@article{gimeno_shaw_turner_bremen_cortes_faiz_gonder_robbins_2021, title={Replication of Marek's disease vaccines in turkey embryos and their effect on TLR-3 and IFN-gamma transcripts}, volume={50}, ISSN={["1465-3338"]}, DOI={10.1080/03079457.2021.1882937}, abstractNote={ABSTRACT Understanding the pathogenesis of herpesvirus of turkeys (HVT) in its natural host is necessary before recombinant HVT (rHVT) can be used efficiently in turkey flocks. The objectives of this study were to evaluate when commercial turkey flocks get infected with wild type HVT, to study replication of HVT (conventional and recombinant rHVT-Newcastle disease, rHVT-ND) and other Marek’s disease (MD) vaccines (SB-1 and CVI988) in turkey embryonic tissues, and to evaluate the expression of TLR-3 and IFN-γ in the lung and spleen of one-day-old turkeys after in ovo vaccination with MD vaccines. Our results demonstrated that commercial turkeys got exposed to wild type HVT within the first days of life; therefore, there is a potential of interaction between wild type HVT and rHVT when administered at day of age. On the other hand, all evaluated vaccines (especially HVT and rHVT-ND) replicated very well in turkey embryonic tissues. In ovo vaccination with HVT and CVI988 increased transcription of TLR-3 in the spleen of one-day-old turkeys. However, no effect on the transcription of TLR-3 or IFN-γ in the lungs and IFN-γ in the spleen in newly hatched turkeys was detected in the present study. Because of the limitations of evaluated genes, timepoints, and studied tissues, future studies are warranted to better understand the effect of MD vaccines on the turkey embryo immune responses. RESEARCH HIGHLIGHTS Commercial turkey flocks get infected with wild type HVT within the first days of life. HVT and rHVT replicates readily in turkey embryonic tissues. SB-1 and CVI988 also replicate in turkey embryonic tissues, but at lower rates than HVT and rHVT. HVT and CVI988 increase transcription of TLR-3 in the spleen.}, number={3}, journal={AVIAN PATHOLOGY}, author={Gimeno, I. M. and Shaw, W. N. and Turner, A. and Bremen, J. and Cortes, A. L. and Faiz, N. M. and Gonder, E. and Robbins, K.}, year={2021}, month={May}, pages={227–233} }
 @article{robbins_suyemoto_lyman_martin_barnes_borst_2012, title={An Outbreak and Source Investigation of Enterococcal Spondylitis in Broilers Caused by Enterococcus cecorum}, volume={56}, ISSN={["0005-2086"]}, DOI={10.1637/10253-052412-case.1}, abstractNote={SUMMARY. Enterococcus cecorum was isolated from spondylitis lesions in broilers from two flocks in North Carolina that were experiencing increased mortality. Affected birds showed paresis and paralysis, clinical signs characteristic of enterococcal spondylitis (ES). Affected birds rested on their hocks and caudal abdomens with legs extended forward and were unable to stand or walk. Necropsy examination of affected birds revealed firm to hard inflammatory masses involving the vertebral bodies at the level of the free thoracic vertebra that bulged dorsally and compressed the spinal cord. When opened, lesions contained pale, tan to yellow caseonecrotic material. Microscopically, necrosis and fibrinoheterophilic spondylitis with intralesional gram-positive bacteria were seen. Heavy growth of E. cecorum recovered from vertebral lesions confirmed the diagnosis of ES. To investigate possible sources of the organism for one of the flocks bacterial cultures were made from the environment, water lines, mice trapped on the farm, cecal/cloacal swabs from one of the parent broiler breeder flocks, egg residue, hatching eggs, and the hatchery environment. Except for cecal/cloacal swabs from the breeders, E. cecorum was not isolated from any of these samples. When compared phenotypically and genotypically, cecal/cloacal isolates of E. cecorum from the breeders differed from isolates from spondylitis lesions in the broilers. The source of E. cecorum for the broiler flocks was not determined, but vertical transmission appears unlikely.}, number={4}, journal={AVIAN DISEASES}, author={Robbins, Kabel M. and Suyemoto, M. Mitsu and Lyman, Roberta L. and Martin, Michael P. and Barnes, H. John and Borst, Luke B.}, year={2012}, month={Dec}, pages={768–773} }
 @article{borst_suyemoto_robbins_lyman_martin_barnes_2012, title={Molecular epidemiology of Enterococcus cecorum isolates recovered from enterococcal spondylitis outbreaks in the southeastern United States}, volume={41}, ISSN={["1465-3338"]}, DOI={10.1080/03079457.2012.718070}, abstractNote={Enterococcus cecorum, a normal intestinal inhabitant, is increasingly responsible for outbreaks of arthritis and osteomyelitis in chickens worldwide. Enterococcal spondylitis (ES) is a specific manifestation of E. cecorum-associated disease in which increased flock morbidity and mortality result from chronic infection involving the free thoracic vertebra. In this study the genetic relatedness and antimicrobial resistance of isolates recovered from ES-affected flocks in the southeastern United States were determined. ES outbreaks from 2007 to 2011 were investigated in North Carolina (15 flocks, 13 farms, four integrators), South Carolina (one flock, one farm, one integrator) and Alabama (six flocks, six farms, one integrator). From these 22 epidemiologically distinct outbreaks, 326 isolates of E. cecorum were recovered. Isolates from spinal lesions and caeca of affected birds (cases) and caeca of unaffected birds (controls) were genotyped using pulsed-field gel electrophoresis; phenotyped using both GenIII MicroPlate™ (Biolog; Hayward, CA, USA) microbial identification plates and antimicrobial sensitivity testing; and compared with each other. Isolates from spinal lesions were incapable of mannitol metabolism and the majority of these isolates were genetically clonal. In contrast, caecal isolates from control birds varied in their ability to metabolize mannitol and were genetically diverse. Isolates from both case and control birds had high levels of antimicrobial resistance. These findings indicate that the increase in E. cecorum-associated disease in the southeast United States is due to the emergence of new clones with increased pathogenicity and multidrug resistance.}, number={5}, journal={AVIAN PATHOLOGY}, author={Borst, Luke B. and Suyemoto, M. Mitsu and Robbins, Kabel M. and Lyman, Roberta L. and Martin, Michael P. and Barnes, H. John}, year={2012}, pages={479–485} }
 @article{robbins_ye_fletcher_2011, title={Identification of Ascaridia numidae in Guinea Fowl (Numida meleagris) and Association with Elevated Mortality}, volume={55}, ISSN={["1938-4351"]}, DOI={10.1637/9587-102110-case.1}, abstractNote={SUMMARY. An outbreak of ascaridiasis occurred in 10-wk-old guinea fowl (Numida meleagris) on a commercial farm. Birds had exhibited elevated mortality (11.66%) in the previous week, as well as increased water consumption, weakness, anorexia, and stunted growth. Numerous nematodes, occasionally occluding the intestinal lumen, were present in the jejunum and ileum and were identified as Ascaridia numidae based on microscopic morphology. Ribosomal DNA 18S and 28S D3 sequences of the nematode were deposited into GenBank and found to be most similar to Ascaridia galli and Toxocara vitulorum, respectively; sequences for A. numidae had not been previously reported. Treatment with piperazine sulfate significantly reduced the number of adult worms in the intestines, greatly decreased eggs per gram of feces, relieved clinical signs in the flock, and returned the flock mortality back to expected levels. All findings implicate A. numidae as the cause of elevated mortality in this flock.}, number={1}, journal={AVIAN DISEASES}, author={Robbins, Kabel M. and Ye, Weimin and Fletcher, Oscar J.}, year={2011}, month={Mar}, pages={151–154} }