Reduced reproductive performance of lactating cows is strongly associated with environmental and pathogenic stressors. This review summarizes the most recent knowledge on the effects of acute or chronic heat stress (HS) and acute or chronic intramammary infection (IMI) on ovarian function. It also offers various approaches for improving the fertility of cows under chronic HS or IMI. Comparing the 2 stressors reveals a few similarities in the mode of alteration in the hypothalamus–pituitary–ovarian axis, in particular, in the follicle and its enclosed oocyte. Both HS and IMI cause a reduction in the preovulatory LH surge, with a pronounced effect in cows with IMI, and consequently, ovulation is being delayed or inhibited. Both stresses induce changes in follicular growth dynamics, reduce follicular steroidogenesis, and disrupt follicular dominance. Unlike their effects on follicular function, the effects of mastitis and HS on corpus luteum (CL) function are debatable. Under chronic summer thermal stress, several, but not all, studies show reduced progesterone secretion by the CL. Subclinical mastitis does not affect CL function, whereas the effect of clinical mastitis is controversial; some show a reduction in progesterone, whereas others do not. Both stresses have been found to impair cytoplasmic and nuclear maturation of oocytes, associated with reduced embryonic development. These findings have provided insights into the mechanism by which HS and IMI compromise fertility, which enable developing new strategies to mitigate these effects. For instance, treatment with GnRH and PGF2α to induce follicular turnover successfully improved conception rate in subpopulations of HS cows during the summer, in particular, primiparous cows and cows with high BCS. The “Ovsynch” program, also based on the use of GnRH and PGF2α, has been shown to improve conception rate of subclinical mastitic cows, most likely due to better synchronization of timing of ovulation with that of AI. Supplementing progesterone after AI improves conception rate of HS cows, particularly those with postpartum uterine disease and low BCS. It should be noted that similarities between the 2 stressors do not necessarily suggest a shared mechanism. Although not clear enough, an additive deleterious effects of HS and IMI on reproduction is suggested.