Etiology

• A hereditary predisposition has been implicated in dairy cattle and incidence is associated with negative energy balance and stress factors in high producing dairy cows.
  • A genetic predisposition to partition glucose into the udder to prioritise lactose synthesis and milk production is characterized by insulin resistance in Holstein cattle Holstein.
• In normal proestrus, regression of the Corpus Luteum (CL) coincides with development and  maturation of a selected dominant follicle and other follicles are inhibited.
• In cystic ovarian disease (COD) there is failure of the positive feedback of follicular estrogen on the hypothalamus, via estrogen receptor ‘a’, to release sufficient Gonadotrophin Releasing Hormone (GnRH) to trigger an LH surge.
  • IGF-1 acts as a ‘co-gonadotroph’ amplifying the positive feedback to the hypothalamus, depending on appropriate positive metabolic signals.
  • Ovulation therefore fails to occur and the dominant follicle continues to enlarge.
  • Other follicles may grow and form multiple cysts and there may be luteinization of the structure.
• The cystic ovary remains capable of steroidogenesis and its products vary from estrogens to progesterone and androgens.
  • The actions of the hormones produced are responsible for the changes seen in the genital tract body conformation and behavior of affected cows.
• In the development of a luteal cyst, the release of LH may be greater than when follicular cysts develop, so that luteinization of the follicle occurs but the level is still insufficient to cause ovulation.

Predisposing factors

General

• Genetic selection for high milk production has led to a degree of ‘insulin resistance’ in dairy breeds such as Holstein Holstein.
• Negative energy balance and metabolic compromise associated with insufficient glucose availability is critical.
• Poor transition management that leads to excessive fat mobilization and fatty liver syndrome Fatty liver syndrome contributes to an increased risk of COD.