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Foot-and-mouth disease (FMD), a highly contagious viral disease caused by FMD virus (FMDV) that threatens Egypt’s livestock industry. FMDV causes severe economic losses in the livestock, with restriction of international trade from endemic regions. Surveillance for FMDV serotypes circulating in Egypt is urgently needed to assess the epidemiological situation in the country. FMD outbreaks reported in Egypt in between December 2016 and January-March 2017. A cross-sectional study was conducted to identify the FMDV serotypes responsible for the outbreaks and to collect information on the virus’s morphopathological effects. Postmortem tissue and clinical samples (oral swabs, vesicular fluids from ruptured vesicles, and blood) were collected from recently deceased and infected animals. Pathological examination revealed classical FMD lesions as vesicular and erosive lesions on epithelial tissues with non-suppurative lymphoplasmacytic myocarditis. Phylogenetic and sequencing analyses demonstrated that FMDV serotype O, EA-3 topotype, VP1 is the prevalent serotype responsible for the pathological alterations and the high mortality in young calves, adult cattle, and water buffalo. The outcomes indicate continuous mutations in the circulating FMDV, which result in the occasional failure of vaccination. Based on these findings, extensive continuous monitoring and serotyping of the existing circulating FMDV isolates and regular vaccination with reevaluation of the currently used vaccine in Egypt are recommended to prevent the recurrence of such outbreaks.

Background Cadmium is a highly toxicant heavy metal that poses serious risks to aquatic organisms, animals, and humans. Recent studies have investigated using biological chitosan nanoparticles (Bio-CHNPs) as a potential solution to alleviate the harmful effects of Cd exposure, particularly in aquaculture. Bio-CHNPs have gained attention for their applications in drug delivery and biomedical research, indicating their potential utility in addressing environmental toxicity. Objective This research aims to explore the effectiveness of Bio-CHNPs in mitigating cadmium chloride (CdCL 2 ) toxicity in African catfish ( Clarias gariepinus). Methods One hundred and twenty (n = 120) catfish were divided into 4 groups; G1 (control); G2, intoxicated with 10% LC 50 of CdCL 2 ; G3 received 3 g/kg of Bio-CNPs; G4, treated with 10% LC 50 of CdCL 2 and Bio-CNPs 3 g/kg feed. Results CdCl 2 exposure resulted in severe liver, intestine, and kidney damage, which was evidenced by alterations in biochemical parameters, hormonal imbalance, DNA damage, and micronucleus formation. Antioxidant defense mechanisms were compromised, as the activities of Superoxide Dismutase (SOD), Total Antioxidant Capacity (TAC), and Catalase (CAT) were reduced. mRNA expression levels of inflammatory cytokines such as IL-1β, IL-8, and LBP were also significantly elevated following CdCl 2 exposure. Conversely, Bio-CHNPs treatment showed antioxidant and anti-inflammatory effects, greatly lowering the biochemical, genotoxic, and histopathological effects induced by CdCl 2 . Conclusion The outcomes of this study are indicative of the potential of Bio-CHNPs as a promising aquaculture feed supplement, with a dual advantage of antagonizing the toxicity of environmental pollutants like Cd and imparting antioxidant and immunomodulatory effects. Bio-CHNP supplementation can be a viable strategy for remedying aquatic environmental heavy metal pollution, with the ultimate safeguarding of human health and ecosystem balance.

[This corrects the article DOI: 10.3389/fphar.2024.1394557.].

Introduction: Isoproterenol (ISO) is regarded as an adrenergic non-selective β agonist. It regulates myocardial contractility and may cause damage to cardiac tissues. Alchemilla vulgaris (AV) is an herbal plant that has garnered considerable attention due to its anti-inflammatory and antioxidant bioactive components. The present investigation assessed the cardioprotective potential of AV towards ISO-induced myocardial damage. Methods: Four groups of mice were utilized: control that received saline, an ISO group (85 mg/kg, S.C.), ISO + AV100, and ISO + AV200 groups (mice received 100 or 200 mg/kg AV orally along with ISO). Results and discussion: ISO induced notable cardiac damage demonstrated by clear histopathological disruption and alterations in biochemical parameters. Intriguingly, AV treatment mitigates ISO provoked oxidative stress elucidated by a substantial enhancement in superoxide dismutase (SOD) and catalase (CAT) activities and reduced glutathione (GSH) content, as well as a considerable reduction in malondialdehyde (MDA) concentrations. In addition, notable downregulation of inflammatory biomarkers (IL-1β, TNF-α, and RAGE) and the NF-κB/p65 pathway was observed in ISO-exposed animals following AV treatment. Furthermore, the pro-apoptotic marker Bax was downregulated together with autophagy markers Beclin1 and LC3 with in ISO-exposed animals when treated with AV. Pre-treatment with AV significantly alleviated ISO-induced cardiac damage in a dose related manner, possibly due to their antioxidant and anti-inflammatory properties. Interestingly, when AV was given at higher doses, a remarkable restoration of ISO-induced cardiac injury was revealed.

Subcutaneous nodular onchocercosis was detected and investigated in 17 Japanese Sika deer ( Cervus nippon ), captured in Gifu and Shiga Prefectures/Japan, in the period between 2016 and 2017. The worms were found in all the seventeen deer within characteristics subcutaneous nodules dispersed mainly in the back (especially in the lumbar region and flanks), with few scattered nodules were located at the forelimbs and neck. The all collected nodules were examined stereo-microscopically. The parasites were extracted from the nodules and identified through morphological and histopathological examinations. Molecular identification through sequencing of the following genes; internal transcribed spacer subunit 2 (ITS2)–28S ribosomal RNA (28S rRNA), cytochrome c oxidase subunit 1 (cox1) and mitochondrially encoded NADH dehydrogenase subunit 2 (NAD2) were performed. The histopathological, molecular and phylogenetic analysis demonstrated that, the filarial nematode isolated from Gifu and Shiga Prefectures in Japan is O. flexuosa . This is the first report about presence of O. flexuosa in Japanese Sika deer ( Cervus nippon ) in Gifu and Shiga Prefectures.

Heavy metals including cadmium (Cd) are one of the major persistent and non-biodegradable wastewater pollutants. However, Cd reaches the aquatic ecosystem via industrial and agricultural waste discharges and causes serious deterioration in the welfare status of aquatic animals. The use of feed supplements with immune-stimulants to mitigate the toxic influences of heavy metals including Cd is a much more intriguing point. Thus, the current experiment used the bio-synthetized chitosan nanoparticles derived from Bacillus subtilis (Bs-CNPs) as a feed supplement and evaluated its ameliorative impacts on the growth and welfare status of Cd-intoxicated Nile tilapia ( Oreochromis niloticus ). Bifactorial design (3 Bs-CNPs levels × 3 Cd levels) was used in the current study where Nile tilapia fingerlings (58–63 g) were fed on 0.0, 2, and 4 g Bs-CNPs/kg feed alongside with exposing to 0.0, 0.392, and 0.784 mg Cd/L for 60 days to represent nine treatments as follows: T1: control group (no Cd exposure; no Bs-CNPs supplement); T2 and T3: fish were intoxicated with 0.784 and 0.392 mg Cd/L, respectively; T4 and T5: fish fed on 2 and 4 g Bs-CNPs/kg feed, respectively; T6 and T7: fish were fed on 2 g Bs-CNPs/kg feed along with exposure to 0.784 and 0.392 mg Cd/L, respectively; and T8 and T9: fish were fed on 4 g Bs-CNPs/kg feed along with exposure to 0.784 and 0.392 mg Cd/L, respectively. It is noted that the Cd-intoxicated fish exhibited significant retardation in growth performance and digestive enzyme activities with a decline in their survival rate compared to the control group (T1). The results also revealed that exposing fish to Cd toxicity alone with no feed supplement (T2 and T3) experienced abnormal clinical signs and behavioral changes. Compared with the control group (no Cd with no Bs-CNPs), highest values of cortisol, glucose, aspartate and alanine aminotransferase, and acetylcholine esterase activity were found in fish fed on the control diet along with exposure to 0.784 mg Cd/L. Higher Cd restudies in liver, intestine, gills, kidney, and muscles tissues were detected in fish exposed to 0.784 mg Cd/L alone and the sequence order of Cd levels in different fish organs is intestine > gills > liver > kidney > muscles. Remarkable pathological alterations in hepatic and intestinal tissues were also observed. On the other hand, feeding Nile tilapia on Bs-CNPs-enriched diets alone with no Cd exposure enhanced their growth performance, digestive enzyme activities, and hematological parameters with no Cd residues in fish organs. Interestingly, feeding the Cd-intoxicated fish on diets with Bs-CNPs (4 g/kg feed) returned their growth, digestive enzymes, hematological, and biochemical parameters to approximate those of the control group. Furthermore, these treatments showed histopathological alteration recovery in the intestine and liver tissues is similar to those in the control group (no Cd with no Bs-CNPs). Fish fed on Bs-CNPs levels with no Cd exposure showed no Cd residues in different fish organs. The Cd levels in different organs of fish exposed to 0.392 mg Cd/L along with feeding on Bs-CNPs (4 g/kg feed) were lower than those in Cd-exposed fish treatments. Consequently, the current study evoked that feeding Nile tilapia fingerlings on Bs-CNPs (4 g/kg feed) could enhance their growth performance and protect the fish from the Cd toxicity that may occur in the aquatic ecosystem.

Ulcerative colitis (UC) is a chronic colonic inflammation with a significant health hazard. Aspergillus awamori (A. awamori ) is a microorganism with various bioactive compounds with natural antioxidant and anti-inflammatory properties. The present work aimed to elucidate the protective and therapeutic effects of varying concentrations of A. awamori against acetic acid (AA)-induced ulcerative colitis (UC) in rats. Nine groups of albino male rats were established: a control negative group (G1), a control positive group (G2,AA), and preventive protocol groups (including G3A, G4A, and G5A) that received 100 mg, 50 mg, and 25 mg/kg b.w, respectively, of A. awamori orally and daily from the 1st day of the experiment and for 7 consecutive days. Then, they were subjected to one dose of AA intrarectally on day 8th. G3B, G4B, and G5B were termed as curative protocol groups that received one dose of AA on day 8th and then administered 100 mg, 50 mg, and 25 mg/kg b.w. of A. awamori, respectively, on day 9th and continued receiving these doses daily until day 16th. Rats in the AA group exhibited marked histopathological alterations of the distal colon, with an exaggeration of the DAI. In addition, a remarkable increase in oxidative stress was represented by the elevation of MDA and NO levels with a decline in SOD and GPx activities. In addition, upregulation of TNF-α, IL-6, and IL-1β mRNA expressions and downregulation of Muc2 and Nrf2 levels were detected. Unambiguously, a remarkable anti-inflammatory effect was noticed either in A. awamori prevented or treated groups expounded by reducing and regulating TNF-α, IL-6, and IL-1β with improved pathological lesion scoring. The Muc2 , Nrf2 , and bcl-2 gene levels were upregulated and restored also. In summary, the findings in this work reveal that A. awamori supplementation successfully alleviated the UC induced by AA, which had a better effect when administered before colitis induction.

The prevalence of Gallibacterium anatis in poultry production has increased over the last two decades. However, only a few studies have explored the pathogenicity of this bacterium in commercial layer chickens. This trial studied the aspects of the pathogenicity of a Gallibacterium anatis biovar haemolytica local Egyptian isolate (previously registered as strain B14 with GenBank accession no. KJ026147). We used 500 base pairs of a 16S ribosomal RNA gene and the 16S-23S ribosomal RNA intergenic spacer, partial sequence in an experimental infection trial in commercial White Shaver layer chickens aged 19 wk. The hens were divided into three groups of 40 birds each. The hens in Groups 1 and 2 were experimentally infected through the intranasal (IN) and intravenous (IV) routes, respectively, with a dose of 0.2 ml/bird containing 1.2 × 109 colony-forming units/ml. In contrast, Group 3 was kept as a noninfected control group. Both IN and IV infections resulted in a delayed egg laying for 1 wk and a significant (P ≤ 0.05) drop in egg production by 7.81% and 10.28% compared with the control group over 7 wk. Severe lesions in the form of hemorrhagic pneumonia, catarrhal tracheitis, ovarian follicle and oviductal regression, and septicemia were evident on necropsy, demonstrating the pathogenicity of G. anatis as a primary pathogen.