Claw horn lesions in mid-lactation primiparous dairy cows under pasture-based systems: Association with behavioral and metabolic changes around calving.

The objectives of this study were to describe the lying behavior of primiparous dairy cows under pasture-based systems during the pre- and postcalving period and characterize the association of lying behavior and analytes related to energy metabolism during this period with claw horn disruption lesion development later in lactation. Our convenience sample included 39 primiparous Holstein cows from 3 commercial farms that were assessed for body condition score (BCS; 5-point scale, 0.25-point increments) and had blood collected at wk -3, -2, -1, 1, 2, and 3 relative to calving date. Blood samples were assayed for nonesterified fatty acids, ß-hydroxybutyrate (BHB), and cholesterol concentrations. Electronic data loggers (HOBO Pendant G Acceleration, Onset Computer Corporation, Bourne, MA) recorded lying behavior at 1-min intervals from 3 wk before calving to 3 wk after calving. Starting at 4 wk after calving and until 16 wk after calving, cows were examined for claw lesions at approximately 4-wk intervals. Sole lesions and white line lesions were scored on a 0 to 10 scale. Of the 39 primiparous cows, 19 cows scored 0 at all exams during the entire study period and 20 cows had at least 1 severe lesion (score ≥4) between 8 and 16 wk after calving. Time spent lying before calving averaged 10.3 ± 0.3 h/d, but declined to 7.3 ± 0.3 h/d after calving (least squares means ± standard error). At calving, we noted an increase in the number of lying bouts (12.9 ± 0.45 bouts/d) compared with the pre- and postcalving averages of 11.6 (±0.53) and 9.1 (±0.47) bouts, respectively. Cows that developed claw lesions later in mid lactation spent less time lying down than cows without lesions during wk 3 after calving compared with healthy cows (7.29 ± 0.22 vs. 8.51 ± 0.16 h/d). Lesion cows had fewer lying bouts per day, and these bouts were of longer duration than no-lesion cows after calving. Increased odds of lesion were found to be associated with shorter lying times and fewer number of lying bouts during wk 3 (odds ratio = 1.23). Nonesterified fatty acids (747 ± 58 vs. 990 ± 86.85 µmol/L) and BHB (0.77 ± 0.06 vs. 0.60 ± 0.04 mmol/L) concentrations during wk 1 were greater in cows that developed claw lesions relative to cows that did not develop lesions. The BHB concentrations also remained higher in wk 2 for cows that developed claw lesions (0.63 ± 0.04 vs. 0.46 ± 0.03 mmol/L) compared with cows that did not develop any lesions. Cows that developed lesions experienced greater losses in BCS from wk -3 to 3 than cows without lesions (0.74 ± 0.01 and 0.61 ± 0.01 BCS change, respectively). In summary, changes in lying behavior and energy metabolic status after calving were associated with claw horn disruption lesions in mid-lactation primiparous cows under pasture-based systems.

Nociceptive threshold, blood constituents and physiological values in 213 cows with locomotion scores ranging from normal to severely lame.

The aim of this study was to investigate associations between mechanical nociceptive threshold, blood constituents, physiological measurements and locomotion score (LS) in dairy cattle with a range of LS from 1 (normal) to 5 (severely lame). The study used 213 Friesian/Friesian cross dairy cows from 12 farms. There were 40-50 cows each with LS 1-4 and 22 cows with LS 5. Each cow was restrained and her temperature and respiratory and cardiac rates were measured. Nociceptive threshold, plasma concentrations of haptoglobin, ß-hydroxybutyrate (ß-HB), cortisol, glucose, lactate, creatinine kinase activity, packed cell volume and white blood cell counts were determined. Mixed effect models were used to investigate associations between the variables measured and LS. Parity and stage of lactation were forced into all analyses and the model fit was checked by investigation of residuals. After accounting for parity and stage of lactation, nociceptive threshold was significantly lower in cattle with LS 3-5 compared with LS 1 in a dose response manner, indicating increasing hyperalgesia with increasing LS. Haptoglobin concentration was raised in all cattle with LS>1, demonstrating an inflammatory response with all levels of lameness. Cortisol and glucose concentrations were lower and ß-HB concentrations higher in cows with LS 2 compared with cows with other scores, possibly signifying metabolic challenge. Heart and respiratory rate and rectal temperature were significantly higher only in cows with LS 5, suggesting that these measurements were insensitive measures of pain or stress. It was concluded that hyperalgesia increases with increasing severity of lameness and that nociceptive pressure and haptoglobin were sensitive measures of pain from lameness.

D-lactic acid interferes with the effects of platelet activating factor on bovine neutrophils.

D-lactic acidosis occurs in ruminants, such as cattle, with acute ruminal acidosis caused by ingestion of excessive amounts of highly fermentable carbohydrates. Affected animals show clinical signs similar to those of septic shock, as well as acute laminitis and liver abscesses. It has been proposed that the inflammatory response and susceptibility to infection could both be caused by the inhibition of phagocytic mechanisms. To determine the effects of d-lactic acid on bovine neutrophil functions, we pretreated cells with different concentrations of D-lactic acid and measured intracellular pH using 2',7'-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein acetoxymethyl ester (BCECF-AM) and calcium flux using FLUO-3 AM-loaded neutrophils. Reactive oxygen species (ROS) production was measured using a luminol chemiluminescence assay, and MMP-9/gelatinase-B granule release was measured by zymography. CD11b and CD62L/l-selectin expression, changes in cell shape, superoxide anion production, phagocytosis of Escherichia coli-Texas red bioparticles, and apoptosis were all measured using flow cytometry. Our results demonstrated that D-lactic acid reduced ROS production, CD11b upregulation and MMP-9 release in bovine neutrophils treated with 100 nM platelet-activating factor (PAF). D-lactic acid induced MMP-9 release and, at higher concentrations, upregulated CD11b expression, decrease L-selectin expression, and induces late apoptosis. We concluded that D-lactic acid can interfere with neutrophil functions induced by PAF, leading to reduced innate immune responses during bacterial infections. Moreover, the increase of MMP-9 release and CD11b expression induced by 10mM D-lactic acid could promote an nonspecific neutrophil-dependent inflammatory reaction in cattle with acute ruminal acidosis.

Risk factors for bulk milk somatic cell counts and total bacterial counts in smallholder dairy farms in the 10th region of Chile.

We investigated the principal management factors that influenced bulk milk somatic cell count (BMSCC) and total bacterial count (TBC) of smallholder dairy farms in the 10th region of Chile. One hundred and fifty smallholder milk producers were selected randomly from 42 milk collection centres (MCCs). In April and May of 2002, all farms were visited and a detailed interview questionnaire on dairy-cow management related to milk quality was conducted. In addition, the BMSCC and TBC results from the previous 2 months' fortnightly tests were obtained from the MCCs. The mean BMSCC and TBC were used as the dependent variables in the analyses and were normalised by a natural-logarithm transformation (LN). All independent management variables were categorised into binary outcomes and present (=1) was compared with absent (=0). Biserial correlations were calculated between the LNBMSCC or LNTBC and the management factors of the smallholder farms. Management factors with correlations with P0.05) factors. A random MCC effect was included in the models to investigate the importance of clustering of herds within MCC. In the null model for mean LNTBC, the random effect of MCCs was highly significant. It was explained by: milk collected once a day or less compared with collection twice a day, not cleaning the bucket after milking mastitic cows versus cleaning the bucket and cooling milk in a vat of water versus not cooling milk or using ice or a bulk tank to cool milk. Other factors that increased the LNTBC were a waiting yard with a soil or gravel floor versus concrete, use of plastic buckets for milking instead of metal, not feeding California mastitis test (CMT)-positive milk to calves and cows of dual-purpose breed. The final model explained 35% of the variance. The model predicted that a herd that complied with all the management practices had a mean predicted TBC of 105 colony forming units (cfu)/ml, whereas a herd that did not comply with any of these management factors had a predicted TBC of 59 x 10(9)cfu/ml. The model of mean LNBMSCC explained 18% of the variance; the random effect of MCC was not significant. Management factors that decreased the mean LNBMSCC were: using the CMT for 1 year versus using the test for more than 1 year or not at all, absence of a concrete waiting yard, not filtering the milk or using filters other than a plastic sieve to filter the milk, milking cows with mastitis last, and sometimes or always examining the udder before milking. A herd that complied with all of these management factors had a BMSCC of approximately 46,166 cells/ml, whereas a herd that did not comply with any of the management practices above had a mean BMSCC of 2 x 10(6)cells/ml.

Risk factors associated with BMSCC greater than 200 000 cells/ml in dairy herds in southern Chile.

A cross-sectional survey of 523 dairy farms in the south of Chile was carried out to quantify risk factors associated with bulk-milk somatic-cell count (BMSCC) >200 x 10(3)cells/ml. Questionnaires followed by one reminder were sent to 3710 dairy farms via the 11 milk-processing plants that they supplied in October 1998. The response proportion was 14.1%. The median BMSCC was 289 x 10(3) cells/ml (range: 74 x 10(3) to 1800 x 10(3)cells/ml). The median herd size was 70 cows (range: 7-616); herd size was not associated with BMSCC. The annual milk yield of 33.2% of the herds was <4000 l and 53.4% had an annual milk yield of 4 x 10(3) to 6 x 10(3) l. Clinical-mastitis records were kept by 55.3% of the farmers. Seventy-six percent of the farmers (377/499) reported <10 clinical cases of mastitis in the year prior to the questionnaire. Logistic multiple regression indicated that BMSCC >200 x 10(3)cells/ml was more likely when foremilking was practised, and when cows were collected in a yard before milking. BMSCC was less likely to be >200 x 10(3)cells/ml when teats were washed with water containing disinfectant compared with plain water; when the udder and teats were always checked before milking compared with, sometimes or never; when cows with mastitis were milked first compared with any other ordering, and when farmers recorded individual-cow somatic-cell count (ICSCC) compared with when ICSCC was not recorded.

A serological survey of leptospirosis in sheep in Chile.

In order to investigate exposure to Leptospira spp. in sheep in the Xth Region in the south of Chile, 629 ovine serum samples were collected from 11 convenience selected sheep farms, using within farm random sampling. The sera collected were examined for antibodies to the following serovars; icterohaemorrhagiae, autumnalis, hardjo, pomona, ballum, and canicola, using the Microscopic Agglutination Test. Ten out of eleven flocks had sheep which were seropositive for at least one Leptospira spp. Positive tests, the majority at low titres, were obtained from 36/629 (5.7%) of all the serum samples tested. The most frequently detected serovars were, in descending order: icterohaemorrhagiae, autumnalis and hardjo. The greatest proportion of positive samples came from sheep which were over 30 months old.

Case control study of risk factors for toxic mastitis in 26 dairy herds.

A retrospective case control study of farm level risk factors for toxic mastitis was carried out in November and December 1996. Twenty-six farms from mid-Somerset were visited: 13 case farms (had had a cow with toxic mastitis in the previous year) and 13 geographically matched controls (no case of toxic mastitis). The farmers were interviewed and the buildings were examined. Information was collected on the type and quality of housing, usual milking routines, milk quality and mastitis prevalence in the previous year. All the data were collected on to pretested recording sheets and loaded into a database. Simple and complex analysis was done. The following variable were significantly (P < 0.05) associated with an increased risk of toxic mastitis in the simple analysis: housing cows in October rather than November; a low number of calving boxes per cow; a high proportion of cows with intermediate body condition and low herd bulk milk somatic cell counts (HBMSCC). In the final model low HBMSCC and a high proportion of cows with intermediate body condition remained significant. The authors conclude that, despite the small size sample, the results of this study are consistent, plausible and support the information from previous experimental and observational studies about the role of somatic cell counts in toxic mastitis.