Acute Salpingitis And Pelvic Inflammatory Disease Pathogenesis and Microbiology

PID usually begins with cervical infection that is caused by C. trachomatis, N. gonorrhoeae, or both. Acute salpingitis and PID occur after extension of the infection from the lower parts of the female genital tract to higher structures. Organisms infecting the cervix can spread to involve the uterus and fallopian tubes in two ways: by causing a transient endometritis that extends to involve the endosalpinx or by reaching the tubes via lymphatic spread. Acute salpingitis and PID may be gonococcal or nongonococcal, according to the presence or absence of associated endocervical gonorrhea. Acute pelvic salpingitis and PID is predominantly a disease of young sexually active nonparous females.

The recovery of N. gonorrhoeae from the upper genital tract is variable. Many species of aerobes and anaerobes that are related to the normal vaginal flora can be isolated. Chlamydiae and mycoplasmae also have been implicated. It is generally suspected that sexually transmitted pathogens paves the way to polymicrobial aerobic-anaerobic PID and that the cervical bacteria travel through the endometrium and salpinges to the TOA junction (30). Presumably, it explains the rarity of pelvic infections during the full-term pregnancy. The isolation of gonococci from the endocervix does not necessarily account for upper genital tract disease. Moreover, the eradication of gonococci may not be an adequate treatment for acute salpingitis. The morbidity and sequelae of both gonococcal and nongonococcal salpingitis may be attributed to repeated ascending infection by the aerobic and anaerobic microorganisms that are secondary invaders.

The polymicrobial etiology of acute salpingitis is well documented (30-32). Culdocentesis and laparoscopy have revealed mixed aerobic and anaerobic bacterial flora in addition to gonococci in patients with acute salpingitis. The most frequent pathogens appear to be gonococci and anaerobic bacteria (most commonly Peptostreptococcus and Bacteroides spp.). Anaerobes are present in the upper genital tract during an episode of acute PID, with the prevalence dependent on the population under study (33). Vaginal anaerobes can facilitate acquisition of PID and cause tissue damage to the fallopian tube, either directly or indirectly through the host inflammatory response.

Brook studied 57 culdocenthesis aspirates of PID, 15 of which were in adolescent females (34). There were 93 anaerobes and 90 aerobes (1.6/specimen each). The predominant anaerobes were Bacteroides spp. (33, including 16 B. fragilis group) and anaerobic cocci (32). The predominant aerobes were Enterobacteriaceae (31), N. gonorrhoeae (13), Streptococcus spp. (16), and S. aureus (7). BLPB were isolated in 29 (51%) patients. These included all 16 of the B. fragilis group, 6 of 7 S. aureus and 7 of 31 Enterobacteriaceae.

A characteristic pattern has evolved from these studies. In approximately one-third of patients, only gonococci could be recovered from the intraabdominal site; another third had gonococci plus anaerobic and aerobic bacteria; and the final third had both aerobic and anaerobic bacteria, but not gonococci, recovered from their abdominal cavities (4,25,33). Animal studies demonstrated the synergistic relationship between N. gonorrhoeae and Bacteroides spp. (35). Mixture of aerobic bacteria and AGNB were inoculated subcutaneously and intrapentonealy in mice. The growth of each component of the mixed infection was enhanced when these were present together in a subcutaneous abscess in mice. Furthermore, the emergence of encapsulated strains was enhanced in these infections (35). This synergy may enable the organisms to cause more severe local and systemic damage to the host.

Of particular interest was the observed ability of encapsulated N. gonorrhoeae to induce the conversion of slightly encapsulated Bacteroides spp. to heavily encapsulated ones (35). This phenomenon may represent the events that occur after cervical N. gonorrhoeae infection, which may lead to tubal or pelvic inflammation. In this fashion a nonvirulent Bacteroides that is part of the normal vaginal flora can become virulent after exposure to N. gonorrhoeae; however, the N. gonorrhoeae that eventually did not survive in the abscess were able to induce encapsulation of the Bacteroides spp. Similarly, the conversion of nonencapsulated N. gonorrhoeae after coinoculation with an encapsulated Bacteroides isolate may explain the increased virulence of N. gonorrhoeae isolates recovered from the tubes or cul-de-sac (36,37).

C. trachomatis has also received attention as an etiologic agent in acute salpingitis. Studies show a 30% incidence of Chlamydia isolation from the fallopian tubes of patients with acute salpingitis (38). Serologic studies suggest that C. trachomatis is associated with 40% to 60% of acute salpingitis cases (39). The presence of the major outer-membrane protein of C. trachomatis was associated with chronic salpingitis and/or salpingitis isthmica nodosa with tubal occlusion (40).

Mycoplasmae have frequently been recovered from the lower genital tract of females with salpingitis and is associated serologically with salpingitis and tubal factor infertility (41). Hinonen and Miettnen recovered C. trachomatis significantly more frequently from the fallopian tubes among cases with severe PID (42), thus confirming role of C. trachomatis as the leading cause of PID in both laparoscopically mild and severe PID.

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