SUMMARY: Leptospirosis is a zoonosis of worldwide distribution, caused by infection with pathogenic spirochaetes of the genus Leptospira. The wild boar (Sus scrofa), an important hunting species in Europe, seems to play a significant role in the epidemiological cycle of leptospirosis. A total of 101 serum samples from wild boar hunted in Northern Portugal were analysed for leptospiral antibodies detection by microscopic agglutination test. Sera were collected during hunting seasons (2011–2013) and tested with 17 different pathogenic serovars of Leptospira. Antibodies against nine serovars were detected in 66 (65·4%) of these sera. Serovars Tarassovi and Altodouro exhibited the highest seroreactivity rates (23·8% and 16·8%, respectively), followed by Autumnalis (7·9%) and Bratislava (6·9%). Age and district of origin were found to be risk factors for the presence of leptospiral antibodies in contrast to gender. From a One Health perspective, this study revealed that wild boar should be considered as a potential source of leptospirosis dissemination for humans and animal species (domestic and wild) in shared environments, particularly in the Trás-os-Montes region.

Introduction: The olfactory system acts as an interface between the environment and the brain. Its direct neural connection makes it a target for xenobiotics and a suitable model for studying olfactory dysfunction and related neurotoxic effects. This study aimed to characterize an animal model of olfactory dysfunction induced by nose-to-brain (NTB) delivery of vanadium pentoxide (V₂O₅).Methods: Rats received 182 or 273 μg intranasally, thrice weekly over 4 weeks, followed by behavioral, histological, and biochemical analysis of the olfactory epithelium (OE), olfactory bulbs (OBs), and hippocampus.Results: Behavioral tests showed significant olfactory deficits, longer latencies, and reduced investigation times in exposed groups. Histological analysis revealed coagulative necrosis in the OE, disrupted cellular organization, reduced number and size of OB glomeruli, and hippocampal neuronal loss with gliosis. Immunohistochemistry revealed increased proliferating cell nuclear antigen (PCNA) expression in the OE, dopaminergic neuron loss and astroglial proliferation in the OB, and hippocampal astroglial proliferation at the highest dose. Myelin basic protein (MBP) expression remained unchanged. Oxidative stress markers were largely unaltered, except for increased superoxide dismutase (SOD) in OBs and glutathione S-transferase (GST) in the hippocampus, especially at the high dose.Discussion: The results reveal dose-dependent vanadium-induced neurotoxicity in the olfactory system. The higher dose induced pronounced structural damage, neuroinflammation, and oxidative stress, resulting in olfactory and cognitive impairments relevant to advanced olfactory dysfunction and neurodegeneration. The lower dose induced milder yet significant effects, supporting its use in early-stage dysfunction studies. This NTB-based model offers a valuable tool for investigating olfactory dysfunction mechanisms in toxicological and neurodegenerative contexts.

Pseudogymnoascus destructans(Pd), the emergent fungus causing bat “White-Nose Syndrome”, responsible for ∼6 million mortalities in the United States (US), is thought to expand clonally in North America and Europe. Presence of distinct mating-types in Europe led to numerous research attempts searching for population sexuality worldwide. This study not only presents the first evidence of genetic recombination in Pd but also detects recombination in Pd genotype data generated by previous studies in Europe and North America, through clone-corrected linkage disequilibrium analysis. Portuguese and other European populations are apparently reproducing through sex between two mating-types. Seeming parasexual recombination in the invasive single mating-type US population rings alarms for the North American bat populations and deserves urgent attention. This study emphasizes on clone-correction in linkage disequilibrium analysis.One Sentence Summary: Clone-correction yielded signs of elusive recombination in the global “clonal” populations of white-nose syndrome pathogen.

The intranasal route enables direct delivery of multiple substances from the nose to the brain, through olfactory and trigeminal pathways, bypassing the blood–brain barrier and avoiding systemic absorption. Despite the potential of this route, the various administration approaches make data reproducibility and interpretation challenging, emphasizing the necessity to establish a consistent methodology. Considering this, the aim of our study was to assess and compare the distribution of two dye volumes (30 µl and 50 µl) in the nasal cavity of rat cadavers. We employed three distinct methods of intranasal delivery: nose drops, by pipette tip, or cannula inserted into the nasal cavity. The results indicated that for both volumes, using the nose drops and the pipette tip methods, the dye dispersion occurred mainly in the vestibule, respiratory and olfactory regions, without reaching the olfactory bulbs. Using the cannula method, the deposition predominantly occurred in the respiratory and olfactory regions, with the dye reaching 66.7% and 100% of the olfactory bulbs, respectively, to low and high volume. Furthermore, the results demonstrated differences between the two volumes, in the pharynx, larynx, trachea, septal window, and incisive papilla, where an increased dye presence was observed with the 50 µl instillation across all three methods. According to our results, the intranasal delivery with a cannula was the most effective method for dye deposition in the olfactory region. However, further studies in live animals will be necessary to determine and refine the administration method that consistently allows specific deposition in the olfactory system.

Olfactory dysfunction is increasingly recognized as an important consequence of exposure to environmental toxicants, owing to the anatomical and functional characteristics of the olfactory system, which allow inhaled toxicants to reach the central nervous system via the olfactory pathway. Experimental rodent models provide valuable tools for investigating the mechanisms underlying toxicant-induced olfactory injury under controlled conditions. In particular, intranasal vanadium exposure has emerged as a relevant experimental approach because it reproduces an environmentally relevant route of exposure while inducing pathological changes throughout the olfactory system. This review integrates current knowledge derived from experimental rodent models of intranasal vanadium exposure, covering the anatomy and physiology of the olfactory system, intranasal delivery strategies, the cellular and molecular mechanisms underlying vanadium-induced injury, and the associated histopathological, biochemical, behavioural and functional alterations. Vanadium-induced injury is characterized by oxidative stress, mitochondrial dysfunction, neuroinflammation, dysregulation of intracellular signalling pathways, and neuronal degeneration, leading to structural and functional alterations throughout the olfactory pathway. Finally, the review identifies current knowledge gaps regarding olfactory epithelial regeneration and functional recovery following toxic injury and highlights priorities for future research to improve experimental models of environmentally induced olfactory dysfunction.