Disease of the Bovine Ovary
The disease arises from the failure of mature follicles to ovulate. It occurs most often before the first postpartum ovulation. Approximately 45–60% of animals that develop anovulatory follicular cysts will reestablish normal ovarian cycles spontaneously. Cystic follicles may also develop after postpartum ovarian cycles have been established, and these cysts are more likely to persist if effective treatment is not instituted.
The cause of cystic ovarian disease is not understood in any species.
The disease in cattle occurs more frequently after parturient or postparturient disease, and there is evidence that intrauterine infections and mastitis play a role in the pathogenesis of the disease. There is clearly a genetic predisposition to the disease in certain families. The daughters of cows that have had cystic ovaries have a substantially increased risk of developing the disease as compared to the general population. The disease tends to involve primarily dairy cows, but it can occur in cattle of any breed if they are withheld from breeding for a prolonged period of time. One of the factors that has made the understanding of the disease difficult is the definition of the disease itself. Follicular cysts in cattle are usually defined as follicles greater than 2.5 cm in diameter that fail to ovulate and may persist, usually longer than 10 days. By the time a follicle can meet the criteria to be defined as cystic, the conditions that led to its formation have passed and are not available for study. To offset this difficulty, anovulatory ovarian disease has been produced by a variety of experimental techniques. Unfortunately it is not known whether any, or all, of the experimental manipulations induces anovulatory cystic disease by the mechanisms that operate in the natural disease.
Cows that develop cystic ovaries as the result of estrogen and progesterone treatment have an increased mean basal concentration of luteinizing hormone secretion with increase in the frequency and amplitude of pulses, but the characteristic preovulatory luteinizing hormone surge is deficient. This increase in luteinizing hormone secretion is thought to be due to aberrant hypothalamic function altered experimentally by steroids or naturally by ovarian secretion.
Cattaneo L, Signorini ML, Bertoli J, Bartolome JA, Gareis NC, Dıaz PU, Bo GA, Ortega HH. (2014) Epidemiological Description of Cystic Ovarian Disease in Argentine Dairy Herds: Risk Factors and Effects on the Reproductive Performance of Lactating Cows. Reprod Dom Anim 2014; 49: 1028-1033
There is a long running contention that cystic corpus luteum is a cause of infertility.
Vincze B, Kátai L, Deák K , Nagy K, Cseh S, Kovács L. Pregnancy Rates of Holstein Friesian Cows with Cavitary or Compact Corpus Luteum. Veterinary Sciences 2024: 11: 246
Bovine alphaherpesvirus 1 (BoHV-1) is of the family Herpesviridae, genus Varicellovirus and is the cause of infectous bovine rhinotracheitis, and infectious pustular vulvovaginitis and infectous balanoposthitis. It is known to produce ovarian disease experimentally. The ovaries of innoculated cattle develop necrosis and inflammation particularly of the corpora lutea.
There is evidence that vaccines of BoHV-1 may reduce follicular numbers.
Widener CL, Graves WM, Alward KJ, Bohlen JF. Influence of a bovine respiratory disease vaccine with a temperature-sensitive modified live or killed infectious bovine rhinotracheitis component on oestrous cycle parameters and anti-Müllerian hormone concentration in nulliparous heifers. Reprod Domest Anim. 2019; 54: 1470-1476.
Van der Maaten MJ, Miller JM, Whetstone CA. Ovarian lesions induced in heifers by intravenous inoculation with modified-live infectious bovine rhinotracheitis virus on the day after breeding. Am J Vet Res. 1985; 46: 1996-1999.
Ali et al (2105) reports on a cow that appears to be spontaneously cured of a granulosa-theca tumor by necrosis and single cyst formation.
Teh et al (2021) reported on a case series of cows.
27 had sex cord stromal tumors. 26 were granulosa cell tumors and 1 was a thecoma. They did extensive immunohistochemistry and identified different patterns (macrofollicular, microfollicular, diffuse, insular, trabecular, pseudopapillary). There was no followup information or indication of metastatic potential.
The macrofillicular pattern as a dominant or significant pattern was seen in 12 cases, The microfollicular in 10, the trabecular pattern in 10, the diffuse pattern in 1, the insular pattern (tightly packed island or nests) in 6, and the pseudopapillary pattern in 1. 14 had combinations, 12 were a pure pattern.
Immunohistochemistry results were given. All tumors stained for AMH. Only those with a follicular pattern (macro or micro follicular) stained for Inhibin alpha (10 of these had only 10% of cells staining). There was cytokeratin staining (AE1/AE3) in macrofollicular, microfollicular and trabecular cells. Often times, less than 10% of cells stained. The thecoma stained for AMH but did not stain for inhibin or cytokeratin.
Belotti et al (2021) reported on a cow with what they called an incipient granulosa cell tumor. This tumor was 6 x 7 mm and had multiple cystic structures with Call Exner like bodies.
El-Sheikh Ali H, Kitahara G, Torisu S, Nibe K, Kaneko Y, Hidaka Y, Osawa T. Evidence of Spontaneous Recovery of Granulosa-Theca Cell Tumour in a Heifer: A Retrospective Report. Reprod Domest Anim. 2015 50:
Dobson H, Kerby MJ, Chantrey J, Smith RF. Long-term outcome for two heifers with a granulosa-theca cell tumour Vet Rec 2013, 172: 581-582
Belotti EM, Sacco SC, Stassi AF, Notaro US, Angeli E, Etchevers L, Chiaraviglio JA, Ortega HH, Salvetti NR. Characterization of an incipient granulosa cell tumour in a Holstein cow: Steroid hormone receptors and coregulators expression. Anat Histol Embryol. 2022; 51: 62-68.
Teh APP, Kitahara G, Izzati UZ, et al. Immunohistochemical and Morphological Features of Bovine Granulosa Cell Tumours in Relation to Growth Pattern and Folliculogenesis. J Comp Pathol. 2021;187:40-51. doi:10.1016/j.jcpa.2021.06.008