Equine infertility Flashcards
What are some DDx for causes of infertility in a mare? (8)
True temporary anoestrus (e.g. seasonal)
True permanent anoestrus
Transitional oestrus
Silent oestrus/behavioural anoestrus
Irregular oestrous cycles
Ovarian tumours (GTCT)
Endometritis (4 types)
Retention of endometrial cups
What is a silent oestrus in a mare? What are some causes?
Cycle (±OV) w/o showing behavioural/overt signs of oestrus
- foal at foot > lactational anoestrus dt concern for foal
- any stress = transport, introduction into a new flock
What actions can be taken in a mare suspected of having silent heats?
Adjust teasing technique
Synchronise cycle (PGF2a)
AI (if OV is dx’d by US)
What are some causes of true temporary anoestrus in mares?
Seasonal anoestrus (winter)
Systemic disease
Anabolic steroid tx (illegal in racehorses)
GnRH vaccine
What causes retention of endometrial cups? Why does this cause acyclic activity?
Loss of a foal after d35 of pregnancy (when cups form)
- cups cause accessory CL growth > maintain high P4 until d120 of pregnancy
- mare won’t cycle that season
How is retention of endometrial cups dx’d in both:
- a mare who has just lost a foal?
- a mare who lost a foal last season?
A - Blood eCG test + ovary US (accessory CLs)
B - hysteroscopy (–> tx by ablation of cups)
What are some causes + associated clinical signs of true permanent anoestrus?
Chromosomal abnormalities (if never cycled before) = masculine behaviour, external genital abnormalities
What is the most common ovarian neoplasia in mares? Are these tumours generally hormonally active or inactive?
Granulosa theca cell tumour (GTCT)
Active tumours secrete:
- testosterone OR oestrogen
- inhibin
- AMH
What are some clinical signs of a GTCT?
Behavioural changes (dependent on what hormones are produced)
- testosterone → stallion-like behaviour
- oestrogen → nymphomaniac
- none → anoestrus
How are GTCTs diagnosed? what test + what signs?
Physical exam + behavioural signs
Examine ovaries by rectal palpation/US
- GTCT = enlarged, polycystic/honeycomb, no OV fossa
- other ovary = very small (dt inhibin prod’n by GTCT)
Blood tests = inhibin (+++), AMH (+++)
What mechanism causes the unaffected ovary to be hypoplastic in a horse w a unilateral GTCT?
Neoplastic inhibin prod’n → suppression of FSH prod’n in anterior pituitary → no follicular activity in unaffected ovary
What is the treatment for a GTCT?
Prognosis for breeding soundness?
Unilateral ovariectomy (mid-ventral laparotomy)
Good Px but takes 6-8wks for cyclicity to resume (TF may lose the season)
Ddx for enlarged ovaries
GTCT (benign)
Teratoma - contain teeth/hair
Ovarian adenocarcinoma (malignant)
Ovarian haematoma
Ddx for irregular oestrus cycles
Transitional oestrus (at beginning of the breeding season)
Anovulatory haemorrhagic follicles (AHF)
Persistent CL
What is an anovulatory haemorrhagic follicle (AHF)?
Dominant follicles which fail to ovulate then fill with unclotted blood + P4-producing luteal cells
Why does blood in an AHF fail to clot?
Anticoagulants in follicular fluid
- this differentiates an AHF from a corpus haemorrhagicum (clotted blood)
What are some risk factors for an AHF?
Older mares
Transitional oestrus
What is the tx for an AHF?
PGF2a injection to induce luteolysis
- may take longer to respond than a regular CL TF ≥ 1 dose may be necessary
What is a persistent CL?
Any CL which lasts longer than 13-16 days (length of luteal phase in mares) → failure to come back into heat
What are the 3 possible causes of a persistent CL?
Dioestral ovulation
Chronic endometrial disease (no endometrial fcn = no PGF2a)
EEL following conception (CL persists til d70)
What is the tx for a persistent CL?
Induce luteolysis = PGF2a
What pathogens are most commonly involved in endometritis in mares?
Opportunistic pathogens = commensals of genitals of mare/stallion
- Streptococcus equi zooepidemicus
- E. coli
Venereally-tm’d pathogens =
- Taylorella equigenitalis (CEM)
- Klebsiella pneumoniae
- P. aeruginosa
When/how do pathogens gain entry to the uterus to cause endometritis?
Veterinary uterine exams (if poor asepsis)
Poor MCT during AI procedure
Joining to a stallion
What are some non-bacterial causes of endometritis?
Fungal infections - Candida, Aspergillus, Mucor
Iodine/ABs
Air (pneumovagina)
Urine (urovagina)
What uterine defence mechanisms protect against infectious endometritis?
In what stage of the oestrous cycle are these mechanisms impaired + why?
PMNs (Mø + neuts) = phagocytic cells
Cilia of endometrial cells
Secretory Ab (IgM/IgA)
Muscle contractions = ejection of uterine contents
Impaired in dioestrus:
- P4-induced immunosuppression
- Closed cervix/no muscle contraction/no flushing = no drainage
What anatomical barriers protect against infectious agents reaching the uterus?
Vulval lips
Vestibulo-vaginal sphincter
Cervix
What methods of Dx of endometritis are available?
Breeding history of infertility
Clin signs = vaginal discharge (often on tail)
Clitoral swabs (any time) → cytology/C&S (only excludes STIs as many commensals in clit fossa)
Endometrial swabs (during dioestrus) → cytology/C&S (dx of all agents - should be sterile environment)
Endometrial Bx → histopathology
Tx of endometritis
- timing during cycle?
- when to next breed?
Flush uterus w saline (+ OXT to contract uterus)
- tx during oestrus = open cervix + good defences
- when flush runs clear → antimicrobial tx
- intrauterine NS ABs
- systemic BS ABs (TMS)
- antifungals
- povidone-iodine flush (vs. fungi)
- breed mare on same oestrus (using MCT)
What is endometrosis?
What Dx method?
What are the consequences?
Degenerative endometrial changes dt chronic endometritis
- irreversible
- fibrosis stroma
- degeneration of endometrial glands
Dx = Bx/histopathology
Leads to poor endometrial blood supply + formation of endometrial cysts
What do endometrial cysts indicate in a mare?
Poor lymphatic drainage dt fibrosis of the endometrium
What is the end-stage consequence of endometrial fibrosis?
Transluminal adhesions
What is persistent mating-induced endometritis (PMIE)?
Persistence of endometrial inflammation > 4-5d post-service
- normal endometrial inflamm following joining lasts 1-2d
- bacteria on stallions penis + spermatozoa
- cleared by uterine defences
- persistence = inflammatory uterine environment → embryo can’t survive when it enters at d4-5 post-OV
What is a ‘susceptible mare’?
Any mare which does not clear uterine infllammation by 2d post-joining
- Premature PGF2a release → short inter-OV interval
- Persistent endometritis = infertility (as embyro can’t survive inflamed environment)
