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Copyright of Equine Veterinary Journal is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

It is well established that the plasma metabolite profile changes during metabolic dysfunction, such as elevated non-esterified fatty acid (NEFA) release when body reserve mobilization is excessive in early lactation cows. Relationships between changes in plasma concentrations of metabolites caused by a metabolic impairment and the status of vitamins, such as folates and vitamin B12, have barely been studied in cattle. This study was undertaken to assess relationships between peripartum plasma concentrations of folates, vitamin B12, NEFA, and beta-hydroxybutyrate (BHB). Longitudinal data of 48 multiparous Holstein cows from 5 studies were taken from days −14 to 21 relative to calving. Blood samples were taken weekly before calving and either twice or thrice per week postpartum, and plasma was analyzed for folate, vitamin B12, NEFA, and BHB concentrations. Postpartum plasma NEFA and BHB concentrations were negatively related to plasma folate concentration at days −14 and −7 relative to parturition, whereas the opposite relationship was noted for the plasma vitamin B12:folate ratio. The plasma folate and NEFA areas under the curve from the whole studied period were negatively associated, and the opposite was observed with the association between the plasma vitamin B12:folate ratio and NEFA as well as the BHB areas under the curve. The results suggest that there is an increased use of folate for metabolic functions during elevated concentrations of plasma NEFA and BHB. Future research should focus on finding an optimal plasma vitamin B12:folate ratio to favor cow health during the challenging period of parturition. [ABSTRACT FROM AUTHOR]

Summary: Background: There is a knowledge gap about how equine MFC subchondral radiolucencies (SR) arise and evolve. Osteoclasts are believed to have a role but have not been studied in situ. Objectives: To measure and compare osteoclast density and the percentage of chondroclasts in healthy and MFC SR specimens from juvenile Thoroughbreds. Study design: Cadaveric study. Methods: Medial femoral condyles (MFC) from a tissue bank of equine stifles were studied. Inclusion criteria were MFCs (≤8 months old) with a computed tomography SR lesion and histological focal failure of endochondral ossification (L group). Contralateral, lesion‐free, MFCs were a control group (CC). Osteochondral slabs were cut through the lesion (L), a healthy site immediately caudal to the lesion, (internal control; IC) and the contralateral, site‐matched controls (CC). Histological sections were immunostained with Cathepsin K for osteoclast counting. Osteoclasts in contact with the growth cartilage (chondroclasts) were also counted. The sections were segmented into regions of interest (ROI) at different depths in the subchondral bone: ROI1 (0‐1 mm), ROI2 (1‐3 mm) and ROI3 (3‐6 mm). Osteoclasts were counted and the bone area was measured in each ROI to calculate their density. Chondroclasts were counted in ROI1. Results: Sections were studied from L and IC (n = 6) and CC sites (n = 5). Osteoclast density was significantly higher in ROI1 when compared with ROI3 in all groups. Although higher osteoclast density was measured in ROI1 in the L group, no significant differences were detected when compared with control ROIs. The proportion of chondroclasts in ROI1 was lower in the L sections when compared with controls but no significant differences were detected. Main limitations: Limited sample size. Conclusions: Osteoclasts are important actors in MFC subchondral bone development, digesting both growth cartilage (chondroclasts) and bone, but the pathophysiology of early MFC SRs cannot be explained solely by an increased osteoclast presence in the subchondral bone. [ABSTRACT FROM AUTHOR]

Copyright of Canadian Journal of Animal Science is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: The aetiology of equine medial femoral condyle (MFC) subchondral bone radiolucencies (SR) is unknown. Objectives: Characterise the microstructural structural features of MFC SR in juvenile Thoroughbreds with microcomputed tomography (μCT) and histology. Study design: Cross‐sectional post‐mortem study. Methods: Distal femurs were collected at post‐mortem. Conventional tomodensitometry was employed to scout for MFCs with and without SR lesions (SR+ and SR−, respectively). Group 1 were CT MFC SR+ and Group 2 age‐matched SR− controls. Both underwent μCT and histological analysis. Group 3 CT MFC SR− foals, <6 months, were selected to search for chondronecrosis. Histological sections, processed from the lesion (Group 1) and a corresponding site in Groups 2 and 3, were assessed for chondronecrosis, fibrin, fibroplasia and osteochondral separation. Group 3 sections were surveyed for chondronecrosis alone. Results: A total of 178 femurs from 89 Thoroughbreds were harvested. Of these horses 19.1% (95% CI: 10.9%‐27.3%) were CT MFC SR+ (17/23; 7.46 ± 4.36 months) and met the inclusion criteria for Group 1. Group 2 included 30 CT MFC SR− specimens (5.00 ± 2.73 months) and Group 3 had 44 CT MFC SR− s (2.68 ± 1.74 months). SR were located axially in foals <7 months of age, and centrally thereafter. All SRs had areas of thickened cartilage on histology and separation at the osteochondral junction containing fibrin (acute event) and fibroplasia (chronicity) in 73.9% (17/23; 95% CI: 56%‐91.9%). In Group 1 specimens, chondronecrosis was present in 82.6% (19/23; 95% CI: 67.1%‐98.1%) but four MFC SR+ had no evidence of chondronecrosis. Chondronecrosis was not detected in the Group 3 foal MFCs. Main limitations: No longitudinal follow‐up. Conclusions: The absence of chondronecrosis, pathognomic of osteochondrosis, in four MFC SR+s and in all of the CT MFC SR− foals suggests that osteochondrosis is not the cause, or the only cause, of these lesions and favours trauma as an alternate aetiological hypothesis. [ABSTRACT FROM AUTHOR]

Abstract Background Actinobacillus pleuropneumoniae is the etiological agent of porcine pleuropneumonia, a respiratory disease which causes great economic losses worldwide. Many virulence factors are involved in the pathogenesis, namely capsular polysaccharides, RTX toxins, LPS and many iron acquisition systems. In order to identify genes that are expressed in vivo during a natural infection, we undertook transcript profiling experiments with an A. pleuropneumoniae DNA microarray, after recovery of bacterial mRNAs from serotype 5b-infected porcine lungs. AppChip2 contains 2033 PCR amplicons based on the genomic sequence of App serotype 5b strain L20, representing more than 95% of ORFs greater than 160 bp in length. Results Transcriptional profiling of A. pleuropneumoniae recovered from the lung of a pig suffering from a natural infection or following growth of the bacterial isolate in BHI medium was performed. An RNA extraction protocol combining beadbeating and hot-acid-phenol was developed in order to maximize bacterial mRNA yields and quality following total RNA extraction from lung lesions. Nearly all A. pleuropneumoniae transcripts could be detected on our microarrays, and 150 genes were deemed differentially expressed in vivo during the acute phase of the infection. Our results indicate that, for example, gene apxIVA from an operon coding for RTX toxin ApxIV is highly up-regulated in vivo, and that two genes from the operon coding for type IV fimbriae (APL_0878 and APL_0879) were also up-regulated. These transcriptional profiling data, combined with previous comparative genomic hybridizations performed by our group, revealed that 66 out of the 72 up-regulated genes are conserved amongst all serotypes and that 3 of them code for products that are predicted outer membrane proteins (genes irp and APL_0959, predicted to code for a TonB-dependent receptor and a filamentous hemagglutinin/adhesin respectively) or lipoproteins (gene APL_0920). Only 4 of 72 up-regulated genes had previously been identified in controled experimental infections. Conclusions These genes that we have identified as up-regulated in vivo, conserved across serotypes and coding for potential outer membrane proteins represent potential candidates for the development of a cross-protective vaccine against porcine pleuropneumonia.

Objective: To measure the nerve fiber density in synovial membranes from healthy and OA equine joints and to investigate the relationship between synovial innervation and OA severity, synovial vascularity and synovitis.Design: Twenty-five equine metacarpophalangeal joints were collected post-mortem. The joints were dissected and the macroscopic lesions of the articular cartilage were scored. Synovial membrane specimens (n = 50) were harvested, fixed, sectioned and scored histologically. Immunohistochemical staining and immunofluorescence with S-100 protein, that identifies nerve fibers, and ⍺-actin, that stains vascular smooth muscle, were also performed on site-matched specimens and the relationships between these tissues was interrogated.Results: The nerve fiber density was higher in the superficial layer (≤200 μm) of the synovium when compared to the deeper layer in control equine joints (mean difference (95% C.I.): 0.054% (0.018%, 0.11%)). In osteoarthritic joints, synovial innervation decreased in the superficial layer with increasing macroscopic OA score (β (SEM), 95% C.I.: -0.0061 (0.00021), -0.0011, -0.00017). The blood vessel density was also higher in the superficial layer of the synovium compared to the deep layer in the control (mean difference (95% C.I.): 1.1% (0.36%, 2.3%)) and OA (mean difference (95% C.I.): 0.60% (0.22%, 1.2%)) equine joints. Moreover, considering all synovial specimens, higher nerve fiber density in the deep layer positively correlated with blood vessel density (β (SEM), 95% C.I.: 0.11 (0.036), 0.035, 0.18).Conclusion: The reduction in nerve fiber density with advanced cartilage degeneration suggests that peripheral neuropathy is associated with equine OA. Whether this link is associated with neuropathic pain, requires further investigation. [ABSTRACT FROM AUTHOR]