Handbergpierce4767

LT1 or PepT1 mRNA in enterocytes. These results demonstrate that RSS, which can be induced by different etiologies, can show differences in the expression of the stem cell marker Olfm4.Infectious bronchitis is a respiratory disease of chickens caused by a gammacoronavirus named infectious bronchitis virus (IBV). In addition to affecting the respiratory tract, IBV may also induce urogenital infections, leading to nephropathogenic disease, false layer syndrome in laying hens, and epididymal lithiasis and epididymitis in males. Here, we report a case of decreased reproductive efficiency due to male infertility in 33- to 38-wk-old broiler breeders. At necropsy, the males presented with urates deposited on the skin around the vent and testicular asymmetry due to marked unilateral atrophy. Histopathology revealed lymphocytic epididymitis, epididymal lithiasis, and orchitis. IBV antigen was detected within collecting and efferent ducts of epididymides by immunohistochemistry. IBV strain DMV/1639 was detected by reverse transcription-quantitative PCR in pools of testes, oviducts, tracheas, cecal tonsils, and kidneys from a 37-wk-old affected flock. This report shows evidence of the role of IBV in male chicken infertility and highlights the importance of performing molecular surveillance of IBV to monitor vaccine strains and to detect emerging variants that can potentially hinder production.Currently, there is no available vaccine against hemorrhagic enteritis virus (HEV) in Australia. Although it is assumed that subclinical HEV infections occur and may be associated with an increase in colibacillosis in Australian commercial turkey flocks, the prevalence of infection with this virus in the country is largely unknown. The aims of this study were to determine the extent of HEV infection in commercial flocks in Australia and to investigate the diversity of Australian HEV strains. Serum and spleen samples were collected from breeder and grower turkeys and serum was collected from breeder and grower chickens by the two major poultry integrator companies in Australia. Of the turkey samples, 727/849 (86%) sera were positive for anti-HEV antibodies by ELISA. HEV DNA was detected in 215/278 (77%) spleen samples positive by PCR. Of the meat chicken sera, 115/144 (80%) samples were seropositive. Sequencing the whole genome of three HEV field isolates showed that the Australian strains are highly similar and cluster separately from strains from other geographic regions although several point mutations were shared with HEV strains considered to be virulent. In conclusion, HEV infection is ubiquitous in Australian commercial poultry flocks. The impact of the many genomic point mutations detected in Australian HEV strains on virus pathogenicity is unclear.In 2018, a national recall of shell eggs in the United States occurred due to human illness caused by Salmonella Braenderup. Although previous studies have identified Salmonella Braenderup in laying hens and the production environment, little is known about the ability of this Salmonella serovar to infect laying hens and contaminate eggs. The objective of this study was to examine the invasiveness of Salmonella Braenderup in laying hens as well as its ability to persist in the production environment. Specific-pathogen-free laying hens (four trials; 72 hens/trial) were orally challenged with 107 colony-forming units of Salmonella Braenderup. On day 6 postinoculation, half of the challenged hens were euthanatized, and samples of ileocecal junction (sections above and below it, and portions of both ceca), liver, spleen, ovary, and oviduct tissues were collected and cultured for Salmonella Braenderup. Egg and environmental (nest box swaps and substrate (litter)) samples were collected days 7-20 postinoculation (Trials 1 and 2; excluding weekends) and days 7-27 postinoculation (Trials 3 and 4; excluding weekends) to detect Salmonella Braenderup. Recovery of Salmonella Braenderup was highest in ileocecal tissue samples (11.1%-33.3%; P less then 0.05), with little to no recovery in other collected tissue samples. Salmonella Braenderup was detected in a small number of shell emulsions (0%-2.9%; P less then 0.01) and recovered in Trial 1 at a high rate (92.5%; P less then 0.0001) in the substrate composite samples; however, recovery of Salmonella Braenderup was low in the other egg and environmental samples. These trials indicate that Salmonella Braenderup is not an invasive Salmonella serovar for cage-free laying hens, especially when compared to serovars of concern to the egg industry. Sodium oxamate clinical trial However, it may persist in the environment at low levels.Marek's disease (MD) vaccine does not provide sterilizing immunity that prevents subsequent MD virus (MDV) replication and shedding in vaccinated birds. It is hypothesized that cell-mediated immunity is critical to control the virus replication in chickens because MDV exists in cell-associated forms in the host. To improve the MD vaccine efficacy, particularly cell-mediated immunity, we constructed recombinant v301B/1-IL-15, an MDV serotype 2 vaccine strain 301B/1 expressing chicken interleukin-15 (IL-15), a cytokine which promotes T-cell proliferation and enhances T-cell responses. We examined the vaccine efficacy of v301B/1-IL-15 given as a bivalent MD vaccine in combination with turkey herpesvirus (HVT) against a very virulent MDV challenge. The expression of IL-15 did not interfere with virus stability and the growth of recombinant v301B/1-IL-15. However, the protective efficacy of v301B/1-IL-15 was not significantly different from that of v301B/1, the parental virus used to construct v301B/1-IL-15. Shedding of challenge virus was slightly reduced at Day 21 (16 days postchallenge) in the v301B/1-IL-15 plus HVT vaccinated group, with no statistically significant difference to that of the v301B/1 plus HVT vaccinated group, and thymus atrophy was observed to be less severe in the v301B/1-IL-15 plus HVT vaccinated group. Overall, the protection of v301B/1-IL-15 was not differentiable from v301B/1 against very virulent MDV challenge, but there is no interference with bivalent MD vaccine efficacy.Growing demand for poultry meat and eggs labeled as organic, cage free, or pasture raised has increased the number of producers that manage chickens outdoors. In these open environments, there are likely diverse enteric parasites sustained by fecal-oral transmission or passage through intermediate invertebrate hosts (e.g., worms and insects) that chickens consume. Enteric parasites can reduce chicken health and productivity, but there are few published data describing the identities or prevalence of these parasites on farms that use open environments in the United States. We surveyed 27 poultry farms with open environments that were situated across a wide geographic range, including California, Oregon, Idaho, and Washington. These farms did not use anticoccidial drugs, coccidia vaccines, or parasiticides. Flock size, enclosure area, flock density, flock rotation frequency, and average flock age were highly correlated for all the farms in this study. We analyzed how enclosure size and flock rotations per year creased by 0.03%. Furthermore, for every additional rotation per year, the odds of detecting A. galli decreased by 1.3%. For every additional rotation per year, the odds of detecting tapeworm species increased by 2.2%. We found no evidence that flock spatial management affected prevalence of the other parasites observed on the farms. Farming practices and parasite responses in these systems are highly varied, which makes it difficult to identify potential management interventions for reducing these infections.The intestinal disease coccidiosis, caused by parasitic Eimeria species, severely impacts poultry production, leading to an estimated $14 billion in annual losses worldwide. As the poultry industry moves away from antibiotics as a treatment for diseases, a better understanding of the microbiota is required to develop other solutions such as probiotics, prebiotics, and nutritional supplements. This study aimed to investigate the effects of Eimeria tenella infection on luminal (cecal contents [CeC]) and mucosal (cecal epithelial scrapings [CeS]) microbial populations in 288 Ross 708 broiler chickens at multiple time points postinfection (PI). By use of 16S rRNA amplicon sequencing, it was revealed that microbial diversity differed in infected (IF) chickens in comparison to the control (C) in both CeC and CeS microbiota at the peak of infection (7 days PI), when simultaneously IF birds saw reduced body weight gain and a higher feed conversion ratio. Infection resulted in a significant differential abundance of some bacterial taxa, including increases in potential secondary pathogens Escherichia coli, Enterococcus, Clostridium, and Proteus and a decrease in the short chain fatty acid-producing family Lachnospiraceae. Predicted metagenomic pathways associated with E. coli, such as those responsible for amino acid biosynthesis, were differentially expressed in IF birds. In conclusion, our results show that E. tenella infection disturbs luminal and mucosal microbiota balance in chickens. Moreover, the luminal microbiota seems to be more susceptible to prolonged imbalance due to IF, whereas the mucosal microbiota appeared to be affected only in the short term, demonstrating the importance of researching both the luminal and mucosal microbiota of the cecum.The objectives of this study were to evaluate whether a preinfection of Eimeria adenoeides (EAD) or Eimeria tenella (ET) could affect the severity of subsequent histomoniasis in turkeys (Experiment 1) and if previous exposure to EAD infection, when a single or multiple inoculations of EAD were administered with sufficient time for complete cecal recovery, would affect the severity of HM incidence and lesions (Experiment 2). In Experiment 1, 200 poults were assigned to 1 of 5 groups, as follows unchallenged negative control, positive challenge control inoculated with 105 HM, EAD at 500 oocysts/bird and Histomonas meleagridis (HM), EAD at 2500 oocysts/bird and HM, or ET at 9 × 106 oocysts/bird and HM. ET and EAD were inoculated on day 15 and HM on day 20. In Experiment 2, the trial consisted of two different challenge ages to evaluate short- or long-term EAD effects before HM challenge. Poults (n = 260) were assigned to either early-HM-challenged groups (HM on day 19 challenge control or EAD at 2500 oocysts/bird on day 14 with HM on day 19) or late-HM-challenged groups (HM on day 35 challenge control, EAD at 2500 oocysts/bird on day 14 and HM on day 35, or EAD at 100 oocysts/bird every 2-3 days during the first 3 weeks and HM on day 35). An unchallenged negative-control group was used for both the early- and late-challenge phases in Experiment 2. Mortalities were recorded, and surviving poults were scored for histomoniasis-related hepatic and cecal lesions. In Experiment 1, preinfection with both doses of EAD reduced the mortality as well as the cecal and hepatic lesions caused by histomoniasis. In Experiment 2, neither short- nor long-term preinfection with EAD had an effect on histomoniasis-related mortality or lesions. Differences between Experiments 1 and 2 may be due to the level of infection caused by the prechallenge with EAD and the resulting destruction of cecal tissue.