acute pelvic inflammatory disease. N. Engl. J. Med., 1975; 293: 166.
10. Sweet, ItL Anaerobic infections of the female genital tract. Am. J. Obstet. Gynecol., 1975; 122: 891.
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.