Avian reovirus (ARV) infections of broiler and turkey flocks have caused significant clinical disease and economic losses in Pennsylvania (PA) since 2011. Most of the ARV-infected birds suffered from severe arthritis, tenosynovitis, pericarditis and depressed growth or runting-stunting syndrome (RSS). A high morbidity (up to 20% to 40%) was observed in ARV-affected flocks, and the flock mortality was occasionally as high as 10%. ARV infections in turkeys were diagnosed for the first time in PA in 2011. From 2011 to 2014, a total of 301 ARV isolations were made from affected PA poultry. The molecular characterization of the Sigma C gene of 114 field isolates, representing most ARV outbreaks, revealed that only 21.93% of the 114 sequenced ARV isolates were in the same genotyping cluster (cluster 1) as the ARV vaccine strains (S1133, 1733, and 2048), whereas 78.07% of the sequenced isolates were in genotyping clusters 2, 3, 4, 5, and 6 (which were distinct from the vaccine strains) and represented newly emerging ARV variants. In particular, genotyping cluster 6 was a new ARV genotype that was identified for the first time in 10 novel PA ARV variants of field isolates.
The survival or clearance of the avian influenza virus (AIV) of subtype H7N2 in its chicken host was evaluated using experimentally infected specific pathogen free (SPF) chickens of different age groups. Birds of different ages were successfully infected with infectious doses ranging between 10(4.7) and 10(5.7) ELD50 per bird. In infected birds, the infective virus was undetectable usually by the third week following exposure. The infectivity or inactivation time of the H7N2 AIV in various environmental conditions was studied using chicken manure, heat, ethanol, pH, and disinfectants. The H7N2 AIV was effectively inactivated by field chicken manure in less than a week at an ambient temperature of 15-20 degrees C. At a pH 2, heating at 56 degrees C, and exposure to 70% ethanol or a specific disinfectant, the AIV infectivity was destroyed in less than 30 min.
Nephropathogenic infectious bronchitis (NIB) was diagnosed in 28 infectious bronchitis virus (IBV)-vaccinated commercial chicken flocks in Pennsylvania from December 1997 to July 2000. Early dinical signs were increased flock mortality and urinary water loss (polyuria and pollakiuria) leading to wet litter. Daily mortality ranged from 0.01% in layers to 2.45% in broilers, with total broiler mortality as high as 23%. Severe renal swelling and accumulation of urates in the tubules were commonly seen. Visceral gout and urolithiasis were less frequently observed. Histopathologic changes included characteristic tubular epithelial degeneration and sloughing with lymphoplasmacytic interstitial nephritis. Minimal respiratory disease signs were noted in broilers. Egg production and shell quality declined in layers. Confirmatory diagnosis of NIB was made by IBV antigen-specific immunohistochemical staining of the renal tubular epithelium and virus isolation. Sequencing of the S1 subunit gene of 21 IBV isolates showed the NIB outbreak to be associated with two unique genotypes, PA/Wolgemuth/98 and PA/171/99. The cases from which the genotypes were isolated were clinically indistinguishable. The NIB viruses were unrelated to previously recognized endemic strains in Pennsylvania and were also dissimilar to each other. Genotype PA/Wolgemuth/98 was isolated almost exclusively during the first 14 mo of the outbreak, whereas PA/171/99 was recovered during the final 18 mo. The reason for the apparent replacement of PA/Wolgemuth/98 by PA/171/99 is not known.
Marek's disease (MD) is a lymphomatous and neuropathic disease of domestic fowl caused by an alphaherpesvirus, designated Marek's disease virus (MDV), belonging to the genus
Between 1997 and 1999 several cases of a new disease in Muscovy ducks were reported in Pennsylvania, USA. The cases were characterized by locomotor dysfunction, weakness, recumbency, 40 to 60% morbidity and 10 to 40% mortality. The most characteristic microscopic lesions were moderate to severe degenerative rhabodomyopathy. In order to characterize the aetiological agent, virus isolation was attempted from the spleen, liver, heart, skeletal muscle and intestine by inoculation of 14-day-old Muscovy duck embryos with tissue homogenates. Deaths occurred on the second egg passage and parvoviruses were isolated by serial passage of allantoic fluid from dead embryos and then in Muscovy duck embryo fibroblast (MDEF) cultures. Parvovirus particles were observed in allantoic fluids and supernatants of MDEF cultures by transmission electron microscopy. Two genomic fragments, comprising 1108 nucleotides of the right open reading frame that codes for the structural viral proteins 1, 2 and 3, were amplified by polymerase chain reaction from one of the isolates, Muscovy duck parvovirus (MDPV)/PSU-31010. Comparison of this fragment with available sequences of other MDPV and related goose parvovirus (GPV) isolates showed that it had only 84.5% sequence identity with other MDPV isolates and 84.6% identity with the GPV isolates. This region shares over 99% identity among previously sequenced MDPV isolates and 95% identity among the related GPV isolates. This suggests that MDPV/PSU-31010 is divergent from all other sequenced MDPV and GPV isolates, and may represent a new group of avian parvoviruses.
The evolutionary history of avian paramyxovirus serotype 1 (PMV1), which includes the agents of Newcastle disease (ND), is characterized by a series of strain emergence events since viruses in this family were first recognized in the 1920s. Despite the importance of ND to the poultry industry, little is known about PMV1 strain emergence events and the subsequent dispersal and evolution of new strains. The genotype VI-PMV1 was first identified in the 1980s and has been named pigeon paramyxovirus-1 (PPMV1) because of unusual host specificity with Columbiformes (Collins et al., 1996); it has been responsible for panzootics in both chickens and pigeons during that time. Here, we used evolutionary analyses to characterize the emergence of this contemporary PMV1 lineage. We demonstrate that GVI-PMV1 arose through cross-species transmission events from Galliformes (i.e. chicken) to Columbiformes, and quickly established in pigeon populations. Our studies revealed a close association between the time of viral emergence and panzootic events of this virus. The virus appeared first in Southeastern Europe and quickly spread across the European continent, which became the epicenter for global virus dissemination. With new viral gene sequences, we show that GVI-PMV1 viruses currently circulating in North America resulted from multiple invasion events from Europe, one associated with an exotic European Columbiformes species, and that extant lineages have diversified locally. This study extends our understanding of successful viral emergence subsequent to cross-species transmission and dispersal patterns of newly emerged avian viruses, which may improve surveillance awareness and disease control of this and other important avian pathogens.
The objective of this field trial was to evaluate the effect of a vaccine protocol using a commercially available trivalent vaccine designed for intranasal use. Experimental challenge studies have demonstrated varying efficacies of vaccines administered via the intranasal route. A total of 468 calves from 3 herds were enrolled and randomized into 3 treatment groups (positive control, PC, n = 211; intranasal vaccine, IN, n = 215; negative control, NC, n = 42) and followed for 8 to 12 wk. The PC consisted of one dose of commercially available multivalent injectable vaccine against bovine respiratory syncytial virus, infectious bovine rhinotracheitis, parainfluenza 3, and bovine viral diarrhea administered subcutaneously at 6 wk of age. The IN was administered at enrollment and 6 wk of age, and contained antigen against bovine respiratory syncytial virus, infectious bovine rhinotracheitis, and parainfluenza 3. The NC was sterile saline administered intranasally and subcutaneously at enrollment and 6 wk of age. Clinical illness was assessed using systematic respiratory scoring, and thoracic ultrasonography was used to identify the lung consolidation associated with pneumonia. Rib fractures were identified in 6% of calves, and an association was observed between rib fractures and calving ease. Overall, 54% of the calves had at least one episode of an abnormal respiratory score (ILL). Vaccination protocol did not affect the occurrence of ILL. Similarly, 54% of the calves had at least one episode of lung consolidation ≥3 cm (CON). Vaccine protocol affected the odds of CON. The odds of CON in PC were 1.63 (95% confidence interval: 1.04-2.56) times the odds of CON in IN, and 0.38 (95% confidence interval: 0.16-0.93) times the odds of CON in NC. The odds of CON in IN were 0.23 (95% confidence interval: 0.09-0.59) times the odds of CON in NC. The outcomes ILL and CON were associated; however, the measure of agreement was only fair (kappa = 0.38). Multivariable linear regression revealed an interaction between vaccine protocol and herd on average daily gain (ADG); therefore, these data were stratified. In herd 1, IN (0.53 ± 0.03 kg/d) decreased ADG compared with PC (0.63 ± 0.03 kg/d). In herd 2, IN increased ADG (0.41 ± 0.03 kg/d) compared with PC (0.38 ± 0.03 kg/d). In contrast, none of the protocols affected ADG at herd 3. In conclusion, this commercially available trivalent IN vaccine protocol did not alter the incidence of ILL, reduced the risk of lung lesions associated with pneumonia, and improved the ADG of the calves in one of the commercial study herds.
Marek’s disease, a disease primarily affecting immature chickens, is a worldwide problem that has on at least three occasions threatened the poultry industry in the United States. A rich dataset to study the epidemiology of this disease is available because the United States Department of Agriculture has required mandatory inspections of all commercially sold poultry of significant scale since the mid-20th century with over 99% of all chickens inspected. This dataset includes monthly totals aggregated by state since 1961 of the number of “young chickens” inspected and the number with “leukosis”, a condemnation category that is almost always associated with Marek’s disease in this category of birds. The objective of this study was to analyze temporal and spatial patterns in this condemnation data to gain insight into the ecology and epidemiology of the causative virus. We extracted visual patterns in the data using seasonal trend decomposition, and we tested for statistical significance using extended linear modeling techniques. The analysis confirmed previous findings that there are differences in leukosis condemnation rates between states, across years, and within years. The analysis also revealed several patterns not previously highlighted, including spatial and temporal autocorrelations in leukosis condemnation, changes to the amplitude of seasonality over time, and increasing within-year variation in condemnation rate over time. These patterns suggest that locally shared farm practices, virus transmission between farms, or viral persistence may be important to understanding the dynamics of the disease. We also discuss the plausibility of other potential explanations for these patterns.
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