On the causation of pelvic inflammatory disease

Abstract

The classic descriptive model of pelvic inflammatory disease (PID) omits any direct statement that sexual intercourse leads to the development of the lower genital or cervical infection which ultimately leads to upper genital or tubal infection. Despite this, clinicians treating patients with PID frequently, either implicity or explicitly, link its onset to sexual activity. In the past decade numerous authors have commented on the strong association between the widespread changes in sexual attitudes and behavior (without describing them in detail) and the enormous rise in sexually transmitted diseases and PID. With the advent of the case control study, the epidemiologist viewed sexual activity as only 1 of many risk factors for the development of PID. Yet, the clinician often maintanied that this relationship was too obvious to require case control studies to prove the point. The sum, the classic hypothesis on the pathogenesis of PID has remained virtually unchanged for nearly 8 decades in spite of its limitations, such as the failure to consider the endogenous and exogenous risk factors for the development of PID in a given patient. Possibly the greatest defect of the classic theory is its failure to address the precise mechanisms by which the infectious agents that cause PID travel from the lower to the upper genital tract. Existing literature suggests that 3 mechanisms may be operative. The 1st mechanism is that motile trichomonads are capable of ascending from the vagina to the level of the fallopian tubes and may carry with them a variety of infectious agents. The 2nd suspected mechanism for transport of microorganisms to the fallopian tubes is by attachment to sperm. If this occurs, then clearly spermatozoa may serve as vectors of pelvic infection. Abundant evidence exists to support the concept that sperm intimately associate with a variety of infectious agents, many of which are unrecognized as pathogens in the female. The 3rd suspected mechanism for transport of bacteria from the lower to the upper genital tract in the female appears to be that of passive transport. The literalture lacks reference to bacteria per se gaining entrance to the uterus but contains abundant references to the transport of particular matter and sperm. The current orientation of most American textbooks and much of the literature in regard to the pathogenesis of PID is oversimplified. More attention must be devoted to the mechanisms by which infectious agents arrive at the fallopian tubes.