Veterinary Pathology最新文献

Malignant catarrhal fever (MCF) is an often fatal, sporadic gammaherpesvirus-induced disease of ruminants with global relevance. Ovine gammaherpesvirus-2 (OvHV-2), with sheep as its reservoir host, is a major cause of MCF in susceptible species. Despite extensive research on the molecular aspects of the disease, its pathogenesis is not yet fully understood. The present study re-established the Syrian golden hamster (Mesocricetus auratus) as an amenable animal model of MCF and applied complementary in situ approaches to confirm recent findings in natural disease that could shed new light on pathogenic aspects of MCF. These showed that systemic OvHV-2 infection is associated with T-cell and macrophage-dominated mononuclear infiltrates and vasculitis in various organs. Both T-cells and monocytes/macrophages harbor the virus, and infected leukocytes are abundant in the infiltrates. The results also indicate that OvHV-2 has a broader target cell spectrum, including vascular endothelial cells and selected squamous epithelia. The former supports the interpretation that the inflammatory processes develop due to circulating, activated, infected T-cells and monocytes that home to tissues and emigrate from vessels prone to leukocyte emigration, possibly with direct interaction between virus-infected leukocytes and endothelial cells. The latter supports the hypothesis of graft versus host disease scenario, without viral cytopathic effect on epithelial cells but infiltration of the mucosa by infected T-cells and macrophages. The disease processes are accompanied by evidence of expansion of the T-cell compartments and the monocyte/macrophage pool in lymphatic tissues and bone marrow.

Liver-type fatty acid-binding protein (L-FABP) is expressed by several tissues, plays a role in fatty acid metabolism, and has antioxidant effects. Its renal expression is upregulated by stress. Urinary L-FABP (uL-FABP) is a promising kidney biomarker in people for detection of early acute and chronic kidney disease (CKD) and as a marker for progression in patients with glomerulonephritis. However, data on canine uL-FABP are currently limited. This prospective study was designed to examine canine tissue expression of L-FABP and to validate an ELISA to quantify uL-FABP in older dogs with or without early signs of CKD. Tissues of 4 recently euthanized dogs and 117 urine samples of 73 client-owned older dogs undergoing health screening were evaluated in the study. Immunohistochemistry was performed on kidney and liver tissues. Analytical validation of a commercially available ELISA for measurement of L-FABP in canine urine was performed (limit of detection, imprecision, specificity). The ELISA was used to measure L-FABP in stored urine samples from a cohort of older dogs. Dogs were found to express L-FABP, mostly in proximal tubular epithelial cells and in the periportal hepatocytes of the liver. Assay validation revealed poor sensitivity and imprecision for measurement of canine uL-FABP. Of the 117 urine samples analyzed, 98 were below the limit of detection (LOD; 7.30 ng/mL) and a further 5 were below the limit of quantification (LOQ; 16.20 ng/mL). The proximal tubules of dog kidneys express L-FABP, but the value of uL-FABP as tubular marker in older dogs warrants further study.

Equine spinal neurodegenerative conditions are frequently encountered in sport and racing horses and may be career-ending diagnoses. To further define the spatial transcriptomic landscape of equine dorsal root ganglia (DRG) in healthy adult horses, we investigated gene expression differences in distinct DRG regions using the GeoMx Digital Spatial Profiling from NanoString. Four human cell markers demonstrated high fidelity for equine cells; microtubule-associated protein 2 (MAP2), myelin basic protein (MBP), allograft inflammatory 104 factor 1/ionized calcium-binding adaptor molecule 1 (IBA1/AIF1), and Syto83 nuclear marker. Geometric regions of interest were then selected as MBP-rich, IBA1-high, and IBA1-low, and gene expression was compared. Experimental validation was achieved, with genes involved in myelination enriched in MBP-rich regions, and the identification of glia-specific genes enriched in IBA1-high regions. Thus, spatial transcriptomics with human cell markers was successful in equine DRG and can now be applied to determine cell-specific transcriptional changes during disease states.

Intoxication of sheep and cattle by Astylus atromaculatus recently occurred in Uruguay and Argentina in association with severe drought. Although the disease was experimentally reproduced in sheep in the 1970s, there is limited information on clinical and pathologic findings of sheep experimentally intoxicated by this beetle. Here, we described the clinical, gross, and microscopic findings in 3 sheep orally dosed with A. atromaculatus (treatment group, TG) and in 2 control sheep (control group, CG) dosed with distilled water. Anorexia, lethargy, ruminal stasis, reluctance to move, prolonged recumbency, and bruxism were observed in the TG but not the CG sheep. Gross postmortem lesions were only observed in TG sheep and included fibrinonecrotizing enteritis affecting the duodenum, jejunum, and ileum, and multifocal hemorrhages in rumen, omasum, and abomasum. Microscopically, all 3 TG animals had multifocal necrosis in the small intestine; the lesions were most severe in the jejunum. Multifocal necrosis was seen in the mucosa of the rumen, omasum, and abomasum. No significant gross or microscopic abnormalities were observed in the 2 CG sheep. The study supports the role of A. atromaculatus in acute, fatal gastrointestinal disease like that previously described in experimental and spontaneous cases in sheep.

Acute pancreatitis (AP) is a life-threatening condition, with a higher mortality rate in men than women and in which estrogens might play a protective role. This study aimed to investigate sex-dependent differences in a mouse model of caerulein-induced AP. Thirty-six C57BL/6J mice (19 females and 17 males) were treated intraperitoneally with phosphate-buffered saline or caerulein, and sacrificed 12 hours, 2 days, or 7 days after the last injection. Blood was collected for amylase, lipase, and glucose determination. Severity and extent of inflammation, apoptosis, and acinar to ductal metaplasia (ADM) in pancreatic tissue were scored histologically and total macrophages, major histocompatibility complex (MHC)-II+ cells, M2 macrophages, T and B cells, neutrophils, apoptosis, and ADM were marked immunohistochemically and quantified by digital image analysis. Serum amylase had a peak at 12 hours, without differences between the sexes. In females, pancreatitis reached a peak at 12 hours with a fast recovery while, in males, the peak was delayed to day 2 with residual apoptosis still present. Macrophages were the main inflammatory cell population, followed by T cells, B cells and neutrophils, without differences between sexes. In males, CD206+ cells and apoptosis were higher at both days 2 and 7, and cytokeratin-19+ (CK19+) ADM was higher at day 7 compared with females. The results of this study revealed a faster onset and resolution of caerulein-induced AP in female mice compared with male mice, supporting a sex-dependent modulation of acute pancreatitis.

Coiled-coil domain containing 85c (Ccdc85c) is a causative gene for genetic hydrocephalus found in hemorrhagic hydrocephalus (hhy) mice. The Ccdc85c knockout (KO) rat has subcortical heterotopia with frequent brain hemorrhage as seen in hhy mice. In this study, we report aberrant alpha-smooth muscle actin (α-SMA) expression in the wall of lateral ventricle of the Ccdc85c KO rats. The α-SMA-positive cells were distributed at the dorsal, medial, and lateral regions of the lateral ventricle of KO rats. The expression of α-SMA was first observed on postnatal day 20 (P20) and became noticeably stronger at P26 when hydrocephalus was prominent. Double immunofluorescence showed co-expression of α-SMA with nestin, vimentin, and glial fibrillary acidic protein in the ventricular lining of KO rats. Therefore, we conclude that α-SMA-positive cells may represent an immature subpopulation of cells at adult age around the lateral ventricle of Ccdc85c KO rats.

The present study aimed to evaluate the histologic, histochemical, and immunohistochemical changes in buffalo livers with cystic echinococcosis. Noninfected and infected livers were collected from the freshly slaughtered buffalo at the Aligarh abattoir. Small pieces of both infected and noninfected livers (n = 5) were cut and processed for histologic and histochemical studies. Immunohistochemistry was performed using rabbit anti-CD3, CD19, and CD117 antibodies. The results revealed the presence of brood capsules and germinal and laminated membranes surrounded by a fibrous adventitial layer, followed by moderate and diffused infiltration of eosinophils, monocytes, neutrophils, lymphocytes, and marked focal infiltration of mast cells. The infected livers also had mild dilation of central veins and sinusoids, mild and focal necrosis of hepatic tissue, and congestion of central and portal veins. Periodic acid-Schiff reaction revealed marked glycogen depletion in the infected liver. Masson's trichrome stain showed marked deposition of collagen fibers in the portal area, adventitial layer, and between the hepatocytes compared with the noninfected liver, where deposition was found only in the portal area. The T-cell response was more pronounced than the B-cell response in infected liver. Thus, it can be concluded that hydatid cyst infection causes several pathological and biochemical changes and increased infiltration of inflammatory cells in the infected livers, suggesting the involvement of nonspecific immune responses against hydatid cysts. The T-cell response was more pronounced than B-cells, indicating the involvement of cell-mediated immunity against cystic echinococcosis. These findings may help to understand the local immune responses to cystic echinococcosis.

Canine high-grade oligodendrogliomas (HGOGs) exhibit a high expression of platelet-derived growth factor receptor-α (PDGFRA). We examined PDGFRA mutations and gain of PDGFRA and their association with the PDGFRA expression and proliferation of tumor cells in canine HGOG cases and cell lines. Polymerase chain reaction and sequence analysis revealed expected pathogenic mutations in PDGFRA exons 7 and 8 in 16/34 (47%) cases. However, these mutations were not associated with PDGFRA expression, as examined by mRNA in situ hybridization (ISH) and immunohistochemistry, or proliferation activity, as examined by the Ki-67 labeling index (LI). Chromosomal ISH performed in 16 cases revealed PDGFRA and endoplasmic reticulum membrane protein complex subunit 2 (EMC2) gains in 15 cases (94%). PDGFRA gain was moderately correlated with PDGFRA mRNA expression (ρ = 0.54, P = .04) and were moderately correlated with PDGFRA H-score, which is the score based on immunolabeling intensity (ρ = 0.44, P = .09). However, PDGFRA gain was not correlated with the Ki-67 LI (ρ = 0.23, P = .38). The canine HGOG cell line with PDGFRA gain showed higher PDGFRA mRNA expression (P < .01), H-score (P < .01), and Ki-67 LI (P < .01) than the cell line without PDGFRA gain in vitro. The gain of PDGFRA and EMC2 suggests polysomy of canine chromosome 13, where both genes are located. The in vitro analysis results suggested that chromosome 13 polysomy is associated with increased PDGFRA expression and cell proliferation in canine HGOG. Chromosome 13 polysomy may be involved in canine gliomagenesis by increasing PDGFRA expression and inducing tumor cell proliferation.

This report describes cardiovascular and renal soft tissue mineralization and renal intratubular crystals in 13 out of 16 guinea pigs that were given very hard drinking water for 9 months. These animals, aged 14 to 20 months, were experimentally naïve. No clinical symptoms were observed, but 1 guinea pig was found dead in its cage. Necropsy did not reveal any gross findings; however, histologic examination revealed mineralization and crystal formations. Despite no known changes in the feed sourcing or formulation, the possibility that the incident was feed-related was considered. The most recent analysis of the feed obtained from the manufacturer during this period, which was conducted by an accredited laboratory authorized by the Ministry of Agriculture and Forestry, was appropriate. No similar lesions were reported at other centers using the same feed; however, drinking water analysis for total dissolved solids revealed extremely hard water, with elevated levels of calcium and calcium carbonate and low magnesium levels, due to a malfunctioning water treatment system. After installing a new system to balance calcium and magnesium, no new cases appeared over the next 2 years. It was determined that the mineralization and crystal formations were most likely caused by water hardness. This study demonstrates that mineralization typically attributed to feed in guinea pigs can also result from high calcium content in drinking water, highlighting the importance of water analysis in such cases.

Collection of coral for histologic examination requires holding of samples in seawater for a time before they are fixed for histologic processing. This could adversely affect the interpretation of morphologic changes during histologic examinations. We evaluated the microscopic morphology of Porites evermanni and Montipora capitata held (0-120 minutes) in seawater prior to fixation in Z-Fix formulated with raw or artificial seawater. We saw no evident effects of treatments on microscopic morphology. However, among 88 statistical comparisons, and after accounting for false discovery rate, holding time prior to fixation was associated with a significant increase in degree of mucosity of basal body walls.