Search

Background: Malignant (intra-) nasal tumors (NTs) are the most common cause of chronic nasal discharge in dogs. Besides radiation therapy, palliative therapy is necessary in some dogs. Therefore, studies on receptor expression have supported the utility of tyrosine kinase inhibitors (TKI) in dogs with nasal carcinomas. However, studies on receptor expression in nasal sarcomas are lacking. Materials and methods: This study evaluated the expression of vascular endothelial growth factor receptor-2 (VEGFR-2), epidermal growth factor receptor (EGFR), cyclooxigenase-2 (COX-2), Ki-67, survivin and E-cadherin in nasal carcinomas and sarcomas and compared it with tumor (T) categories based on computed tomography (CT). Results: In 26 dogs with NTs, cross sectional imaging and upper airway endoscopy with guided biopsy collection were performed, followed by histopathological examination of NTs, revealing 19 epithelial and 7 mesenchymal tumors. While EGFR and E-cadherin were only expressed by carcinomas, the following markers were expressed by both carcinomas and sarcomas without significant differences between tumor types and T-categories: VEGFR-2 (carcinomas and sarcomas 100%), COX-2 (carcinomas 63%, sarcomas 57%), survivin (carcinomas 100%, sarcomas 86%) and Ki-67 (median expression of 28.5% in carcinomas and 17.3% in sarcomas). Conclusion: Based on similarities in marker expression between canine carcinomas and sarcomas, clinical studies should further elucidate the use of TKI or COX-2 inhibitors as additional therapy in dogs with nasal sarcomas. [ABSTRACT FROM AUTHOR]

Background: Ancillary diagnostic methods to enhance the accuracy of viability assessment have not been established for use in clinical practice. Objectives: To assess intestinal microperfusion measured by Laser Doppler Flowmetry and Spectrophotometry (LDFS) in naturally occurring small intestinal strangulations of different origins and to compare this between viable and non‐viable segments. Study design: Prospective clinical trial. Methods: Forty horses undergoing colic surgery for naturally occurring small intestinal strangulations were included. Tissue oxygen saturation (tSO2), haemoglobin (tHB) and blood flow (tBF) were determined by LDFS before and after release of the strangulation. Intestinal biopsies were taken in cases that underwent intestinal resection or intraoperative euthanasia and assessed using a semi‐quantitative mucosal injury score (MIS). The LDFS measurements were compared between the different categories of strangulation causes and histopathological injury using parametric and non‐parametric tests (p < 0.05). Results: Strangulations by pedunculated lipomas had lower tBF (13.9 ± 18 arbitrary units [AU]) than epiploic foramen entrapments (65.2 ± 61 AU; CI −1.697 to −0.2498; p = 0.005). Segments with MIS > 5 showed lower tBF during strangulation than segments with MIS < 4 (mean difference 61.1 AU; CI −1.119 to −0.07361; p = 0.03). This did not differ significantly following release of strangulation. Furthermore, there was a positive correlation between the inflammatory cell count and tBF during strangulation (r 0.34; CI 0.01 to 0.60; p = 0.04). The tSO2 and tHB did not differ between the different categories of lesions or injury. Main limitations: No biopsies could be taken from the intestinal segments that did not undergo resection. The duration of strangulation could not reliably be ascertained. Conclusions: Blood flow measurements in naturally occurring strangulating lesions show a varying degree of ischaemia in different causes of strangulation. Intestinal blood flow measurements prior to release of the strangulation could potentially contribute to the identification of mucosal injury, yet a high individual variability and other contributing factors need to be considered. [ABSTRACT FROM AUTHOR]

Influenza A virus (IAV) infections in swine are usually subclinical, but they can reach high morbidity rates. The mortality rate is normally low. In this study, six vaccinated, spontaneously deceased sows revealed IAV infection and enhanced neutrophilic bronchopneumonia with unexpectedly large numbers of infiltrating eosinophils. The purpose of this study was to characterize these lung lesions with special emphasis on the phenotypes of inflammatory cells, the presence of eosinophilic peroxidase (EPO), and neutrophil extracellular traps (NETs). The number of Sirius red-stained eosinophils was significantly higher in the lungs of IAV-infected sows compared to healthy pigs, indicating a migration of eosinophils from blood vessels into the lung tissue stimulated by IAV infection. The detection of intra- and extracellular EPO in the lungs suggests its contribution to pulmonary damage. The presence of CD3+ T lymphocytes, CD20+ B lymphocytes, and Iba-1+ macrophages indicates the involvement of cell-mediated immune responses in disease progression. Furthermore, high numbers of myeloperoxidase-positive cells were detected. However, DNA-histone-1 complexes were reduced in IAV-infected sows, leading to the hypothesis that NETs are not formed in the IAV-infected sows. In conclusion, our findings in the lungs of IAV-infected vaccinated sows suggest the presence of so far unreported field cases of vaccine-associated enhanced respiratory disease. [ABSTRACT FROM AUTHOR]

Mutations within the ectodysplasin A (EDA) gene have been associated with congenital hypotrichosis and anodontia (HAD/XHED) in humans, mice, dogs and cattle. We identified a three-generation family of Fleckvieh cattle with male calves exhibiting clinical and histopathological signs consistent with an X-linked recessive HAD (XHED). Whole genome and Sanger sequencing of cDNA showed a perfect association of the missense mutation g.85716041G>A (ss2019497443, rs1114816375) within the EDA gene with all three cases following an X-linked recessive inheritance, but normal EDAR and EDARADD. This mutation causes an exchange of glycine (G) with arginine (R) at amino acid position 227 (p.227G>R) in the second collagen triple helix repeat domain of EDA. The EDA variant was associated with a significant reduction and underdevelopment of hair follicles along with a reduced outgrowth of hairs, a complete loss of seromucous nasolabial and mucous tracheal and bronchial glands and a malformation of and reduction in number of teeth. Thermostability of EDA G227R was reduced, consistent with a relatively mild hair and tooth phenotype. However, incisors and canines were more severely affected in one of the calves, which correlated with the presence of a homozygous missense mutation of RNF111 (g.51306765T>G), a putative candidate gene possibly associated with tooth number in EDA-deficient Fleckvieh calves. [ABSTRACT FROM AUTHOR]

Mycobacterium avium subsp. hominissuis is an opportunistic pathogen with zoonotic potential (1,2) that is present in soil and dust. Animals are seen as a reservoir and potential threat for human [...]

Summary: Background: Ischaemic postconditioning (IPoC) has been shown to ameliorate ischaemia reperfusion injury in different species and tissues. Objectives: To assess the feasibility of IPoC in equine small intestinal ischaemia and to assess its effect on histomorphology, electrophysiology and paracellular permeability. Study design: Randomised in vivo experiment. Methods: Experimental jejunal ischaemia was induced for 90 min in horses under general anaesthesia. In the control group (C; n = 7), the jejunum was reperfused without further intervention. In the postconditioning group (IPoC; n = 7), reocclusion was implemented following release of ischaemia by clamping the mesenteric vessels in three cycles of 30 seconds. This was followed by 120 minutes of reperfusion in both groups. Intestinal microperfusion and oxygenation was measured during IPoC using spectrophotometry and Doppler flowmetry. Histomorphology and histomorphometry of the intestinal mucosa were assessed. Furthermore, electrophysiological variables and unidirectional flux rates of 3H‐mannitol were determined in Ussing chambers. Western blot analysis was performed to determine the tight junction protein levels of claudin‐1, claudin‐2 and occludin in the intestinal mucosa. Comparisons between the groups and time points were performed using a two‐way repeated measures analysis of variance (ANOVA) or non‐parametric statistical tests for the ordinal and not normally distributed data (significance P <.05). Results: IPoC significantly reduced intestinal microperfusion during all clamping cycles yet affected oxygen saturation only during the first cycle. After reperfusion, Group IPoC showed significantly less mucosal villus denudation (mean difference 21.5%, P =.02) and decreased mucosal‐to‐serosal flux rates (mean difference 15.2 nM/cm2/h, P =.007) compared to Group C. There were no significant differences between the groups for the other tested variables. Main limitations: Small sample size, long‐term effects were not investigated. Conclusions: Following IPoC, the intestinal mucosa demonstrated significantly less villus denudation and paracellular permeability compared to the untreated control group, possibly indicating a protective effect of IPoC on ischaemia reperfusion injury. [ABSTRACT FROM AUTHOR]