Journal of Veterinary Diagnostic Investigation最新文献

Junctional epidermolysis bullosa (JEB) is a congenital blistering skin disorder with clefting within the lamina lucida of the basement membrane zone. We describe the clinical and morphologic features of JEB in a 4-mo-old domestic shorthair kitten and identify the underlying genetic variant. The kitten was presented with blistering lesions affecting friction-prone areas of haired skin, mucocutaneous junctions, and oral mucosa. Histopathology revealed extensive subepidermal cleft formation in affected tissues. Periodic acid-Schiff (PAS) staining showed a thin, PAS-positive line along the dermal side of the cleft, consistent with retention of the lamina densa. Transmission electron microscopy confirmed separation at the level of the lamina lucida with intact basal keratinocytes. Whole genome sequencing identified a homozygous 2-bp deletion in exon 7 of COL17A1, predicted to result in loss of function and disrupted binding domains. Our findings support a diagnosis of JEB associated with a novel COL17A1 variant.

Ovine pulmonary adenocarcinoma (OPA), caused by Jaagsiekte sheep retrovirus (JSRV; family Retroviridae, taxon species Betaretrovirus ovijaa), is a viral oncogenic lung disease in sheep. Its metastatic potential remains under-evaluated. We investigated macrometastases (MACs), micrometastases (MICs), and isolated tumor cells (ITCs) in regional draining lymph nodes (DLNs) using histopathology and immunohistochemistry (IHC). Samples from 41 lung tumors and their regional DLNs were obtained from slaughtered Țurcană sheep. Histologically, all cases were diagnosed as OPAs. The classical or mixed OPA was observed in 37 of 41 (90%) cases; the remaining tumors were the atypical form. In 10 cases, myxoid growths were also detected. For IHC, anti-multicytokeratin, thyroid transcription factor 1, and JSRV antibodies were used to detect metastatic cells within DLNs. Neoplastic cells were identified in 16 of 41 (39%) DLNs, including 2 MAC, 7 MIC, and 7 ITC cases. Lung tumors >7 cm were significantly associated with lymph node metastasis (p < 0.05). A random forest model incorporating tumor volume, necrosis, mitotic count, and Ki67 index achieved the best performance (AUC = 0.70; accuracy = 62.5%; F1 = 0.57) for metastasis prediction. A benign epithelial inclusion was found within a DLN in one case, which has not been reported previously, to our knowledge. We found that OPA has a higher metastatic potential than previously recognized, particularly in larger tumors. Multivariate analysis, including additional tumor markers, likely would improve metastasis prediction. Our findings advance our understanding of OPA progression and its relevance as a comparative model for human lung adenocarcinoma.

Interstitial lung diseases of sheep and goats, which are caused by a range of infectious, parasitic, and toxic agents, have substantial negative health and welfare impacts globally. Within this category of pulmonary disease, entities such as peste des petits ruminants (PPR) can undermine the livelihood of farming communities in sub-Saharan Africa and Southeast Asia; enzootic pneumonia, maedi, and ovine pulmonary adenocarcinoma compromise the productivity of farm enterprises where sheep are housed for prolonged periods. I detail the pathogenesis and lesions caused by a range of viral, bacterial, parasitic, and toxic agents that target the pulmonary interstitium in small ruminants, ultimately resulting in parenchymal damage and clinical disease. These lesions range from the progressive distortion of alveolar walls by infiltrating lymphocytes and macrophages following small ruminant lentiviral infection, to the acute impact of alveolar septal thromboembolism in Bibersteinia trehalosi infection, and eosinophil-mediated necrosis of alveolar walls triggered during the migratory larval stages of parasitism by Dictyocaulus filaria. In addition, I review the pathologic impact of neoplastic type II pneumocytes extending over the interstitial scaffold in cases of sheep pulmonary adenocarcinoma (jaagsiekte) and the toxic injury induced by plants (Trema and Crotalaria sp.) and other toxins (carbolic dips, 3-methyl indole) on the pulmonary interstitium.

A 5-wk-old, 10.6-kg, intact female Leonberger dog was presented for evaluation of a mass on the left ventrolateral thorax that had been present since birth. A biopsy of the mass revealed an invasive, unencapsulated spindle-cell population arranged in bundles and concentric whorls (pseudo-onion bulb formations) with multifocal melanocytic differentiation. Neoplastic cells in pseudo-onion bulbs immunolabeled strongly for glial acidic fibrillary protein and PGP9.5 and moderately for S100 and Sox10. The supporting matrix had strong immunolabeling for laminin. Cells had multifocal immunolabeling for NeuN, melan A, and PNL2. Collectively, these histopathologic characteristics support a diagnosis of congenital nerve sheath tumor, which is rarely described in dogs.

An 11-mo-old, intact male captive kinkajou (Potos flavus) was submitted for postmortem investigation because of emaciation and hindlimb overgrooming. Histologically, alveolar airspaces were filled with fungal structures that were morphologically and histochemically consistent with Pneumocystis spp. PCR of pulmonary tissue was negative for canine distemper virus and positive for Pneumocystis spp. Molecular testing yielded amplification of the Pneumocystis spp. mitochondrial large-subunit rRNA (mtLSU rRNA, 510 bp) and the small-subunit rRNA (mtSSU rRNA, 565 bp). Phylogenetic analysis suggested a potentially novel Pneumocystis lineage associated with P. flavus. Additional nuclear loci are required to confirm its taxonomic status. Gastric and colonic histologic findings included concurrent candidiasis and colonic nematodosis. An underlying immunosuppressive disease was suspected. Further investigation is required to clarify the role of kinkajous in the ecology of fungal pathogens and the causes of immunosuppression in this species, particularly in the context of human-wildlife interactions. Enhanced surveillance and interdisciplinary collaboration are essential to evaluate potential zoonotic risks and inform conservation and public health strategies.

Marker-assisted selection has increasingly relied on single-nucleotide polymorphisms (SNPs) as robust genetic markers, particularly in livestock breeding programs. In pig farming, embryonic mortality significantly affects litter size, and SNPs in reference genes have been implicated as potential causal factors. We developed and optimized a tetra-primer amplification refractory mutation system (T-ARMS) PCR assay for rapid, cost-effective detection of SNPs in 3 candidate genes-TADA2A, PORL1B, URB1-that are associated with embryonic lethality and reproductive performance. Primer sets were designed based on known mutation sites and validated using synthetic gene constructs and porcine genomic DNA from pigs of Duroc and Landrace breeds. Optimization of annealing temperatures and primer concentration ratios yielded distinct and reproducible allele-specific amplicon patterns that were corroborated by PCR-RFLP and Sanger sequencing. Our T-ARMS PCR protocol, which requires minimal equipment and reduces processing time to <3 h, had high specificity and efficiency in differentiating wild-type, heterozygous, and homozygous mutant genotypes in 20 Duroc and 20 Landrace pigs. Our Tetra-ARMS PCR assay is a robust and economically viable tool for SNP genotyping in pig breeding programs, potentially contributing to the reduction of embryonic lethality and the improvement of overall reproductive outcomes.

Neonatal interstitial lung disease occurs within the first 3 wk of life and includes any disease process that affects alveolar septa and, in some species, interlobular septa. Postmortem diagnosis of neonatal interstitial lung disease is challenging because of our incomplete understanding of normal postnatal lung development, especially in altricial species such as dogs and cats, which are born with morphologically and physiologically immature lungs. Most altricial species are born with lungs in the saccular stage of development and continue development to the alveolar stage in the postnatal period. I address normal postnatal lung development in dogs and cats, structural immaturity of the lung, neonatal respiratory distress syndrome, and sepsis. Histologically, neonatal lungs are easily mistaken for infectious pneumonia or structural immaturity based on their thick alveolar septa and hypercellularity. However, by determining the stage of lung development and considering factors such as gestational age, birth weight, and age at death, the degree of lung development may be entirely appropriate for that animal. Neonatal respiratory distress syndrome is a clinical term for inadequate gas exchange. The underlying cause is surfactant dysfunction, which can be primary or secondary. Mature surfactant is essential for neonatal survival but is extremely difficult to assess in a postmortem lung. Sepsis is the leading cause of death in canine and feline neonates; histologic lesions are often subtle given the acute nature of the disease.

Four beef cows grazing in a mountainous grassland area had acute onset of drooling, frothy oral discharge, hyperemic mucous membranes, diarrhea, anorexia, dyspnea, and recumbency. Two cows died within 7-8 h of the onset of signs; the remaining 2 cows succumbed 24 h later. Scattered, 3-6-mm, gray-white solids were found on the grassland, suggesting potential contamination. Postmortem examination found abdominal distension, nasal hemorrhage, and distended rumens containing undigested forage. Hemorrhagic lesions were observed in the reticulum, omasum, abomasum, jejunum, and ileum. Yellow, 2-3-mm granular solids were identified in the rumen contents. Toxicologic analysis using scanning electron microscope-energy dispersive X-ray spectroscopy and high-performance liquid chromatography-inductively coupled plasma-mass spectrometry detected high concentrations of trivalent arsenic [As(III), up to 1,070 mg/kg] and pentavalent arsenic [As(V), up to 1,180 mg/kg] in the rumen contents and grassland solids. Elemental analysis revealed magnesium, aluminum, calcium, arsenic (As), silicon, carbon, and oxygen in the residues, suggesting industrial byproducts from As removal processes.

Between 2008 and 2024, fowl adenovirus (FAdV) genotypes were determined by hexon gene sequencing for 1,362 samples: 1,234 from 9 Canadian provinces and 128 samples from the United States. Most genotyped samples were from Ontario (681), followed by Alberta (243), Nova Scotia (116), British Columbia (77), Quebec (58), Saskatchewan (21), Manitoba (20), Newfoundland (16), and Prince Edward Island (2). Most samples (1,285) were related to inclusion body hepatitis (IBH); 77 samples were submitted for other reasons. Four FAdV genotypes (FAdV2, FAdV8a, FAdV8b, FAdV11) were associated with IBH-related submissions. Between 2008 and 2014, the most common strains associated with IBH outbreaks were FAdV11 and FAdV8a. However, since 2015, the identity of FAdVs involved in IBH outbreaks has shifted, with FAdV8b becoming the most frequent IBH-associated strain, largely displacing FAdV8a and FAdV11. In a much smaller group of 77 samples from non-IBH submissions, 10 FAdV genotypes were detected: FAdV1, FAdV2, FAdV3, FAdV4, FAdV6, FAdV7, FAdV8a, FAdV8b, FAdV9, and FAdV11. Although FAdV4 is a recognized causative agent of hepatitis-hydropericardium syndrome worldwide, no association with clinical disease was reported in the birds included in our study. Our comprehensive 17-y analysis of FAdV circulation patterns will support the development of control measures and vaccination programs to reduce the impact of FAdV-related outbreaks.

Two Actinobacillus pleuropneumoniae (APP) isolates from clinical cases of porcine pleuropneumonia in Japan, positive for ApxIA, ApxIIA, and ApxIVA, were nontypeable using the agar gel diffusion (AGD) test but positive in the capsular serovar 1-specific PCR assay. Nucleotide sequence analysis revealed that gene clusters involved in the biosynthesis of the capsular polysaccharide (CPS) and lipopolysaccharide O-polysaccharide of the isolates were identical to those of serovar 1 reference strain 4047. The main difference found in the CPS loci was a loss of 7 nucleotides at the 3'-end of the cps1D gene in the atypical isolates, which is responsible for the defect in CPS production. Consistent with the serologic and molecular findings, transmission electron microscopic analysis confirmed the absence of detectable capsular material in the 2 atypical isolates. Collectively, our results suggest that this type of APP, defective in CPS production, may severely hamper serologic typing of the pathogen.