Subacute ruminal acidosis (SARA) is likely to arise when an easily palatable, high-energy diet meets a ruminal environment not adapted to this type of substrate. Increase of short-chained fatty acids (SCFA) will occur. Eventually, this may result in a transient nadir of ruminal pH below 5.5. Two situations are likely to represent the risk of SARA. First, fresh lactating cows are confronted with a diet considerably differing from that in the dry-period. A diet change carried out too rapidly or without proper transition management will put the animals at risk. Secondly, further in lactation, inaccurate calculation of dry-matter-intake (DMI) leading to wrong roughage/concentrate ratio, an inadequate content of structure within the diet or mistakes in preparing of total mixed rations may produce SARA. The consequences of SARA are diverse and complex. Laminitis is regularly connected to SARA and the negative impact of organic acids on the ruminal wall may lead to parakeratosis enabling translocation of pathogens into the bloodstream provoking inflammation and abscessation throughout the ruminant body. Moreover, milk-fat depression (MFD) can be related to SARA. In order to achieve a proper diagnosis, SARA has to be understood as a herd-management problem. A screening of the herd for SARA by means of a rumenocentesis, performed on a sample-group, preferably 12 individuals, may reveal the presence of SARA. The herd screening should include the risk group suspected, preferably. The prevention of SARA applies to the principles of ruminant feeding. Careful transition management from the dry to the lactation period and control of fibre-content and ration quality should be more yielding than the use of buffers or antibiotic drugs.U.S.

-This review addresses the suggestion that the decline in dairy reproductive performance, as increasingly observed these days, may be due to a hampered process of metabolic adaptation in early lactating cows. In our opinion, adaptation to the negative energy balance is a gradual process. Because almost all cows do adapt in the long run, it is not possible to classify animals as adapted or non-adapted. The use of risk factors is more appropriate in this case and is discussed in this review. Among them are the body condition score and its derivatives, feed intake, the calculated negative energy balance, and metabolic parameters like the plasma concentration of insulin or the triacylglycerol content in the liver. Moreover, factors that play a role in the link between declined reproductive performance and the metabolic situation of the cow during the early lactating period are discussed. Among these are insulin, insulin-like growth factors, leptin, neuropeptide Y, nonesterified fatty acids, thyroïd hormones, urea, and ammonia. fertility / dairy / periparturient metabolic adaptation / physiopathology / periparturition

A total of 4368 first lactation records for Holstein cows from 30 herds was used to estimate genetic parameters for yield, conformation traits, and the binary coded disease traits of udder edema, milk fever, retained placenta, metritis, displaced abomasum, ketosis, cystic ovary, mastitis, and lameness. Data on health, parentage, and yield came from an on-farm program for record keeping and management. Test day production data were obtained from British Columbia DHI. Type classification data were received from the Holstein Association of Canada. Heritabilities of disease traits were low ranging from 0 to 0.05. Exceptions were lameness (0.16) and ketosis (0.39). Correlations of disease traits with 305-d milk yield and of selected type traits with retained placenta, displaced abomasum, mastitis, and lameness were estimated. Phenotypic correlations did not substantially differ from 0 except for the correlation between lameness and rear leg set (0.37). Genetic correlations between disease traits and milk yield were mostly positive (0.02 to 0.44). Only retained placenta had a negative genetic correlation with milk yield (-0.28). Genetic correlations ranged from 0 to 0.37 between udder conformation traits and mastitis, from -0.38 to 0.09 between leg conformation traits and lameness, and from -0.11 to 0.38 between rump conformation and retained placenta. The results suggest that selection based solely on yield may increase the incidence of disease. Selection on conformation traits can help reduce the incidence of disease, although genetic correlations are low.

A longitudinal study in 15 herds, with a total of 2157 cows, was conducted to examine the relationship between teat-end callosity (TEC) and the incidence of clinical mastitis. During the 1.5-yr study period, clinical mastitis was diagnosed by the farmers based on clinical signs. Teat-end callosity was scored every month according to a teat-end callosity classification system, which discriminates between teat-end callosity thickness (TECT) and roughness (TECR). Differences in TECT between healthy and clinical mastitis quarters within infected cows were small but significant 3 mo before (0.13 higher), in the month during which the clinical mastitis occurred (0.08 higher), and in the following 2 mo (0.06 and 0.05 higher). To compare TECT and TECR between cows with and without clinical mastitis, 199 cows with clinical mastitis were paired with control cows based on herd, days in milk, and parity. Clinical mastitis cows had more TEC than their healthy herd mates, particularly when clinical mastitis occurred between the second and fifth months of lactation. Clinical Escherichia coli mastitis in the second or third month of lactation occurred in cows with less TEC than in cows with clinical mastitis caused by other pathogens. Clinical culture-negative, yeast, Klebsiella pneumoniae, and Enterobacter aerogenes mastitis cows had more TECT and TECR than other cows with clinical mastitis in the same month of lactation. Pointed teat ends had higher TECT and TECR than flat or inverted teat ends. Teat-end callosity thickness increased with a higher milk yield at peak production.

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