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Cystic Ovarian Disease

Dr. D. A. ColemanWest Virginia University

As early as 1831, abnormally large ovarian folliclesthat failed to ovulate (release an egg) werereported to result in altered cyclic activity,abnormal sexual behavior and reduced fertility.

This condition, termed cystic ovarian disease,occurs in 5 to 10% of dairy cows nationally.

In a study of 2532 health records in West Virginia,7% of the cows had cystic ovaries. Cows thatexperienced cystic ovaries had calving intervalsnearly 2 months longer than herdmates withoutcysts. Each day a dairy cow remains open past day85 postpartum represents an estimated loss of$2.50 to $3.00. Thus, approximately $180.00 ofpotential income is lost per year for each cow thatdevelops an ovarian cystover $1200 per year fora 100-Cow herd. Occurrence in one West Virginiaherd is 28%. This herd loses an estimated $5000each year because of cystic ovarian disease.

Because of financial consequences associatedwith ovarian cysts in dairy cows, scientists havestudied the disease for over 100 years.Future research may determine why some folliclesdevelop into cysts, factors or traits that make acow more likely to develop cystic follicles andmethods for treatment of cystic cows to minimizeextra days open. The following is a brief summaryof current knowledge concerning cystic ovariandisease in dairy cattle.

Ovarian cysts are characterized by rectal palpationas structures greater than 2.5 cm (approximately 1inch) in diameter remaining on an ovary for more

than 10 days. Major categories of cysts includefollicular cysts, Iuteinized follicular cysts andcystic corpora lutea.

Follicular cysts result from failure of ovulation andIuteinization. (Luteinization is the structural andbiochemical changes that occur in cells andtissues of a follicle when it releases the egg.Follicular cells that once produced estrogenchange into luteal cells of the new corpus Iuteum(CL, also called a yellow body) that secreteprogesterone. Follicular cysts are blister-likestructures, flaccid to the touch.

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Luteinized cysts apparently fail to ovulate, butsome Iuteinization occurs. Because of the varyingdegree of Iuteinization, Iuteinized cysts are firmerto 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 inpregnant cows and reasoned that cystic CL couldnot support pregnancy. However, researchers atCornell University report that a CL needs toproduce only approximately 100 gof progesteroneto support pregnancy. Therefore, a cystic CL couldmaintain pregnancy. In the absence of pregnancy,cystic CL regress and are considerednonpathological.

Symptoms

An abnormal pattern of estrous behavior is themost noticeable sign of cystic ovarian disease.A cow with an ovarian cyst might exhibit constanestrus (nymphomania), no estrus (anestrus) or anerratic combination of estrus and anestrus.Ratios of estrus to anestrus vary among studiesfrom 74%:26% to 17%:83%.

Detection of cysts in the early postpartum periodmight account for the reported predominance ofanestrous behavior. Sexual activity does notnormally accompany follicular maturation duringthis time. A predominance of nymphomania wasreported in many early studies when more bulls

were present on farms. A greater proportion ofcows with cystic ovaries will be classified asnymphomanic where good estrous detectionpractices are used.

Other general symptoms of cystic ovarian diseaseinclude: 1) lack of muscle tone in the vulva, vagina,cervix and uterus; 2) passive prolapse of the vaginaand/or excessive discharge of mucus; 3) relaxationof sacroiliac and sacrosciatic ligaments of thepelvis (resulting in the sterility hump appearance


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of the tail head); 4) changes in generalmetabolism; 5) erratic changes in milk production;6) rough dry hair coat; 7) nervous tension;8) disturbed feeding and rumination and9) progressive emaciation.

Etiology

Numerous studies have determined the

anatomical, physiological and biochemicalchanges that occur during normal developmentand ovulation of follicles. With this knowledge, itshould be possible to determine what went wrongwhen a cyst develops. However, many eventsleading to the rupture of a follicle and release ofan egg depend on small changes in moleculeswithin cells that line the inner (granulosa cells)and outer (theca cells) tissue layers of the follicle.These changes occur rapidly, and timing of theseevents varies among cows. Research in this areahas awaited development of new techniquessensitive enough to study these minute cellularand biochemical changes.

Cyclic development and ovulation (rupture) offollicles requires proper timing of release ofseveral hormones from both the ovary and brain.See Fig. 1 for the known general interactions ofthese hormones. When properly timed, thesechanges result in release of an egg approximatelyevery 3 weeks in cattle.

Briefly, ovarian follicles begin to develop andenlarge rapidly under the influence of folliclestimulating hormone (FSH) from the pituitarygland. As follicles grow, they secrete an increasingamount of estrogen into the blood. The increasedestrogen concentration is necessary for thedisplay of estrus. In addition, the elevatedestrogen level causes the brain to releasegonadotropin-releasing hormone (GnRH).

GnRH causes the pituitary to release a surge ofIuteinizing hormone (LH) and FSH. This surge ofLH is responsible for ovulation of the follicle andIuteinization of the cells lining the follicular wall.Cells that once provided estrogen now secreteprogesterone, and the resulting structure is calleda CL.

Circulating progesterone from the CL reducesuterine contractions and inhibits the surge releaseof FSH and LH. If pregnancy does not occur,prostaglandin F2 from the uterus causes the CL to

regress on about day 16 or 17 of the cycle. As theCL regresses, progesterone decreases and FSHand LH again are released in greater amounts,culminating in an estrogen induced ovulatorysurge of gonadotropins, and the initiation of a newcycle.

See Fig. 2 for known hormonal and biochemicalchanges that occur within the preovulatory follicleafter stimulation with LH. Cystic follicles coulddevelop if any of the steps shown in Figs. 1 or 2fail. The actual cause(s) of cystic ovarian diseaseis (are) unknown. However, the apparentlysuccessful treatment of cystic cows with GnRH(discussed later) suggests that ovarian cysts resultfrom an inadequate or improperly timed release ofGnRH from the brain.

Predisposing Causes

Development of cysts has been associated withmany factors. In the late 1800s, it was proposedthat occurrence of cysts was influenced bygenetics or occurred secondary to uterineinfection. Subsequent studies discredited theuterine infection theory and further supported agenetic predisposition.

Estimates of heritability vary considerably from 5%to as high as 43% when the data set is limited todams and daughters with at least four service

periods each. Estimates of repeatability range from6 to 27%; recurrence varies from 15 to 75%.

Cystic ovarian disease was more common inHolstein-Friesians than in Jersey, Guernsey orAyrshire cows and varied among sire-lines withinbreed. Culling bulls whose daughters had a highincidence of cystic ovaries reduced occurrence ofcysts in Sweden from 10.8% in 1954 to 5.1% in1961.

In several studies, more cysts were found in highproducing cows compared to their herdmates.Higher levels of peripheral estrogen were found incows with cysts. Furthermore, cows fed

diethylstilbestrol (a synthetic estrogen) producedmore milk compared to their identical-twincontrols. These findings suggest that an elevatedlevel of estrogen in cows with follicular cystsmight cause higher milk yield.

In at least one study, however, cows with cystsaveraged 1.2 years older than cows without cystsand, therefore, would be expected to produce moremilk. Other studies have found no relationshipbetween cystic ovarian disease and level ofproduction. Some cystic follicles continued togrow without producing estrogen, and lessestrogen was found in follicular fluid from cysticfollicles compared to normal follicles.

In another study, there was no relationshipbetween content of estrogen in fluid from cysticfollicles and behavior of the cow. In addition, lowermilk yields were found in nymphomanic cows(having presumably more estrogen) than inanestrous cows. Thus the relationship betweenovarian cysts and level of production of milk still isnot well documented.

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Fig. 1. Hormonal interactions between the ovary and brain.

Older cows have a higher incidence of ovariancysts with a cumulative rate of 50% over 11 years.Incidence increases up to the fourth or fifthlactation in dairy cows. Beef cows develop cystsafter 4 to 6 years of age even if never bred. Yet, norelationship was found between lactation numberand incidence of cystic ovaries in 324 cows in theuniversity herd in another study. Presumably,different culling practices for reproductiveinefficiency removed many cows predisposed tocystic development before it occurred.

The greatest incidence of ovarian cysts occurswithin the first 45 to 60 days postpartum andduring October through February.

Treatments

Manual rupture of cysts was practiced byScandinavian veterinarians in the late 1800s.This crushing of the ovary, repeatedly if necessary,was promoted in the United States at thebeginning of the century. However, because offrequent excessive hemorrhaging and possibleadhesions, manual rupture of cysts is notpresently recommended.

The functional relationship between the ovariesand the pituitary gland was established in the1920s. In 1942, 11 of 13 nymphomanic cows cyclednormally after treatment with an extract of theanterior pituitary gland or with pregnant maresserum gonadotropin (PMSG) which contains asimilar compound. Conception was reported in 9 10 cows that were bred. Shortly thereafter,Wisconsin researchers reported 49 of 71nymphomanic cows with normal genital tractsbegan cycling after treatment with unfractionedpituitary extract from sheep; 38 of the 49 becamepregnant.

Following characterization and purification, humachorionic gonadotropin (hCG) also was usedsuccessfully to treat cows with cystic ovaries.However, frequent treatment of cows with hCG orPMSG resulted in development of antibodies tothese large molecules, and many cows would notrespond after a few treatments.

Isolation, characterization and synthesis of thenaturally occurring brain molecule GnRH in theearly 1970s provided a substance capable ofinducing a surge release of LH without inducing


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Fig. 2. Effects of LH on cells that line thepreovulatory follicle.

an immune response.cysts to Iuteinize and

The surge of LH causedthen regress after an interval

similar to the lifespan of a normal CL.

Experimental results obtained at Columbia,Missouri, indicate that approximately 75-80% ofcows treated with GnRH recover from the cyst andbegin cycling within 23 days. Combining manualrupture with hormonal therapy has no additionalbenefit, and administration of drugs by intravenousand intramuscular routes is equal in effectiveness.Treatment of cows with progesterone or estradiolhas had few benefits. Treatment with adrenalcorticoids can result in development of additionalovarian cysts.

Prophylactic administration of GnRH atapproximately 2 weeks postpartum reportedlydecreased calving interval by stimulating ovarianactivity early postpartum. This also resulted inlower occurrence of cystic ovaries and less cullingof cows with no detrimental effect on services perconception or days open. However, otherinvestigators found no benefit with routineprophylactic treatment.

Many cows with cystic ovaries recoverspontaneously without treatment (range 30-71%).Herds that were examined every 2 weeks werefound to have a greater incidence of cysts thanherds examined at intervals of 4 weeks. Thissuggests that some cysts develop and thenregress spontaneously in less than 30 days.Development of and self-recovery from cysticovarian disease is more common early in thepostpartum period.

A major factor in assessing actual or perceivedcystic ovarian disease is the expertise of theperson palpating the cows ovaries. As early as1919, W.L. Williams wrote on the difficulty of

distinguishing by rectal palpation cystic ovarianfollicles from normal ovarian structures near thetime of ovulation. In a recent field study involving28 herds and the 10 veterinarians who regularlyserved the herds, there was no benefit of treatmentwith GnRH over saline in 40 cows diagnosed ascystic from a single examination. The studypointed out possible inaccuracies of someindividuals when diagnosing ovarian cysts by asingle rectal palpation. Using a milk progesteroneassay to determine hormonal activity of ovarianstructures, Japanese researchers found a highincidence of unnecessary or inappropriatetreatment of misdiagnosed cystic cows.

Recommendations

Based on current knowledge of cystic ovariandisease and on a computerized economic decisionanalysis system, it is recommended to wait untilapproximately one month post-calving beforeattempting to diagnose cystic ovarian disease.After this time, cows diagnosed by an experiencedpalpater as having an ovarian cyst should betreated with GnRH at first diagnosis. Cows shouldbe palpated a second time within 7 to 10 days ifpossible and retreated if necessary.

Trade or brand names are mentioned only for information.The Cooperative Extension Service intends no endorsement norimplies discrimination to the exclusion of other products whichalso may be suitable.

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