The poultry industry is a critical source of affordable protein worldwide; however, it faces continuous threats from various poultry diseases that significantly impact public health, economic stability, and food security. Knowledge of and examination of the transmission routes, risk factors, and environmental survival characteristics of the most important pathogens affecting poultry populations, as well as the importance of strict biosecurity, are pivotal. Transmission routes are split into direct and vector-borne pathways, and indirect ways, which include infections via contaminated surfaces and vector-borne pathways, including insects and rodents. Avian influenza virus and Newcastle disease virus spread through respiratory droplets, and their transmission risk increases with increasing stocking density. While other pathogens (e.g., infectious bursal disease virus and Salmonella spp.), to persist long-term in the environments, for example, feed and litter, increasing the probability to persist long-term in the environments, for example, feed and litter, increasing the probability of infection. The long-term resilience of pathogens in multiple pathogens in various environmental conditions highlights the role of biosecurity, sanitation, and hygiene controls in preventing disease outbreaks. High stocking density in production systems, suboptimal ventilation, and inadequate biosecurity controls further increase transmission risks. This paper summarizes important disease transmissions and reinforces the need for strict biosecurity protocols and routine health monitoring to prevent the spread of pathogens within and beyond poultry facilities. These strategies can support safe poultry production, address growing global demand, and ensure food safety and public health.

Air pollution is a foremost public health problem worldwide. The pulmonary effects of air pollution have been well established for decades, and substantial epidemiological evidence is consistently showing that both acute and chronic exposure to air pollution is linked to cardiovascular morbidity and mortality. The underlying cause for this link is, however, still unknown, and many questions remain open. Most of the epidemiological studies focusing on health consequences of exposure to urban air used data from air monitoring stations or—when applying personal sampling or monitoring—measured a limited number of components to assess the exposure. On the other hand, studies conducting a decent exposure characterization and measuring a relatively large number of components with personal sampling had little or no focus on the effects and investigated only a few biomarkers. The number of research studies on this topic is huge, but at the same time, it seems as if there was no need for a comprehensive examination of the effects of urban air pollution on health. Researchers and research supporting organizations, in their fascination with the search for “novelty” and “beyond state-of-the-art”, do not seem to be aware of that they will never be able to assemble the whole picture from the puzzle pieces of research activities focusing only on certain aspects. Without a comprehensive investigation, we might never be able to answer such questions as (i) which of the urban air pollutants are forerunners in causing health effects, especially cardiovascular effects? (ii) Which biomarkers have the best predictor performance in early effects? (iii) Are there biomarkers or combinations of biomarkers that can help determine the degree of individual susceptibility and sensitivity and the dependence of these by different factors (e.g., age, gender, and physical activity)? The authors of this article aim to go through the already investigated—at the same time, essential—elements of the topic and propose a more comprehensive study, which, of course, can be expanded, debated, and improved.

Background: Avian influenza (AI), caused by orthomyxoviruses, is a globally significant disease affecting avian and non-avian species. It manifests in two variants, according to the two biovariants of the virus differentiated as highly pathogenic avian influenza (HPAI) and low pathogenic avian influenza (LPAI) strains, both of which compromise animal welfare, reduce productivity, and cause substantial economic loss. The zoonotic potential of HPAI strains, particularly the currently dominant clade 2.3.4.4b, raises concerns about public health and epidemic risks. This review assesses the results of current vaccine trials targeting HPAI clade 2.3.4.4b, emphasizing these studies because most outbreak strains in domestic poultry currently belong to this dominant clade. Methods: Multiple scientific databases comprised reports of research trials on vaccine efficacy against HPAI clade 2.3.4.4b. The Boolean term “Clade 2.3.4.4b AND vaccine” was entered into the following databases: PubMed, PubAg, Scopus, Cochrane Library, and ScienceDirect. Results: The resulting papers were analyzed. Studies revealed that antigenic similarity between vaccine and field strains enhances protective efficacy (PE), reduces viral shedding, and improves hemagglutination inhibition titers. While multivalent vaccines showed potential, results were inconsistent and varied depending on strain compatibility. Single-dose vaccines may provide sufficient PE for poultry, though ducks and geese often require multiple doses, and long-term PE is yet unknown. It was discovered that vector vaccines can provide appropriate PE against clade 2.3.4.4.b. Conclusions: Further analysis is needed as their effects may be short-lived, and subsequent doses may be required. Limited research exists on the long-term efficacy of these vaccines and their effectiveness in many avian species. Addressing these gaps is crucial for optimizing vaccination strategies. A re-evaluation of vaccination strategies is recommended but essential to implement adequate biosecurity measures on in poultry farms. This review synthesizes current evidence and may assist veterinarians and authorities in deciding whether to apply or license vaccines to reduce economic losses caused by AI.

Background: Escherichia coli is a bacterial species widely distributed among mammals and avian species, and also a member of the normal intestinal microbiota. However, some E. coli strains of different pathotypes can cause disease in both humans and animals. Atypical enteropathogenic E. coli (aEPEC) can infect both animals and humans or influence the severity of other ongoing infections. Results: In the present study, a total of 332 samples were collected from ducks, geese, turkeys, chickens, and pigeons from the Hungarian Veterinary Diagnostic Directorate, two slaughterhouses, two pigeon keepers and one backyard chicken farm. E. coli was isolated and verified from 319 samples. The isolates were screened by PCR for diarrheagenic E. coli pathotypes. Altogether seven atypical enteropathogenic E. coli (aEPEC) strains were identified: two from four-week-old dead turkeys, two from force-fed geese, and three from pigeons. No further pathotypes were identified in the collection. The atypical EPEC strains were classified phylogenetically to B1, B2, and F, and four out of the seven aEPEC isolates proved to be multidrug resistant. Serotypes of aEPEC strains were uniform collected from same farms and showed diversity between their origins with O76, O145, O109 serogroups. Conclusions: This is the first report in the literature about aEPEC in goose (Anser anser domestica). Furthermore, this is the first isolation of aEPEC from turkeys and pigeons in Hungary. The uneven distribution of aEPEC in different age groups of poultry suggests that aEPEC disappears with growing up, but stress (e.g.: force-feeding) and concurrent diseases might promote its reappearance in the intestine.

Bisphenol A (BPA) is a synthetic compound utilized in industry for the production of various plastics. BPA penetrates into the environment and adversely affects living organisms. Therefore, the influence of various BPA dosages on the neurochemical characteristics of nerve fibers located in the aortic branch wall was investigated in this study utilizing a double immunofluorescence method. It was found that BPA in concentration of 0.5 mg/kg body weight/day causes a clear increase in the density of nerves within aortic branch walls immunoreactive to cocaine- and amphetamine-regulated transcript (CART), calcitonin gene-related peptide (CGRP), neuronal isoform of nitric oxide synthase (nNOS), pituitary adenylate cyclase-activating peptide (PACAP), and vasoactive intestinal polypeptide (VIP). Nerves containing galanin (GAL) and/or somatostatin (SOM) did not change when BPA was introduced into the system. Changes noted after administration of BPA at a dose of 0.05 mg/kg body weight/day were less visible and concerned fibers immunoreactive to CART, CGRP, and/or PACAP. The obtained results show that BPA affects the neurochemical coding of nerves in the aortic branch wall. These fluctuations may be the first signs of the influence of this substance on blood vessels and may also be at the root of the disturbances in the cardiovascular system.

In this study, we investigated the bioaccumulation of 17 heavy metals—titanium, vanadium, chromium, manganese, iron, cobalt, nickel, copper, zinc, arsenic, selenium, molybdenum, antimony, cadmium, tin, mercury, and lead—in the liver and kidney tissues of the least weasel, based on samples (n = 129) collected from adjacent intensive agricultural environments in Hungary and Austria. To explore the structure of the bioaccumulation data, principal component analysis (PCA) was performed. The PCA score plot based on national-level elemental profiles revealed no differentiation between Austria and Hungary. In contrast, a clear and unambiguous distinction was observed between the two examined tissues within individuals for Ti, Mn, Fe, Co, Zn, Se, Mo, Cd, and Hg (p < 0.001), as well as for Pb (p < 0.05). The biological relevance of the accumulation results was adjusted using the MCID approach. As heavy metal accumulation in the least weasel has not yet been investigated, our results could only be compared with concentrations reported for predatory mammals occurring in similar habitats. Based on the relevant literature, we highlight predominantly anthropogenic exposure pathways affecting agroecosystems—organic and mineral fertilizers, plant protection products, wastewater, and fossil fuels—which underscore the necessity of regular biomonitoring studies in agricultural landscapes.