Behavioral and conformational manifestations of follicular cystic ovary disease vary considerably, as does the overall clinical picture. However, all the signs relate to the focal primary lesions, namely, thin-walled cysts in the ovary and the disruption of the normal endocrine events of the estrous cycle.
Cystic ovary disease primarily affects dairy cattle, although it has been reported occasionally in beef cattle. This difference is due to the more intensive management and treatment of individual dairy cows. The disease is more common among certain family lines within breeds, which implicates hereditary factors in the etiology.
The cystic ovary syndrome is commonly thought to be caused by high milk production. The observation is biased, however, because higher-producing cows are more likely to be examined, more likely to be treated if found to have cystic ovary disease, and more likely to be allowed to remain in the herd despite some decrease in reproductive performance. Evidence indicates that cystic ovary disease causes cows to produce more milk rather than that high production causes cows to develop cystic ovary disease. Incidence increases with age. Most cases occur within 3–8 wk of parturition at the first attempted postpartum ovulation, coinciding with peak daily milk production and rapidly decreasing body condition. The reported herd incidence is 5–25% per lactation, or higher in some problem herds, and can be influenced by herd-health programs in which examination and detection are emphasized.
Etiology and Pathogenesis
Hereditary predisposition has been implicated in dairy cattle; eg, daughters of previously cystic cows had a higher incidence of cystic ovary disease than did daughters of unaffected cows. Periparturient stress apparently serves as a trigger. The mechanism by which stress elicits the hypothalamic and pituitary defects in genetically predisposed cows is most commonly thought to be a relative deficiency in the release of luteinizing hormone (LH) at estrus. This may be a reflection of failure of hypothalamic release of gonadotropin-releasing hormone (GnRH). Another mechanism that can exist in some cows with cysts is a deficiency of LH and follicle-stimulating hormone receptors in developing follicles.
During normal proestrus, regression of the CL coincides with development of a selected follicle, while the growth of any additional follicles is inhibited. In animals developing cystic ovary disease, ovulation fails to occur and the dominant follicle continues to enlarge. An important component of the etiology is the inappropriate release, or lack of release, of GnRH during estrus. The mechanism may be a hypothalamic defect that results in failure of follicular estrogen to cause a release of GnRH. The end result is a lack of ovulation at the time of estrus. This defect appears to involve the estrogen receptor α. Moreover, other follicles may grow and form multiple cysts either bilaterally or unilaterally.
Grossly, follicular cysts resemble enlarged follicles, varying in size from 1.7 to 5–6 cm in diameter. The size and form of an affected ovary depends on the number and size of cysts present. The cystic ovary is capable, at least initially, of steroidogenesis, and its products vary from estrogens to progesterone to androgens. The actions of the various hormones produced or the absence of the stabilizing action of high progesterone from the normal CL during ~75% of the estrous cycle (or both) are responsible for the changes seen in the genital tract, body conformation, and general behavior.
Behavioral aberrations range from frequent, intermittent estrus with exaggerated monosexual drive to bull-like behavior (bulling), including mounting, pawing the ground, and bellowing. This behavior may be accompanied by masculinization of the head and neck. Relaxation of the vulva, perineum, and the large pelvic ligaments, which causes the tail head to be elevated, can occur in chronic cases. Some affected cows show these signs, but others may be sexually quiescent; anestrous cows are the most common presentation. This variation is due to the duration of the condition and the nature of the hormone signals or lack thereof from the diseased ovary.
The affected ovaries generally are enlarged and rounded, but their size varies, depending on the number and size of cysts. Their surface is smooth, elevated, and blister-like, particularly when cysts exceed 2.5–3 cm in diameter. Cysts frequently are multiple and may approach 4–6 cm in diameter. Under the influence of hormones produced by the cystic ovary or the lack of hormones (especially progesterone) normally present during estrous cycles, the uterus undergoes palpable changes, which in turn vary with the duration of the cystic condition. Thus, during the first week, the uterine wall is thickened and edematous as an extension of the preceding estrus. Toward the end of the first week, the uterine wall develops a sponge-like consistency. In chronic cases, atony and atrophy of the uterine wall are common. Occasionally, the uterine horns become markedly shortened. Some degree of mucoid to mucopurulent vaginal discharge is common. Hydrometra, a fluid-filled, extremely thin-walled uterus, is seen occasionally.
Palpation of the uterus is helpful to differentiate a follicular cyst from a dominant preovulatory follicle; only the estrous cow has a coiled, extremely turgid uterus and a follicle. As noted earlier, cystic cows fail to ovulate a preovulatory follicle after undergoing CL regression and, on examination of the reproductive tract, they present with a large follicle, absence of a CL, and absence of a turgid uterus. Ultrasound technology per rectum can be used to differentiate cysts from corpora lutea and may be helpful in diagnosing cyst type (ie, follicular vs luteal). Larger, multiple cysts are easily identified by rectal palpation. History, conformation, and uterine changes, when present, provide supplemental diagnostic evidence.
The disease responds readily to an LH-type hormonal treatment. In the past, human chorionic gonadotropin (hCG) was commonly used. It is most effective at 10,000 USP units IM, although success with lower doses given IM or IV has also been reported.
Hormone therapy with GnRH is effective at 100 μg and less antigenic than hCG. To hasten the onset of the first estrus after treatment, prostaglandin (PG) F2α products can be given 7 days after hCG or GnRH. Ovulation synchronization protocols, such as OvSynch, combine GnRH and PGF2α to control follicular dynamics, luteolysis, and ovulation. They allow for fixed timed artificial insemination (TAI) of cattle without the need for estrus detection, and have been successfully used to treat cows with cystic ovaries. This protocol consists of giving GnRH, then PG 7 days later, then a second administration of GnRH 48 hr later, and finally TAI 0–24 hr later. The claim that breeding on the first estrus is prone to produce twins has not been substantiated. In fact, breeding on the first estrus reduces danger of recurrence by establishing pregnancy as soon as possible.
The potential danger of traumatizing the ovary and causing hemorrhage with subsequent local adhesions should not be overlooked, but manual rupture has been used often without problems. This method should be weighed against the cost of hormone therapy.
After therapy with an LH-type hormone, a normal, fertile estrus can be expected in 15–30 days. With GnRH therapy, 25% of cases required a second treatment, and 5% required a third. One-third of the cases treated for the third time failed to respond. Spontaneous recovery is possible and is most common in cases arising during the first 50 days after calving. Each successfully treated cow is more likely to require treatment after the next parturition than are previously unaffected cows. Likewise, successful treatment encourages perpetuation of the disease in the herd if the offspring are used for breeding. While cystic ovary disease in cattle clearly has a genetic component, it is unlikely that a single farm using artificial insemination can significantly influence the incidence. In Sweden, progress has been made in reducing the condition through culling and selection procedures for bulls used in artificial insemination, but affected cows are still treated.
Cystic Ovary Disease as a Herd Problem
Occasionally, individual herds experience exceptionally high rates (~50%) of cystic ovary disease over a period of months. Determining the cause of these episodes is not easy, but the following questions should be addressed: 1) Is the diagnosis accurate, ie, are the structures being identified as cysts really cysts? This can be established via second opinion diagnoses, determination of milk or plasma progesterone levels, ultrasound examination of the ovaries in suspected cases, observing ovarian changes and time of estrus activity after treatment with prostaglandin products, and/or improving diagnostic skills by continuing education. 2) Has the palpation examination schedule for the herd changed? Initiating routine postpartum examinations for all cows and increasing frequency of herd visits can result in an increased apparent incidence. 3) Has the herd incidence of periparturient complications and stress increased? Cows having problems around calving (such as twins, milk fever, dystocia, retained placenta, ketosis, etc) are much more likely to develop cysts. Attempts to reduce these complications are indicated. 4) Have herd genetics been considered? It is well accepted that ovarian cysts are more common in certain lines. 5) Has the nutritional program of the herd been evaluated? Nutritional problems are frequently implicated as causing cows to develop cysts, but rarely have these concerns been confirmed in controlled studies. Inadequacies or imbalances involving calcium and phosphorus, vitamin E and selenium, and energy are most often implicated. Moldy feed or roughages that contain high concentrations of estrogenic substances are also frequently suspected, but better testing methods are needed. Proper nutritional management of dairy herds is always warranted. Monitoring the effects of the nutritional program via a body condition scoring program should be used as part of the effort to reduce ovarian cysts in problem herds.
Last full review/revision July 2011 by Carlos A. Risco, DVM, DACT