Histology and pathology

The spread of infection from the cervix to the endometrium leads to an acute, predominately polymorph mediated endometritis [14]. Transcervical suction biopsy of the endometrium allows assessment of the endometrial inflammation which correlates well with salpingitis [14]. Unfortunately the usefulness of this approach to diagnose PID is limited by the risk of introducing infection during the procedure, the time delay in fixing and staining the sample, and the uncertain significance of isolated endometritis.

The inflammatory response seen in the fallopian tubes depends on the underlying pathogen. Gonorrhoea infects the non-ciliated epithelial cells but production of tumour necrosis factor and gamma interferon soon lead to collateral damage to the surrounding tissue and invasion of the submucosa. The tissue damage associated with chlamydia is mediated primarily by the immune response to the infection occurring as a result of a delayed type hyper-sensitivity reaction to one of the chlamydial heat shock proteins. This is characterized by a low-grade lymphocytic response compared with the acute neutrophil response of gonococcal salpingitis.

Recurrent infection with chlamydia causes further immune stimulation possibly mediated by a cross reaction between chlamydial and human heat shock proteins 60 [15]. This exaggerated immune response following re-exposure to chlamydia may explain the exponential increase in the risk of tubal damage which occurs with repeated infection.

Severe inflammation is associated with tubal occlusion and the production of a tubo-ovarian abscess or hydrosalpinx. Healing following acute inflammation may produce chronic fibrosis with associated damage to the ciliated epithelium, tubal blockage and pelvic adhesions. Histologically this chronic damage produces lymphoid follicles and a mononuclear cell infiltrate.

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