Journal of Veterinary Diagnostic Investigation最新文献

With the revision of the World Organisation for Animal Health (WOAH) Terrestrial Manual on equine rhinopneumonitis in 2024, 3 recommended qPCR primer-probe sets were added for the detection of equid alphaherpesvirus 1 (EqAHV1; formerly equine herpesvirus 1 [EHV1]; family Orthoherpesviridae, taxon species Varicellovirus equidalpha1), also known as equine abortion virus. We compared the sensitivity and specificity of the 3 qPCR primer-probe sets to determine the most reliable set. Sets gB1H and gB1P, which target the glycoprotein B (gB) gene of EqAHV1, detected all 10 copies and even lower copy numbers. In contrast, set gC1 (ISO 17025-accredited method used at the WOAH reference laboratory), which targets the glycoprotein C (gC) gene, failed to detect ≤10 copies of EqAHV1. Our results showed the lower sensitivity of gC1, which was not improved by modification of primer and probe concentrations. gB1P detected not only EqAHV1 but also equid alphaherpesvirus 4 (EqAHV4; Orthoherpesviridae, Varicellovirus equidalpha4), likely owing to an erroneous amplification of the homologous EqAHV4 gB gene, indicating that gB1P is not suitable for the detection of EqAHV1 with high specificity. We then compared gB1H with gB1D, a set recommended in the previous version of the Manual, using 120 nasal swabs collected from febrile horses. gB1H had slightly higher sensitivity than gB1D. gB1H proved to be the most reliable primer-probe set for detecting EqAHV1, with high sensitivity and specificity. Nevertheless, individual laboratories are encouraged to validate these methods under their own conditions before implementation.

Since ~1980, the Animal Health Laboratory (AHL) in Ontario, Canada, has isolated animal mollicute species by culture. Data for the most recent 17 y (2007-2024) captures over 90,000 test results. Advancements in PCR, qPCR, and DNA sequencing have shifted the percentage of testing by PCR from 18.7% in 2007 to 91.1% in 2024. The bulk of this shift is due to the uptake of molecular testing as a screening tool for clinically normal animals, but this shift has not been universal, particularly for ureaplasma testing. Culture remains the gold standard for the detection and identification of rare pathogens and plays a key role in research through our mycoplasma cryobank, which includes 40+ y of isolates. Synergizing the microbiologic and molecular techniques developed over the AHL's multi-decade history has presented novel opportunities for detection, characterization, and local eradication of animal mollicutes, including the development of new assays, tracking of historical trends for antimicrobial resistance (AMR), and identifying AMR-associated mutations in Mycoplasmopsis (Mycoplasma) bovis.

Equine meningoencephalomyelitis is an important cause of morbidity and mortality and is associated with a wide variety of infectious etiologies. Because of the lack of large retrospective studies, the prevalence and incidence of these diseases are unknown. Here we describe 171 cases of meningoencephalomyelitis in horses submitted to the Section of Anatomic Pathology at the New York State Animal Health Diagnostic Center (Cornell University, Ithaca, NY, USA) from 1996-2023. Neuroinflammatory disease was identified in 5.4% of submitted horses with a wide breed, age, and sex distribution. A parasitic cause was identified in 32 (19%) cases, with protozoa in 18 (11%) cases and metazoa in 14 (8%) cases. A viral cause was identified in 31 (18%) cases, corresponding to infection by equid alphaherpesvirus 1 (EqAHV1; 12 of 31, 39%), eastern equine encephalitis virus (10 of 31; 32%), West Nile virus (5 of 31; 16%), and rabies virus (4 of 31; 13%), followed by 14 bacterial (8%) cases and 7 fungal (4%) cases. Of the remaining 87 of 171 (51%) cases, 20 (23%) had some histologic features, although not conclusive, of protozoal disease, and 8 (9%) of EqAHV1 infection. However, 59 (68%) cases did not have any neuropathologic changes that would support a definitive diagnosis. Although we found the expected causes of equine meningoencephalomyelitis in our study, the large number of cases with unknown etiologic diagnoses highlights the challenges of definitively proving causes of neuroinflammation in the horse and supports the need for improved ante- and postmortem testing.

An 11-y-old male lionhead rabbit (Oryctolagus cuniculus) was presented with progressive hindlimb weakness and right-sided neurologic deficits, and was subsequently euthanized due to poor prognosis. Autopsy revealed a 1.6 × 1.1 × 1.0-cm, well-circumscribed, extra-axial mass compressing the occipital lobe and affecting both telencephalic hemispheres. Histologic and immunohistochemical analyses demonstrating positivity for synaptophysin and neuron-specific enolase, along with a Ki67 proliferative index of ~20%, were highly suggestive of a high-grade pineal parenchymal tumor (PPT). The tumor was densely cellular with marked atypia and frequent binucleation, and lacked pineocytomatous rosettes-features most consistent with a pineal parenchymal tumor of intermediate differentiation in humans. No evidence of metastasis was observed. Pineal tumors are exceptionally rare in domestic animals, with limited documentation in species such as dogs, horses, goats, cattle, and birds. To our knowledge, PPT has not been reported previously in a rabbit, underscoring the diagnostic challenges associated with intracranial neoplasms in this species.

Canine interstitial pulmonary fibrosis has been described in dogs, almost exclusively in terrier breeds. Here, we present a unique case of spontaneous pneumothorax in a Labrador Retriever that was presented to an emergency clinic in severe respiratory distress. Despite resuscitation efforts, the animal died and was submitted for autopsy, which revealed severely collapsed lungs bilaterally and bullae along the pleural surface, with at least one ruptured bulla observed grossly. Histopathology of the lung revealed coalescing areas of interstitial fibrosis throughout most of the lung tissue examined. A pan-herpesvirus PCR assay was negative on fresh lung tissue. Based on our findings, we propose that the fibrosis and bullae developed sequentially, and the fibrotic interstitium likely decreased the elasticity in the respective alveoli, leading to increased alveolar wall tension in normal alveoli, which caused the formation of bullae. Our case adds to the body of literature regarding canine interstitial lung disease by describing a unique presentation of canine idiopathic interstitial fibrosis in a non-terrier breed.

Chronic interstitial lung disease (cILD) is uncommon in dogs and little is known of the pathogenesis, apart from the condition in West Highland White Terriers. This study aimed to characterize histologic lesions of canine cILD, compare the lesions and clinical features, and classify the histopathologic patterns according to criteria used in humans. The study included 24 postmortem cases of subacute or chronic ILD in >6-month-old dogs with respiratory signs. Histologic lung lesions included attenuated bronchiolar epithelium, alveolar edema, type II pneumocyte proliferation, fibrosis of alveolar septa, fibrin or fibrous tissue within alveoli or bronchioles, and hyaline membranes. Of the 24 cases, 8 were classified as organizing diffuse alveolar damage, 4 as organizing pneumonia, and 3 as acute fibrinous and organizing pneumonia; 9 were unclassifiable and considered as nonspecific interstitial lung disease. None fulfilled criteria for usual interstitial pneumonia. Potential causes included aspiration of gastric or foreign material, prior acute respiratory distress syndrome, or failed healing of pneumonia. Left-sided heart failure was identified in 12 of 24 cases but was not considered to directly cause the interstitial lung lesions. Gross lesions of cor pulmonale were associated with organizing pneumonia and longer clinical duration. The cases had diverse histologic lesions and patterns of lung fibrosis, but the results suggested that these may represent divergent responses to overlapping causes of lung injury rather than distinct diseases. These findings clarify the pathogenesis of cILD in dogs, the mechanisms of initial damage, and the future development of approaches to delay or predict disease progression.

We report here 6 cases of bovine eurytrematosis on 2 farms (dairy and beef cattle) in southeastern Brazil. The cattle had different primary lesions that explained their clinical conditions; however, upon autopsy, common to all animals were abnormalities in the pancreas and the presence of Eurytrema spp. All parasitized pancreases were swollen, firm, and tan to yellow-pink. Upon dissection, numerous parasites were observed, the pancreatic ducts were thickened and dilated, and the parenchyma was fibrotic. Histopathologic findings were multifocal-to-diffuse chronic interstitial pancreatitis. Despite clinical signs, such as low body condition score, compatible with eurytrematosis, it was challenging to determine whether these signs were caused primarily by the pancreatic lesion or by the primary disease affecting the cows. Bovine eurytrematosis may be associated with other underlying conditions, making its diagnosis difficult and potentially impacting the prognosis of the affected animals. Our findings underscore the harmful nature of Eurytrema coelomaticum as a parasite and emphasize that it may be more than an incidental finding at autopsy.

Nine days after a surgical intervention due to an injury of the left hind hoof capsule, a 9-y-old, 538-kg female Wielkopolski horse was found recumbent in its stall with an unplugged permanent intravenous catheter positioned in the left jugular vein. Despite immediate resuscitation attempts, the animal died within minutes. Suspecting venous air embolism, radiographic imaging and detailed postmortem examinations were performed. However, visualization of the heart by radiography was hindered by the animal's body mass and postmortem changes. The autopsy followed a modified Richter method, originally developed for diagnosing air embolism in humans. The horse was positioned in left lateral recumbency to allow in situ access to the atria and venous sinuses. Gas bubbles observed in the right atrium and ventricle confirmed venous air embolism as the cause of death. Venous air embolism is a rarely documented cause of death in veterinary pathology. We present here an autopsy protocol for diagnosis of venous air embolism in large animals, which is primarily a macroscopic diagnosis.

Congestive heart failure (CHF) in feedyard cattle is of increasing concern among producers and can be difficult to diagnose definitively postmortem. In a cross-sectional observational study, we evaluated gross pathology findings, various heart measurements, and subjective heart scores (1-5 scale: 1 = normal, 5 = severely remodeled) to identify heart disease postmortem. In postmortem examinations of 346 feedyard deaths, we classified 106 (30.6%) cases as cardiac enlargement or misshapen ventricle (CEMV) when there was an abnormal heart shape or dilated ventricle(s), and no signs of infectious heart disease. CHF was defined as a CEMV case with chronic passive congestion of the liver (i.e., nutmeg liver) and ≥2 of the following lesions: serous or serosanguineous pleural, pericardial, or peritoneal effusion. Eleven of the 346 autopsied cattle were classified as having CHF. Descriptive statistics and multivariate models were used to identify statistical associations between objective heart measurements or subjective heart scores and the prevalence of CEMV or CHF. CEMV cases had significantly increased heart widths, thinner left ventricular free walls, and expanded right ventricular lumen areas (p <0.05). The CHF model did not converge because we had too few cases to be able to evaluate associations between CHF and variables of interest.