Pelvic inflammatory disease is a polymicrobial infection. Gonorrhoea and chlamydia are the most frequently recognized pathogens but a wide variety of other bacteria and viruses can also be isolated from the fallopian tubes of women with PID (Table 42.1).
Neisseria gonorrhoeae is a gram negative diplococcus which means that when a sample of cervical discharge is spread and fixed on a slide the bacteria can be seen on microscopy as pairs of red kidney-shaped organisms, mostly sitting within polymorphs. Gonorrhoea causes about 5% of PID in the UK [5,6].
N. gonorrhoeae initially infects the cervix but ascends to the upper genital tract in 10-20% of untreated cases. Around half of women with gonorrhoea are asymptomatic, but when symptoms are present the vaginal discharge tends to be thick and purulent. Although isolating gonorrhoea from the cervix supports a diagnosis of PID, its absence in the lower genital tract cannot exclude infection in the fallopian tubes or ovaries.
Chlamydia trachomatis is an unusual bacterium as it requires a host cell to grow (obligate intracellular organism), behaving in some ways more like a virus. To detect the organism therefore, the optimal specimen needs to contain cells and should be collected by gently rubbing against the endocervix with a swab. The use of sensitive nucleic acid amplification tests (NAAT) also allows the use of other more accessible samples to detect chlamydia, for example, vulval swabs (which the patient can take herself after appropriate instruction) or first pass urine. Light microscopy is not useful since C. trachomatis is too small to be seen.
Chlamydia, like gonorrhoea, initially infects the cervix and sometimes also the urethra. It is the commonest identified cause of PID in the UK accounting for 30% of cases  and causes a more chronic low-grade infection than gonorrhoea. Over two thirds of women with chlamydial infection are asymptomatic.
Evidence for the role of Mycoplasma genitalium in causing PID is growing. It has been isolated from the cervix, endometrium and, in a single case, from the fallopian tubes of women with PID . Tubal factor infertility is strongly associated with past infection with M. genitalium and inoculation of the lower genital tract with mycoplasma causes PID in female monkeys . Unfortunately no reliable routine test for M. genitalium is currently available.
Anaerobic bacteria are of particular importance in women with severe PID, and can often be isolated from tubo-ovarian abscesses. Their role in mild to moderate PID is less clear. Bacteroides fragilis, peptostreptococci and peptococci can all be isolated from the genital tract of women with PID and the production of mucinases and sialidases by anaerobic bacteria may break down cervical mucous, thus facilitating the passage of other bacteria into the upper genital tract.
Actinomyces israeli is occasionally detected in women with an intrauterine contraceptive device (IUCD) in situ. If there are no symptoms of vaginal discharge, intermenstrual bleeding or pelvic pain then the woman should be advised that neither treatment nor removal of the IUCD is required, but she should be reviewed in 6 months or earlier if symptoms develop. If symptoms are present then at least a 2-weeks therapy with a penicillin, tetracycline or macrolide antibiotic is indicated and the IUCD should be removed.
Tuberculous PID is largely limited to patients from developing countries. Pelvic infection usually occurs secondary to haematogenous spread from an extra genital source but occasionally Mycobacterium tuberculosis can be transmitted sexually . Usually it is not possible to detect the organism in the lower genital tract and samples should be obtained by uterine curettage or from the fallopian tubes at laparoscopy to be sent for culture or nucleic acid testing. Standard quadruple anti-tuberculous therapy with isoniazid, rifampicin, ethambutol and pyrazinamide is effective but surgical intervention may be required for extensive disease.
A number of viruses have been isolated from the upper genital tract in women with PID (Table 42.1) but their role in pathogenesis is unclear.
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