Cystic Ovary Disease:

Cystic Ovary Disease                                              : 

Among domestic animals, cystic ovary disease is most common in cattle, particularly the dairy breeds, but it occurs sporadically in dogs , cats, pigs, and perhaps mares. When diagnosing the reproductive status of mares, it must be remembered that normal follicle size during estrus is 4-6 cm in diameter. Ovulation failure can also be found in mares that are having irregular estrous cycles during the spring or fall transition phases of the reproductive cycle, but this situation is not treated in the same way as the cystic ovary disease condition of cattle.

 The granulosa cell tumor condition in mares causes marked enlargement of one ovary but differs from cystic ovary disease of cattle .

Three ovarian structures in cattle include the term cyst: follicular cysts, luteal cysts, and cystic corpus luteum (CL). In contrast to the other 2, the structure described as a cystic CL arises after normal ovulation. Cystic CL are known to be a normal stage or variation of CL development because they are found in normally cycling and pregnant cows without concurrent abnormal reproductive performance. Cystic CL have a soft, mushy core area, due to presence of fluid from a degenerating blood clot, compared with the homogeneous, liver-like consistency of the base of a typical CL.

Cystic CL are most often detected 5-7 days after estrus when the structure is nearing the end of the corpus hemorrhagicum or growth phase. The cystic CL as well as the typical CL may or may not have an ovulation crown or papilla at its apex. Absence of this ovulation crown or papilla should not be considered diagnostic of the cystic condition because 10-20% of functional, normal CL fail to develop this feature. The two pathologic forms of bovine cystic ovary disease, follicular cysts and luteal cysts, are etiologically and pathogenetically related but differ clinically.

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—especially absence of the negative feedback of progesterone from the CL on the hypothalamus and pituitary.
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:


 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. Moreover, other follicles may grow and form multiple cysts either bilaterally or unilaterally. Grossly, follicular cysts resemble enlarged follicles, varying in size from 2.5 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.

**Clinical Findings:

Behavioral aberrations range from anestrus to frequent, intermittent estrus with exaggerated monosexual drive to bull-like behavior, including mounting, pawing the ground, and bellowing. This behavior often is 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, is common in chronic cases. Some affected cows show these signs, but others may be sexually quiescent. 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.


Larger, multiple cysts are easily identified by rectal palpation. History, conformation, and uterine changes, when present, provide supplemental diagnostic evidence. Palpation of the uterus is helpful for differentiation between a single follicular cyst and a mature graafian follicle; only the estrous cow has a coiled, extremely turgid uterus. Ultrasound technology per rectum can be used in differentiating cysts from corpora lutea and may be helpful in diagnosing cyst type (ie, follicular vs luteal).


From one viewpoint, the disease responds readily to treatment, be it mechanical (manual rupture) or hormonal. The success rate of manual rupture, when measured in terms of conceptions within 24 days, is ~50%; hormone therapy (see below) may be somewhat more successful but is more expensive. Aberrant behavior ceases soon after successful therapy. This is followed by normal conformation of the ovary; a normal, fertile estrus can be expected in 4-7 or 15-25 days after manual rupture and in 15-30 days after LH-type hormonal therapy. 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.

That, and the observation that spontaneous recovery involves the same sequence of events as recovery in response to hormonal therapy, suggests caution in evaluating therapeutic efficiency. 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 the cystic ovary condition 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.


The oldest and least expensive treatment is manual rupture—the ovary is grasped and moderate pressure applied with finger pads, not tips, against the palm until the cyst bursts. After successful rupture, some have recommended that the ovary be compressed briefly to minimize hemorrhage; however, hemorrhage is rarely a sequela of rupture of correctly diagnosed follicular cysts. Hemorrhage probably occurs most often when the condition is misdiagnosed, and rupture of a CL or corpus hemorrhagicum is attempted. 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.

Of several hormone preparations recommended and used in the past, human chorionic gonadotropin (HCG) remains the only one still available and commonly used. It is most efficacious at 10,000 USP units IM, although success with lower doses given IM or IV has also been reported.

Newer hormone therapy includes GnRH or LH-releasing hormone products, which are efficacious at 100 µg, IM. GnRH products are equally effective but less antigenic than HCG. The 2 products may be alternated when retreatment is necessary. To hasten the onset of the first estrus after treatment, prostaglandins can be administered 9-10 days after HCG or GnRH. 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.
Progesterone (or its analogs) has been given parenterally and PO to cows that do not respond to HCG and GnRH therapy, but in the USA these products have been removed from the cattle market or are not approved for use in lactating dairy cows. Progesterone treatment has been continued at least 10-12 days, if not 20, in expectation of a normal estrus on withdrawal.

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