Journal of Veterinary Diagnostic Investigation最新文献

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.

Interstitial pneumonia and lymphocytic bronchiolitis with interstitial emphysema is an unusual reaction pattern in fetal and neonatal calves. These changes often are thought to suggest a chronic bacterial infection acquired in utero, and an associated placentitis is expected. Viral agents can also be implicated. Specific known pathogens that can induce a similar inflammatory response include Ureaplasma diversum, Mycoplasmopsis bovis, Brucella abortus, bovine viral diarrhea virus, and bovine parainfluenza virus 3. We describe a series of 15 cases of interstitial pneumonia and lymphocytic bronchiolitis with interstitial emphysema in fetal and early neonatal (up to 3-d-old) beef calves collected over 10 y in Alberta, Canada. Where reported, calves appeared small, weak, and occasionally were dyspneic. On autopsy, lungs appeared diffusely voluminous with interstitial emphysema, bulla formation, and rarely mediastinal emphysema and pneumothorax. A few calves had additional features of bacterial infection, such as pericarditis. Placenta was not received. Histologic lung findings in the affected calves included alveolar septa expanded by mononuclear cells, sparse neutrophils and macrophages within alveoli, variable lymphocytic and histiocytic peribronchiolar cuffing, prominent lymphoid aggregates surrounding bronchioles, occasional vascular necrosis, and subpleural and interlobular emphysema. PCR testing and immunohistochemistry for the previously noted pathogens were negative, and the cause of this unique condition, although presumably infectious, remains unknown.

Interstitial and bronchointerstitial pneumonias of undetermined etiology in young foals are relatively common in autopsy services with an equine focus. Unknown viruses, toxins, hyperthermia, surfactant or alveolar macrophage function deficiency, certain antibiotics, and aberrant responses to Rhodococcus equi or other bacteria have been proposed as causes. We performed a retrospective study of autopsies on foals with a diagnosis of interstitial or bronchointerstitial pneumonia with an unidentified etiology. Forty-one foals (median age: 3-mo-old) were included. Most were received in summer (n = 28) and spring (n = 10). The most frequently reported clinical signs were dyspnea and/or tachypnea (n = 28) and fever (n = 19). Antibiotic treatment was reported in 21 cases, and the most frequently used antibiotics were penicillin (n = 9) and gentamicin (n = 8). Grossly, most of the lungs were diffusely rubbery-to-firm (n = 35) and did not collapse (n = 22). Histologically, combinations of exudative (E; hyaline membranes), proliferative (P; type II pneumocyte hyperplasia), and fibrotic (F; fibroplasia) phases were common (E + P, n = 15; E + P + F, n = 13) in the interstitial component. Necrosis of the bronchiolar epithelium was rare (n = 4), concurrent suppurative bronchopneumonia was common (n = 22), and a few foals (n = 5) had pulmonary pyogranulomas. Pneumocystis spp. organisms were observed in 8 cases using Grocott-Gomori methenamine silver stain. Bacteria were recovered from the lungs in 22 cases, with R. equi (n = 7) and E. coli (n = 6) being the most common isolates. No unequivocal viral causes were identified during the regular diagnostic work-up and after using novel diagnostic approaches such as herpesvirus consensus PCR and viral metagenomics in a subset of the cases.

Highly pathogenic avian influenza (HPAI) A(H5N1) virus, clade 2.3.4.4b, genotype 3.13, was first confirmed in dairy cattle in March 2024 in a Texas dairy herd and has since spread to other states, likely via movement of subclinically affected cattle. On 2024 May 5, a backyard poultry farm in Idaho reported sick and dying chickens. This pasture-based farm included 1,100 chickens, 32 ducks, 18 alpacas, 13 yaks, 3 cats, 3 dogs, 1 llama, and 1 goat. Most animals had direct access to a pond filled by the stream bordering the property. Additional dairy premises in the same county had been confirmed with HPAI during the same timeframe. The poultry were depopulated on May 10, the same day the first alpaca abortion was observed. Overall, 4 abortions occurred among the alpacas. In one of the abortions, HPAI A(H5N1) virus was isolated from fetal tissues. Additional testing documented seroconversion in several alpacas and detection of HPAI A(H5N1) virus in milk from an alpaca with a cria. To our knowledge, HPAI A(H5N1) virus, clade 2.3.4.4b, has not been reported previously in alpacas.

An 18-mo-old Aberdeen Angus steer was unable to rise without assistance; and, when standing, the steer walked with flexed forelimbs. Due to the poor prognosis, it was euthanized and autopsied. Grossly, the cervical spinal cord was markedly enlarged at C5-C6 by a yellow, soft, well-demarcated nodule that affected ~70% of the parenchyma. Microscopically, the expansive, multinodular, unencapsulated neoplasm affected mostly the white matter and consisted of 2 distinct cell populations. Small, pleomorphic cells with scant cytoplasm predominated; nuclei were positive for oligodendrocyte transcription factor 2 (OLIG2) and cytoplasm was negative for glial fibrillary acidic protein, compatible with oligodendrocytes. A second population of large round cells with abundant cytoplasm had positive cytoplasmic staining for S100 protein and synaptophysin (SYN), compatible with mature neurons. We diagnosed a spinal cord ganglioglioma in this steer based on histologic features and OLIG2 and SYN immunolabelling.

Bovine botulism is a lethal disease caused by Clostridium botulinum neurotoxins (BoNT). In cattle, the most frequent form of this disease in several South American countries and elsewhere is caused by BoNT type D, which has been associated with phosphorus deficiency, leading to pica and osteophagy. An outbreak of botulism occurred in a fully vaccinated 600-steer herd of cattle. The cattle were grazing on native pasture in a paddock in which several decomposing animal carcasses were found; the animals had performed osteophagy. The first 2 deaths were recorded in November 2016, and the number of fatalities increased to 84 through April of 2017. All the cases had similar clinical signs, which were consistent with botulism. The affected animals had hypophosphatemia and rear-leg weakness, ataxia, progressive flaccid paralysis of several muscles, recumbency, and death. Autopsies were performed on 3 animals; gross findings included hydropericardium, congestion of the cerebellum, and bone fragments and stones in the rumen and reticulum. Botulism was confirmed in the 3 animals by detecting BoNT type D by mouse bioassay. A large outbreak of botulism in vaccinated cattle associated with phosphorus deficiency and osteophagy has not been reported previously in Argentina, to our knowledge. Our case demonstrates that, even in vaccinated herds, rigorous carcass management is essential to reduce the risk of environmental contamination and to prevent fatal botulism outbreaks, especially in phosphorus-deficient areas. Improved reporting of similar cases is vital to refine prevention strategies and reduce the economic impact of the disease.