of the stallions associated with above average rates of EPL, the underlying problem
is embryonic chromosome abnormalities arising either from karyotypic abnormalities
of the stallion or from DNA damage or instability in his sperm.8
‘Deficiencies of the maternal environment’ is a broad concept encompassing diverse
factors such as insufficient maternal progesterone, inadequate provision of nutrients
from an aged, degenerate or inadequately synchronised endometrium (e.g. after
embryo transfer) and infection/inflammation as a result of unresolved post-breeding
endometritis, endometritis acquired subsequently (i.e. ascending or by ‘reactivation
of dormant micro-organisms’) because, for example, of inadequate closure of the
cervix, the vestibular-vaginal ‘sphincter’ and/or the vulva. Uterine infection can also
be induced during emb ryo transfer, either because the embryo was recovered from
an infected mare or because of the accidental introduction of bacteria during transfer;
the limited ability of the diestrus uterus to combat bacterial proliferation explains the
relative ease with which contamination at this time results in an active infection. EPL
due to endometritis may present as the accumulation of uterine fluid, or widespread
and marked uterine edema, despite the presence of a conceptus, where subsequent
conceptus death will result either from direct infection of the embryo or via luteolysis
due to PGF2a release from an inflamed endometrium.
While it is tempting to assume that inadequate maternal progesterone is a major
contributor to EPL, there is little evidence to support this assumption.2 Indeed, even
when maternal recognition of pregnancy and maintenance of the CL do fail, the
failure is often paired with abnormal conceptus development (e.g. ‘small for dates’
vesicle) such that it is impossible to determine cause and effect. Nevertheless, luteal
failure certainly does occur and can, for example, be induced by PGF2a release from
organs other than the uterus, e.g. in the case of systemic disease involving
endotoxemia.9 Moreover, it appears that the day 18-35 pregnant mare is particularly
vulnerable to luteolysis because the inhibition of endometrial PGF2a release that
underlies maternal recognition of pregnancy wanes after the cessation of conceptus
mobility on day 17.5 Indeed, various manipulations (e.g. twin aspiration) and
hormones (e.g. oxytocin, oestrogen, hCG) have been shown to elicit endometrial
PGF2a secretion during the day 18-35 period. While this PGF2a release rarely results
in complete luteolysis, it is possible that there is a mare-specific minimum threshold
for progesterone concentrations below which pregnancy may be endangered
because, for example, the uterus is no longer able to provide the nutrients required
for conceptus development. Age-related endometrial degeneration can also
markedly affect the supply of nutrients to a conceptus, and while this classically
leads to fetal compromise later in gestation, EPL can result if endometrial
degeneration is severe, or if large lymphatic cysts impede conceptus migration or
nutrient uptake. Finally, there are reports that stress in the form of pain, systemic
disease, weaning, transport, changes in group structure, poor nutrition or extremes
of temperature can predispose to pregnancy loss.10,11 Although the extent to which
stress contributes to EPL is not known, it is nevertheless prudent to minimise
exposure to the potential stressors listed above during early pregnancy.
Treatment or prevention of pregnancy loss
Many of the measures that can be taken to reduce the risk of EPL are non-specific
and involve attention to good breeding management (e.g. prevent post-breeding
endometritis, and correct anatomical defects predisposing to pneumo or urovagina),
Proceedings
of
the
South
African
Equine
Veterinary
Association
Congress
2016
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