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Managing the mare with small ovaries

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01 August 2009, at 12:00am

Dr JONATHAN PYCOCK discusses ovarian problems in mares

OVARIAN problems are relatively common in mares and small ovaries may be due to a permanent developmental condition (e.g. chromosomal abnormality), transient physiologic condition (e.g. seasonal anoestrus) or an acquired pathological condition (e.g. Cushing’s disease).

In summary, small or inactive ovaries in mares may be caused by: 

■ Seasonal anoestrus 

■ Lactation related anoestrus

■ Age 

■ Equine Cushing’s disease 

■ Chromosomal abnormality 

■ Exogenous hormone administration

Seasonal anoestrus 

Since the early nineteenth century, when 1st January was declared the official birthdate for thoroughbred foals, irrespective of their actual birth dates within that year, veterinarians have been plagued with problems attempting to breed mares in the winter and early spring outside their most fertile period.

Mares are seasonally polyoestrous, and environmental and other factors can exert a profound effect on reproductive function particularly during the transitional period between winter anoestrus and the onset of cyclical activity in the spring. The onset of cyclic activity is stimulated by increased day length.

On rectal palpation or transrectal ultrasound imaging both ovaries will be small (<3 x 2 x 2cm), and in some mares there will be a number of small follicles (Figure 1). Plasma progesterone concentrations are less than 1ng/ml.><3 x 2 x 2cm), and in some mares there will be a number of small follicles (Figure 1). Plasma progesterone concentrations are less than 1ng/ml.

Although increasing day length is the primary controlling factor, ensuring freedom from disease and good body condition by stabling, adequate nutrition, anthelmintic therapy and attention to dental conditions can hasten the onset of cyclical ovarian activity.

Thus, prolonged anoestrus can be prevented by good management and exposing mares to artificial light during winter. The simplest regime is to provide 16 hours of natural and artificial light with eight hours of darkness. This exposure needs to be applied for 50 to 60 days.

Several pharmacological protocols including pituitary extracts, gonadotrophin-releasing hormone, dopamine antagonists and progestagens have been designed to reduce the length of light exposure necessary.

The progestagen altrenogest (Regumate) is given over a 10-15 day period in mares that are in middle to late transition. This is typically mares with at least 25mm follicles (Figure 2) and an oedema pattern in the uterus (Figure 3).

Currently, treatment with an equine Follicle Stimulating Hormone (eFSH) product during the transitional phase to increase follicular development and production of steroidogenically competent follicles sooner is being developed. Recombinant eFSH and equine Luteinising Hormone (eLH) have been developed and may become available commercially shortly.

Lactation-related anoestrus 

Lactation-related anoestrus is commonest in mares foaling early in the season. Affected mares may have a normal post-partum oestrus after 6- 12 days, but fail to return to oestrus at the end of the first dioestrus. Alternatively they may not even have a normal “foal heat”. The ovaries resemble those of a mare in deep winter anoestrus, i.e. small and inactive; the condition can last for several months. Originally it was thought to be due to prolactin suppressing pituitary gonadotrophin release, but this is now in doubt. Affected mares should be teased and examined weekly per rectum to assess their ovarian status.

Treatments similar to those described above for winter anoestrus have been used, but with little success. Twice daily injections of 0.04mg (10ml) of a synthetic gonadotrophin-releasing hormone agonist (buserelin; Receptal) have been found to induce the development of a follicle within 7-14 days of commencing therapy. Oral administration of the dopamine antagonist domperidone (Motilium 10mg tablets) at a dose rate of 1mg/kg daily for 10 days may be effective. The mare may return to anoestrus following the induced ovulation if she fails to conceive. Weaning may be the only effective way the mare can resume cycling.

Age

Small and inactive ovaries are normally found in prepubertal mares. In the mare, the age at which puberty occurs is influenced by the effect of the season of the year. A filly born early in the year, say January or February, may have her first cycle in May or June of the following year, i.e. when she is 16 or 17 months old. 

A filly foal born late in the year may not develop large, pre-ovulatory follicles until she is 22 or 23 months old. Aged mares may rarely exhibit ovarian senescence. No effective treatments are currently available in the mare for promoting follicular growth in senescent ovaries. The incidence of Cushing’s disease is increased in older mares and may be the cause of the small ovaries. 

Equine Cushing’s disease 

Cushing’s syndrome (pituitary pars intermedia dysfunction) has been associated with a variety of medical and reproductive problems, usually in aged mares. 

This is presumably due to destruction of the cells secreting FSH and LH leading to small ovaries. 

Chromosomal abnormality 

The normal chromosome complement for the domestic horse is 64 chromosomes including two sex chromosomes, XX in females and XY in males. The karyotype of a normal female is 64, XX and 64, XY in males. 

Various sex chromosome anomalies have been described in the horse, and whilst not common, must not be overlooked as a cause of small ovaries. The incidence of chromosomal abnormalities is difficult to assess, but must be suspected in maiden mares with small, inactive ovaries and an immature tubular genital tract once winter anoestrus has been eliminated as a cause of acyclicity. However, some genetically normal young fillies in training can be acyclic, and thus they must be given more time to mature reproductively and karyotyping must be performed before making a final diagnosis. 

The main karyotypic abnormality of such mares is the 63, XO genotype termed X monosomy or equine Turner’s syndrome. Examination detects very small ovaries (< 1 cm in diameter), and a poorly developed tubular genital tract which is difficult to palpate. The external genitalia are typically normal. These mares are usually small for their age and do not cycle, although occasionally may show passive oestrous signs. Definitive diagnosis requires cytogenetic analysis of a blood sample. 

The author submits samples to UCD Veterinary Genetics Laboratory in California. They are able to accept samples from UK with the appropriate paperwork. More information is available at www.vgl.ucdavis.edu/services/h... /karyotyping.php . There is no treatment and the mare is sterile. 

Some infertile mares have XY ovarian dysgenesis and in a maiden mare, once winter anoestrus has been eliminated as a cause of acycliclity, must be considered as a possible cause of infertility. Affected mares present with normal external genitalia, small, inactive ovaries and an immature tubular genital tract. 

Examination of the reproductive system detects very small ovaries (<1cm in diameter), and a poorly developed tubular genital tract, which is difficult to palpate. This is similar to mares with 63, XO genotype (Turner’s syndrome). 

There is no treatment and the mare is sterile. Other chromosome abnormalities include ovarian hypoplasia and testicular feminisation. These are also rare, but must be considered in female horses with irregular cycles and small ovaries during the breeding season.  

Another variation of numerical sex chromosome abnormalities is X chromosome mosaicism. Depending on how many cells have different numbers of sex chromosomes, affected mares have a variety of the syndromes described above and may have abnormal external genitalia such as clitoral hypertrophy and a reduced vulval length (Figure 4). 

Confusingly, such mares can very rarely conceive and deliver a live foal. Cytogenic evaluation is essential for accurate diagnosis and prognosis. 

Exogenous hormone administration 

 Anabolic steroid administration to fillies inhibits ovarian activity by suppressing pituitary gonadotrophin secretion. This results in failure of follicular development and ovulation. Some fillies develop clitoral hypertrophy following use of anabolic steroids. The use of anabolic steroids should be avoided in fillies and mares intended to be used for breeding.