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
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