Our objective was to determine the effects of mastitis during early lactation on the reproductive performance of Jersey cows. From 1986 to 1997, quarter foremilk samples were collected every 4 to 8 wk during lactation, at drying off, near calving, and when clinical mastitis was diagnosed and were evaluated microbiologically to identify causative bacteria. Services per conception, days open, and days to first service were obtained from DHIA records on 752 cows. Cows were separated by mastitis type (clinical, n = 186; subclinical, n = 240; control, uninfected or infected after confirmed pregnancy, n = 326). Cows were reclassified based on the time of clinical or subclinical mastitis as follows: period 1, before first service (n = 374); period 2, between first service and pregnancy (n = 52); and period 3, after confirmed pregnancy or uninfected (control; n = 326). Milk production did not differ for any group separations. Reproductive performance did not differ between gram-negative or gram-positive mastitis pathogens. Cows with clinical or subclinical mastitis before first service had increased days to first service (77.3+/-2.7 and 74.8+/-2.7 d), days open (110.0+/-6.9 and 107.7+/-6.9 d), and services per conception (2.1+/-0.2 and 2.1+/-0.2) compared with controls (67.8+/-2.2 d, 85.4+/-5.8 d, 1.6+/-0.2; P < 0.05). Days to first service were not increased in cows with clinical or subclinical mastitis during period 2 (70.6+/-3.3 and 61.2+/-7.8 d). However, days open (143.6+/-8.5 d) and services per conception (3.0+/-0.2) were increased (P < 0.05) in cows with clinical mastitis during period 2, but not in cows with subclinical mastitis (90.9+/-20.2 d and 2.1+/-0.5). Cows initially diagnosed subclinical that became clinical during period 2 exhibited increased days to first service (93.9+/-10.1 d), days open (196.0+/-26.2 d), and services per conception (4.3+/-0.7) compared with control animals (P < 0.05). In conclusion, subclinical mastitis reduced reproductive performance of lactating cows similar to clinical mastitis. Subclinical mastitis followed by clinical mastitis resulted in the most severe loss in reproductive performance.

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The objective of the study was to determine if experimentally induced clinical mastitis before ovulation resulted in alterations of endocrine function, follicular growth, or ovulation. On d 8 (estrus = d 0), cows were challenged (TRT; n = 19) with Streptococcus uberis or were not challenged (control; n = 14). Forty-eight hours after induction of luteal regression on d 12, blood samples were collected to determine estradiol-17beta, LH pulse frequency, and occurrence of the LH surge. Ovaries were scanned to monitor follicular growth and ovulation. Cows with clinical mastitis (n = 12) had elevated rectal temperatures, somatic cell counts, and mammary scores. Estrus and ovulation occurred in 4 of 12 clinically infected cows and in all control cows. Cows that were challenged but did not develop clinical mastitis (n = 5) displayed estrus and ovulated. Due to differences in expression of estrus, cows were further subdivided for analyses into 4 groups: control, TRT-EST (infected cows that displayed estrus; n = 4), TRT-NOEST (infected cows that did not display estrus; n = 8), and NOMAS (cows that were inoculated but did not develop mastitis; n = 4). Ovulation rate was 100% for CON, NOMAS, and TRT-EST compared with 0% for TRT-NOEST cows. Size of the ovulatory follicle ("presumed" ovulatory follicle in TRT-NOEST cows) was similar for all groups. Frequency of LH pulses was decreased in TRT-NOEST compared with CON, TRT-EST, and NO-MAS. Estradiol-17beta increased over time in CON, NO-MAS, and TRT-EST cows, but did not increase in TRT-NOEST cows. Cows with clinical mastitis may exhibit estrus and ovulate normally or have disruptions in normal physiology including decreased LH pulsatility, absence of an LH surge and estrous behavior, suppressed estradiol-17beta, and failure to ovulate.

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