Abstract

Summary. Mastitis has a deleterious effect on reproductive responses and fertility of dairy cows, which depends on whether it occurs before or after artificial insemination (AI). Subclinical intramammary infection (IMI) before AI reduced steroid concentrations in the preovulatory follicle of approximately one third of lactating cows, and was associated with low expression of major steroidogenic genes. Consequently, IMI induced an attenuated LH surge and delayed ovulation in 30% of cows with subclinical IMI; the remaining 70% exhibited normal responses. The reason for the diversity in reproductive responses of individual cows to subclinical IMI is unclear. Mastitis induced by Gram-negative or Gram-positive bacteria disrupted the developmental competence of the pool of oocytes at the germinal vesicle stage, resulting in low blastocyst rates. The specific immune/inflammatory molecules involved in impairment of reproductive responses in subclinical mastitic cows are poorly documented. Exposure of small antral follicles to subclinical mastitis induced by Gram-positive bacterial toxins had a long-term effect by reducing estradiol concentrations of preovulatory follicles. Unlike chronic subclinical mastitis, the disruptive effect of short-term clinical IMI before AI is time-dependent and involves lowered conception when IMI occurs close to the time of insemination. The effect of clinical intramammary infection on corpus luteum function is equivocal. In a recent study, inter-estrus interval and progesterone concentration were unaltered in most (95%) E. coli-mastitic cows treated with anti-inflammatory drugs. Fertility studies showed that fertility of subclinical mastitic cows is improved by the Ovsynch program, probably because of synchronized timing of ovulation relative to AI in cows that could otherwise exhibit delayed ovulation.

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