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when do most observed abortions in mares occur?
after 4th month of gestation
how many abortions are due to infectious causes?
16.2-47.5% of abortions due to infectious causes
why are non-infectious pregnancy losses more common in early gestation?
more likely to see abortion in first 40-50 days because this isn't until when endometrial cups form
the initial pregnancy is dependent upon the initial CL, and if anything happens to this CL= pregnancy loss
what external factors may cause/contribute to embryonic death?
stress
transport
inadequate nutrition
what is the relationship between endotoxemia and early pregnancy loss?
Endotoxins from the gut (or anywhere else) get into systemic circulation and release prostaglandins- prostaglandin release causes luteolysis
what is the consequence of endometrial fibrosis?
-leads to glandular nesting and dilation of lymphatic stasis
-fibrosis may predispose cysts to develop
-fibrosis limits nutrients to the foal
what are the 2 types of endometrial cysts associated with endometrosis?
1. endometrial gland cysts (<10mm)
2. lymphatic (lacunae) cysts (>10mm)- usually bigger than endometrial gland cysts
what is the most common non-infectious cause of abortion in mares?
twins
75% of abortions involving twins occur 8months-full term
do caudal or cranial uterine body pregnancies have a better prognosis of survival to term?
cranial uterine body pregnancies
what pathologies are mares with twins predisposed to?
1. prepubic tendon ruptures
2. broad ligament hematomas
3. dystocia
4. retained fetal membranes
5. subsequent infertility
what are the chances a mare ovulates (day 0) and has dizygotic twins?
20% chance
for dizygotic twins, what is the chance of survival during days 11-15 of gestation (mobility phase)?
for both: 49% of survival
for one embryo: 42% of survival
9% chance neither embryo survives
is there a higher chance of dizygotic twins fixating in the same or different uterine horns on day 16?
70% of twins will fixate in the same horn, 30% will fixate in separate horns
for dizygotic twins in the same horn, what is the chance of survival at day 40 of gestation for both embryos?
17% chance of survival for both embryos
83% chance only one embryo survives (the other embryo is reduced w/o intervention)
for dizygotic twins in different horns, what is the chance of survival at day 40 of gestation for both embryos?
100% chance of survival for both embryos if in different horns
are twins more or less likely to survive if synchronous and asynchronous ovulation occur within 24 hours of each other?
twins are more likely to survive bc they will be more similar in size
(twins dissimilar in size are more likely to have natural reduction of 1 embryo)
what is the defined end of the embryo stage?
day 40 of gestation
what is the deprivation hypothesis?
embryo reduction and time of reduction depend upon the amount of contact between the endometrium and embryo vascular wall
when is the best time to detect twins?
begin the twin search early in the mobility phase, days 11-12 after 1st ovulation
-->however, may be difficult to crush this early, may have to wait until just before fixation (before day 16)
if fixation of twins occurs and embryos are bilateral/unilateral, should manual intervention occur to reduce?
if bilateral, rupture one immediately
if unilateral, consider natural reduction odds
what are different techniques used for managing/reducing twins?
1. ultrasonic disruption if over 25 days ('dribbling' embryo with U/S probe)
2. thoracic crush (firm downward pressure on embryo with U/S probe until heart beat no longer detected)
3. transvaginal U/S-guided allantoic aspiration
4. transrectal or intrabdominal cervical dislocation
5. transabdominal U/S-guided cardiac injection
why is it important to know the difference between an endometrial cysts and a developing embryo?
to help avoid the misdiagnosis of twins
is altrenogest (regumate) measured in a serum progesterone quantitative test?
no, altrenogest does not cross react with progesterone
this allows for progesterone levels in the mare to still be monitored without artificial increases from altrenogest
can progesterone levels be tested for with serum from a serum-separator tube?
no- the 'goo' in the SST binds progesterone, and will give artificially low results
when do the highest incidences of ascending placentitis occur during gestation?
between 5-10 months
what is usually the first clinical signs of ascending placentitis?
premature mammary development
why does premature mammary development occur with ascending placentitis?
placentitis causes hormonal shifts to occur early when they should be happening at parturition, and causes the mare to think she is going into labor
what are the most common bacterial causes of placentitis?
*** s. zooepidemicus (most common)
also e. coli, s. aureus, p. aeuroginosa, k. pneumoniae
what is the relationship between estrone sulfate and progesterone in late gestation?
in late gestation, progesterone levels will increase and estrone sulfate will decrease
how can monitoring estrone sulfate and progesterone be useful for assessing placentitis?
with placentitis, hormonal shifts will occur prematurely
if estrogen decreases and progesterone increases way to soon, assume placentitis
what is combined uterine placental thickness?
ultrasound-guided measurement of placental thickness taken between the uterine artery and the allantoic space
why is the combined uterine placental thickness clinically important?
should be 1mm less than the month of gestation (should never go above 12mm in thickness)
if too thick= placentitis
where is the characteristic lesion of ascending bacterial placentitis?
characteristic placental lesion at the cervical star
what drugs can be used to treat placentitis?
1. SMZs/TMS (crosses placenta and accumulates in fetal fluids)
2. doxycycline
3. altrenogest
4. ECP (estradiol cyionate)
5. firocoxib
6. pentoxifylline
what are the etiological agents of nocardioform abortion (aka equine focal mucopurulent placentitis) in mares?
1. crossiella equi
2. amycolatopsis kentuckyensis
3. stenotropomonas maltophilia
what is the characteristic lesion of nocardioform abortion in mares?
characteristic placental lesion at junction of uterine body and base of gravid horn
what is the most common lepto serotype causing abortion in mares?
lepto. interrogans serovar subtype kennewicki
which drug can be used to increase the number of organisms found in the urine of mares with lepto?
furosemide
what is the treatment of leptospiral abortion in mares?
procaine penicillin G (PPG) or oxytetracycline
is treatment of leptospiral abortion in mares with PPG or oxytet effective?
tx may not eliminate shedding, but it may prevent fetal infection
is there a vaccine available for lepto in mares?
yes, there is an approved vaccine, but it is for Pomona (labelled for recurrent uveitis)
which herpes virus is most commonly responsible for equine abortion in the US?
equine herpes virus-1
how is EHV-1 transmitted?
via inhalation or ingestion
can survive for 14-42 days outside of horses
how does latency of EHV-1 cause abortion storms?
infection with EHV-1 persists in the latent state and is reactivated during periods of stress (pregnancy)
aborted tissue is a source of infection, and mares may shed the virus via respiratory routes as well
what is the pathognomonic gross lesion of EHV-1 in aborted fetuses?
pulmonary edema, hydrothorax, and hepatic necrotic foci
what is the pathognomonic histologic lesion of EHV-1 in aborted fetuses?
viral eosinophilic intranuclear inclusions in necrotic foci in liver, lung, thymus, adrenals and lymph nodes
why are EHV-1 vaccines recommended at least 3 times during pregnancy?
immunity to vaccination is short lived and of limited efficacy
vaccination does not offer 100% protection against abortion but will reduce incidence of abortion
during which months of gestation should mares be vaccinated for EHV-1?
months 5, 7, and 9
if there is an outbreak, vx at 3 months as well
what is equine herpesvirus-3?
equine coital exanthema
-does not cause abortion of systemic illness
-causes an infectious venereal disease which is usually self-limiting
which breeds is equine viral arteritis most prevalent in?
standardbreds (due to genetic predisposition)
is equine viral arteritis a reportable disease?
yes
how is equine viral arteritis transmitted?
1. respiratory (most common)
2. venereal infection from stallions
what are carriers of equine viral arteritis?
30-35% of stallions are long term carriers due to the virus having high affinity for ampulla fibrocytes and macrophages
what is the pathogenesis of equine viral arteritis causing abortion?
pathogenic to endothelial cells causing vasculitis
abortion occurs from severe necrotizing myometritis, placental detachment, decreased P4 and increased PGF2a
in addition to abortion, what are the clinical signs of equine viral arteritits?
limb edema (esp. in hind limbs, ventral abdomen, scrotum, and prepuce)
also fever, leukopenia, nasal and ocular d/c, rhinitis, coughing, dyspnea
when does abortion due to equine viral arteritis occur?
most occur 5-10 months gestation
why is it recommended that all animals be tested for EVA before vaccination?
the vaccine is a modified live vaccine, and antibodies will create positive results
we want to know which animals are actually negative and which are positive to no negative animals are bred to infected/carrier animals
what is the etiologic agent for mare reproductive loss syndrome?
eastern tent catipillars