Birth weight threshold for identifying piglets at risk for preweaning mortality.

Several studies have suggested there is a critical relationship between piglet birth weight and preweaning mortality. Thus, the objective of the current work was to identify a birth weight threshold value for preweaning mortality. Birth weight and survival data from two studies involving a combined total of 4,068 piglets from 394 litters on four commercial farms (three European, one U.S.) were compiled for a pooled, multistudy analysis. Overall preweaning mortality across the two studies was 12.2%. Key variables used in the analysis were piglet birth weight (measured within 24 h of birth) and corresponding survival outcome (dead or live) by weaning at 3-4 wk of age. A mixed effects logistic regression model was fit to estimate the relationship between preweaning mortality and birth weight. A random effect of study was included to account for overall differences in mortality between the two studies. A piecewise linear predictor was selected to best represent the drastic decrease in preweaning mortality found as birth weight increased in the range of 0.5-1.0 kg and the less extreme change in weight above 1.0 kg. The change point of the birth weight and preweaning mortality model was determined by comparing model fit based on maximizing the likelihood over the interval ranging from 0.5 to 2.3 kg birth weight. Results from the analysis showed a curvilinear relationship between birth weight and preweaning mortality where the birth weight change point value or threshold value was 1.11 kg. In the combined data set, 15.2% of pigs had birth weights ≤1.11 kg. This subpopulation of pigs had a 34.4% preweaning mortality rate and represented 43% of total preweaning mortalities. These findings imply interventions targeted at reducing the incidence of piglets with birth weights ≤1.11 kg have potential to improve piglet survivability. Additional research is needed to validate 1.11 kg as the birth weight threshold for increased risk of preweaning mortality.

Inflammatory biomarkers are associated with ketosis in periparturient Holstein cows.

Ketosis is a prevalent periparturient metabolic disorder and we hypothesize that lipopolysaccharide (LPS) infiltration may play a key role in its etiology. Study objectives were to characterize biomarkers of inflammation during the transition period in healthy and clinically diagnosed ketotic cows. Cows were retrospectively categorized into one of two groups: healthy and clinically diagnosed ketotic. Two data sets were utilized; the first dataset (Study A) was obtained as a subset of cows (n=16) enrolled in a larger experiment conducted at the Iowa State University Dairy utilizing Holstein cows (8 healthy; 8 ketotic), and the second dataset (Study B; 22 healthy; 22 ketotic) was obtained from a commercial farm. For both experiments, blood samples were collected prior to and following calving. Ketotic cows in both studies had reduced milk production compared to healthy cows (P<0.01). Post-calving, ketotic cows had increased serum amyloid A (4.2 and 1.8 fold in studies A and B, respectively; P=0.03 and P=0.04), haptoglobin (>6 fold and ~4 fold; P=0.04 and P=0.03), and lipopolysaccharide binding protein (66 and 45%; P<0.01 and P=0.02) compared with their healthy counterparts. Antepartum circulating LPS in ketotic cows was increased (2.3 fold; P=0.01) compared to healthy cows in Study B. In summary, increased biomarkers of inflammation appear to be closely associated with ketosis in transition dairy cows.

Effects of Zeranol upon luteal maintenance and fetal development in peripubertal gilts.

Eighty gilts were utilized to determine whether zeranol implants could maintain hCG-induced corpora lutea (CL) in peripubertal gilts and to examine the effects of a Zeranol implant on fetal development. Crossbred gilts (171+/-0.3 days of age, 109.1+1.4 kg) were blocked by weight and ancestry to control (n=40) or treatment (n=40) groups. To induce ovulation and CL maintenance, treated gilts received 500 IU of hCG i.m. and a Zeranol ear implant (Ralgro, 36 mg; day 0). All gilts were checked once daily for estrus with a mature boar from days 3-58 of the experiment. On day 42, treated gilts received two 10 mg injections of Lutalyse (PGF(2)alpha) spaced 6 h apart. Treated gilts not displaying estrus within 7 days of PGF(2)alpha received two additional 10 mg of PGF(2)alpha spaced 6 h apart on day 49. On days 44-58, gilts detected in estrus were inseminated twice, 24 h apart with pooled semen via AI. Blood samples were obtained on days 0, 7, 18 and 42 and analyzed for serum progesterone (P(4)). Bred gilts were slaughtered on days 58-62 of gestation. Ovulation, as determined by serum concentrations of P(4) on day 7 of the experiment, was induced by hCG in 79.5% of treated gilts. Zeranol implants, however, failed to increase (P>0.05) the proportion of gilts available for breeding (treated, 21/39; control, 18/40). Of gilts inseminated on days 44-58, 16/21 treated gilts and 16/18 control gilts were pregnant at slaughter on days 58-62 of gestation. Number of fetuses (7.5 versus 12), fetal weight (83 versus 121 g), fetal length (117 versus 132 mm) and fetal survival (45% versus 78%) were reduced (P<0.001) by Zeranol implants. These data indicate that treatment of peripubertal gilts with a 36 mg Zeranol implant did not increase the proportion of gilts available for breeding while causing deleterious effects upon the fetuses.