Cystic ovarian disease

Ovarian cysts are characterized as structures greater than 2.5 cm (approximately 1 inch) in diameter remaining on an ovary for more than 10 days. Major categories of cysts include follicular cysts, luteinized follicular cysts and cystic corpora lutea.

Follicular cysts result from failure of ovulation and luteinization. (Luteinization is the structural and biochemical changes that occur in a follicle after ovulation. Follicular cells that once produced estrogen change into luteal cells of the new corpus luteum (CL) that secrete progesterone. Follicular cysts are blister-like structures, flaccid to the touch.

Luteinized cysts apparently fail to ovulate, but some luteinization occurs. Because of the varying degree of luteinization, luteinized cysts are firmer to the touch than follicular cysts though not as solid as CL.

Cystic CL are CL with a fluid filled center. Several early researchers did not find cystic CL in pregnant cows and reasoned that cystic CL could not support pregnancy. However, Cornell University researchers reported that a CL producing only 100 µg of progesterone can support pregnancy. Therefore, a cystic CL could maintain pregnancy. In the absence of pregnancy, cystic CL regress and are considered nonpathological.


Abnormal estrous behavior patterns are the most noticeable sign of cystic ovarian disease.

A cow with an ovarian cyst might exhibit “constant” estrus (nymphomania), no estrus (anestrus) or an erratic combination of estrus and anestrus. Ratios of estrus to anestrus vary among studies from 74%:26% to 17%:83%.

Other general symptoms of cystic ovarian disease include: 1) lack of muscle tone in the vulva, vagina, cervix and uterus; 2) passive prolapse of the vagina and/or excessive discharge of mucus; 3) relaxation of sacroiliac and sacrosciatic ligaments of the pelvis (resulting in the “sterility hump” appearance of the tail head); 4) changes in general metabolism; 5) erratic changes in milk production; 6) rough dry hair coat; 7) nervous tension; 8) disturbed feeding and rumination and 9) progressive emaciation.


Cyclic development and ovulation (rupture) of follicles requires proper timing of release of several hormones from both the ovary and brain. When properly timed, an egg is released approximately every 3 weeks in cattle.

Briefly, ovarian follicles begin to develop and enlarge rapidly under the influence of follicle stimulating hormone (FSH) from the pituitary gland. As follicles grow, they secrete an increasing amount of estrogen into the blood. The increased estrogen concentration leads to display of estrus. In addition, the elevated estrogen level causes the brain to release gonadotropin-releasing hormone (GnRH).

GnRH causes the pituitary to release a surge of Iuteinizing hormone (LH) and FSH. LH is responsible for follicle ovulation and Iuteinization of the cells lining the follicular wall. Cells that once provided estrogen now secrete progesterone, and the resulting structure is called a CL.

Circulating progesterone from the CL reduces uterine contractions and inhibits surges of FSH and LH. If pregnancy does not occur, prostaglandin F2α from the uterus causes the CL to regress on about day 16 or 17 of the cycle. As the CL regresses, progesterone decreases and FSH and LH again are released in greater amounts, culminating in an estrogen induced ovulatory surge of gonadotropins, and the initiation of a new cycle.

Cystic follicles could develop if any of the steps described above fail. The actual cause(s) of cystic ovarian disease is (are) unknown. However, the apparently successful treatment of cystic cows with GnRH (discussed later) suggests that ovarian cysts result from an inadequate or improperly timed release of GnRH from the brain.

Predisposing Causes

Development of cysts has been associated with many factors.

Genetic predisposition for cystic ovarian disease is well documented. Estimates of heritability vary considerably from 5% to as high as 43%. Estimates of repeatability range from 6 to 27%; recurrence varies from 15 to 75%.

Cystic ovarian disease was found to be more common in Holstein-Friesians than in Jersey, Guernsey or Ayrshire cows and varied among sire-lines within breed.

In several studies, more cysts and accompanying higher levels of peripheral estrogen were found in high producing cows compared to their herdmates. In at least one study, however, cows with cysts averaged 1.2 years older than cows without cysts and, therefore, would be expected to produce more milk. Other studies have found no relationship between cystic ovarian disease and level of production. Some cystic follicles continued to grow without producing estrogen, and less estrogen was found in follicular fluid from cystic follicles compared to normal follicles. The relationship between ovarian cysts and level of production of milk still is not well documented.

Older cows have a higher incidence of ovarian cysts with a cumulative rate of 50% over 11 years. Incidence increases up to the fourth or fifth lactation in dairy cows. Beef cows develop cysts after 4 to 6 years of age even if never bred. Yet, no relationship was found between lactation number and incidence of cystic ovaries in 324 cows in the university herd in another study. Presumably, different culling practices for reproductive inefficiency removed many cows predisposed to cystic development before it occurred. The greatest incidence of ovarian cysts occurs within the first 45 to 60 days postpartum and during October through February.


The previously recommended practice of manual rupture of is not presently recommended due to risk of frequent excessive hemorrhaging and possible adhesions.

Experimental results obtained from University of Missouri, indicate that approximately 75-80% of cows treated with GnRH recover from the cyst and begin cycling within 23 days. Combining manual rupture with hormonal therapy had no additional benefit. Administration of drugs by intravenous and intramuscular routes is equal in effectiveness. Treatment of cows with progesterone or estradiol has had few benefits. Treatment with adrenal corticoids can result in development of additional ovarian cysts.

Prophylactic administration of GnRH at approximately 2 weeks postpartum reportedly decreased calving interval by stimulating ovarian activity early postpartum. This also resulted in lower occurrence of cystic ovaries and less culling of cows with no detrimental effect on services per conception or days open. However, other investigators found no benefit with routine prophylactic treatment.

Many cows with cystic ovaries recover spontaneously without treatment (range 30-71%). Herds that were examined every 2 weeks were found to have a greater incidence of cysts than herds examined at intervals of 4 weeks, suggesting that some cysts develop and then regress spontaneously in less than 30 days. Development of and self-recovery from cystic ovarian disease is more common early in the postpartum period.

A major factor in assessing actual or perceived cystic ovarian disease is the expertise of the person palpating the cow’s ovaries. In a recent field study involving 28 herds and the 10 veterinarians who regularly served the herds, there was no benefit of treatment with GnRH over saline in 40 cows diagnosed as cystic from a single examination. The study pointed out possible inaccuracies of some individuals when diagnosing ovarian cysts by a single rectal palpation. Using a milk progesterone assay to determine hormonal activity of ovarian structures, Japanese researchers found a high incidence of unnecessary or inappropriate treatment of misdiagnosed “cystic” cows.


Based on current knowledge of cystic ovarian disease and economics, it is recommended to wait until approximately one month post-calving before attempting to diagnose cystic ovarian disease.

After this time, cows diagnosed with an ovarian cyst should be treated with GnRH at first diagnosis. Cows should be palpated a second time within 7 to 10 days if possible and retreated if necessary.


D.A. Coleman

D.A. Coleman
1 articles

West Virgina University

West Virgina University