Nipah virus (NiV) infection is a viral disease caused by a Henipavirus, belonging to the Paramyxoviridae family, responsible for a zoonosis. The course of the disease can be very serious and lead to death. NiV natural hosts are fruit bats (also known as megabats) belonging to the Pteropodidae family, especially those of the Pteropus genus. Natural infection in domestic animals has been described in farming pigs, horses, domestic and feral dogs and cats. Natural NiV transmission is possible intra-species (pig-to-pig, human-to-human) and inter-species (flying bat-to-human, pig-to-human, horse-to-human). The infection can be spread by humans or animals in different ways. It is peculiar how the viral transmission modes among different hosts also change depending on the geographical area for different reasons, including different breeding methods, eating habits and the recently identified genetic traits/molecular features of main virus proteins related to virulence. Outbreaks have been described in Malaysia, Singapore, Bangladesh, India and the Philippines with, in some cases, severe respiratory and neurological disease and high mortality in both humans and pigs. Diagnosis can be made using different methods including serological, molecular, virological and immunohistochemical methods. The cornerstones for control of the disease are biosecurity (via the correct management of reservoir and intermediate/amplifying hosts) and potential vaccines which are still under development. However, the evaluation of the potential influence of climate and anthropogenic changes on the NiV reservoir bats and their habitat as well as on disease spread and inter-specific infections is of great importance. Bats, as natural reservoirs of the virus, are responsible for the viral spread and, therefore, for the outbreaks of the disease in humans and animals. Due to the worldwide distribution of bats, potential new reports and spillovers are not to be dismissed in the future.

West Nile virus (WNV) is an important zoonotic pathogen belonging to the Flaviviridae family, which is endemic in some areas and emerging in others. WNV is transmitted by blood-sucking mosquitoes of the genus Culicoides, Aedes, and Anopheles, and the infection can cause different clinical symptoms. The most common and benign illness in humans is West Nile fever (WNF), but a lethal neurological disease (WNND), related to the neuro-invasiveness of WNV lineage 2, represents the highest health risk of WNV infection. The neuro-clinical form is recognized in mammals (land and cetaceans), particularly in humans (elderly or immunosuppressed) and in horses, avian species, and wildlife animals ranging free or in a zoological setting. This review highlights the most relevant data regarding epidemiology, virology, pathogenesis and immunity, clinical signs and differential diagnosis, pathology and imaging, histopathology and gross pathology, economic impact, influence of climate change, and surveillance of WNV. Climate change has favored the wide spread of WNV in many areas of the globe and consequent One-Health and Eco-Health emergencies, influencing the health of human beings, animals, and ecosystems.

An 8-month-old intact male domestic shorthair cat was referred to the Emergency Service of the Veterinary Teaching Hospital (VTH) of the Department of Veterinary Science of the University of Parma (Italy) from the Parma municipal multi-cat shelter, during the winter season (January 2023), for lethargy, anorexia, hypothermia, and hypoglycemia. At the VTH, upon cardiologic examination, an increase in heart rate, under normal blood pressure conditions, was detected. Signalment, clinical history, basal metabolic panel (BMP), ultrasound investigations, and cytological findings were all consistent with a diagnosis of feline infectious peritonitis (FIP). FIP was confirmed in the effusive abdominal fluid by a molecular genetic test (real-time PCR for feline coronavirus RNA). The molecular genetic investigation also detected an FCoV S gene single-nucleotide mutation: biotype M1058L. At necropsy, an effusive collection was recorded in the abdomen, thoracic cavity, and pericardium sac. White parenchymal nodules, of about 1 mm diameter, were found on the surface and deep in the lungs, liver, kidneys, and heart. Histopathology revealed the typical FIP pyogranulomatous vasculitis and IHC confirmed the presence of the FIP virus (FIPV) antigen. The most relevant histopathological finding was the myocarditis/myocardial necrosis associated with the presence of the S gene-mutated FCoV (M1058L biotype). This is the first case of myocarditis in a cat positive for the FCoV/FIP M1058L biotype. Further studies are necessary to support the mutated FCoV M1058L biotype, as an uncommon, but possible, causative pathogen of myocarditis in FCoV/FIP-positive cats. Studies including several FCoV/FIP M1058L-positive cases could allow us to make a correlation with heart gross pathology, histopathology, and immunolocalization of the FCoV/FIP M1058L biotype in the myocardium. The investigation will potentially allow us to determine the effective tropism of the FCoV/FIP M1058L biotype for myocardiocytes or whether myocardiocyte lesions are evident in the presence of concomitant causes related to the patient, its poor condition, or external environmental distress such as cold season, and whether the aforementioned concomitant events are correlated.

The review deals with the current knowledge on the global panzootic spread of highly pathogenic avian influenza viruses (HPAIVs), with an emphasis on the H5N1 clade 2.3.4.4b virus. It describes the viral structure, replication, pathotypes and molecular determinants of host range, including sialic-acid receptor usage and key genetic mammalian-adaptation markers (PB2-E627K and PB2-D701N mutations). The host spectrum nowadays extends from wild waterfowl and poultry including seabirds, terrestrial and marine mammals and, based largely on experimental studies or molecular detection, reptiles, amphibians, and fish. Recently, the H5N1 clade 2.3.4.4b virus has shown marked tropism for lactating mammary epithelium in dairy cattle, with virions shed in raw milk. The review reports epidemiology, geographical expansion, clinical presentation, pathogenesis and pathology, diagnosis, immune responses and vaccination approaches across species. It also analyses European Union (EU) and Italian regulatory frameworks, surveillance strategies and biosecurity measures from a One-Health perspective. The review highlights how climate change, wildlife–livestock interfaces, intensive farming and global trade favor viral persistence and genomic reassortment and concludes by stressing strategic actions to limit further host adaptation and panzootic/pandemic risks.

Background: Vulvar squamous cell carcinoma (VSCC) has been recently associated with Equus caballus papillomavirus type 2 (EcPV2) infection. Still, few reports concerning this disease are present in the literature. Objective: To describe a case of naturally occurring EcPV2‐induced VSCC, by investigating tumour ability in undergoing the epithelial‐to‐mesenchymal transition (EMT). Study design: Case report. Methods: A 13‐year‐old Haflinger mare was referred for a rapidly growing vulvar mass. After surgical excision, the mass was submitted to histopathology and molecular analysis. Histopathological diagnosis was consistent with a VSCC. Real‐time qPCR, real‐time reverse transcriptase (RT)‐qPCR and RNAscope were carried out to detect EcPV2 infection and to evaluate E6/E7 oncogenes expression. To highlight the EMT, immunohistochemistry (IHC) was performed. Expression of EMT‐related and innate immunity‐related genes was investigated through RT‐qPCR. Results: Real‐time qPCR, RT‐qPCR and RNAscope confirmed EcPV2 DNA presence and expression of EcPV2 oncoproteins (E6 and E7) within the neoplastic vulvar lesion. IHC highlighted a cadherin switch together with the expression of the EMT‐related transcription factor HIF1α. With RT‐qPCR, significantly increased gene expression of EBI3 (45.0 ± 1.62, p < 0.01), CDH2 (2445.3 ± 0.39, p < 0.001), CXCL8 (288.7 ± 0.40, p < 0.001) and decreased gene expression of CDH1 (0.3 ± 0.57, p < 0.05), IL12A (0.04 ± 1.06, p < 0.01) and IL17 (0.2 ± 0.64, p < 0.05) were detected. Main limitations: Lack of ability to generalise and danger of over‐interpretation. Conclusion: The results obtained were suggestive of an EMT event occurring within the neoplastic lesion.

Canine cognitive dysfunction (CCD) is a common age-related neurodegenerative disorder in dogs that shares several pathological and clinical features with human Alzheimer’s disease (AD). In both species, β-amyloid (Aβ) accumulates within the brain parenchyma and cerebral vessel walls and is associated with synaptic loss, oxidative stress, mitochondrial dysfunction, and chronic neuroinflammation, ultimately leading to progressive cognitive decline. Increasing evidence indicates that impairment of brain clearance mechanisms, particularly the glymphatic system, represents a central pathogenic mechanism in both CCD and AD. The glymphatic system is a glia-dependent perivascular network involved in the clearance of Aβ and other metabolic waste products from the brain. Its function declines with aging, vascular disease, and astrocytic alterations, including changes in aquaporin-4 distribution. Reduced glymphatic and periarterial drainage promotes the retention and aggregation of Aβ and tau proteins. Compared with AD, tau pathology in CCD is generally less extensive, supporting the interpretation of CCD as an Aβ-predominant condition and a partial pathological analog of Alzheimer’s disease. Clinically, CCD is characterized by a constellation of behavioral changes including, disorientation, altered social interactions, sleep–wake cycle disturbances, a loss of housetraining, changes in activity levels, and increased anxiety, commonly summarized by the DISHAA acronym. Overall, CCD represents a valuable spontaneous large-animal model for investigating neurodegenerative mechanisms and clearance-related therapeutic targets relevant to both veterinary and human medicine.