SAEVA Proceedings 2016 | Page 14

  Persistent mating induced endometritis During the last 10 years, it has also become increasingly clear that endometritis is not always initiated by pathogens. Indeed, it is now accepted that a transient uterine inflammation is a normal physiological response to the intrauterine deposition of semen, and that the sperm themselves potently stimulate the inflammatory reaction, probably as a part of the normal process to aid their subsequent elimination from the mare’s reproductive tract. A normal mare will resolve this inflammation promptly (within 48 hours post-mating) thanks to a battery of intrinsic uterine defence mechanisms, which include the influx of neutrophils to phagocytose ‘unwanted’ sperm, and enhanced uterine contractility to aid expulsion of both non-fertilising sperm and inflammatory debris through a relaxed cervix. In mares ‘susceptible’ to post-breeding endometritis, however, the normal uterine defence mechanisms are compromised such that the clearance of sperm and inflammatory debris is not completed within 48 hours, and the initially physiological inflammation develops into a more persistent, pathological c ondition known as ‘persistent post-breeding endometritis’ (PBE: Troedsson et al, 1999). Predispositions to post-breeding endometritis include reduced myometrial contractility in older mares, a pendulous uterus in multiparous mares and a fibrotic cervix incapable of relaxing sufficiently to allow effective uterine clearance, classically in aged maiden mares. It is also thought that artificial insemination with semen from which most of the seminal plasma has been removed (e.g. frozen-thawed semen) may predispose to PBE because seminal plasma contains factors capable of enhancing uterine clearance, either by stimulating myometrial contractions or by promoting neutrophil migration and phagocytosis. In practice, it is important to identify mares likely to be susceptible to PBE so that they can be intensively monitored around the time of insemination, firstly to minimise uterine exposure to semen and bacteria and, following breeding, to ensure the rapid clearance of sperm and the resolution of inflammation. However, while a thorough history and clinical reproductive examination will identify many potentially susceptible mares, others may only become evident following the first insemination. In susceptible mares, intensive monitoring of follicle development combined with the use of an ovulation-inducing agent should help limit uterine exposure to semen to a single mating/insemination per cycle, while timing the insemination as far prior to ovulation as is compatible with fertilisation will allow extra time to resolve the uterine inflammation before the combination of rising progesterone concentrations, cervical closure and imminent arrival of the embryo in the uterus limit the therapeutic options. The early (6-12 hours post-mating) identification and removal of inflammatory fluid using a combination of large volume uterine lavage, uterotonic agents such as oxytocin or PGF2a analogues and cervical dilation, is also essential to limiting the uterine inflammatory response. On the other hand, since current evidence suggests that PBE is not primarily a result of bacterial colonisation, the use of ‘prophylactic’ antibiotic therapy is questionable and, in mares with significant uterine fluid accumulation, is unlikely to be effective. With respect to the uterotonic drugs, recent studies suggest that lower doses of oxytocin (5-10 IU) may be more effective in promoting uterine clearance than higher doses (>20 IU), because the latter provoke a non-productive uterine ‘spasm’ rather than waves of contraction (Madill et al, 2002). And while PGF2a analogues have become popular alternatives to oxytocin because of their longer duration of action (4-5 hours Proceedings  of  the  South  African  Equine  Veterinary  Association  Congress  2016   13