Reproductive tract infections are common and impede reproduction by reducing per cycle fertilization, increasing pregnancy loss, and impairing neonatal survival. They therefore increase risk of culling and are expensive. Infection may interfere with reproduction by directly causing anatomical damage that prevents normal reproduction. Most effects are mediated by components or products of infectious organisms (such as lipopolysaccharide - LPS, endotoxin), or indirectly by inflammatory mediators, such as cytokines, eicosanoids, nitric oxide and oxidative stress affecting gamete production and function, follicular function, ovulation, fertilization, embryonic development, implantation, or survival of the conceptus. For example, bacteria and leukocytes in semen damage sperm cell membranes, mitochondrial function, sperm motility and even DNA integrity. Bacterial infection impairs ovarian follicular function, both directly and by effects on the hypothalamo-pituitary-gonadal axis, prolonging anovulation and leading to decreased concentrations of steroid hormones. Inflammation affects microtubule assembly and chromosomal structure in oocytes, preventing fertilization. Zygotes resulting from fertilization of oocytes with sperm subjected to oxidative stress are less likely to develop to the blastocyst stage. Inflammation affects endometrial adhesion molecule expression, resulting in implantation failure and inflammation may result in pregnancy failure. Extragenital inflammation (e.g., mastitis) may also impair reproductive functions and outcomes. These observations make it clear that direct and indirect effects of infection and inflammation, even in locations remote from the reproductive tract, can interrupt successful reproduction at several crucial stages.