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Dog circovirus (DogCV) was identified in an outbreak of enteritis in pups in Italy. The disease was observed in 6 young dachshunds pups of a litter from a breeding kennel and caused the death of 2 dogs. Upon full-genome analysis, the virus detected in one of the dead pups (strain Bari/411-13) was closely related to DogCVs that have been recently isolated in the USA. The present study, if corroborated by further reports, could represent a useful contribution to the knowledge of the pathogenic potential of DogCV and its association with enteritis in dogs.

Rotavirus (RV) is a leading pathogen causing diarrhea in children. In this study, a total of 51 fecal samples from children with RV enteritis, 29 post-treatment fecal samples, and 38 fecal samples from age-matched healthy controls were collected. Microbial DNA was isolated from the samples followed by high throughput Illumina sequencing targeting 16 S rRNA gene. Compared to the healthy group, the RV-infected group exhibited reduced microbial diversity. Both groups shared Firmicutes as the dominant phylum. Additionally, the abundance of Proteobacteria increased significantly in the RV-infected group. At the genus level, among the top 50 most abundant genera, 34 showed significant differences, with these differential genera correlating with certain clinical indicators such as dehydration levels and C-reactive protein (CRP). Notably, there were no significant differences in the microbiota before and after treatment in RV-infected children. Only 8.82% (3/34) of the differential genera in the post-treatment group showed a recovery trend towards the healthy state. This study enhances the understanding of how RV infection alters the gut microbiota structure in children and provides a scientific basis for improving clinical diagnosis and treatment strategies.

Feline bocavirus-1 (FBoV-1) was identified in cats from different households with hemorrhagic enteritis during outbreaks of an unusual clinical presentation of feline panleukopenia virus (FPLV) in Thailand. Use of polymerase chain reaction revealed the presence of the FBoV-1 DNA in several tissues, suggesting hematogenous viremia, with the viral nucleic acid, detected by in situ hybridization (ISH), was localized in intestinal cells and vascular endothelium of intestinal mucosa and serosa, and in necrosis areas primarily in various lymph nodes while FPLV-immunohistochemical analysis revealed viral localization only in cryptal cells, neurons, and limited to leukocytes in the mesenteric lymph node. Full-length coding genome analysis of the Thai FBoV-1 strains isolated from moribund cats revealed three distinct strains with a high between-strain genetic diversity, while genetic recombination in one of the three FBoV-1 strains within the NS1 gene. This is the first report identifying natural genetic recombination of the FBoV-1 and describing the pathology and viral tropism of FBoV-1 infection in cats. Although the role of FBoV-1 associated with systemic infection of these cats remained undetermined, a contributory role of enteric infection of FBoV-1 is possible. Synergistic effects of dual infection with FPLV and FBoV-1 are hypothesized, suggesting more likely severe clinical presentations.

Canine parvovirus (CPV) is the most important viral cause of acute canine enteritis leading to severe damage of the intestinal barrier. It has been speculated that dogs might develop chronic disorders after surviving CPV infection. However, no studies regarding the long-term implications of CPV infection have been published to date. The aim of this study was to evaluate whether dogs that have survived CPV infection will have an increased risk for developing chronic gastroenteritis, atopic dermatitis, or cardiac disease. Dogs that had been treated at the Clinic of Small Animal Medicine, LMU Munich, for CPV infection for which a follow-up of at least 12 months was available, were included in the study. Owners completed a questionnaire on the presence of chronic gastrointestinal and cutaneous signs, cardiac disease, and other potential disorders. An identical questionnaire was sent to owners of matched control dogs during the same time period. Seventy-one questionnaires of dogs with CPV infection and 67 of control dogs were analyzed. Significantly more CPV-infected dogs (30/71) compared to control dogs (8/67) had developed chronic gastrointestinal signs later in their lives (P < 0.001). No significant differences were observed regarding skin diseases (P = 1), cardiac problems (P = 0.160), or any other diseases (P = 0.173) later in life. Results of this study suggest that dogs that survive CPV infection have a significantly higher risk (odds ratio = 5.33) for developing a chronic gastrointestinal disease. Further prospective studies to identify the trigger for the development of chronic diarrhoea and possible targeted treatment strategies are needed.

Duck enteritis virus (DEV) may lead to vascular injury, gastrointestinal mucosal erosion, lymphoid organ injury, and Polyinosinic-polycytidylic acid (Poly I:C) has an antiviral effect by inducing low levels of interferon. The purpose of this study was to explore the pathogenesis of DEV-induced intestinal injury in ducks and to verify the therapeutic effects of different concentrations of Poly I:C. In this study, duck enteritis model was established by infecting healthy Pekin ducks with DEV. Duck intestinal tissues were extracted from normal control group, model group, and treatment group with different doses of Poly I:C. In vivo, HE and TUNEL staining were used to observe the morphological changes and apoptosis. In vitro, the proliferation and apoptosis of duck intestinal epithelial cells were evaluated by MTT assay, TUNEL staining, and flow cytometry. The results showed that Poly I:C protected ducks from DEV toxicity by improving intestinal morphology and inhibiting apoptosis. In addition, the antiviral effect of Poly I:C on DEV was found in a dose-dependent manner, with a more relatively obvious effect at a high dose of Poly I:C. All in all, these results demonstrated that Poly I:C played a vital role in the apoptosis induced by DEV in ducks and modest dose of Poly I:C treatment worked well and may provide important reference for the development of new antiviral drugs in the future.

Abstract Background The trace elements copper (Cu), zinc (Zn), and selenium (Se) have been the focus of research into their potential roles in the prognosis of gastrointestinal disorders in humans. Objective Evaluation of the predictive potential serum concentrations of Cu, Zn, Cu/Zn, Se, and cobalamin as possible prognostic indicators in dogs with parvoviral enteritis (CPV). Animals Client-owned dogs diagnosed with CPV (n = 20) and healthy controls (n = 10). Methods A case-controlled study. Serum concentrations of Cu and Zn were measured using a spectrophotometric method; serum Se levels were determined by mass spectrophotometry; and serum cobalamin concentrations were assessed using a chemiluminescent immunoassay method. The Mann–Whitney U test was employed to compare subgroup medians. Results Upon admission, surviving dogs with CPV (n = 10) exhibited higher serum Cu concentrations (median = 154.24; range = 60.15–188.46 μg/dL) and Cu/Zn ratios (median = 1.52; range = 0.67–2.45), alongside lower serum Zn concentrations (median = 88.05; range = 51.3–129.2 μg/dL) and cobalamin levels (median = 252.5; range = 111–396 pg/mL), compared to the control group (Cu, median = 72.12; range = 47.04–90.26 μg/dL), Zn (median = 184.2; range = 73.0–262.7 μg/dL), Cu/Zn (median = 0.37; range = 0.26–0.73), cobalamin (median = 638.5; range = 306.0–1016 pg/mL). Additionally, non-surviving dogs (n = 10) exhibited markedly higher serum Cu concentrations (median = 193.5; range = 125.0–229.0 μg/dL) and Cu/Zn ratios (median = 5.45; range = 1.95–9.23), and significantly lower serum Zn (median = 37.75; range = 24.8–71.6 μg/dL), Se (median = 52.45; range = 21.27–91 μg/L), and cobalamin levels (median = 52.2; range = 20.0–147.0 pg/mL) compared to both survivors and controls. Conclusions and Clinical Importance Statistical variations in serum concentrations of Cu, Zn, and cobalamin, alongside Cu/Zn ratios, were observed among survivors, non-survivors, and controls (control-survivor and survivor-non-survivor: p < 0.05 and control-non-survivor: p < 0.01), which might suggest their potential prognostic value in CPV.

Young pigs are often coinfected with porcine circovirus 2 (PCV2) and porcine epidemic diarrhea virus (PEDV). This study aimed to determine the impact of coinfection of pigs with PCV2 and PEDV. Forty 16-day-old crossbred mixed-sex piglets were assigned to four groups (  = 10/group, NEG-CONTROL, PCV2-CONTROL, PCV2+PEDV, and PEDV-CONTROL). At day postinoculation (dpi) 0, NEG-CONTROL pigs were inoculated with saline, PCV2-CONTROL pigs were inoculated with PCV2, PCV2+PEDV pigs were inoculated with PCV2 and PEDV, and PEDV-CONTROL pigs were inoculated with PEDV. No clinical signs were observed in the NEG-CONTROL and PCV2-CONTROL group pigs throughout termination of the study at dpi 21. Other than mild to moderate diarrhea, which lasted for about 7 days, no other clinical signs associated with PEDV or PCV2 infection were observed in the PEDV-CONTROL and PEDV+PCV2 groups. Coinfection of PEDV and PCV2 had no effect on virus shedding, serum antibody profile, and macroscopic or microscopic lesions.

Background and aims Runting-stunting syndrome (RSS) in chickens, also known as malabsorption syndrome, which is characterized by mild to severe enteritis and diagnosed through typical histopathologic examination as well as clinical signs, results in considerable economic losses. Despite the many studies carried out over decades to determine the etiologic agents of RSS involved in the disease, several outbreaks remained without the elucidation of, potentially multiple, etiologies involved. Methods We performed comparative analysis of viral metagenomes from four chicken flocks affected with RSS using next-generation sequencing. Primers for the detection of chicken enteric viruses were designed from the sequencing data obtained with metagenomics. Multiplex reverse transcription–polymerase chain reaction (PCR) and PCR were performed to detect a variety of etiological agents previously described in natural cases of RSS. Results The most abundant viral families identified in this study were Astroviridae , Picornaviridae , Parvoviridae , Caliciviridae , Reoviridae and Picobirnaviridae . Chicken astrovirus sequences were present in all four samples, suggesting an association between chicken astrovirus and RSS and chicken astrovirus as a candidate pathogen responsible for RSS. Picobirnavirus and the newly identified chapparvovirus were found in chickens in the Republic of Korea for the first time, and the genetic diversity of enteric viruses and viral communities was showed. Conclusions Chicken astrovirus was consistently detected in broilers affected with RSS and the result of this study may contribute to knowledge of enteric diseases and viruses in chickens.

Since 2017, goose astrovirus (GoAstV) has been widely prevalent in various provinces of China, causing economic losses in the goose industry, with outbreak mortality rates ranging from 10 to 60%. Notably, a goose farm in Sichuan Province has faced an outbreak of infectious disease in 1–3 weeks old goslings, with a mortality rate of approximately 30%. Viral metagenomic analysis of fecal samples identified Goose astrovirus genotype 1 (GoAstV-1), and PCR analysis confirmed the presence of GoAstV-1. Furthermore, we successfully isolated a GoAstV-C1 strain using goose embryos named AAstV/Goose/CHN/2023/C1 (GenBank No. PP108251), and its viral titer was calculated as 10^4.834 ELD 50 /0.5 mL using the Reed-Muench method. The genome size of GoAstV-C1 was about 7,261 nucleotides through amplifying with Sanger sequencing and assembling with SeqMan software. Phylogenetic analysis revealed that GoAstV-1 strains are classified into three major subtypes: A, B, and C, with the GoAstV-C1 strain identified as a unique variant within subtype B, characterized by distinct genetic divergence features. Experimental inoculation of one-day-old goslings with the virus resulted in a mortality rate of 5 out of 15 ( p- value = 0.0421) and a significant reduction in weight gain compared to controls ( p- value = 0.005). Pathological examination revealed that GoAstV-C1 infection caused severe damage to the liver, spleen, and kidneys. Interestingly, unlike most GoAstV, which leads to characteristic gout symptoms, our isolates GoAstV-C1 caused obvious intestinal damage characterized by necrosis, inflammatory infiltration, and crypt architectural disruption. We indicated that GoAstV-C1 displays a unique intestinal tropism rather than characteristic gout symptoms and elucidated genomic features and evolutionary relationships of GoAstV strains. These findings help advance our knowledge of the epidemiology and pathogenicity of GoAstV-1, and the predicted structure of capsid protein could serve as a potential target for designing novel antiviral drugs or vaccines against GoAstV-1.

Chronic active Epstein–Barr virus infective enteritis (CAEBV enteritis) is rare and has not been well described yet. Therefore, we reported the clinicopathologic features of 11 patients with chronic active Epstein–Barr virus infective enteritis and their differences from inflammatory bowel disease. The major clinical presentations of chronic active Epstein–Barr virus infective enteritis were intermittent fever over 39 °C (100%), diarrhea (73%), abdominal pain (64%), lymphadenopathy (64%), splenomegaly (64%), and hepatomegaly (27%). The main endoscopic findings included numerous shallow, small, and irregular ulcers, mainly involving colon and small intestine together, no cobble-like appearance, and longitudinal ulcers. Compared to inflammatory bowel disease patients, the frequency of intermittent fever, hepatomegaly, splenomegaly, lymphadenopathy, the value of C-reactive protein, and serum Epstein–Barr virus DNA (EBV DNA) were significantly higher in chronic active Epstein–Barr virus infective enteritis patients ( p  < 0.01). The histologic findings show transmural inflammation with extended lymphoid infiltration, fissuring ulcers, and intraepithelial lymphocytosis. But chronic active Epstein–Barr virus infective enteritis lacked granulomas and connective tissue changes such as neural hypertrophy and thickened muscularis mucosae. Three chronic active Epstein–Barr virus infective enteritis patients died within 5 years of disease onset, and those three patients have received total colectomy, two of them died within 1 month after surgery. In this study, clinicopathologic features have been summarized to better recognize chronic active Epstein–Barr virus infective enteritis. There are resemblances between chronic active Epstein–Barr virus infective enteritis and inflammatory bowel disease, but some symptoms, signs, and indexes like intermittent fever, hepatomegaly, splenomegaly, lymphadenopathy, and elevated C-reactive protein, Epstein–Barr virus DNA are characteristics to differentiate chronic active Epstein–Barr virus infective enteritis and inflammation. Histopathological features also help the discrimination. Serum Epstein–Barr virus DNA and intestinal tissue in situ hybridization for Epstein–Barr virus-encoded RNA are recommended to exclude chronic active Epstein–Barr virus infective enteritis.