Journal of Veterinary Diagnostic Investigation最新文献

Canine leishmaniosis is a widespread, potentially fatal disease caused by infection with Leishmania infantum. We evaluated 5 commercial point-of-care tests (POCTs) for the detection of L. infantum antibodies in dog sera and compared their performance with the immunofluorescence assay (IFA) as the reference method. We tested serum samples from 160 dogs that either had lived in or traveled to leishmaniosis-endemic areas using the following immunochromatography POCTs: the trüRapid Leish (Biotech), FASTest Leish (Megacor), Leishmania Ab (Bionote), and Uranotest Leishmania 2.0 and 3.0 (Uranovet). Practicality, sensitivity, specificity, positive predictive value, and negative predictive value were determined. The prevalence of L. infantum antibodies in all dogs was 28.1% as determined by IFA. The highest sensitivity among POCTs was achieved by the Leishmania Ab and the Uranotest Leishmania 2.0 (88.9%), followed by the trüRapid Leish (86.4%), the Uranotest Leishmania 3.0 (84.4%), and the FASTest Leish (48.9%). The highest specificity was achieved by the FASTest Leish (100%) followed by the Leishmania Ab (98.3%), the trüRapid Leish (96.5%), the Uranotest Leishmania 3.0 (94.8%), and the Uranotest Leishmania 2.0 (90.4%). Given its comparatively high sensitivity and specificity, the Leishmania Ab may be considered for screening dogs from endemic areas and for confirming Leishmania infection in clinical dogs.

Reactive proliferative vascular disorders of the CNS are poorly documented in veterinary medicine. Here, we describe widespread CNS hemangiomatosis in a 1-y-old female donkey with weakness, recumbency, and lifelong unthriftiness. Elevated serum creatine kinase and aspartate aminotransferase activities were consistent with skeletal muscle injury attributed to prolonged recumbency. Despite supportive care, the donkey remained unable to stand and was euthanized 5 d after presentation. Gross findings consisted of poor body condition and multiple gastric ulcers. Histologically, clusters of sometimes tortuous, redundant leptomeningeal and neuroparenchymal capillaries and small- to medium-sized arterioles and venules were present throughout the CNS. These changes were more pronounced in the spinal cord and cerebellum. Immunohistochemistry highlighted these vascular proliferations, with membranous labeling of endothelial cells for CD31 and cytoplasmic labeling for factor VIII-related antigen. Vascular myocytes had cytoplasmic labeling for smooth muscle actin. Although CNS development appeared undisturbed, other neuroparenchymal changes included Purkinje cell degeneration and necrosis with dendritic and axonal swelling and gliosis; white matter vacuolation and microgliosis (with occasional early, mildly vacuolated macrophages) of the ventral funiculi and the dorsal portion of the lateral spinal cord, cerebellum, and cerebrum; and white and gray matter vacuolation and gliosis of the thalamus and brainstem. Inflammatory cells within these areas had cytoplasmic labeling for ionized calcium-binding adaptor molecule 1. Moderate-to-severe skeletal muscle degeneration, atrophy, and fibrosis affected the dorsal sacrocaudal muscle. Our findings are consistent with congenital, widespread CNS hemangiomatosis.

Idiopathic pulmonary fibrosis (IPF) describes a severe, progressive, and ultimately fatal end-stage lung disorder in dogs and cats. The term IPF was coined in dogs and cats for 2 reasons: 1) the cause of the fibrosis at the time of diagnosis was unknown (i.e., presumed idiopathic); and 2) the condition was believed to resemble human IPF, the most common type of progressive fibrotic lung disease in people. However, pulmonary fibrosis in dogs and cats is not a single homogeneous disorder, does not consistently resemble all histologic features of human IPF, and is rarely exhaustively evaluated for an underlying cause. Fibrosis is a response to injury, and knowledge of the type of injury has critical implications for disease management, especially if identified before end-stage lesions occur. We offer an approach to a thorough diagnostic evaluation, including clinical, imaging, laboratory, and pathology data, which sets the stage for multidisciplinary discussions. Given that thoracic computed tomography (CT) is increasingly utilized to identify features compatible with pulmonary fibrosis in dogs and cats, we describe these CT patterns and their pitfalls. Diagnostic respiratory evaluations should investigate possible inciting causes, provide information about disease extent and severity, and identify comorbid disorders. Such evaluations will allow optimized therapy, including avoiding treatments that may have adverse effects or be overtly harmful. Importantly, although end-stage fibrotic lungs currently have no viable treatment, early recognition of known triggers of fibrosis could ultimately enable novel targeted therapy while there is still time to alter the clinical course.

Tritrichomonas foetus infection can cause reproductive losses and subsequent economic losses in cow-calf herds. Our objective was to determine if 0.9% sterile saline (saline) was noninferior to PBS as a transport medium for T. foetus reverse-transcription real-time PCR (RT-rtPCR) testing. Transport tubes were prepared with either 1.6 mL of PBS with preputial washing (n = 30) or 1.6 mL of saline with preputial washing (n = 30) and inoculated at 3 different concentrations of T. foetus organisms (high = 100 org/100 µL; moderate = 10 org/100 µL; low = 1 org/100 µL) for a total volume of 1.7 mL/tube. Samples were submitted to a diagnostic laboratory for RT-rtPCR analysis. The effect of concentration and medium on mean Ct values was tested using linear regression. Normalized means were used to conduct a noninferiority t-test, with a noninferiority margin of 1 Ct. For all analyses, α = 0.05. Mean Ct values (high = 18.5; moderate = 22.7; low = 30.4) differed by concentration (p <0.0001), whereas medium (p = 0.67) and the interaction of medium and concentration (p = 0.87) were not significant. The normalized mean Ct for PBS was 22.6 (min = 16.2; max = 27.0), and for saline was 22.8 (min = 20.9; max = 26.4). The normalized mean Ct of saline was noninferior to PBS (p = 0.037). The use of saline as a transport medium for T. foetus RT-rtPCR should not affect Ct results.

African horse sickness (AHS) is the only equine disease for which the World Organisation for Animal Health (WOAH) gives official disease-free status, given that it poses a major threat to the equine industry. The disease is caused by AHS virus (AHSV; family Sedoreoviridae, taxon species Orbivirus alphaequi), which is endemic in sub-Saharan Africa. Reverse-transcription quantitative real-time PCR (RT-qPCR) is a rapid, sensitive detection method used in the diagnosis of AHS and the certification of animals as negative for AHSV for the purpose of movement. Genetic variability of AHSV may influence the accuracy of RT-qPCR detection methods because of possible mispriming and/or probe binding failures. We evaluated the diagnostic accuracy of the current WOAH-recommended RT-qPCR assays for the detection of AHSV, namely the Agüero et al. and Guthrie et al. methods. Utilizing 150 AHSV-positive diagnostic samples, we performed in vitro analysis using both assays. The Agüero assay failed to detect AHSV in 13 samples (8.7% false-negative rate). The AHSV VP7 genes of the 13 negative samples, and publicly archived sequences were used to perform in silico analysis, and we incorporated minor changes into the primers and probes of modified Guthrie and modified Agüero assays. A second in vitro analysis yielded 100% sensitivity for both assays. Differences in both the in silico and in vitro analyses highlight the need for continuous monitoring of the efficacy of molecular protocols used for the detection of AHSV.

The pulmonary consequences of congestive heart failure in domestic animals, particularly from clinical and gross morphologic perspectives, have been described. However, the full spectrum of mechanistic and microscopic alterations, especially at the molecular and cellular levels, remains less well integrated in the context of veterinary pathology. We examine the pathogenesis and consequences of pulmonary hypertension secondary to left heart failure, in which chronic elevation of hydrostatic pressure triggers complex molecular, physiologic, and morphologic responses. These include the epithelial and endothelial stress response, molecular signaling, and interstitial remodeling. Although pulmonary edema is often referred to as the ultimate consequence of pulmonary venous hypertension, other critical yet underappreciated aspects also exist, such as pulmonary remodeling. We also explore the molecular mechanisms that can be activated during venous hypertension, offering a framework for understanding the continuum from reversible congestion to irreversible parenchymal injury. Describing the physiologic and morphologic patterns associated with cardiogenic lung disease not only enhances diagnostic precision, but also promotes a shared vocabulary for use among pathologists, clinicians, and cardiologists.

A 4-y-old, male English Mastiff with a history of inflammatory neuromuscular disease developed progressive tetraparesis, ataxia, and severe temporal muscle atrophy, culminating in non-ambulatory status and euthanasia. The autopsy revealed diffuse muscle atrophy and pale pulmonary nodules. Histologically, polyphasic myositis was evident, with apicomplexan organisms within skeletal muscle myofibers. Encephalomyelitis, myocarditis, and hepatitis with protozoal cysts and tachyzoites also were observed. Immunohistochemistry of brain tissue was strongly positive for Neospora caninum and Toxoplasma gondii, but PCR testing confirmed N. caninum and excluded T. gondii, establishing a diagnosis of disseminated neosporosis. Despite extensive tissue involvement, N. caninum antibody titers were below the diagnostic cutoff. Our case highlights that non-positive serologic results do not exclude neosporosis in clinically compatible cases, particularly in dogs undergoing corticoid therapy, and underscores the diagnostic value of histopathology with confirmatory molecular testing for definitive diagnosis.

A panzootic caused by highly pathogenic avian influenza (HPAI) A(H5N1) virus, clade 2.3.4.4b, has affected many animal species around the world since 2021. In March 2024, genotype B3.13 of this virus was identified in dairy cattle in the United States, following a spillover event from wild birds. Mammary gland lesions were a key finding in infected cows, with infectious virus detected in their milk. Raw milk is sold legally in retail establishments in multiple US states, including California. In November 2024, HPAI A(H5N1) virus, clade 2.3.4.4b, genotype B3.13, was detected in raw milk sold commercially in California and then in bulk milk tanks. The affected product later was recalled. We describe an 8-mo-old cat with a history of severe illness after consuming this raw milk before it was recalled. The cat was euthanized and submitted for postmortem examination and diagnostic workup. Autopsy and histopathology revealed icterus, nasal discharge, hydrothorax, gliosis, and necrotizing pneumonia, hepatitis, and salpingitis, among other lesions. Immunohistochemistry for influenza A virus revealed intralesional immunolabeling in many organs. Molecular detection was positive for HPAI A(H5N1) virus, clade 2.3.4.4b, genotype B3.13. To our knowledge, HPAI A(H5N1) virus has not been reported previously in cats after consuming raw milk purchased from a retail establishment, nor has salpingitis been associated with HPAI A(H5N1) virus infection in a mammal. Hepatic damage and icterus were prominent findings in our case rather than primary involvement of the CNS.

Teratomas originate from pluripotent germ cells and differentiate into the 3 germ cell layers: endoderm, mesoderm, and ectoderm. Hence, these tumors arise most often in the gonads. Extragonadal teratomas are rare in veterinary medicine. Congenital oropharyngeal teratoma, also known as epignathus, is a neoplasm that has been reported in humans and a few veterinary species. We describe the clinical, gross, cytologic, and histopathologic features of an oropharyngeal teratoma in a neonatal Boer × Nigerian Dwarf goat that died within 4 h of birth, and briefly review extragonadal teratomas in veterinary species.

Enzootic nasal adenocarcinoma (ENA) is a contagious neoplasm of the ethmoid turbinate mucosa in sheep, caused by enzootic nasal tumor virus 1 (ENTV1; family Retroviridae, unclassified Betaretrovirus). We report an outbreak of ENTV1-associated ENA in a sheep flock in South Dakota, USA. Affected animals had dyspnea, unilateral nasal discharge, and progressive weight loss. Postmortem examination revealed unilateral nasal masses that were diagnosed histologically as invasive nasal adenocarcinoma. PCR amplification followed by Sanger sequencing of the gag and env gene regions confirmed the presence of ENTV1. Our proviral genome assembly via next-generation sequencing is only the second ENTV1 sequence submitted to GenBank from the United States. Our isolate clustered within the ENTV1 clade and was closely related to the reported U.S. and Canadian isolates, indicating a shared evolutionary lineage. To further investigate tumor biology, we established 3-dimensional organoids derived from the nasal adenocarcinoma, which maintained the histologic features of the primary tumor and tested positive for ENTV1. These organoids also had an invasive phenotype, demonstrating their potential utility as a novel in vitro model for studying ENA pathogenesis and evaluating therapeutic interventions.