Pregnancy Loss Causes and Consequences Flashcards

1
Q
  • Gala Girl starts foaling at 332 days after breeding
  • She was restless and flank watching for 3 hours before starting active abdominal contractions which have now been present for 30 minutes
  • Are these events normal?
  • What can you see now?
  • What does this indicate?
  • Do you need to take any actions, if so what?
  • If the foal is delivered alive might there be any consequences?
A
  • Failure of progression
  • Need to know normal mare parturition timeline
  • Some signs
  • Mare – short uterine before abdominal (1 hours, and 3 hours is deffo upper limit)
  • After 30 mins of straining would expect part of the foal to be devliered
  • Red bag devery – breaking of the placenta; being pushed out before the foal but should come out through the star
  • Yes we need to act as this as been going on for too long and the foal is likely to be hypoxic
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2
Q

What does fetal loss usually results in?

A

Abortion

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3
Q

Why does fetal mummification not happen very often?

A

Fetal mummification does not occur in the absence of twins since usually after death there is abortion. Most causes of death occur late in pregnancy and after the switch from luteal to placenta. Placenta supporting progesterone loss – expel fetus

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4
Q

What is the exception to fetal mummfication happening?

A

cervical abnormality which prevents expulsion

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5
Q

What causes persistence of endometritits?

A

•Presence of bacteria or inflammatory products within the uterus as a result of mating-induced endometritis creates a hostile uterine environment and prevents the mare from staying pregnant (when the conceptus enters the uterus on day 5/6)

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6
Q

What is the pregnancy rate after the following durations of endometritis after ovulation?
1 day?

2 day?

3 days

4 day?

5 days?

A

75%

65%

32%

11%

0%

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7
Q

What is the effect of venereal pathogens on embryonic death?

A

•Mares with any of the venereal pathogens may get pregnant but may fail to stay pregnant because of a hostile uterine environment as discussed earlier

•Venereal more likely to cause endometritis which then causes pregnancy loss! In terms of later pregnancy loss these pathogens aren’t so relelvant

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8
Q

When does early inter embryo inhibition occur? (3)

What is the mechanism?

A

–This appears to be a natural method of reduction of one of twins

–It only occurs post fixation

–It only occurs when fixation occurs within the same horn

–The mechanism appears to be some specific inter-embryo inhibition

–The twins that go on to abort later usually originate from conceptuses that have fixed in opposite horns so that this mechanism has not occurred

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9
Q

How liekly is it for a luteal insufficiency to cause embryonic death?

A

Theory - low progesterone

little evidence of this in the mare! Supplementing progesterone is probably of little benefit. Risk period can be before endometrial cups at the end of the CL! But is it needed the rest of the time when there are multiple CLS?

–Much anecdote on low progesterone concentrations causing pregnancy loss in mares

–Many mares especially in USA are given large doses of altrenogest (Regumate) over many days to ‘prevent’ this

–Some of these mares may have previously had pregnancy loss but in most the cause has never been documented as low progesterone

–One might consider when any risk period would likely be (perhaps day 20 to 40? – why?)

–In GE’s view the practice is bogus in the majority of cases

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10
Q

What can the secondary problem of a luteal insufficiency (low progesterone) be?

A

–Specific inflammatory or stressful situations may result in PG release

–This can threaten progesterone concentrations

–In some cases Altrenogest may be considered to help ‘protect’ the pregnancy (e.g. the early pregnant mare undergoing anaesthesia, mare with placentitis)

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11
Q

What is the Pregnancy loss rates for mares that have reached the stage of endometrial cup formation?

A

10%

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12
Q

Even tho non infectious is most comon, what needs to be considered as a primary concern?

A

Infectious

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13
Q

What is our next diagnostic step if there is a fetal abortion?

A

•Appropriate samples (fresh whole fetus, membranes and mare’s serum) should be sent to appropriate pathologist

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14
Q

Wat do we d if there is a suspicion of an infectious cause of abortion?

A

abortion plans must be implemented to isolate the infected mare and to prevent movement onto and off the stud

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15
Q

What are the non infectious causes of fetal abortion? (2)

A
  • Multiple conceptuses
  • Umbilical cord abnormalities
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16
Q

What is the incidence of multiple ovulations?

A

20%

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17
Q

What is the prevalence of twins at 14 days?

A

10% •(less in some breeds) – some may naturally resorb

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18
Q

What can an incorrect diagnosis at 14 days be caused by? (3)

A

–Incomplete examination of the uterus (conceptuses are mobile)

–Failure to recognise twins

–Confusion of endometrial cysts

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19
Q

What is the outcome of multiple conceptuses?

A
  • Outcome is rarely successful as a result of competition for placental attachment area (see case in Week 1)
  • Competeing for the placenta and the attachment sites
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20
Q

When do we plan examinations for multiple conceptsues?

A

–Day 14 and if suspicion of twins then re-examine 2 days later

–Day 21

–Day 35

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21
Q

How can you deal with twins? (2)

A

–Abolish whole pregnancy with PG?

•But likely to occur again at next pregnancy

–Manual rupture of one conceptus at day 14/15

  • The smaller conceptus is normally chosen
  • Early conceptuses are not difficult to crush
  • After day 21 greater pressure is required and more fluid is released
  • Mare should be examined again 2 days later to ensure singleton remains
22
Q

What can be seen?

A

Crushing twin by pressure of transducer and subsequent appearance of crushed conceptus

23
Q

What is this?

A

Fetal death associated with umbilical cord torsion

Torsion of UC = fetal death

•In some cases it is longer than normal and may be twisted (obstruction) or may constrict around a fetal extremity resulting in fetal death

24
Q

What are the infectious causes of equine abortion? (3)

A
  • Equine herpes virus
  • Equine viral arteritis
  • Bacterial/fungal placentitis

–Ascending placentitis

–Aetiology - mares with poor vulval conformation= bacterial load in vagina and cervix

–Can do caslicks to reduce the risk

25
Q

Which herpes virus causes abortion?

A

1 and rarely 4

26
Q

When are most abortions with EHV?

A

•Most abortions within 60 days of infection but most are seen after 250 days

–Common presentation: mare has respiratory disease and is then well until an unexpected abortion. Fetus normally delivered within the membranes and mare remains well

–In herds tend to get spread of abortions rather than a ‘storm’

27
Q

Can mares become carriers EHV?

A

•Some mares remain latent carriers with recrudescence when stressed (pregnant) so in a herd are a risk to other mares (there is no test for carriers)

28
Q

What is this?

A

Abortion of fresh fetus within fetal membranes associated with EHV1 infection

29
Q

What are the different types of alpha herpes virus ? (7)

A
  • Bovine herpesvirus 1 (Infectious bovine rhinotracheitis virus IBR, infectious pustulvaginitis IPV)
  • Equine herpesvirus 1 (equine abortion herpesvirus)
  • Equine herpesvirus 3 (coital exanthema virus)
  • Equine herpesvirus 4 (equine rhinopneumonitis virus)
  • Pseudorabies virus (Aujesky’s disease virus)
  • Canine herpesvirus
  • Feline herpesvirus
30
Q

What are the 3 types of gamma herpes virus?

A
  • Equine herpesvirus 2 (? respiratory disease)
  • Bovine herpesvirus 4 (? respiratory disease)
  • Alcephine herpesvirus 1 (malignant catarrha fever virus)
31
Q

What advice do we give for a horse found to have aborted due to EHV? (4)

A

•Aborting mare should be isolated from others as the aborted material is infectious

–Often isolation of the mare at the time of abortion does not reduce a herd outbreak as most mares were infected at the same time (some time earlier)

•Advise that mares are kept in groups according to stage of pregnancy

–Foals born alive may also shed virus for 1 week

  • Isolate new arrivals before introducing to pregnant herd
  • Control is normal via vaccination of pregnant mares at 5, 7 and 9 months of pregnancy (Equip EHV 1,4)

–Vaccination works but failures are not uncommon

32
Q
  • One of a group of 30 unvaccinated national park ponies aborts in late pregnancy.
  • Examination of the fetus confirms that this is Equine herpesvirus 1
  • The ponies cannot be isolated except in adjacent outdoor paddocks.
  • Somebody should do something about it. What can be done?
A
  • Thckened oedema placenta – typical of herpes. Check for ascending placentitis (problem likely to be focussed around cervix)
  • Here we have a late term pregnancy and an animal which is potential infectious and can spread to other incontacts. Need a regime to manage infection so need to manage mare to mare transmission.
  • This foal could be infected – in a herd of abortion. There is a risk the foal has herpes which it will transmit. The foal may surcum to neonate disease
  • Many of the herd animal are likely to have been infected some time previously.
  • Only thing available to vaccinate in face of an abortion outbreak - once identified you would isolate and vaccinate
33
Q

How is equine viral arteritis transmitted? (2)

A

•Transmitted both via respiratory tract route and also venereally (including chilled semen)

34
Q

What are the clinical signs of EAV? (4)

A

•Classic disease is flu-like but with significant conjunctivitis, (pink eye) focal dermatitis, limb and ventral oedema

35
Q

How does the EAV infect the male?

A

•Organism excreted at this time and in the stallion may infect the accessory glands and result in a persistent infection (mares clear infection within 1 month and develop immunity)

36
Q

What happens to pregnant mares with EAV?

A

•Pregnant mares that get infected may abort (abortion may relate to degree of immunity or pathogenicity of virus strain)

37
Q

What is seen with the dead fetus with EAV?

A

•Aborted fetuses appear partially autolysed (unlike fresh foetuses seen with EHV) however still need appropriate pathological examination

38
Q

What is seen in a hrse with EAV?

A

Raised nodular lesions

Ventral and scrotal oedema

Occular swelling

39
Q

What is the disease spread of EVA like?

A

•sporadic and often respiratory tract route

40
Q

How do mares infect others when they have been affected with EVA venereally?

A

•Mares infected venereally are mainly a risk in that they develop respiratory tract infections that infect other mares which is pregnant abort

41
Q

What is the procedure to prevent EVA?

A

•Killed vaccine available in the UK (Equip Artervac)

–Administration to stallions must be accompanied by blood sampling to show sero-negative status prior to vaccination and sero-positive status post vaccination since vaccine response and infection response cannot be differentiated and without documenting vaccine response importation of stallion or his semen will be prevented

–Although could be widely given to mares the most common procedure on a stud is demonstration of negative serology in mare prior to accepting on stud

42
Q

What is placentitis? and what is the effect?

A
  • Ascending infection possibly associated with poor perineal conformation
  • Reduces placental efficiency producing growth retardation of fetus
43
Q

What is the effect if placentitis spreads to the fetus?

A

Septicaemia

44
Q

What is seen with placentitis?
How can we detect?

A

•Usually vulval discharge, mammary changes and then abortion

Placentitis can be detected by vaginal palpation and scooping, ultrasound examination

45
Q

How can you treat placentitis?

A

•Treatment is culture/sensitivity but usually systemic potentiated sulphonamide and consideration of progesterone supplementation

46
Q

What are stillbirths commonly associated with? (3)

A
  • Prolonged parturition
  • Umbilical cord obstruction during parturition (see previous slides)
  • Premature placental separation

–Cause uncertain

–Separation rather than rupture at cervical star

  • Termed ‘Red-bag’ presentation
  • Cervical star intact on examination of placenta
47
Q

What is this?

A

Intact cervical star where placenta should rupture and the foal leaves within amnion

48
Q

What is the law on EVA in the UK?

A

•EVA is notifiable by law under the Equine Viral Arteritis Order 1995

–Under the Order, anyone who owns, manages, inspects or examines a horse must notify the Divisional Veterinary Manager (DVM) of DEFRA when:

  • They suspect the disease in a stallion, either on the basis of clinical signs or following blood or semen testing;
  • They suspect disease, either on the basis of clinical signs or following blood testing, in a mare that has been mated or artificialy inseminated within the past 14 days
  • If the lab finds blood or fetus as EVA positive they will report
49
Q
  • Sophie is 12 year old primigravida at 290 days of pregnancy. She has poor vulval conformation managed when 21 d pregnant with a Caslick procedure
  • Currently she has a purulent vulval discharge. Trans-abdominal ultrasound shows the combined thickness of the uterus and placenta to be 18 mm
  • What is likely going on?
  • What treatment are appropriate?
  • Are there any risks with the treatments you propose?
  • At what gestational age would the foal likely survive?
A
  • Thick placenta
  • Caslick used to prevent ascending placentitis
  • She has got a placentitis
  • 40 days to go
  • Foal will be struggling due to abnormal placenta. Foal may be septic.
  • Would induce parturition butfoal unlikely to survive.
  • Want to try to manage to keep foal in the mare to allow it to grow and survive
  • Could then induce parturition closer to term
  • Give antibiotics I/U through cervix but don’t want to penetrate the friable oedematous placenta!
  • Pus will come out
  • Antibiotic pessary or tablet and digitally poke through the cervix
  • Some put on progesterone
  • Systemic AB will have limited penetration
  • Then induce when ready (use eye size to estimate age)
  • 310-315 days should survive (ish). Better to work out gestational age by size.
50
Q

What is the normal combined placenta uterine thickness at day:

150-270?

271-300

301- 330

331+

In pregnancy

A