INFECTIOUS AND INFLAMMATORY CAUSES

Infection and inflammation, both local and systemic in the reproductive tract, are important factors that can reduce ovarian function and trigger delayed ovulation in cows [101]. These mechanisms act through negative effects on the HPO axis, elevated proinflammatory cytokines, and direct disruption of follicular development and oocyte quality [91].

Subclinical endometritis is a major cause of ovulatory dysfunction in postpartum cows [102]. Although asymptomatic, this condition is characterized by inflammatory cell infiltration of the uterine mucosa and increased cytokines such as IL-1β, Interleukin-6 (IL-6), and TNF-α [103]. Diagnostic thresholds are commonly defined by polymorphonuclear neutrophil (PMN) proportions: ≥18–20% PMN at 21–33 days postpartum and ≥5–10% PMN after 34–47 days postpartum, depending on sampling method and herd conditions [103]. These cytokines can enter the bloodstream, inhibit GnRH activity in the hypothalamus, reduce the frequency of LH pulses, and disrupt granulosa cell proliferation in the dominant follicle [104]. Subclinical endometritis also alters the uterine environment, increasing prostaglandin production, which affects ovarian function and can inhibit post-ovulatory CL formation [105]. Together, these effects prolong the follicular phase and increase delayed ovulation risk [106].

Viral reproductive diseases, particularly infectious bovine rhinotracheitis (IBR) and bovine viral diarrhea (BVD), significantly impact estrous cyclicity and ovulation [107]. IBR can cause oophoritis and granulosa cell necrosis, disrupting preovulatory follicle development [108], whereas BVD causes immunosuppression and decreases ovarian sensitivity to FSH and LH [109]. Acute BVD infection also reduces estradiol levels and impairs the positive feedback necessary to trigger the LH surge [110]. Effective herd vaccination programs mitigate these effects by reducing viral circulation, systemic inflammation, and the likelihood of ovulatory disruption [111].

Systemic inflammation from mastitis, clinical metritis, pneumonia, or metabolic stress also contributes to delayed ovulation [112, 113]. Elevated cortisol suppresses GnRH secretion, decreases LH pulse amplitude, and impairs ovarian steroidogenic enzyme activity [114]. Inflammatory cytokines can induce granulosa cell apoptosis, inhibit estradiol synthesis, and disrupt oocyte–granulosa communication, impairing oocyte maturation [115]. Timely antimicrobial or anti-inflammatory interventions, particularly during the early postpartum period, are critical for limiting uterine and systemic inflammation, preserving LH surge dynamics, and preventing delayed ovulation [2].

Preventive and herd level control strategies include maintaining strict vaccination protocols, monitoring for subclinical uterine infections, timely postpartum interventions, and management practices that minimize stress and inflammation. These measures reduce systemic and local inflammatory challenges, thereby supporting normal HPO axis function and timely ovulation [112].

Figure 3 summarizes the major interacting risk factors associated with delayed ovulation in cattle.